Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
260 Cards in this Set
- Front
- Back
What is eczema skin like?
|
Vesicles due to intercellular swelling. The vesicles are filled with fluid that leaked through the the cells.
|
|
What is the acute phase eczema?
|
*oozing and crusting due to swelling b/w cells
*bulla on skin *basal cell inflamm. on histo |
|
What is the chronic phase of eczema?
|
Lichenification
|
|
What is the atopy triad with which eczema is associated?
|
Eczema, asthma, hayfever
|
|
What Ig and what immune cell is elevated in the eczema pt's serum?
|
IgE and eosinophils
|
|
What MUST you have to be dx with eczema?
|
pruritis (itchy skin)
|
|
what parts of the skin does eczema involve?
|
skin creases--elbow folds, back of the knees, ankles, neck
|
|
What are the dxstic guidelines of eczema?
|
*involvement with creases
*hx of having the atopic triad (IgE hyperactivity) *hx of general dry skin *Flexural eczema (eczema on cheek/forehead/outer limbs in kids under 4) *onset under age 2 |
|
What is a bad se of topical steroids?
|
Thins the epidermis. Therefore don't use for more than 2-3 weeks at a time.
|
|
Where do you want to avoid steroid crm use and why?
|
Places where systemic absorption of the drug is increased. Avoid this because you can get a cushingoid like state due to high systemic steroids.
|
|
Class I steroids are the most potent Class VI steroids are the least potent
|
TRUE
|
|
Class I drug?
|
Temovate (Clobetasol)
|
|
Class II drugs?
|
Lidex and Topocort
|
|
Class IV drug?
|
Elocon
|
|
Class VI drug?
|
Desowen
|
|
What do you tell a pt to stop the itching fast?
|
*Cool water/milk compresses
*ASA--b/c itch and pain ride on the same nerve |
|
What do you tell a pt to stop the itching fast?
|
*Cool water/milk compresses
*ASA--b/c itch and pain ride on the same nerve |
|
Small pox vaccines can be given to eczema pts?
|
NO! NO! no no no no no no!
|
|
What is the mechanism of GI toxicity induced by NSAIDs and how prevalent is this se?
|
Prostaglandin inhibition. PGs are necessary for mucus production that protects the GI tract.
20% |
|
MOA of action of NSAIDs vs. DMARDs?
|
*NSAIDS affect sxs only by inhibiting PG
*DMARDS can change the course of dz by stabilizing golgi lysosomes. |
|
How are APAP and ASA diff?
|
APAP doesn't have anti-inflammatory activity.
|
|
What does Enbrel do?
|
TNF R inhibitor and therefore blocks inflamm. response.
|
|
What does minocycline do?
|
blocks metalloproteinase and therefore blocks CT breakdown.
|
|
Which drug is used to treat acute gouty arthritis and why?
|
Indomethacin because it inhibits uric acid formaxn.
|
|
Acute Urticaria resolves completely within how many weeks?
|
six. Anything greater is considered chronic urticaria.
|
|
Describe the urticaria lesion
|
Annular/papular with erythematous border.
|
|
What are causes of urticaria?
|
*IgE mediated (allergies)
*Compliment *Mast Cell degranulation |
|
What causes compliment mediated urticaria?
|
Serum sickness, angiodema (subcutaneous edema)
|
|
What % of urticaria is idiopathic?
|
more than 75%
|
|
How do hives arise?
|
Inciting agent causes mast cell degranulation--> histamine causes capillary permeability--> protein and fluid extravasate into interstitum--> swelling
|
|
What is the defn of dermographism?
|
Hypersensitivity to touch. Anything that lightly strokes the skin can cause urticaria. Ex: running a pencil across your arm.
|
|
What is solar urticaria?
|
Urtic. in response to UVA and UVA light.
|
|
What is cholinergic urticaria?
|
Urtic. caused by cholines in response to:
exercise emotional stress increased environmental temperature |
|
Cold urticaria is?
|
urtic. due to cold!
|
|
Something that looks like urticaria but is NOT is found on muscle bx to be urticarial vasculitis. What is this?
