Pharm: platelets: clotting

Platelet activation:
Receptors are long and sticky and binds to fibrinogen and little platelets stick together and that’s aggregation. These little bonds are the process of platelet aggregation. So what causes platelet aggregation? One biggy is collagen. No gaps or nicks, but as soon as vessels is injured hter ie exposure of sub endothelium and collagen sticks to injured spot. Collagen is great platelt acivator.
TXA2,
ADP-AdenosineDiphosphate,
PAF-platelet activating factor
Thrombin
GP: Glycoprotein

A clot is created but it is not stable. NO reinfocement and the clot might fall off if its not stabilized so the next step is coagulation which is the formation of fibrin and this is stringy fibers that reinforces the clot. There is an intrinsic pathway and an extrinsic pathway and it is a cascade. So once it starts it cascades to the final product.
Intrinsic pathway: all of the factors needed for cascade are already present intrinsically to the vascular system. What happens, is you have a factor activated to active factor: Factor A. And on goes a chain of stimulation. Last one is Factor 10.
Reponse to injury: thromboplastin is released. This stimulates a factor 7 to factor 7A, which stimulates factor 10 to become factor 10A.
KNOW: What intrinsic factor is, and that it means that it’s got factors already in the vasculator. Extrinsic needs thermoplastic form outside. And both of these converge on factor 10A.
What we are trying to produce is fibrin and factor 10A stimulates protrombinm to become thrombin. Thrombin stimulates fibrinogen to become fibrin. And all this fibrin is what goes to the clot to reinforce it.
Trigger pathway downstream. Body has set up mechanism to captivate and activate them if they wander away from the tissue site and that enzyme is called Antithrombin. It can inactivate 10A and Thrombin. It inactivates all of those little activated factors if they tend to wander away and that’s when heparin is going to come in.
Aterial Thrombus vs. Venus thrombus
Aerteria thrombus: starts from tissue injury, happens in arteries pretty locally since arteries are going out the the tissues. Tends to be a local effect. The injury stimulates platelet aggregation. Clot occludes the artery.

But If it’s a Venus thrombus, we treat with platelet drugs. So ant platelet drugs help with myocardial infarction and venus thrombus in the coagulation pathway: venus stasis. Some women get DVT in their legs because the blood flow has slowed down the the point the coagulation pathway has slowed down. Treat with anticoagulants like heparin.
KNOW: these drugs…
1. Heparin:
-animal bovine protiene. A long chain with a little active site in the middle.
-binds with ant thrombin and makes it better at inactivating thrombin and factor 10A. So heparin binds with ant thrombin which is the protein that inactivates all of these little factors and makes ant thrombin better, including most importantly 10 a and thrombin.
So here’s how it works….drawing of mechanism of action.

Kinetics and Dynamics of Heparin.
-Big molecule
-highly polar with ltos of negative charges
-PO: will not work, wont’ go through GI membranes
-Does not cross placenta. Due to membrane negative charge-
-No CNS
-Immediate onset of action. Short halflife of 1.5 hours. Give in repeated doses often.
-Variable and non-specific binding.: hard to tell how much active and available heparin you have. Hard to decide how much will be enough for pts.
-Hepatically metabolized: hepatic disease must be closely monitored.
-Renally excreted.
-Use: keep veins open, for initial treatment of DVT or PE (Pulmonary Embolus when a piece of clot breaks off and travels to lungs.) Venus problems can travel a long way, but arterial problems don’t travel so far.
-Side Effects: Bleeding in 10% of pts. Can be mild-severe, and can happen in any site in the body. Will see lots of bruises. Tachycardia. In situations where there is waay to much heparin there is an antidote called Protamine. This his positive charges, and it binds together with negative charge of heparin, and then it can’t do anything.
Heparine Induced Thrombocytopenia: Drop in Platelets. DON”T learn the mechanism. Know that a drop in platelets can be this, which can be fatal.
Hypersensitivity: Heparin is derived from animal extracts and this can cause a protein anaphylaxis reaction. There is a significant chance for fever, chills, etc…
IF there are two steps to hemostasis and blocking pathway, so if I give drugs that block platelet aggregation then pt is at much higher risk. Careful of anti-platelet and heparin. They have no way to coagulate anything. Aspirin/heparin, etc…
Monistering. Difficult to preduct how much is enough. APTT: Activated Partial trothomboplastin time. Typically this is 40%. Don’t memorize how to give it daily. Also moniter platelets.

