NationStates Jolt Archive

My daughter just came home from the college clinic and let us know she is being tested for any number of diseases. She has had purple blotches around her ankles for several years, but lately they have been blistering. Her calves and ankles have been swelling, as well. One of the things the hematologist is looking for is the type of purpura that is present in her blood.

I've looked at WebMD and found very little. Short of going to a medical library, I'd like to find out some more information about purpura. Are there some online resources that can give me a decent description of what purpura is and how many different types there are?

Thanks.

Oh oh, me too, let me ask:

Should I go to the doctor for intermittant testicle pain and an oddly painful patch roughly around the right artery that runs along the neck (odds on lymph node swellage, but that's a guess, and I can't feel it).

I had this little patch of dry skin for a while and it flaked a bit and now it feels normal, but it's lighter than the surrounding skin. Should I be concerned about this?

Should I go to the doctor for intermittant testicle pain and an oddly painful patch roughly around the right artery that runs along the neck (odds on lymph node swellage, but that's a guess, and I can't feel it).
Oh, don't worry. Thats just the last stages of Scrotial-Cranial Placement Inversion.
I mean, it is ultimately lethal, but at this point there isn't anything anyone can do to help, so you might as well enjoy what you've got left. Oh, and if yourr ears start trickling blood, it might be for the better if you weren't within sight of any children. Emotional Scarring and all that.

Anyway, toodlepip and a nice day for you indeed.

Fass is an MD?

I had this little patch of dry skin for a while and it flaked a bit and now it feels normal, but it's lighter than the surrounding skin. Should I be concerned about this?
That is just the reptilian skin graft taking shape. Eventually that whole section will shear off and the graft will become visible. It is better if you don't seek medical help, because then we might have to kill you to keep the whole thing hush-hush.

Oh yes, and to the original poster, purpura is just a relatively minor flesh eating disease. I'm sure that it won't get any worse for sometime! And I understand that the complete internal organ liquification is (through mind rendingly painful and horrible) relatively fast. No more than 5-6 minutes.

Oh, don't worry. Thats just the last stages of Scrotial-Cranial Placement Inversion.
I mean, it is ultimately lethal, but at this point there isn't anything anyone can do to help, so you might as well enjoy what you've got left. Oh, and if yourr ears start trickling blood, it might be for the better if you weren't within sight of any children. Emotional Scarring and all that.

Anyway, toodlepip and a nice day for you indeed.
Damnit, Diet Pepsi!

Fass is an MD?
Yeah I didn't know that. I can hardly imagine that. He's a bit too young as well.

i've had a cut in my rear end that bleeds off and on... it'll bleed a bit when I do #2, maybe for a few days... then it seems to heal up.

right now there is no blood, which has put my mind at ease.

do i have a hemorrhoid?

if so, is the blood a sign of danger... or i mean as long as i'm not passing out from it is it more or less okay, so long as it heals up (again) eventually?

(it seems like i do something to tear it open, whereupon there's blood for a few days... then it seems to heal up for a while... and somehow, at some point, the cycle starts over again).

My stool is normal-looking -- not like coffee grinds, and there isn't blood in the stool itself. this blood is coming from tissue inside (near the opening of) my anus. It is bright-red, presumably arterial, blood.

(sorry, i know it sounds gross, but i've been worried about it a bit when it acts up from time to time)

I'm also somewhat worried about the opportunity for infection in the cut (when it's open), given its environment.

any advice/diagnosis would be greatly appreciated. thanks, Fass.

<snip, for the love of God!>
First of all, no one is that interested in your ass. If we were so concerned, we would say "Hey, Frangland, how is your stool today?", but no, we say, "How are you doing."
Second of all, I'd say that your ass is grass. Quite literally, in fact, as of the moment it is slowly turning into plantlife. However, the changes aren't evident on the outside until near the end of the process, until then you will see rents, and occassional greeness.
Eventually you'll have a stick up your butt and you'll start voting Republican (yes, even if you aren't in the U.S.), but that will take a while. Until then, I suggest you enjoy your last visits to the rest room and have fun analyzing your stool (apparently you enjoy doing this, but I am merely a "fyiskal doktor" not a "hed shreenkir", like Freud, so I can't officially tell you how much you want to have sex with your mother based on that) because eventually that will just get converted straight into fertillizer.

My daughter just came home from the college clinic and let us know she is being tested for any number of diseases. She has had purple blotches around her ankles for several years, but lately they have been blistering. Her calves and ankles have been swelling, as well. One of the things the hematologist is looking for is the type of purpura that is present in her blood.

I've looked at WebMD and found very little. Short of going to a medical library, I'd like to find out some more information about purpura. Are there some online resources that can give me a decent description of what purpura is and how many different types there are?

