Colds and Allergies (Chapter 10) + Bermon Paper on URTI + Bonus Lecture Flashcards
What are the two main types of viruses?
rhinoviruses and coronaviruses
What are two diseases that colds are confused with often ?
Allergic rhinitis, or bacterial URTI
If someone has symptoms of a cold with a sore throat, what is it probably ?
Streptococcal infection (bacterial)
How are streptococcal infections spread ?
by airborne nasal discharge (sneezing), contact with hand
what are the complications of common cold ?
bacteria may appear in nose or ear because cavities are blocked
how many days does it take to get better from a cold ?
7-10
how long can viruses stay on inanimate objects for ? what happens to them ?
a few hours
oxygen can damage virus coating
how do viruses survive better ? what does this imply about the way they are usually transmitted ?
they usually survive better in liquids, therefore they need to contact the mucous membranes in order to more easily enter the body.
what is the difference between the way influenza and the common cold is transmitted ?
influenza is usually airborne
what drugs cure the common cold ?
none, they only alleviate the symptoms
what molecule is behind mucus production ? how ?
acetylcholine
released from cholinergic nerve, which increases mucus production
what effect does the common cold have on asthma ?
it may exacerbate asthma symptoms
is it ok to change asthma treatment if one is affected by a cold ?
yes, treatment may need to be increased to combat the increased symptoms
why do people have runny noses ?
mucus secretion trying to get rid of the virus
what is the symptom that may persist even after the end of the cold ?
cough
what is allergic rhinitis
a hypersensitivity reaction to an allergen which combines with an antibody, mainly IgE
explain the mechanism behind allergic rhinitis
antigen/allergen binds with antibody IgE
IgE then combines with mast cells at IgE receptors on the surface of the mast cell and basophils in mucosa of nasal passage. The granules which contain histamine and proteases are released into the outside.
when antigen present, cells degranulate, releasing histamine, prostaglandins, leukotrienes, platelet activating factor, bradykinin (inflammation)
what are the 5 things mast cells release in allergic rhinitis ?
histamine, prostaglandins, leukotrienes, platelet activating factor, bradykinin
why does inflammation occur in allergic rhinitis? what mechanism is behind it ?
tissues express H1 histamine receptor and receptors for leukotrienes, etc.
What do the proteases do in allergic rhinitis ?
The proteases directly kill tissues which release pain and inflammation mediators such as substance P, bradykinin, and arachidonic acid metabolites.
What are the immediate early phase symptoms of allergic rhinitis ?
rhinorrea (runny nose), vasodilation, sneezing, itching of nose and eyes
What are the late phase reactions of allergic rhinitis? What are they due to ?
Sneezing, congestion, enhanced responsiveness of other antibodies
Due to accumulation of the inflammatory cells (mast cells and basophils)
How do genes affect allergic rhinitis ?
If both parents have allergy, child has 50% change of getting allergies
If no parents have allergy, child has 10% chance
What is the counter-regulation theory?
That in developed countries, there are less parasites and infections, so the immune system is more sensitive than in under-developed countries in which the immune system becomes “harder to activate”
What are the three types of allergies ?
Seasonal, perennial, acute
Give examples of seasonal allergies (2)
Pollen: weeds, trees, grasses
Mold spores from decaying vegetation
How many people in the US do seasonal allergies affect ?
35 million
Give 3 examples of perennial allergies
mainly indoor
dust mites, pet dander, cockroaches
what is more common: seasonal or perennial allergies ?
seasonal
what are acute allergies ?
major reaction to allergens, may be deadly
What are heat cramps, heat exhaustion, heat stroke caused by ?
excessive loss of fluid and electrolytes
what is a medical emergency- heat cramps, exhaustion, or stroke?
heat stroke, may lead to coma
what is recommended to drink for an athlete ?