Low molecular weight heparin: smaller molecules
-still has chain
-same activated site where it binds to ant thrombin.
-With short arms, low molecular weight heparin cannot activate thrombin. But it CAN activate factor 10A. It’s arms are too short. Like a T-rex!! It is still as effective as heparin at anticoagulation.
-Adverse effects: bleeding, thrombocytopenia, hypersensitivity. Less risk of all of these, except the risk for bleeding is the same. The differences between unfractionated heparins and low moleuclear weight are thse…
-does not bind indiscriminately to all proteins. Measure by body weight, give dose, and you know how much will be in their plasma. So you don’t need to moniter at all. It doesn’t bind so non-specifically. Much more specific molecule. Much more predictable kinetic profile so you know what you’re gonna get. You can give it on a fixed dose schedule and for heparin, it must be adjusted more or less depending on APTT. Has a longer halflife, so you can give it 1 or 2 times daily. It is sub Q, still not PO, and less likely to cause thrombocytopenia.
Low molecular weight heparin is much more expensive, though. However, pts can be given this and be sent home, and the hospitalization cost of monitoring pts with heparin treatment. So actually, how molecular weight heparin is still cheaper.
KNOW: Advantages of Lowmoleuclar weight heparin over heprain.
Direct Thrombin Inhibitors:
-Don’t need to know the name.
-(Heparin is the indirect thrombin inhibitor, because it must bind to ant thrombin first and then activate thrombin. Also, heparin can only act on Free Thrombin.)
-However, Direct thrombin inhibitors can directly act on free thrombin floating around in blood stream as well as thrombin that’s in a clot.
-Largely used for angioplasty, iv stuff in cardiology unit. Critical Care kind of drug. Extremely expensive. Not more effective than heparin.
-Adverse effects: backpain, decreased BP,

So those are the three types of anticoagulants given IV, SubQ or both.
One PO anticoagulant……
Warfarin:
-Cattle ate some spoiled clover and had a bleeding reaction. WARF came up with a synthetic form of spoiled clover and gave it to animals which caused hemorrhaging there too. Used in rat poison. In early 1950s a guy tried to commit suicide and took allot of rat posion, but didn’t die. But they did find out it had an anticoagulant effect.
-Mechanism of warfarin action is very different from heparin, low moleuclear wight heparin, or direct thombin inhibitors….
*Draws on board* Inactive factor becomes another factor…etc… Vitamin K is necessary to biosynthesize these inactivated factors. So it blocks biosynthesis. That’s a very different mechanism. Warfarin works on one side, and Heparin works on another side of the cascade:
From the intrinsic pathway, once it gets started there are inactive protiens witing to be activated and that activated factor activates another inactivated factor. This is the cascade effect. So one of the components of these factors, in order to be built by body they need vitamin K. Warfarin blocsk this biosynthesis, but warfarin blocsk Vitamin K so these can be synthesized.
-Effects of warfarin are not immediate.
-Once a factor is made and is circulating in the body, warfarin can’t do anything to it. Warfarin only affects factors that are BEING synthesized. So halflife of typical factor is a day or two. So you have to wait for old ones to die to see any effect. Allot of pts you have on Heparin and you have to switch to PO warfarin to get that going. You can gradually wean off the heparin to coumadin, but you can’t just send them out the door because there’s not a peak until several days have passed. Likewise, if a pt is finished taking warfarin, it will be several days until coagulation pathway is back to normal. Wait several days while the body is makin gnew factor. Still at risk for bleeding.
-Adverse effects: Bleeding is #1 problem/ antidote is Vitamin K: overcomes the inhibition of vitamin K from warfarin. Pts who are on warfarin are out in society and they must be advised to use a medical alert bracelet, in case they are in an accident and have a bleeding problem. Also causes birth defects like fetal hemorrhage, central birth defects, etc…because it passes right through the placenta.
-Must moniter the PT:
-prothrombin time. Average pt is 12 seconds. This was normalized to INR. (but you don’t need to know these specifics, like what the INR would be of pt.)
-Moniter also IR: the lab would giv eyou a figure of the Pts prothrombin time vs. the control’s prothrombin time. So institutions have normalized it as INR: normalized prothrombin time. Unanticoagulated blood as an INR of 1. A pt on warfarin you are shooting for 2-3. Some pts should be more than that. If the INR is too high, like 4, you need to cut back on warfarin.
-At home kits are available for pts so they don’t need to come in and get prothrombin time tests at doctor’s.
- Dependent on Cytochrome P450 mechanism.
-Hepatically metabolized.
-99% protein bound, so drug interactions are a major issue
-Non polar: easily absorbed through GI and Placenta. So for OB pts, it is better to give heparin.
-DVT or PE: use
-Every drug that a pt takes in addition must be okayed bythe doctor.
-Nursing considerations:
-Surgury, Peptic ulcer disease, moniter IV sites, moniter platelts, if warfarin moniter INR, educate them to look for bleeding and medical alert bracelets and pregnancy.
*now we draw a little table comparing heparin and warfarin*
HEPARIN
WARFARIN
MOA
Route
Onset