Thanks.

Ignore the abuse....

I did find this.....

http://rarediseases.about.com/cs/purpura/

Ignore the abuse....
What abuse? I am just another humble FD(Fysikal Doktor) doing my best to help those people who want medical advise from the Interweb.
I did find this.....

http://rarediseases.about.com/cs/purpura/
Lying quacks! Not only do they fail to acknowledge the fact that purplewhatsits is a flesh eating disease, but they fail to list anywhere near all the categories! What about people who have the strawberry flavour, what are they going to do?

Ignore the abuse....

I did find this.....

http://rarediseases.about.com/cs/purpura/
Thanks, I figured they were just keeping the thread current in their own ignorant manner.

Though I'm not a physician yet, I am in my last few months of medical school

Here is a website about ITP (http://uuhsc.utah.edu/healthinfo/adult/Hemat/itp.htm) or "Idiopathic Thrombocytopenic Purpura"
and here (http://www.itppeople.com/aboutitp.htm)
and here (http://www.itpsupport.org.uk/american/american_mar2001.htm) :)
and also here (http://www.mosbysdrugconsult.com/WOW/pu007.html)

Also, I didn't know Fass was a doctor :).

EDIT: Ignore my question, you said blotches not spots.

i've had a cut in my rear end that bleeds off and on... it'll bleed a bit when I do #2, maybe for a few days... then it seems to heal up.

I would worry if it stopped bleeding altogether.

My daughter just came home from the college clinic and let us know she is being tested for any number of diseases. She has had purple blotches around her ankles for several years, but lately they have been blistering. Her calves and ankles have been swelling, as well. One of the things the hematologist is looking for is the type of purpura that is present in her blood.

I hope it's nothing of consequence.

This is going to be long and split into two posts. The information has been gathered through different sources, but mainly from Robbin's "Basic Pathology," and I've added small bits here and there for explanatory purposes.

Excessive bleeding can result from increased fragility of vessels, platelet deficiency or dysfunction, derangement of coagulation, and combinations of these.

Tests used to evaluate different aspects of hemostasis (blood clotting) are the following:

* Bleeding time. This measures the time taken for a standardized skin puncture to stop bleeding and provides an in vivo (i.e. an actual patient) assessment of platelet response to limited vascular injury. The reference range depends on the actual method employed and varies from 2 to 9 minutes. Prolongation generally indicates a defect in platelet numbers or function. Bleeding time test is fraught with variability and poor reproducibility. Hence new instrument-based assay systems such as platelet function analyzer-100 (PFA-100) that provide a quantitative measure of platelet function under conditions of high shear stress are being evaluated as replacements for the bleeding time test.

* Platelet counts. These are obtained on anticoagulated blood using an electronic particle counter. The reference range is 150 to 300 × 10^3/μL. Counts well outside this range need to be confirmed by a visual inspection of a peripheral blood smear, as clumping of platelets can cause spurious "thrombocytopenia" during automated counting, and high counts may be indicative of a myeloproliferative disorder.

* Prothrombin time (PT). This assay tests the extrinsic and common coagulation pathways. The clotting of plasma after addition of an exogenous source of tissue thromboplastin (e.g., brain extract) and Ca2+ ions is measured in seconds. A prolonged PT can result from deficiency or dysfunction of factor V, factor VII, factor X, prothrombin, or fibrinogen.

* Partial thromboplastin time (PTT). This assay tests the intrinsic and common clotting pathways. The clotting of plasma after addition of kaolin, cephalin, and calcium ions is measured in seconds. Kaolin serves to activate the contact-dependent factor XII, and cephalin substitutes for platelet phospholipids. Prolongation of the PTT can be due to deficiency or dysfunction of factor V, VIII, IX, X, XI, or XII, prothrombin, or fibrinogen.

More specialized tests are available to measure the levels of specific clotting factors, fibrinogen, fibrin split products, the presence of circulating anticoagulants, and platelet function.

Bleeding disorders caused by vessel wall abnormalities

Disorders within this category, sometimes called nonthrombocytopenic purpuras, are relatively common but do not usually cause serious bleeding problems. Most often, they induce small hemorrhages (petechiae and purpura) in the skin or mucous membranes, particularly the gingivae (gums). On occasion, however, more significant hemorrhages can occur into joints, muscles, and subperiosteal ("under the bone membranes") locations or take the form of menorrhagia, nosebleeds, gastrointestinal bleeding, or hematuria. The platelet count, bleeding time, and results of the coagulation tests (PT, PTT) are usually normal.