|
Urticarial Vasculitis: pts tend to be sicker and the lesions last longer than 24-48h.
|
|
What is tx for urticaria?
|
*HI and H2 blockers (antihistamines)
*steroids (short term, last resort) *avoid the inciting agent |
|
What is a drug eruption?
|
Allergic rxn to Rxs
|
|
What are three forms of drug eruptions?
|
1) exanthem
2) urticarial drug rxn 3) hypersensitivity syndrome |
|
What drug is the most common cause of drug exanthems?
|
Sulfamethoxazole/trimethoprim
|
|
What is the pattern of the lesion seen in drug exanthems?
|
morbilliform with erythema and small papules.
|
|
Pts who have hypersensitivity syndrome to drugs are most sensitive to:
|
anti-convulsants, sulfonamides, and allopurinol
|
|
Hypersensitivity syndrome sxs are:
|
*elevated LFTs
*scaling, vesicles, bullae, and sloughing of the skin *fever *lympadenopathy |
|
What are the viral exanthems and in what population are they seen?
|
Measeles, rubella, erythema infectiosum. Most seen in peds.
|
|
Viral exanthem rashes start where and spread where?
|
Start on the face and spread to the trunk and extremities over the course of a few days.
|
|
Hypersensitivity syndrome:
|
Eyrthema Multiforme
Stevens-Johnson Synd Toxic Epidermal Necrolysis Erythema Nodosum |
|
Erythema multiforme is most often due to
|
HSV.
Less common is URI |
|
What do EM lesions look like?
|
erythematous plaques and papules with targetoid lesion. they are symmetrical
|
|
EM lesions are mostly seen where in the body?
|
Mucus membranes, palms, and soles.
|
|
Patient presents with fever and flu like sxs. They have targetoid lesions all over their body and most signficantly, on their lips. What is likely dx>
|
SJS
|
|
TEN is also a derm emergency. What is it?
|
Diffuse necrosis of the skin that leads to sloughing and loss of skin. Urgently move to burn unit.
|
|
SJS and TEN often overlap as diagnoses. When does SJS become classified as TEN?
|
when there is over 30% of skin sloughing
|
|
When should you NOT use steroids in treating SJS?
When do you use steroids in treating TEN? |
If the SJS is advanced, DO NOT use steroids. Steroids are helpful early in the dz but harmful later.
NEVER use steroids to tx TEN. |
|
What is the most common cause of SJS and TEN?
|
drugs! SMX/TMP
|
|
What is erythema nodosum? What population is it most commonly seen?
|
Nodules deep in the subcuticular tissue.
Young women. |
|
Where in the body is E. Nodosum most seen?
|
Anterior Tibia
|
|
What is vasculitis? How is it manifested in the skin?
|
Inflamm. and necrosis of blood vessels.
It is seen as palpable purpura in the skin. |
|
What is the etiology of vasculitis?
|
Infection, PCN, sulfa, CT dzes such SLE, IBD, hepatitis, cancer
|
|
What is the ddx of vasculitis? How does it present?
|
Schamberg Dz. See little purpura on the lower legs only. Is probably a a capillaritis.
|
|
What is higher frequency and therefore more damaging, UVA or UVB?
|
UVB
|
|
Which wavelength is seen in tanning salons?
|
UVA
|
|
Which wavelength causes burns that are dose dependent?
|
UVB
|
|
If you get an immediate sunburn but it's so mild you don't even know it's there, what wavelength caused it?
|
UVA
|
|
A red haired, fair skin, light eyed girl is what skin type?
|
Type I
|
|
Which kind of tanning is "better" for your skin and why?
|
UVB tanning is better, because it not only darkens existent melanin but it causes new melanin to form (whichis protective). Therefore, tanning salons which only have UVA are less safe.
|
|
Where in the body does vitiligo usu occur?
|
FACE: peri-oral, peri-ocular, and on the lips.