_________________________________________________________________________________
Only works on 10A.
Low moleculular weight heparin.
Know why these LMWH are more convenient and why they are the choice: don’t need to moniter, pts can go home on this drug, has a predicable plasma concentration. Longer halflife. Side effects are same as heparin. Thrombocytopenia which is less than heparin. Direc thrombin inhibitors.

Direct thrombin inhbitors: used in acute care setting
-inactivate thrombin both free and inbedded within.
-Don’t need to know Direct thrombin inhibitors specifically

Warfarin is a biggie. Number one adverse effect is bleeding. Know this drug.
Antiplatlet drugs:
-Aspirin.
-Know which mechanism and its side effect.
EPP
-Receptor antagonists and how those work and glycoprotein II and IIIa and how they work.
Other antipathetic drugs.
Thrombolytics: Don’t know any specifically like names but know what they do and where they are used.
-not in notes
-in anticoagulants worksheet.
-promote conversion of plasminogen to plasmin and that enzyme chews up clots. So if she gives this thormbolyticl ike streptokinase they are clot busters. Zbut you don’t need to know the names of any specifics. Given to babies with clots in their extremities.
Will make a study guide again.
Anemias: read about several. #2 most common and deadly disease in the world. Extremely common. Like iron deficiency. Common in underdeveloped countries. Can affect mortality and morbidity, particularly in vulnerable pts. Renal disease, congestive heart failure, cancer, etc… Can make quality of life awful. For the normal person who has had trauma and lost blood they can get over the hump and be healthy again.
What is anemia?
-The reduction in number of RBCs, size of RBCs or hemoglobin content of RBCs. Normal hemoglobin is 13 for men and 12 for women. Can be due to blood loss, hemolytic, bone marrow disfunciton. Deficincy anemais,
1. Iron
2. B12
3. Folic Acid.
There are two types of deficiency:
1. Microcytic
2. Macrocytic

Iron deficiency is a microcrystal anemia. Low hemoglobin you can’t carry oxygen well to the tissues. Most of the iron the body absorbs goes into the bone marrow. Osme goes to myoglobin and a tiny bit goes to make other enzymes that have iron in them. If a patients iron stores are low the amount of iron their body takes up will be high. IF the stores are high, uptake will be low. If you give allot of iron to a pt who has high iron store, they will not take up much of it. The iron cycle is this:
Iron from your diet binds with ferratin in the small intestine mucosal cells and sometimes it gets stored there. But sometimes it passes through and binds with transferrinand makes complex.
1. About 80% can go to the bone marrow. Then it can go to the bone marrow to make RBCs,
2. can go to the liver for storage for later, Liver is a high iron tissue,
3. it can go tot hmsucles to make myoglobin and
4 it goes to tissues to make enzymes.