The varied clinical conditions in which hemorrhages can be related to abnormalities in the vessel wall include the following:

* Many infections induce petechial and purpuric hemorrhages, but especially implicated are meningococcemia, other forms of septicemia, infective endocarditis, and several of the rickettsioses. The involved mechanism is presumably microbial damage to the microvasculature (vasculitis) or disseminated intravascular coagulation (DIC). Failure to recognize meningococcemia as a cause of petechiae and purpura can be catastrophic for the patient.

* Drug reactions sometimes induce cutaneous petechiae and purpura without causing thrombocytopenia. In many instances, the vascular injury is mediated by drug-induced antibodies and deposition of immune complexes in the vessel walls, leading to hypersensitivity (leukocytoclastic) vasculitis.

* Scurvy and the Ehlers-Danlos syndrome are associated with microvascular bleeding resulting from impaired formation of collagens needed for support of vessel walls. The same mechanism may account for spontaneous purpura commonly seen in the very elderly. The predisposition to skin hemorrhages in Cushing syndrome, in which the protein-wasting effects of excessive corticosteroid ("cortisone") production cause loss of perivascular supporting tissue, has a similar etiology.

* Henoch-Schönlein purpura is a systemic hypersensitivity disease of unknown cause characterized by a purpuric rash, colicky abdominal pain (presumably due to focal hemorrhages into the gastrointestinal tract), polyarthralgia, and acute glomerulonephritis. All these changes result from the deposition of circulating immune complexes within vessels throughout the body and within the glomerular mesangial regions.

* Hereditary hemorrhagic telangiectasia is an autosomal dominant disorder characterized by dilated, tortuous blood vessels with thin walls that bleed readily. Bleeding can occur anywhere in the body but is most common under the mucous membranes of the nose (epistaxis), tongue, mouth, and eyes and throughout the gastrointestinal tract.

* Amyloid infiltration of blood vessels. Systemic amyloidosis is associated with perivascular deposition of amyloid and consequent weakening of blood vessel wall. This is most commonly observed in plasma cell dyscrasias and is manifested as mucocutaneous petechiae.

Bleeding in these conditions is rarely life threatening with the exception of some cases of hereditary telangiectasia. Recognition of the presenting symptoms should prompt further studies to establish a specific diagnosis.

Bleeding related to reduced platelet number ("thrombocytopenia")

Reduction in platelet number constitutes an important cause of generalized bleeding. Normal platelet counts range from 150,000 to 300,000/μL. A count below 100,000/μL is generally considered to constitute thrombocytopenia. However, spontaneous bleeding does not become evident until the count falls below 20,000/μL. Platelet counts in the range of 20,000 to 50,000/μL can aggravate post-traumatic bleeding. Bleeding resulting from thrombocytopenia alone is associated with a prolonged bleeding time and normal PT and PTT. Thes cells are critical for hemostasis, as they form temporary plugs that quickly stop bleeding and promote key reactions in the clotting cascade. Spontaneous bleeding associated with thrombocytopenia most often involves small vessels. The common sites of such hemorrhage are the skin and the mucous membranes of the gastrointestinal and genitourinary tracts. Intracranial bleeding is a threat to any patient with a markedly depressed platelet count.

The many causes of thrombocytopenia can be classified into the four major categories:

* Decreased production of platelets. This can accompany generalized diseases of bone marrow such as aplastic anemia and leukemias or result from diseases that affect the megakaryocytes (the cells that give rise to platelets) somewhat selectively. In vitamin B12 or folic acid deficiency, there is poor development and accelerated destruction of megakaryocytes within the bone marrow (ineffective megakaryopoiesis) because DNA synthesis is impaired.

* Decreased platelet survival. This important cause of thrombocytopenia can have an immunologic or nonimmunologic etiology. In the immune conditions, platelet destruction is caused by circulating antiplatelet antibodies or, less often, immune complexes. The antiplatelet antibodies can be directed against a self-antigen on the platelets (autoantibodies) or against platelet antigens that differ among different individuals (alloantibodies). Common antigenic targets of both autoantibodies and alloantibodies are the platelet membrane glycoprotein complexes IIb-IIIa and Ib-IX. Autoimmune thrombocytopenias include idiopathic thrombocytopenic purpura, certain drug-induced thrombocytopenias, and HIV-associated thrombocytopenias. Alloimmune thrombocytopenias arise when an individual is exposed to platelets of another person, as may occur after blood transfusion or during pregnancy.

Nonimmunologic destruction of platelets may be caused by mechanical injury, in a manner analogous to red cell destruction in microangiopathic hemolytic anemia. The underlying conditions are also similar, including prosthetic heart valves and diffuse narrowing of the microvessels (e.g., malignant hypertension).

* Sequestration. Thrombocytopenia, usually moderate in severity, may develop in any patient with marked splenomegaly, a condition sometimes referred to as hypersplenism. The spleen normally sequesters 30% to 40% of the body's platelets, which remain in equilibrium with the circulating pool. When necessary, hypersplenic thrombocytopenia can be ameliorated by splenectomy.