BODY: knees, groin, armpits, butt. |
|
what is Polymorphic light eruption?
|
skin rash in response to the sun
|
|
what has a faster onset, phototox or photoallergy?
|
phototox
|
|
Elderly patient comes in with large tense bulla in his lip that ruptured. He reports that this happened last month, too, but it spontaneously healed. Likely dx?
|
Bullous Pemphigoid
|
|
What is the Asbo Hanson sign?
|
Lateral spread of the bullous when you press on it
|
|
What ab is involved with dermatitis herpetiformis?
|
IgA
|
|
What GI condition is associated with D. Herpetiformis?
|
Celiac Sprue (gluten insensitivity)
|
|
What is a nevus?
|
a mole. not malignant till they get in the hundreds.
|
|
What shapes are junctional, intradermal, and compound nevi?
|
flat, raised, dome-shaped.
|
|
Describe a recurrent nevus and why it should be excised?
|
Irregular border. It may precede melanoma.
|
|
What is the main cause of melanoma?
|
UV light
|
|
Where do people of color get melanoma?
|
Sole of feet
|
|
Name the clinical features of melanoma
|
assymmetrical, irregular border, varied color, bigger than 6 mm, elevated
|
|
Seborrheic keratosis lesions are benign. What do they look like?
|
Tan/brown scaly plaque
|
|
What is the most common non melanoma skin cancer?
|
Basal Cell Carcinoma
|
|
It is a risk for what people?
|
fair skinned, sun exposed
|
|
What re the three basic kinds of BCC?
Which one is most difficult to tx? |
1) nodular
2) superficial 3) infiltrarting/morphea--hardest to tx |
|
Nodular BCC is the most common. What are the characteristics?
|
Pearly, waxy looking plaques. They may have telangectasias
|
|
What superficial nerve is at risk during surgery to remove a nodule on the periorbital part of the face?
|
temporal N
|
|
How does the superficial kind of BCC differ than the other two?
|
It does not come and go like the others. Instead, it gets bigger over time.
|
|
What does the infiltrating/morphea BCC type look like?
|
White/yellow scar like plaque
|
|
What does a morphea lesion look like?
|
starts out violaceous, then becomes white in the middle with a red/pink surround.
|
|
What In Basal Cell Nevus syndrome, every tx can be used except?
|
radiation. it makes it worse.
|
|
Actinic keratosis is a scaly sun spot. It's a marker for what kind of skin cancer?
|
Squamous cell carcinoma
|
|
What does SCC in situ mean?
|
It is the intermediate stage b/w actinic keratosis and full blown SCC.
|
|
Pt presents with rythematous papules that are rapidly growing and are on the lower lip and ears--places that are sun exposed. Dx?
|
SCC
|
|
What benign lesion mimics BCC?
|
Sebaceous Hyperplasia
|
|
A 13 year old girl presents with a raised, yellow plaque on her scalp. Her mother states that when she was a newborn, this area had no hair. Dx?
|
Nevus Sebaceous
|
|
What benign lesions are found near the eyelid?
|
Syringoma and hydrocystoma
|
|
What benign skin lesion is associated with tuberous sclerosis?
|
angiofibroma
|
|
What benign cyst is located at the nail fold?
|
mucous cyst
|
|
What is an acrochordon?
|
a skin tag
|
|
Rickettsia is a parasite that causes?
|
Rocky Mtn Spotted Fever
|
|
Describe the shape and growth requirements of Rickettsia
|
Coccobaccilli that are obligate intracellular parasites
|
|
What Abx is used to empirically tx RMSF?
|
Doxycycline
|
|
Rickettsia is divided into these two groups:
|
1) spotted fever
2) typhus |
|
Are humans considered reservoirs for Rickettsia?
|
NO! We are only incidental hosts!
|
|
What time during the year would you see Rickettsia?
|
Spring and summer
|
|
What causes the rash in Rickettsia?
|
The parasite proliferates in the endothelial cells of bvs--> vasculitis--> blocks b.f. to skin--> rash and necrosis of skin
|
|
A pt presents with rash, fever, HA, and a hx of hiking or camping where ticks occur. DDx?
|
Rickettsia!
|
|
What state has the most spotted fever?
|
N. Carolina
|
|
In the Spotted Fever subtype, there are 3 subtypes. They are:
|
1) RMSF
2) Boutonnouse Fever 3) Rickettsial Pox |
|
RMSF is caused by a tick that carries what parasite?