water
they won’t lose much electrolytes (dont need Gatorade) unless they are running a marathon
which drugs increases fluid loss or interferes with cooling mechanism, and therefore puts someone more at risk of heat related illnesses such as heat stroke ? (4)
beta blockers
alpha-agonists
anti-histamines
diuretics
how do beta-blockers increase fluid loss or interferes with cooling mechanism
prevent sweating, decrease blood supply to skin
how do alpha-agonists increase fluid loss or interferes with cooling mechanism
what are they used for
constrict blood flow
act as nasal decongestant
how do anti-histamines increase fluid loss or interferes with cooling mechanism
by decreasing sweating
anti-cholinergic
how do diuretics increase fluid loss or interferes with cooling mechanism
increase urine production (dehydration)
what are ways to prevent a cold ?
avoid crowded places
is it ok to stifle a sneeze ?
no
why is it bad to cough into one’s hand ?
because then the hand will touch stuff and the germs will spread
what should one consume if they have a cold
fluids like water or chicken soup
what sort of environment one should be in when they have a cold
moist, so that the humidity will help the mucus and throat deal with colds faster
what are two types of drugs that are used only for colds, not for allergies:
antitussive and expectorants
what is an expectorant ?
enhances the expulsion of mucus by air passages of the lungs
what are two types of drugs used for both colds and allergies ?
antihistamines, decongestants
what are three types of drugs used to treat only allergies, not colds:
corticosteroids, LT modifiers, mast cell stabilizers
what is the target tissue for allergic rhinitis ? what is the implication of this for the drugs used for administration of corticosteroids and mast cell stabilizers
nasal passage rather than bronchial tissue
this means that for allergies, nasal sprays are used rather than inhalers
what generation of antihistamines are desloratadine and loratadine ?
second
what do first generation antihistamines end with ?
-amine
what do second generation antihistamines end with?
-adine
what is histamine ?
a mediator released by mast cells and basophils
what are the receptors usually targeted by antihistamines for allergies ? what are their properties ? what kind of illnesses do drugs target ?
H1 receptor : respiratory tract and near peripheral blood vessels. drugs used as antihistamines
H2 receptor: on stomach cells. drugs used to treat ulcers
what is the H3 receptor ?
histamine receptor in brain, but no drug is known to work on it and we don’t know its purpose
what is the difference between antihistamine early and late second generation drugs
early: off the market
late: commonly used
what are the two main first generation antihistamine drugs ?
diphendramine and chlorphenamine
what are the main two side effects of the first generation antihistamines ?
sedation
anti-cholinergic symptoms
what are 6 anti-cholinergic symptoms?
dry mouth less sweating tachycardia urinary retention blurred vision constipation
what are first generation antihistamines contraindicate
other depressants
how do first generation antihistamines affect athletic performance ?
negatively
how are second generation antihistamines different from first generation antihistamines in terms of structure?
second generation less lipophilic so less likely to cross blood-brain barrier
give two examples of second generation antihistamine drug
Allegra, Claritin
when should anti-histamines be taken ?
before the allergy attack happens, as a preventative measure
how are second generation antihistamines different from first generation antihistamines in terms of action?
less sedation and less anti-cholinergic effects
why can anti-histamines be used in cold ?
because of anti-cholinergic effect of slowing down mucus production, which has the effect of minimizing sniffling.
why are anti-histamines not ideal to take with a lower respiratory tract infection?
anti-histamines have anti-cholinergic effects, meaning they slow down mucus production. however, mucus production can be helpful in treating LRTI
why are anti-histamines used in motion sickness products ?
because they prevent the feeling of vomiting
how is dermatitis treated ?
with anti-histamines
what are the two main active ingredients that are anti-histamine used in allergy and cold medication ?
chlorpheniramine (first generation)
diphehydramine (second generation)
what are two distinguishing characteristics of poison ivy ?
leaves have a tear drop shape
3 leaves attached to stem
what does poison ivy cause ?
dermatitis
what is nasal congestion caused by ?
local vasodilation of nose blood vessels
what is a fancy word for “stuffy nose”
nasal congestion
what is a fancy word for “runny nose”
rhinorrhea
what kind of drugs are used to treat stuffy noses ? why?
stuffy nose= local vasodilation of nose blood vessels
therefore, we need to cause vasoconstriction with drugs that activate the alpha-adrenergic receptor
sympatho-mimetic drugs
what are the 2 active ingredients usually found in nasal decongestants ?