Body loses some iron everyday, but very little. When The liver was discovered that it was iron rich. In early 1920s, Minot was working with iron deficint dogs and fed them raw liver. Minot did the same experiment with people. Both cured.
So when a pt has not a whole lot of iron, the RBCs lack enough iron and they tend to be small, thusmicrocytic anemia. Tend also to be hypo chromic or pale. Changes depending on what the body’s stores are. Most common causes of poisoning are iron poisining. But generally if stores are high the uptake will not be high. What you need to know is adverse effects:
Nausia, vomiting, diarrhea, constipation: will make people non-adherent. Constipation is a big deal. Heartburn, bloating, etc… Tricks to get pts around this issue: GI are not dangerous and become more tolerated over time. Iron supplements wont be taken if it makes them feel awful. Taken with food, and the risk is lower. Not the same adverse effects. Problem is that aborption goes down as well. If they take iron between meals, absorption goes up but also with adverse effects. Start taking drug with meals initially and then after a week take it between meals and that way hopefully the body will have grown accustomed and the side effects wont be quite so bad. Given in eavenly spaced daily doses because the body needs a steady continuous amount. Taken morning, noon, evening. Give moms vitron C. Ascoprbic acid boosts absorption and side effects. Also antacids. Tums or Prilosec and Zantac…that increases PH in stomach, acid content is reduced and iron is not well absorbed. Last one is tetracyclines, which we don’t need to know.
Depending on severity of anemia and causes, recover will take several weeks to several months. Next drug is parenteral. This is a dangerous medication of anyphylaxis. Encourages pts to take the drug Po. And if a pt cannto take po iron because of malabosprtion then they need something parenteral. When blood loss has been huge they can get iron detrate though IV. Po iron should be the best because of anyphylaxis. Can be fatal even when treated.
Vitamin B12 anemia: treating pts with raw liver in 1920s and minot has a student who studied pernicious anemia. Was a fatal disease. Lived 1-3 years. Noticed that pts don thave gastric acid. Pts who received gastric juices and raw hamburger survived.
So humans are dependent on getting B12 from soil, microorganisms, etc.. Anmials that eat the soil and microorganisms get it, and we get it from the animals we eat. Sometimes they live on legumes, etc.. or on leafy vegetables. And allot of strict vegetarians take vitamin supplements anyways. So we need vitamin B12 in order to synthesize dna. Rapidly growing cells are most effective: bone marrow, erythrocytes, plaetelets , wbcs and gi tracts. Rapidly growing cells are most effective.
Mechanism is this: Folic acid is inactive and it needs to become activated and that’s done by vitamin B12. So without, we don’t get active folic acid. And without active folic acid, we can’t synthesize DNA. There is an alternate pathway. This is the marjor and inor pathway. So you can bypass it but not enough to survive. What you need is for vitamin B12 to bind with intrinsic factor and that’s whats in gastric jucie. So vitamin B12 binds with intrinsic factor in the stomach and it can be transported through tissues that way. But if pts do not have any intrinsic factor ad you give them enough b12 youcan get them to absorb it. Elimination of B12 is very slow, so its developed slowly over months. The causes of B12 deficiency are reduced stomach acid, intrinsic factor, diseases like celiac disease which can contibute. Consequece; affects the high growth tissues, oral ulcerations, and bone marrow disfunction and what happens is the dnA replicates and the cell can’t multiply so you have these big cells called macrocytes.
IM, SubQ, pO, and intranasal gel.

Pain: didn’t read chpter 28. But read it before Wed class. On opiods.
What we did read for today, start on pg 54 of notes and down to section of opoids and skip pg. 59. Pain is a huge issue in the hospital. Affects millions of people. Know that pain is very subjective.
IF in doubt, remember rule number 1. If a pt claims pain, you must believe them. Most common pain is lower back pain. Gate controlled theory. Best explanation so far. Go up through the spinal cord and into the brain. Perception and stimulation. Stimulation of the nose receptors causes stimulation in the CNS. Chemicals called
bradykinens
prostoglandins
cytokines
substance P
CGRP
But there are lots of others. A complicated molecular system. After stimulation you’ve got transmission. Pain stimulus travels though spinal cord up into the brain. Third stage is perception.
Ouch that hurts that’s pain perception which happens nthe brain. Laswt is modulation. And what happens ist he brain siulates other nurons which release chemical inhiitorslike norpinephrine, seratonin and endogenous opoids. And those suppress the pain. A or C fibers. Just there for your interest. When you are assessing someones pain, its called the PQRST. P is for palliation, what causes your pain,
Q is quality
R is radiation
S is severity
T is for temporal. What happens over time.
Switch to pg 59.
Nsaids
Acetopmenophen is not an Nsaid. It is not.

Cyclooxygenaseinhibitors. The body take sarachadonic acid and two types of same enzyme. Cox 1 and Cox 2 synthesizes prostoglandins and thromboxine. Prostoglandins one of their functinos is increasing sensitivity to pain. So if we inhibit this enzyme we inhibit prostoglandin s ynthesis and indoing that youreduce the action of prostoglandins and suppress our sensitivity to pain. That’s the though process behind cox inhibitors. Cox 1 is presnt in almost all tissues thoughout the body and it is responbile for housekeeping chores of the body and it has a significan taction in the gastric mucosa and cox 1 is responsible for producing prostoglandins and thomboxanes.
Prostoglandins
-act on the gastric mucusa and increase bicoarbonate secreation, which is a base.
-And in doing sothey decreaes the acid content in the stomach which is protective.
-Also stimulates the rlease of mucus inth stomach which protects the stomach.
-Also decrease acid production
-increase gastric blood flow, perfusion of the stomach.