|
Rickettsia rickettsii
|
|
When this parasite enters your skin, it goes to your_________and then proliferates in your__________
|
lymphatic and blood vessels
endothelial cells |
|
The edema, hemorrhage, and hypovolemia seen in Rickettsiosis is due to:
|
vascular permeability caused by endothelial injury (caused by rickettsii proliferating at cost of endothelial cell)
|
|
What kidney manifestation is seen in RMSF due to the hypovolemia?
|
Pre-renal azotemia
|
|
What other clinical manifestations of RMSF do you see?
|
fever, myalgia, HA, malaise, rash (due to vasculitis), meningoencephalitis, lung problems.
**most impt to think about when making the dx is: RASH and TRAVEL HX to tick area/N. Carolina** |
|
Lab shows normal WBC but low__________
|
bone marrow cells: low plts and RBCs
|
|
Mortality of RMSF is LOW if it is txed early. What do you treat with?
|
Tetracycline, Doxycycline, Chloramphenicol.
|
|
What is the characterisitc skin lesion of Boutonnouse fever?
|
Tarche Noir=black area of necrosis where the tick bit
|
|
T or F: leaving Rickettsialpox untreated is FATAL
|
F. It resolves untreated in 2-3 weeks...but tx with doxycycline anyway until you are sure that you are correct in your dx!
|
|
How do you get Rickettsial pox?
|
House mice!
|
|
Q Fever is caused by a dessication resistant parasite that is acquired by humans when they
|
touch secretions of farm animals--milk, pee, poop, birth fluids
|
|
So Q Fever is an occupational dz of:
|
Farmers and Veterinarians
|
|
How is Q Fever different than the other two Spotted Fever subtypes?
|
No rash!
|
|
Q Fever has a heart complication. What is it?
|
Endocarditis. It's a common cause of aseptic endocarditis...
|
|
Rickettsia prowazekii causes ________
|
Typhus
|
|
Typhus is associated with what kinds of living conditions?
|
War, famine, overcrowding
|
|
What is the typhus vector? the reservoir?
|
body lice=vector.
flying squirrel=reservoir |
|
What is the rash distribution in typhus?
|
centrifugal--it moves from center to periphery
|
|
What is the tx for typhus?
|
doxycycline
|
|
The RMSF rash is centr______while the typhus rash is centr_______
|
centripetal, centrifugal
|
|
What organism causes over 90% of elephantiasis (aka filariasis)?
|
Wucheria Bancrofti
|
|
What kind of living condns do you see filariasis?
|
uncontrolled mosquito breeding in overcrowded cities
|
|
The microfilariae (the egg) of the parasite lives in travels to through the ________ and arrive at the _________ where they mature into adults and live permanently
|
lymphatic vessels, lymph node
|
|
There are 2 stages of filariasis. In the asxtic stage, what is happening with the lymph endothelium and in the immune syst?
|
The lymph endothel. is proliferating and the immune system is downregulated
|
|
In the sxtic stage, what is happening in the lymph nodes?
|
Inflammation in the nodes which leads to fibrosis of the nodes
|
|
Do newcomers to Filariasis endemic areas get ill faster or slower than the native popul?
|
faster!
|
|
What is the diff b/w lymphangitis and lymphadenitis?
|
lymphangitis=INFECTIOUS inflammation of lymph
lymphadenitis=NON-INFECTIOUS inflamm of lymph |
|
In filaria, retrograde lymphadenitis is seen. It's the response to the dying adult worm. What is the pattern of spread?
|
Moves from out toward center of the body
|
|
What are other sxs of filariasis besides retrograde lymphadenitis?
|
*fever
*hydrocele in males *chyluria (milky white urine) *elephantiasis (big, hard tissue due to edema and destruction of lymph tissue) |
|
A pt comes in with mily white urine, big lymph nodes that spread from her hands toward her armpits, and she's had a fever. To make the definitive dx of filariasis, when do you want to draw her blood?
|
late at night
|
|
What is the drug used to tx both individuals and the community for filariasis?