phenylephrine and pseudoephedrine
what drug is used to make crystal meth, and therefore is kept behind the counter ? how does this affect the sale of other drugs ?
pseudoephedrine
therefore, companies usually sell phenylephrine
what kind of 3 side effects does the nasal decongestant pseudoephedrine have ?
side effects related to adrenergic activation, therefore sleeplessness, tremor, agitation
what is rebound congestion ?
when the cold is over, the nasal vessels dilate again as a result of using the spray, therefore congestion becomes worse
what drug should decongestants not be used with
monoamino oxidase inhibitor
what kind of effect does a decongestant have combined with caffeine ?
caffeine has similar effects on CNS as pseudoephedrine
these effects are additive when both drugs are used together, and therefore can be a hazardous combination
why is phenylephrine preferred by companies instead of pseudoephedrine ?
because can’t be converted into crystal meth
what are corticosteroids used for- allergic rhinitis or the common cold ?
topically for allergic rhinitis
what do corticosteroids do ?
reduce all major symptoms (runny nose, itching, sneezing, nasal congestion)
when is it best to use corticosteroids ?
before the anticipated exposure
what are 3 side effects of corticosteroids ?
nasal irritation
headaches
local fungal infections
what is the action of mast cell stabilizers ?
inhibit mast cell degranulation
do you take mast cell stabilizers as a preventative measure or after the symptoms start ?
preventative
how often do mast cells stabilizers have to be taken ?
frequently
what is more effective, mast cell stabilizers or corticosteroids ?
corticosteroids
what do leukotriene modifiers do ?
inhibit leukotriene receptors, or inhibit the synthesis of leukotrienes
what is a side effect of leukotriene modifiers ?
ear infections
if someone has a wet cough, do they need an expectorant ?
no
what do expectorants do ?
lubricate the mucus
why arent expectorants very useful ?
anti-cholinergics and anti-histamines oppose this effect, making this product not very useful
what has the same effect as an expectorant ?
staying hydrated
what is an active ingredient that is an expectorant ?
guaifenesin
if someone has a dry cough, what are the three types of medication they need ?
expectorant
antitussive
analgesic
what do antitussive agents act on ?
the CNS (cough center)
when is coughing productive or not productive ?
productive when it is needed to clear mucus
not productive when it does not move the mucus
what are opioids used as antitussives ? (2)
codeine, hydrocodone
what is a non-opioid drug used an an antitussive
dextromorphan
what are the main issues of taking opioids as antitussives ? (2)
constipation and abuse potential
what are the 4 different types of analgesics used in medication ?
- pillz: acetaminophen, ibuprofen, maybe aspirin
- counter-irritants in lozenges, like menthol
- benzocaine (topical anesthetic)
- vapors (camphor and menthol)
what drugs treat ocular inflammation ? (5)
corticosteroids antihistamines decongestants mast cell stabilizers NSAIDs
are antibiotics of any use to treat allergies or colds ?
not for allergies
not very effective against colds, usually used to treat complications
what are some anti-viral medications
we don’t really have any
what is a vaccine ?
a prophylactic measure whereby an inactivated or synthetic virus component is immunized into a person
how do you know which vaccine to administer in the fall ?
it’s always a guess
why is allergy to vaccines an issue ?
because vaccines are prepared in chicken eggs
what are the effects of immune boosters such as Cold FX
nutritional supplements that could help the immune system fight the infection
what are the three things that work best against a cold?
hydration, vitamins, balanced diet
what is the three ways an AT can be involved in allergy/cold medication
1) adherence to the medication
2) be aware of side effects or complications
3) compliance with banned substance rules
when should someone stop taking the medication ?
wait a bit after symptoms are gone
what are the three kinds of medications that have banned substances ? which ones ?
1) nasal decongestants - sympathomimetic properties
2) antitussive agents - codeine, glucorticoids
3) herbal remedies- ephedrine
with anti-cholinergic drugs what is the main concern for athletes in competition ?
heat exposure since will cause drowsiness and dizziness and blurred vision
What are the three main viruses reported as causes of URTI?
rhinovirus, adenovirus and
para-influenza virus
What is the percentage of URTI reported in studies ?