* Dilutional. Massive transfusions can produce a dilutional thrombocytopenia. Blood stored for longer than 24 hours contains virtually no viable platelets; thus, plasma volume and red cell mass are reconstituted by transfusion, but the number of circulating platelets is relatively reduced.

Immune Thrombocytopenic Purpura (ITP)

ITP can occur in the setting of a variety of conditions and exposures (secondary ITP) or in the absence of any known risk factors (primary or idiopathic ITP). There are two clinical subtypes of primary ITP, acute and chronic; both are autoimmune disorders in which platelet destruction results from the formation of antiplatelet autoantibodies.

Immunologically mediated destruction of platelets (immune thrombocytopenia) occurs in many different settings, including systemic lupus erythematosus, acquired immunodeficiency syndrome (AIDS), after viral infections, and as a complication of drug therapy. These secondary forms of immune thrombocytopenia can sometimes mimic the idiopathic autoimmune variety, and hence the diagnosis of this disorder should be made only after exclusion of other known causes of thrombocytopenia. Particularly important in this regard is systemic lupus erythematosus, a multisystem autoimmune disease that can present with thrombocytopenia.

Chronic ITP is caused by the formation of autoantibodies against platelet membrane glycoproteins, most often IIb-IIIa or Ib-IX. Antibodies reactive with these membrane glycoproteins can be demonstrated in the plasma as well as bound to the platelet surface (platelet-associated immunoglobulins) in approximately 80% of patients. In the overwhelming majority of cases, the antiplatelet antibodies are of the IgG class.

The mechanism of platelet destruction is similar to that seen in autoimmune hemolytic anemias. Opsonized ("coated with antibodies/complement factors") platelets are rendered susceptible to phagocytosis ("ingestion") by the cells of the mononuclear phagocyte system. About 75% to 80% of patients are remarkably improved after splenectomy, indicating that the spleen is the major site of removal of sensitized platelets. Since it is also an important site of autoantibody synthesis, the beneficial effects of splenectomy may in part derive from removal of the source of autoantibodies. Although destruction of sensitized platelets is the major mechanism responsible for thrombocytopenia, there is some evidence that megakaryocytes may be damaged by autoantibodies, leading to impairment of platelet production. In most cases, however, megakaryocyte injury is not significant enough to deplete their numbers.

Chronic ITP occurs most commonly in adult women younger than age 40 years. The female-to-male ratio is 3:1. This disorder is often insidious in onset and is characterized by bleeding into the skin and mucosal surfaces. Cutaneous bleeding is seen in the form of pinpoint hemorrhages (petechiae), especially prominent in the dependent areas where the capillary pressure is higher. Petechiae can become confluent, giving rise to ecchymoses. Often there is a history of easy bruising, nosebleeds, bleeding from the gums, and hemorrhages into soft tissues from relatively minor trauma. The disease may manifest first with melena ("blood in the stool"), hematuria, or excessive menstrual flow. Subarachnoid hemorrhage and intracerebral hemorrhage are serious consequences of thrombocytopenic purpura but, fortunately, are rare in treated patients. Splenomegaly and lymphadenopathy are uncommon in primary ITP, and their presence should lead one to consider other possible diagnoses.

The clinical signs and symptoms associated with ITP are not specific for this condition but rather reflective of thrombocytopenia. Destruction of platelets as the cause of thrombocytopenia is supported by the findings of a low platelet count and normal or increased megakaryocytes in the bone marrow. Accelerated thrombopoiesis often leads to the formation of abnormally large platelets (megathrombocytes), detected easily in a blood smear. The bleeding time is prolonged, but PT and PTT are normal. Tests for platelet autoantibodies are not widely available. Therefore, a diagnosis of ITP should be made only after other causes of platelet deficiencies have been ruled out.

Almost all patients respond to immunosuppressive doses of glucocorticoids, but many eventually relapse and come to splenectomy. Most maintain safe platelet counts postsplenectomy and require no further therapy. A significant minority, however, have refractory forms of ITP that can be very difficult to treat. Various immunosuppressive approaches may be effective in such patients.

Acute Immune Thrombocytopenic Purpura

Like chronic ITP, this condition is caused by antiplatelet autoantibodies, but its clinical features and course are distinct. Acute ITP is a disease of childhood occurring with equal frequency in both sexes. The onset of thrombocytopenia is abrupt and is preceded in many cases by a viral illness. The usual interval between the infection and onset of purpura is 2 weeks. Unlike the adult chronic form of ITP, the childhood disease is self-limited, usually resolving spontaneously within 6 months. Steroid therapy is indicated only if thrombocytopenia is severe. Approximately 20% of the children, usually those without a viral prodrome, have persistent low platelet counts beyond 6 months and appear to have chronic ITP similar in most respects to the adult disease.