|
DEC
|
|
Dracunculiasis will most likely be eradicated in the near future. What is it?
|
A larva of a parasite penetrates the GI tract.
|
|
From the GI tract where does it mature and then migrate?
|
matures in the CT or in the abdomen and then migrates to the skin
|
|
When is the larvae discharged from the skin?
|
whenever the skin gets wet
|
|
how do you remove the dracuncula worm?
|
you have to roll it up with a stick, very carefully, day after day, until it's lifted. that's so weird.
|
|
trichinosis is a parastie in what animal? we eat it when we eat this meat raw or undercooked....
|
pigs! (men are pigs)
|
|
where in the human does the parasite go to encyst and calcify?
|
muscle
|
|
pt presents with myositis, edema around the eyes, and hemorraghes in the retina and in the finger nails. Dx?
How would you treat her? |
trichinella
nothing very useful in the way of tx--steroids and albendazole may help but mostly supportive? |
|
What would you tell her to avoid? What would you tell the farmers who raise the pigs?
|
Avoid bears--they carry trichinella too
Grain feed swine |
|
In cutaneous larval migrans, the larva creeps around the skin causing itchiness. Is it necessary to remove the larva before it causes damage?
|
No. it dies on its own and causes no complications besides pruritis.
|
|
What is cysticercosis? What popul is it most commonly seen in ?
|
Pork tapeworm, seen most in mexican/L. American immigrants
|
|
What is the neural complication of cysticercosis? What is seen on MRI of the brain?
|
seizures! multiple cysts!
|
|
When the larvae of cysticercosis encyst in the muscle, what immune cell tells you it's there? What happens if it encysts in the eye?
|
eosinophils
causes vision loss |
|
What is the chemical name of the histamine ring?
|
Imidazole
|
|
Mast cells store histamine. They turn blue when stained with a special dye...this is called?
|
Metachromasia
|
|
What is the entity in the mast cell that is responsible for metachromasia?
|
the protegoglycan interacts with the basic dye giving a color shift.
|
|
Why is histamine slowly synthesized and slowly metabloized? (slow turnover)?
|
it is tightly bound to vesicles
|
|
Where else is histamine found in the body?
|
GI mucosa and brain. It has a faster turnover in these two locations.
|
|
What two cells mediate the synthesis of nascent histamine?
|
macrophages and plts
|
|
what is the precursor of histamine? What is the enzyme that converts it?
|
L-histidine
Histidine decarboxylase |
|
What is the action of Histidine decarboxylase on L-histidine?
Is it's level high or low in the GI mucosa? |
Histidine decarboxylase removes CO2 from L-Histidine
high levels of this E in the GI mucosa |
|
What are the two pathways by which histamine is metabolized? Which one is dominant?
|
Oxidation and Methylation (dominant)
|
|
What is the E in the oxidation pathway?
|
Diamine oxidase
|
|
What is the E in the methylation pathway? What is the necessary Co-factor it needs?
|
Histamine-N-methyl transferase
SAM (S-adenosyl-L-methionine) |
|
What does this E do to the histamine molecule with SAM?
What is the name of the product? |
It removes the a methyl group from SAM and puts it on the histamine.
N-Methylhistamine |
|
What E acts on N-methylhistamine?
What is the product and how is it excreted? |
Monoamine oxidase (MAO)
MIAA. It's excreted in the urine. |
|
What is a marker of histamine amnts in the tissue?
What is a marker of histamine release? |
Marker in the tissue: Histadine Decarboxylase
Marker of release: amount of MIAA in the urine |
|
There are two Rs of Histamine that we must know: H1 and H2. Which one is fast vasodilation and which one is slow?
|
Hi=rapid vasodilation
H2=slow vasodilation |
|
Which R is found in the heart? What is the effect of stimulating these Rs?
|
H2. Increase in HR, SV, and CO
|
|
Which R is found in the bronchiolar smooth muscle and what is the effect of their stimulation?
|
HI. Constriction--> wheezing
|
|
Which R is found in the gastric mucosa? What is the effect of stim?
|
H2. Increased acid and pepsin secretion.
|
|
Which R is found in the rest of the intestinal tract smooth muscle? Effect of stim?
|
H1. Smooth muscle contraction.
|
|
Both H1 and H2 Rs are found in the skin. They cause the triple response which is what?
|
1) small red spots at the site of injection
2) flare 3) wheal |
|
What causes the wheal and flare rxn?
|
The flush is due to stimulation of the local afferent nerves which fires the efferent nerves-->vasodilation.