Cox 1
-Increase renal blood flow.
-Synthesizes trhomboxane which acauses platlet aggregation.
Cox 2’s prostoglandins
-Tissue injury
-Increased sensitivity to pain and inflammation.
-Affects set point for thermogregulation so those prostoglandins cause fever.
-Presnt in the kidneys and the prostoglanin synthesized from those Cox 2 increase renal blood flow.
NSAIDs.
-Aspirin: only one we need to know
-blocks cox 1 and cox 2
-well absorbed kinetically. Converted to an active metabolite. Elimination is dependent on ph. Aspirn is a weak acid and if you want to get rid of aspirn quickly youcan mekt he urin more basic and that will help get rid of aspirin. If aspirn blocks cox 1 then it would have a role in thromboxine synthesis blocking it, reducing platlet aggregation. Used prophylacitcally. Antiinflammation. Also bocks prostoglanin synthesisis at tissue site reducing pain. Sensitivity reducing paiat injury site and perception of pain in the CNS. Also works since cox two is presntinthe brain it also works as a fever reducer. We do not use aspirn in children at all anymore. Reyes syndrom/.
Dysmennorrea. Reduces pain in smooth muscle of uterous;
____________________________________________________________________

October 8 Wednesday
Lung Cancer and Breast Cancer
Types of Breast cancer: ductal and globular
Ductal Carcinoma in Situ DCIS
-others are being more selective in pt population
Ductal Breast Cancer
-more invasive. Insitu means it hasn’t started to invade the basement membrane. Ductal then has become invasive once its called breast cancer. Large nucleated cells filling the ducts. Once it becomes more advanced moving well beyond the ducts. More advanced. Subcategories of ductal breast cancer. Globular
Carcinoma in situ. Before it penetrates the basement membrane.
-No one treats this as a benign condition.
Infiltrating lobular
Pagets disease
-Description of the nipple. Ductal carcinoma that involves the areaola itself. Itching and oozing a common problem.
Inflammatory Breast cancer:
-Worst possible diagnosis
-Aggressive/Invasive
-Orange-peel skin overlying the tumor.
Half of women will be dead already by the time they reach 85. Chance getting it by 85 is 1:7. Live to age 79, risk is 1:15. Percent of women to die of breast cancer is 2.8% which is similar to chance of dying from a hip fracture. Risk of death by breast cancer decreases when you’re old, but only because you’ll probably die of something else first. May be more on our mind, since it affects younger people and its more on our mind.
Risk factors on pg. 106
Spending more time on genetics than anything else. Age is a risk factor and family history is certiantly a risk, even without knowing anything else about genetics. Definable genetical mutation, which is inherited. Mutation of the BRCA gene #1.
BRCA=breast cancer gene. This particular mutation is not one mutation, there are at least 17 mutations that can affect this gene. Another word is polymorphism. MOre and more when you look at the literature it means that a gene has many many possible mutations. Only a few mutations confer a significant enough risk for breast cancer. There’s a mutation and in different people it means different risks. If you look at BRCA mutation in general which is located on chromosome #17, and found in 1 in 500 women, you have a 40% risk in your lifetime of ovarian cancer.
Options include more frequent screening, diet and exercise, avoiding fatty foods, prophylactice removal of the breasts (both) which is the only kind of surgery where you don’t do anything with the lymph nodes. Gives you a 98% reduction in risk. But this person is also at risk for ovarian cancer, which could be a oopherectomy. Removed primary source of growth factor for breast cancer.
So
-double simple prophylactic mastectomy (cosmetic and breastfeeding issues)
- oopherectomy (no children, osteoperosis, and hot flashes…needing HRT)
-more frequent screening
BRCA 2 is a different gene.
-much higher risk for breast cancer
-not as high a risk for ovarian cancer
-men get this mutation
-increases risk for other cancers too, though.
Indications for Genetic screening in Breast cancer.
-90% is sporadic, rather than inherited. These mutations would be called aquired.
-Know that P53 is a significant risk.
-Women who inheret a BCRA, must be homozygous. Women who don’t inherent these mutations much less commonly aquire one. When you inheret a mutation of a gene you can be vulnerable to other mutations.
What cells in the body are going to have an inherited mutation? ….
Every cell ijn the body. You inheret the same DNA in every cell which makes the same perosn. You find an aquired mutation only in the tumor itself.
Methylation Problems