Drug-Induced Thrombocytopenia: Heparin-Induced Thrombocytopenia

Like hemolytic anemia, thrombocytopenia can result from immunologically mediated destruction of platelets after drug ingestion. The drugs most commonly involved are quinine, quinidine, sulfonamide antibiotics, and heparin. Heparin-induced thrombocytopenia (HIT) is of particular importance because this anticoagulant is used widely and failure to make a correct diagnosis can have severe consequences. Thrombocytopenia occurs in approximately 5% of patients receiving heparin. Most develop so-called type I thrombocytopenia, which occurs rapidly after onset of therapy, is modest in severity and clinically insignificant, and may resolve despite continuation of heparin therapy. It most likely results from a direct platelet-aggregating effect of heparin.

Type II thrombocytopenia is more severe. It occurs 5 to 14 days after commencement of therapy (or sometimes sooner if the patient has been previously sensitized to heparin) and can, paradoxically, lead to life-threatening venous and arterial thrombosis. HIT is caused by an immune reaction directed against a complex of heparin and platelet factor 4, a normal component of platelet granules that binds tightly to heparin. It appears that heparin binding modifies the conformation of platelet factor 4, making it susceptible to immune recognition. Binding of antibody to platelet factor 4 produces immune complexes that activate platelets, promoting thrombosis even in the setting of marked thrombocytopenia. The mechanism of platelet activation is not understood. Unless therapy is immediately discontinued, clots within large arteries may lead to vascular insufficiency and limb loss, and emboli from deep venous thrombosis can cause fatal pulmonary thromboembolism.

HIV-Associated Thrombocytopenia

Thrombocytopenia is perhaps the most common hematologic manifestation of HIV infection. Both impaired platelet production and increased destruction are responsible. CD4, the receptor for HIV on T cells, has also been demonstrated on megakaryocytes, making it possible for these cells to be infected by HIV. Infected megakaryocytes are prone to apoptosis ("cell death") and are impaired in terms of platelet production. HIV infection also causes hyperplasia and dysregulation of B cells, which predispose to the development of immune-mediated thrombocytopenia. Antibodies directed against platelet membrane glycoprotein IIb-III complexes are detected in some patients' sera. These autoantibodies, which sometimes cross-react with HIV-associated gp120, are believed to act as opsonins, thus promoting the phagocytosis of platelets by splenic phagocytes. Some studies also implicate nonspecific deposition of immune complexes on platelets as a factor in their premature destruction by the mononuclear phagocyte system.

Thrombotic Microangiopathies: Thrombotic Thrombocytopenic Purpura (TTP) and Hemolytic-Uremic Syndrome (HUS)

The term thrombotic microangiopathy encompasses a spectrum of clinical syndromes that includes TTP and HUS. TTP, as originally defined, is associated with the pentad of fever, thrombocytopenia, microangiopathic hemolytic anemia, transient neurologic deficits, and renal failure. HUS is also associated with microangiopathic hemolytic anemia and thrombocytopenia but is distinguished from TTP by the absence of neurologic symptoms, the prominence of acute renal failure, and frequent affliction of children. Recent studies, however, have tended to blur these clinical distinctions. Many adult patients with "TTP" lack one or more of the five criteria, and some patients with "HUS" have fever and neurologic dysfunction. The common fundamental feature in both of these conditions is widespread formation of hyaline thrombi, comprised primarily of platelet aggregates, in the microcirculation. Consumption of platelets leads to thrombocytopenia, and the intravascular thrombi provide a likely mechanism for the microangiopathic hemolytic anemia and widespread organ dysfunction. It is believed the varied clinical manifestations of TTP and HUS are related to differing proclivities for thrombus formation in specific microvascular beds.

For many years, the pathogenesis of TTP was enigmatic, although treatment with plasma exchange (initiated in the early 1970s) changed an almost uniformly fatal condition into one that is successfully treated in more than 80% of cases. Recently, the underlying cause of many, but not all, cases of TTP has been elucidated. In brief, symptomatic patients are often deficient in an enzyme called ADAMTS 13. This enzyme is designated "vWF metalloprotease" and it normally degrades very high molecular weight multimers of von Willebrand factor (vWF). In the absence of this enzyme, very high molecular weight multimers of vWF accumulate in plasma and, under some circumstances, promote platelet microaggregate formation throughout the microcirculation, leading to the symptoms of TTP. Superimposition of endothelial cell injury (caused by some other condition) may further predispose a patient to microaggregate formation, thus initiating or exacerbating clinically evident TTP.