The wheal is edema due to fluid leakage from the permeable capillaries. |
|
H1 R raise Ca levels how?
|
H1 Rs are linked to PLC which leads to IP3 and DAG formaxn. IP3 causes an increase in Ca levels.
|
|
H2 Rs effects occur via production of what G protein product?
|
cAMP
|
|
Histamine causes contraction of smooth muscle in the stomach but not in the heart. Why?
|
H1 Rs in the intestinal smooth muscle are physiologically active while H2 Rs in the heart are not.
|
|
Histamine mediates arousal in the brain. In the brain, histamine is made in the?
|
tuberomammillary bodies.
|
|
Hist. release from the mast cells is dependent on which cation?
|
Ca
|
|
What Ig is associated with histamine release? Where does it bind to the Mast cell?
|
IgE. Fc R.
|
|
What are the diff b/w 1st and 2nd generation H1 antagonists?
|
2nd gen. don't cross the BBB, they aren't anti-cholinergic so the s.e.s are less, and they have a longer duration of action.
|
|
What are the generic names of 5 1st generation H1 antagonists?
|
-diphenhydramine
-PYRIBENZAMINE -chlorphenyramine -CYCLIZINE -promethazine |
|
What is the effect of H2 antagonists?
|
lower HR, lower CO, and lower acid secrexn.
|
|
What liver E does cimetidine block?
|
CYP 450
|
|
What is the only containdication of cimetidine?
What Rxs have big interactions with cimetidine? |
gastric cancer
Theophylline, phenytoin, warfarin |
|
What is the MOA of cromolyn? Is it considered an anti-histamine?
|
It stablizes the mast cell membrane and prevents release of histamine. It IS NOT an anti-histamine because it doesn't relax smooth muscle.
|
|
Cromolyn can be used in young asthma pts, including the case of status asthmatics?
|
it CAN be used in asthma pts, but HAS NO VALUE IN STATUS ASTHMATICUS!
|
|
What is another indication of cromolyn?
|
It can be used for allergic rhinitis when used as a spray!
|
|
Tilade is...and is used for....
|
a new Rx that is an anti-histamine release drug...used for asthma
|
|
What do psoriasis lesions look like? Where in the body are they most common?
|
Well demarcated, scaly erythematous plaques. They are most common on the elbows, scalp, and knees.
|
|
What is the major systemic manifestation of psoriasis?
|
Arthritis--sausage fingers
|
|
What is Auspits sign?
|
a dark spot due to Fe from spot bleeding after scratching off a psoriasis plaque
|
|
What is the Koebner phenomenon?
|
Lesions that appear at sites of injury
|
|
In Lichen planus, you can see whitish lines in the plaque. These are called
|
Wickim's striae
|
|
Where in the body do find Lichen Planus lesions the most?
|
trunk
mucus membranes (mouth/lips) pre-tibia |
|
A teenage female presents with one big red scale (fawn-colored) and some satellite scales that surround it. She says this happened last month but resolved on its own. DDx?
|
Pityriasis Rosea.
Secondary Syphilis. |
|
Spaghetti and meatballs is the description that is seen on KOH test for this fungal infection. Is it superficial or deep?
|
Tinea Versicolor. Superficial.
|
|
Syphillis is associated with what tick dz?
|
Lyme Dx. Lyme Dz is syphilllis reborn(??)
|
|
"micacious" and "hyperkeratotic" are buzz words for lesions in what dz?
|
psoriasis
|
|
pustules in psoriasis form due to infiltration of what immune cell?
|
neutrophils (PMNs)
|
|
What is the oil sign?
|
yellowing of the finger nail due to deposition of serum
|
|
Psoriatic arthritis affects these joints:
|
IP joins in the hands
|
|
Why do psoriatic plaques bleed so easily when picked?