30% incidence of URTI
What was the main conclusion of the Bermon Paper as to what causes symptoms of URTI in athletes ?
no identifiable pathogens were either reported or
studied
what population has the highest incidence of reported URTI?
elite athletes
explain the concept of inflammation without infection in elite athletes, as explained by Bermon et al
athletes have symptoms of URTI but in lab studies, it is shown that only 11 out of 37 illness
episodes overall had pathogenic origins, therefore the symptoms of inflammation are, 2/3 of the time, caused without infection
so the Bermon paper shows that in URTI reported by athletes there aren’t always pathogens found in lab studies. what do these lab studies find that is there in resting conditions?
inflammation: increases in airway
neutrophils, eosinophils and lymphocytes
what probably then causes the inflammation in athletes?
pollutants or chlorine-related compounds in swimmers.
what is most frequent reason for consultation in sports medicine clinics, and is the most
common medical condition affecting athletes attending both summer and winter Olympics?
URTI
what is symptomology?
using symptoms to deduce what the infection was
what is pathogenic etiology
testing samples to see what causes the symptoms of the infection
why would hockey players have inflammation without infection ?
carbon and nitrogen oxides, from ice resurfacing (Zamboni)
elite athletes have more inflammatory cells in their lungs, but only when exercising. true or false ?
false
even at rest they have higher levels
there is an increased quantity of this cell that is the most common and consistent feature across many sports. what is it?
neutrophils
can athletes change the airway inflammation and asthmatic symptoms? with what lifestyle choices ?
yes, if they quit the sport the symptoms with decrease. otherwise they will get worse
in sports-related inflammation of URT, what is the most likely mediator ?
The cytokine IL-6, a pro-inflammatory cytokine was the most likely ‘mediator’ of inflammation, this cytokine is part of the bodies danger signal
elite swimmers demonstrated higher levels of what immune cell compared to sedentary control group ?
elite swimmers demonstrated higher levels of exhaled leukotriene B4 compared to sedentary control group
so in a bunch of sports-related URTI cases, no pathogen was found. does that mean there is no pathogen?
no, perhaps cannot be detected like herpes
still higher likelihood that it’s due to environmental factors
how does one ensure a uni-directional flow of lymph?
valves
what are the two types of immunity?
innate and adaptive
what are the 3 cells that are responsible for the 1st line of response (innate)?
macrophages, mast cells, neutrophils
what are the 3 cells that are responsible for the 2nd line of response (adaptive)?
antibodies, B-cells, T-cells
how do phagocytes “call” T-cells?
phagocytes eat and then present pathogen on surface, attracting T-helper cells and activating it
T-cells require what cell to fully be activated ? what does this cause ?
co-stimulatory signal CD28
this causes proliferation and differentiation into subtypes
what are cytokines ?
immune cells secrete cytokines attract more immune cells
what cytokine does Th17 produce ?
IL-17
what cell has been linked to autoimmune inflammatory diseases ?
IL-17
how does one extract T-cells from blood ?
centrifuge blood (top) and Ficoll (bottom) then, goes into layers:
Plasma
White blood cells (natural killer cells, T-cells)
Ficoll
RBC
what is the role of terbutaline ?
beta-2 agonist
what is the role of ICI?
beta-2 antagonist
what is ELISA ?
colorimetric assay that quantifies molecule of interest in sample (cytokines)
the darker the color, the more of the protein of interest we have
what is flow cytometry?
laser based analysis of physical characteristics of single particles to determine what cell in sample
stain cells with markers for Th17 (CD3 and CCR6)
what are two markers for Th17?
CD3 and CCR6
what happens to IL-17 if you add terbutaline into a solution with activated Th17 ?
increase in IL-17
what happens to IL-17 if you add ICI into a solution with activated Th17 ?
decrease in IL-17
what happens to IFN-gamma if you add terbutaline into a solution with activated Th17 ?
decrease in IFN-gamma
how are IFN-gamma and Th1 related?
IFN-gamma is a cytokine produced by Th1
what happens to IFN-gamma if you add ICI into a solution with activated Th17 ?
increase in IFN-gamma
what is the relationship between Th1 and Th17 called ?
reciprocal regulation