The deficiency of ADAMTS 13 may be inherited or acquired. In many patients an antibody that inhibits vWF metalloprotease is detected. Much less commonly the patients have inherited an inactivating mutation in the gene encoding this enzyme. Despite these advances, it is clear that factors other than vWF metalloprotease deficiency must be involved in triggering full-blown TTP, because symptoms are episodic even in those with hereditary deficiency of vWF metalloprotease. It is important to consider the possibility of TTP in any patient presenting with thrombocytopenia and microangiopathic hemolytic anemia, as any delay in diagnosis and treatment can be fatal. Plasma exchange can be life saving by providing the missing enzyme.

In contrast to TTP, most patients with HUS have normal levels of vWF metalloprotease, indicating that HUS usually has a different pathogenesis. One important cause of HUS in children and the elderly is infectious gastroenteritis caused by E. coli strain 0157:H7.60 This strain elaborates a Shiga-like toxin that is absorbed from the inflamed gastrointestinal mucosa. It binds to and damages endothelial cells in the glomerulus and elsewhere, thus initiating platelet activation and aggregation. Affected children present with bloody diarrhea, and a few days later HUS makes its appearance. With appropriate supportive care, affected children often recover completely, but irreversible renal damage and death can occur in more severe cases. HUS can also be seen in adults following exposures that damage endothelial cells (e.g., certain drugs, radiation therapy). The prognosis of adults with HUS is guarded, as it is most often seen in the setting of other chronic, life-threatening conditions.

While DIC and thrombotic microangiopathies share features such as microvascular occlusion and microangiopathic hemolytic anemia, they are pathogenetically distinct. In TTP and HUS (unlike DIC), activation of the coagulation cascade is not of primary importance, and hence results of laboratory tests of coagulation, such as PT and PTT, are usually normal.

Bleeding disorders related to defective platelet functions

Qualitative defects of platelet function can be congenital or acquired. Several congenital disorders characterized by prolonged bleeding time and normal platelet count have been described. A brief discussion of these rare diseases is warranted by the fact that they provide excellent models for investigating the molecular mechanisms of platelet function.

Congenital disorders of platelet function can be classified into three groups on the basis of the specific functional abnormality: defects of adhesion, defects of aggregation, and disorders of platelet secretion (release reaction).

* Bleeding resulting from defective adhesion of platelets to subendothelial matrix is best illustrated by the autosomal recessive disorder Bernard-Soulier syndrome, which is caused by an inherited deficiency of the platelet membrane glycoprotein complex Ib-IX. This glycoprotein is a receptor for vWF and is essential for normal platelet adhesion to subendothelial matrix.

* Bleeding due to defective platelet aggregation is exemplified by Glanzmann's thrombasthenia, which is also transmitted as an autosomal recessive trait. Thrombasthenic platelets fail to aggregate in response to adenosine diphosphate (ADP), collagen, epinephrineView drug information, or thrombinView drug information owing to deficiency or dysfunction of glycoprotein IIb-IIIa, a protein complex that participates in the formation of "bridges" between platelets by binding fibrinogen and vWF.

* Disorders of platelet secretion are characterized by normal initial aggregation with collagen or ADP, but subsequent responses, such as secretion of thromboxanes and release of granule-bound ADP, are impaired. The underlying biochemical defects of these so-called storage pool disorders are varied, complex, and not all that relevant here.

Among the acquired defects of platelet function, two are clinically significant. The first is ingestion of aspirin and other nonsteroidal anti-inflammatory drugs, which significantly prolongs the bleeding time. Aspirin is a potent, irreversible inhibitor of the enzyme cyclooxygenase, which is required for the synthesis of thromboxane A2 and prostaglandins. These mediators play important roles in platelet aggregation and subsequent release reactions. The antiplatelet effects of aspirin form the basis for its use in the prophylaxis of thrombosis. Uremia is the second condition exemplifying an acquired defect in platelet function. Although the pathogenesis of bleeding in uremia is complex and not fully understood, several abnormalities of platelet function are found.

And then there are different kinds of hemophilias, but those are complex, but also easily googled, so I omit them here.

Hope this is of service.

Though I'm not a physician yet, I am in my last few months of medical school.

Also, I didn't know Fass was a doctor :)

Nope, I'm not a doctor. Myrmydonisia must have misunderstood. I'm in med school, so that may be where he got it from. Anyway, he's got a tonne of reading to do and some excellent links to follow, so I think we can be happy that we were all so eager to supply information.

Nope, I'm not a doctor. Myrmydonisia must have misunderstood. I'm in med school, so that may be where he got it from. Anyway, he's got a tonne of reading to do and some excellent links to follow, so I think we can be happy that we were all so eager to supply information.

What year are you in?

What year are you in?