Early menarche or late menopause, high circulating levels of serum estradial or HRT. Estrogen is a growth factor for tumors. When we are talking about HRT we are talking about stimulating a cancer that was already there and making it grow faster. Lifetime exposure cause some carcinogenic effects over a lifetime. High levels of estrogen for 40 years, that may actually be a carcinogenic exposure over that many years. But if a women goes through menopause at age 52, its highly unlikely that estrogen caused the mutations, it was simply a growth factor. Birth control pills have finally been laid to rest as a risk factor for bresat cancer. If anything, the current forms of birth control are protected reducing the risk of breast cancer. With HRT we are stimulating a tumor that’s aready there.
Mitogenesis
-increases cell divisions
Mutogenesis
-of oxidative damage to the DNA.
WHI results: statistics can be a little misleading. If you have tumors and you take estrogens that cause tumor to grow over next few years. Look at the hazard ratio for breast cancer in year five.
No risk with abortions. Oral contraceptive use, and decreased risk of breat cancer with breastfeeding and pregnancy.
…
Pg. 108: Progressive cellular and tissue changes.
Why does pregnancy help prevent? Where the cells are most ready to divide. Cells that are most vulnerable are places where cells are ready to divide anyways. That’s true in the breast also. The portion of the total breast tissue hwere there is the most cell division is Lob 1. Active undifferentiated part of breast with high proliferation rates. Present in geastest amounts between onset of puberty and first child making this the most vulnerable time. Allows the cells to differentiate further into more mature cell types called Lob 2 and Lob 3.
Increased risk in breast cancer is called proliferate breast disease: Fibroadenoma also known as a cyst. Many women have fibro adenomas and cysts int heir breast and this is why…
However if the cyst if full of cells even if they are not cancerous yet they are called atypical hyperplasia this is a significant breast cancer. Women come sin the clinic feeling alump, and mamogram looks funny. They might do a digital mamogram and then an ultrasound. If the lump is full of fluid, they say it’s a cyst don’t worry about it, but if its solid on ultrasound, they are going to biopsy it. That’s how we get clinical evaluation of breats cancer. Past history of breast cancer increases risk for another one.
Gale model: one way women can type in their personal info and get some indication of what hteir risk factors are.
Mutations:
-Formation of oncogenes and mutation of sumor suppressor genes
_Aquired p53 mutation
-BRCA inheritance
-other gene mutations.
Bottom of page. 108: Atypical hyperplasia CIS eventually leading to invasive carcinoma.
Concept of the growth factors in a little bit more detail.
The most important growth factor in breast cancer is estrogen. Required for normal breast cell function. Activation of breast cells at puberty. In neoplastic cells, estrogen stimulation results in over stimulation of growth factor reduction resulting in uncontrolled proliferation.
Estrogen receptor positive…normal cells have estrogen receptors, but if the tumor hast retained its estrogen recetpors it is at least in that way more normal. A better chacne of controlling gtumor, slower growth, and we can block the cancer with Tomoxafin and blocking estrogen synthesiis then those tumors will not progress. That implies about ….
ER negative: Autocrine sitmulation. Don’t need estrogen and don’t care about oopherectomy, tomoxifin or drugs that block estrogen synthesis. That’s when we talk about ER positive and ER negative. Progesterone receptors…tumors are more responsive and slower growing. Insulin-like growth factors don’t have much to do with insulin. All called IGFs. Alpha, beta, gamma, and play a variety in diseases.
Epidermal growth factor: Her2/neu. Treated with HERCEPTIN which blocks the Her receptors and prevents the growth promoting effects of epidermal growth factor. You will see women who are on herceptin for breast cancer.
What we do in looking at brast cancer…usually occurs in upper, outer quadrant. Retaracting and making the breast look asymmetric. Mostly will be found when it’s a little lump. Second most common place is upper, inner. If you look closely you can see that the skin is starting to look different. Regional spread is to the axillary nodes. The amount spread to the nodes is related to how big the primary tumor is. Divided into three regions that help predict prognosis. If you don’t feel nodes, that doesn’t mean that there isn’t cancer there. You have to sample the nodes to make sure they are negative for cnacer.
Sentinal node: injecting dye and watcing for it go to into the sentinal node. If the node is negative, then you are fine. Spreads to lungs, bones, brain, adrenal glands, etc…
MRI better in mammography.
Excisional biopsy
Sentinal node
PET scanning
TNM tumor nodes metastises.