|
The dermal papillae in psoriasis is thickened and extends all the way into the epidermis. When the scale is picked, it exposes the dermis where the bvs are.
|
|
In which dermatitis do patients not scratch because there is no itch relief?
|
Lichen Planus
|
|
How come fungal infections have rings that get bigger on the skin?
|
it consumes keratin and has to move out in order to "eat live skin"
|
|
How do you differentiate b/w syphillis rash and P.R. rash?
|
In syphillis, the rash will go to the palms of hands and feet. Also, see chancres on the genitalia and in oral mucosa
|
|
What food products exacerbate Rheumatoid arthritis?
|
Wheat, citrus, dairy, and nuts.
Also, coffee |
|
What is desired range of Vit D?
Vit D deficiency is considered? |
Above 30 ng/ml
Belove 20 |
|
What is the relationship between Vit D and Ca?
|
Vit D facilitates Ca absorption in the gut
|
|
Vit D Cascade:
Skin-->liver-->kidney--> intestine and bone |
D3-->25(OH)D-->1,25(OH)D--> gut and bones
|
|
What is the affect of anti-oxidants on RA?
|
Anti-oxidants stop oxidative damage and therefore may be protective agains the damage in RA
|
|
Why would low fat diets aggravate RA?
|
Low fat diets are low in Vit E and Vit A, two anti-oxidants that would protect against joint damage.
|
|
The desaturase E converts omega-6 and omega-3 between each other. What factors cause the E to make more omega-6?
|
high etoh
stress diabetes high 6/3 ratio |
|
Supplements to reduce pain and inflamm in RA?
|
Vit D, E, C
Selenium Calcium omega 3 oils olive oil EPA |
|
What would daily caloric and protein requirements be for pts who need to gain weight due to RA?
|
35 kcal/kg of actual weight
1.5-2.0g/kg of ideal weight |
|
Why does prednisone aggravate osteoperosis?
|
It causes increased Ca excrexn and decreased Ca absorpxn
|
|
what is the action of omega-3 on bone resorpxn and inflamm?
|
suppresses osteoclastic activity and pro-inflamm cytokines
|
|
Purposes of bone?
|
biomechanical
metabolism hematopoiesis |
|
What's the diff b/w compact bone and spongy/cancellous bone?
|
Compact bone=structure
Cancellous bone=hematopoiesis |
|
Bone is comprised of three things:
|
1) collagen matrix
2) mineral salts 3) cells |
|
Collagen matrix is composed of:
|
1) type I collagen
2) proteoglycans |
|
Mineral of bone is called hypoxyapetite. It is composed of two elements:
|
1) Ca
2) phosphate |
|
The cells of bone are:
|
osteoclasts, osteoblasts, and osteocytes
|
|
What lines the external surface of bone? what are its two layers called?
|
Periosteum
outer layer=fibrous inner layer=osteoprogenitor cells |
|
What lines the internal surface of bone?
|
Endosteum
|
|
What are the two types of joints and which one allows for movement?
|
1) Diarthroses=allows for free movement
2) Synarthroses=no free movement |
|
Which two factors are cause an increase and Ca absorpxn and breakdown of bone?
|
PTH and Vit D
|
|
PTH responds to a _____in Ca levels. It
|
drop
|
|
What is the defn of simple arthritis?
|
Joint complaints for more than 6 weeks
|
|
What characterizes INFLAMMATORY arthritis?
|
pain, swelling, warmth, erythema, and synovial thickening.
|
|
what are sxs of RA?
|
morning stiffness, multiple joints involved, symmetrical joint involvement, subcutaneous nodules.
|
|
what are systemic sxs of RA?
|
vasculitis and ILD
|
|
in RA, what will the CBC show?
|
high plt count (thrombocytosis)
normocytic, normochromic anemia |
|
ESR is high/normal in RA?
|
high!
|
|
Why does bone form cysts when the cartilage erodes?
|
to increase the surface area so that pressure can be spread out
|
|
Which immune cell recognizes self-peptide as foreign and what cell does it present to?
|
Macrophage. Presents to a T Cell.
|
|
HLA gene complex is on Chromosome #?
|
6
|
|
What is Rheumatoid Factor? Which immune cell makes it? What does it do?
|
RF is an anti-IgG immunoglobulin made by plasma cells. It forms complexes with IgG and then activates complement.