Things work differently here and we don't count it in years, but semesters, so even if I converted it, it would tell you very little. We can say I'm all done with pre-med and the theoretical part of the basic education, am a year or so into the clinical part of it.

Things work differently here and we don't count it in years, but semesters, so even if I converted it, it would tell you very little. We can say I'm all done with pre-med and am a year or so into the clinical part of the education.

Ahhh, so you're technically a year and a half ahead of me :) Lucky.

Ahhh, so you're technically a year and a half ahead of me :) Lucky.

I don't know if I'm that lucky, but, you know, it's taken work. ;)

I don't know if I'm that lucky, but, you know, it's taken work. ;)

I still consider you lucky, these last few months are going to be killers, I just want it to be over with....

I still consider you lucky, these last few months are going to be killers, I just want it to be over with....

Oh, don't remind me! My last exam covered an entire semester (twenty weeks) + bits and pieces from all the previous semesters. I sat for like sex-seven hours writing it and I just don't want to go to that mental place again.

Oh, don't remind me! My last exam covered an entire semester (twenty weeks) + bits and pieces from all the previous semesters. I sat for like sex-seven hours writing it and I just don't want to go to that mental place again.

I just took the first of something like....25 exams/quizzes in my "parasitology and tropical medicine" class, THATS not something I want to think about ever again, haha.

The quiz consisted of slides of microscopic parasites along with a description "A colleague send you a fecal sample...."

Hooray! I get to dig through Dr. ______ fecal sample! Haha...

I just took the first of something like....25 exams/quizzes in my "parasitology and tropical medicine" class, THATS not something I want to think about ever again, haha.

The quiz consisted of slides of microscopic parasites along with a description "A colleague send you a fecal sample...."

Hooray! I get to dig through Dr. ______ fecal sample! Haha...

Hah. I hated those parts and I hated the samples and I hated the bloody annoying names for it all. "Schistosomiasis," "trypanosomiasis," "trychomoniasis," "ochorcersiasis," "entamoeba histlytica," "diphyllobothrium latum," "dracunculus medinensis".... *gaah!* And the thing is, we almost never get any serious parasites here, so it's a real struggle to keep all that stuff fresh in your memory. It slips away so easily.

Hah. I hated those parts and I hated the samples and I hated the bloody annoying names for it all. "Schistosomiasis," "trypanosomiasis," "trychomoniasis," "ochorcersiasis," "entamoeba histlytica," "diphyllobothrium latum," "dracunculus medinensis".... *gaah!* And the thing is, we almost never get any serious parasites here, so it's a real struggle to keep all that stuff fresh in your memory. It slips away so easily.

Memorize....forget....memorize....forget :)

Hah. I hated those parts and I hated the samples and I hated the bloody annoying names for it all. "Schistosomiasis," "trypanosomiasis," "trychomoniasis," "ochorcersiasis," "entamoeba histlytica," "diphyllobothrium latum," "dracunculus medinensis".... *gaah!* And the thing is, we almost never get any serious parasites here, so it's a real struggle to keep all that stuff fresh in your memory. It slips away so easily.
And I liked all that stuff when I was studying medicine. :rolleyes:

I declare Fass the Official NS General Medical resource.

And I liked all that stuff when I was studying medicine. :rolleyes:

Well we can't all like everything, can we? I just hope it is of more use to you. :)

Well we can't all like everything, can we? I just hope it is of more use to you. :)
Actually, no. I reckon that parasites are more of a problem in Russia than in Sweden, but I am a gynaecologist in IVF business. :)

I declare Fass the Official NS General Medical resource.

No, no, Olantia would be much more deserving of that.

Actually, no. I reckon that parasites are more of a problem in Russia than in Sweden, but I am a gynaecologist in IVF business. :)

Well, I guess you might encounter trichomoniasis once in a blue moon, even if you're into the turkey basting side of it all. :p

Well, I guess you might encounter trichomoniasis once in a blue moon, even if you're into the turkey basting side of it all. :p
Yeah, certainly, but thankfully not helmints. :)

My colleague at medical school had an echinococcal cyst in her brain, though...

No, no, Olantia would be much more deserving of that.

You should definately do it, I hear they give you a cute little shirt to wear and everything ;) I'm sure you'd look just fabulous in a shirt with "Offical NS General Medical Resource" on it :)!

You should definately do it, I hear they give you a cute little shirt to wear and everything ;) I'm sure you'd look just fabulous in a shirt with "Offical NS General Medical Resource" on it :)!
Yeah, I vote for Fass too! :)

In any case I have a thesis to write in order to get a Russian equivalent of master's degree, and I am not a frequent poster on NS. :)

Yeah, certainly, but thankfully not helmints. :)

I shudder at the thought of vaginal worms! *ugh* It's such a creepy part of medicine. That's why I dislike it so much; few things make me queezy, but this seriously tests me.