Complement causes the tissue inflamm. and destruction seen in RA |
|
Which immune cell enters the synovium of the joint?
|
neutrophil
|
|
Presence of which Ig gives a poorer px? IgG or IgM?
|
IgM
|
|
Which cytokine mediates joint destruction in RA?
|
TNF alpha
|
|
what are the two main differences b/w OA and RA?
|
in OA, there is non-symmetrical involvement and the stiffness in the a.m. is mild (severe after immobility)
|
|
What is seen in the joint space on X Ray in OA?
|
osteophytes
|
|
What is the most common cause of septic arthritis?
|
bac due to hematogenous spread
|
|
Why is there a wide range of distribution of cortisol secretion among people?
|
Levels of CYP 450 differ b/w people
|
|
Where does the gluct. R receive cortisol in the cell?
|
Cytoplasm. Binding of cort causes a conformation change that brings the R into the nucleus.
|
|
Glucts. are catabolic. They also have waht affect on glucose with respect to the liver?
|
They induce gluconeogenesis
|
|
Addison's dz is too little/too much glucts?
|
too little. these pts have a hard time maintaining blood glucose levels and adapting to stress.
|
|
what are some clinical uses of glucts?
|
skin for allergic rxns
malignancies |
|
ACTH is used to dx primary and secondary adrenal cortical insufficiency. How?
|
If adrenals respond to exogenous ACTH, then the problem does not lie within the adrenal cx itself and is therefore a secondary insufficiency
|
|
Will exogenous administration of glucts. increase or decrease endogenous production?
|
decrease!
Therefore, don't abruptly withdraw the drug. Decrease the amnts gradually so that the HPA axis has time to kick in again. |
|
What corticosteroid is used to tx Crohn's dz and is unique in that it's delivered straight to the terminal ileum?
|
Budesonide
|
|
high levels of corticosteroids will display peripheral mineralocorticoid activity. what sx will indicate that this is happening?
|
salt retention
|
|
Which bone tumor is more common in kids: osteosarcoma or ewings?
|
Ewings in kids under 10. Above age 10, it's most likely osteosarcoma
|
|
What is the first place that bone cancers met?
|
lung!
|
|
Very distal tumors do well with surgery (T/F)
Central tumors do well with surgery (T/F) |
T
F |
|
How do you decide between surgery and radiation?
|
is tumor radiation sensitive?
is it completely resectable? will you kill growth plates in the resection field? will cause a secondary tumor (secondary osteogenic sarcoma)? |
|
What is the defn of a periosteal reaction? How does it give you information about the tumor?
|
it is the response of the periosteum to a stimulus (like growing a tumor).
The shape of the growth tells you how fast it's growingl. For ex, codman's triangle growth is so fast it's more like a tip growing out than a lump |
|
Ewing's sarcoma occurs in the bone ______
Osteosarcomas occur in the bone _____ |
diaphysis (central distribution!)
metaphysis (peripheral distribution!) |
|
Ewing's sarcoma has a neural origin.
PNET is a subtype of Ewing's. Where do PNETs reside? What chromosome is the gene found on? |
PNETs are in soft tissue
chromosome 22 |
|
what is the best tx for Ewing's?
why not surgerical resection? |
Best tx is combo therapy: radiation with Adriamycin + VAC
Resection is usu not successful in Ewings because the cancer has met. by the time of presentation. |
|
Osteosarcoma has an osteoblast origin. When is the peak incidence?
|
Teens and early 20s (time of final bone growth)
|
|
Ewings has excellent response to radiation. Do osteosarcomas respond well to radiation?
What is the best tx option for Osteosarc? |
rarely
chemo....it improves ability to resect |
|
what are some late affects of tx for these two cancers?
|
* secondary sarcoma at site of radiation
* infertility due to chemo |