My colleague at medical school had an echinococcal cyst in her brain, though...

:eek:

Echinococcus granulosus. Do I need to mention why I don't have pets? Not that I'd have a sheep-herding dog or anything... ;) Was she alright in the end? That's some serious stuff.

...

Echinococcus granulosus. Do I need to mention why I don't have pets? Not that I'd have a sheep-herding dog or anything... ;) Was she alright in the end? That's some serious stuff.
The cyst was removed successfully. But she still had to drop out, and later she went to another medical school.

:eek:

Echinococcus granulosus. Do I need to mention why I don't have pets? Not that I'd have a sheep-herding dog or anything... ;) Was she alright in the end? That's some serious stuff.

I shudder to think of the situation in which she contracted the worm to begin with!

The cyst was removed successfully. But she still had to drop out, and later she went to another medical school.

Thank goodness.

I shudder to think of the situation in which she contracted the worm to begin with!

I try to hope in the best in people, so it was probably something completely innocent. I mean, contaminated food perhaps? Or uncareful handling of animal feces? Poor hand hygiene?

For the uneducated, what exactly is Echinococcus granulosus?

I shudder to think of the situation in which she contracted the worm to begin with!
Well, she contacted with farm dogs during our summmer break, and echinococcosis is a not unheard-of thng there. Poor hygiene, perhaps.

For the uneducated, what exactly is Echinococcus granulosus?

Here is a short page with pics. (http://www.biosci.ohio-state.edu/~parasite/echinococcus.html)

For the uneducated, what exactly is Echinococcus granulosus?
To put it simple? A tapeworm that infects mostly dogs. Unfortunately, not only sheep and the like, but also humans can be intermediate hosts. Instead of tapeworm they get a cyst, sometimes a very big one, in which new worms develop.

Oh, and here's the Wikipedia link: http://en.wikipedia.org/wiki/Echinococcus_granulosus

Thank goodness.
I try to hope in the best in people, so it was probably something completely innocent. I mean, contaminated food perhaps? Or uncareful handling of animal feces? Poor hand hygiene?

Food contaminated with.....not a happy thought :).

Here is a short page with pics. (http://www.biosci.ohio-state.edu/~parasite/echinococcus.html)

Damn. That's one nasty ass parasite.

Sorta wants to make me change my major.

Food contaminated with.....not a happy thought :).

Well, if you look to the fecal-oral route, there's never that much happiness, regardless of organism.

Sorta wants to make me change my major.

Which is?

Which is?

Pre-med. Lowly Freshman (First Year), though.

Damn. That's one nasty ass parasite.

Sorta wants to make me change my major.
Alveococcosis is worse... It occurs only in Russia and Japan, if I'm not mistaken, though.

Well, if you look to the fecal-oral route, there's never that much happiness, regardless of organism.

This is true....

And now I'm off to bed, oh what sweet dreams I'll have! Haha...

Alveococcosis is worse... It occurs only in Russia and Japan, if I'm not mistaken, though.

I looked it up, and according to "Medical Microbiology" (Murrey et al.) it's also found in "northern areas" such as Canada, Central Europe, Alaska, Montana, the two Dakotas, Minnesota and Iowa.

I looked it up, and according to "Medical Microbiology" (Murrey et al.) it's also found in "northern areas" such as Canada, Central Europe, Alaska, Montana, the two Dakotas, Minnesota and Iowa.
Thanks... my information was from the 1970s Soviet book; I gather that the worm has been found in many territories since then.

Never thought to find a medical school here...as a german MD, does anyone know about a disease called "aztecs´s ear"? It´s in ICD 10, Q17.3, but up to now nobody could explain it :p

And yes, we have rare cases of alveococcosis, too (northern germany)

Nope, I'm not a doctor. Myrmydonisia must have misunderstood. I'm in med school, so that may be where he got it from. Anyway, he's got a tonne of reading to do and some excellent links to follow, so I think we can be happy that we were all so eager to supply information.
I appreciate the information that you posted earlier. That outdid my expectations by a large margin. I knew you had some medical experience, MD or not, it's close enough for my purposes.

Thanks again to you, Fass, for your scholarly efforts, and to the others for posting the links to ITP and rarediseases.org.

Oh, don't remind me! My last exam covered an entire semester (twenty weeks) + bits and pieces from all the previous semesters. I sat for like sex-seven hours writing it and I just don't want to go to that mental place again.
I remember exam time. The qualifiers for my Physics degree were written and oral. The written part was something close to the history of Physics and the oral part was like trivial pursuit. My thesis defense went a lot better, but was a couple of the longest hours I've ever spent.