減數分裂 MEIOSIS

Heparin and its low molecular weight derivatives (e.g. enoxaparin, dalteparin, tinzaparin) are effective at preventing deep vein thromboses and pulmonary emboli in patients at risk,^[11][12]but there is no evidence that any one is more effective than the other in preventing mortality.^[13] Heparin binds to the enzyme inhibitor antithrombin III (AT) causing a conformational change that results in its activation through an increase in the flexibility of its reactive site loop.^[14] The activated AT then inactivates thrombin and other proteases involved in blood clotting, most notably factor Xa. The rate of inactivation of these proteases by AT can increase by up to 1000-fold due to the binding of heparin.^[15]

HEPARIN = ANTITHROMBIN ACTIVATE

Warfarin inhibits the vitamin K-dependent synthesis of biologically active forms of the calcium-dependent clotting factors II, VII, IX and X, as well as the regulatory factors protein C, protein S, and protein Z.^[2][42] Other proteins not involved in blood clotting, such as osteocalcin, or matrix Gla protein, may also be affected.

Condition	Prothrombin time	Partial thromboplastin time	Bleeding time	Platelet count
Vitamin K deficiency or warfarin	prolonged	prolonged	unaffected	unaffected
Disseminated intravascular coagulation	prolonged	prolonged	prolonged	decreased
Von Willebrand disease	unaffected	prolonged	prolonged	unaffected
Haemophilia	unaffected	prolonged	unaffected	unaffected
Aspirin	unaffected	unaffected	prolonged	unaffected
Thrombocytopenia	unaffected	unaffected	prolonged	decreased
Early Liver failure	prolonged	unaffected	unaffected	unaffected
End-stage Liver failure	prolonged	prolonged	prolonged	decreased
Uremia	unaffected	unaffected	prolonged	unaffected
Congenital afibrinogenemia	prolonged	prolonged	prolonged	unaffected
Factor V deficiency	prolonged	prolonged	unaffected	unaffected
Factor X deficiency as seen in amyloid purpura	prolonged	prolonged	unaffected	unaffected
Glanzmann's thrombasthenia	unaffected	unaffected	prolonged	unaffected
Bernard-Soulier syndrome	unaffected	unaffected	prolonged	decreased

Diazoxide is used as a vasodilator in the treatment of acute hypertension or malignant hypertension.^[2

CAN CAUSE MOST REFLEX TACHY

Mechanism of action

Metoclopramide was first described by Dr. Louis Justin-Besançon and C. Laville in 1964.^[6] It appears to bind to dopamine D₂ receptors where it is a receptor antagonist, and is also a mixed 5-HT₃ receptor antagonist/5-HT₄ receptor agonist.

The anti-emetic action of metoclopramide is due to its antagonist activity at D₂ receptors in the chemoreceptor trigger zone (CTZ) in the central nervous system (CNS)—this action prevents nausea and vomiting triggered by most stimuli.^[7] At higher doses, 5-HT₃ antagonist activity may also contribute to the anti-emetic effect.

The gastroprokinetic activity of metoclopramide is mediated by muscarinic activity, D₂ receptor antagonist activity and 5-HT₄ receptor agonist activity.^[8][9] The gastroprokinetic effect itself may also contribute to the anti-emetic effect.

72 使用下列那一類治療憂鬱症的藥物時，必須限制含乳酪食品的攝取，否則會引起血壓上升的危險？

 Fluoxetine  Imipramine  Bupropion  Tranylcypromine

ANS D

Foods high in endogenous monoamine precursors or exogenous monoamine compounds may cause adverse reactions. The most common example of this, is the hypertensive crisiscaused by the ingestion of tyramine, which is found in foods like aged cheeses, cured meats, tofu and certain red wines. Some, such as yeast extracts, contain enough tyramine to be potentially fatal in a single serving. Spoiled food is also likely to contain dangerous levels of tyramine.

Tranylcypromine (Parnate, Jatrosom) is a drug of the substituted phenethylamine and amphetamine classes which acts as amonoamine oxidase inhibitor (MAOI)—it is a non-selective and irreversible inhibitor of the enzyme monoamine oxidase (MAO).^[1][2] It is used as an antidepressant and anxiolytic agent in the clinical treatment of mood and anxiety disorders, respectively.

：毒蕈素性受體阻斷作用: MUSCARINIC RECEPTOR BLOCKER

• Use of NSAIDs or drugs with anticholinergic properties.THIS CAUSE URINE RETENTION

73 下列有關治療類精神疾病藥物所產生之副作用及其作用可能機制的配對，何者錯誤？

體重增加：組織胺及血清素受體阻斷作用直立型低血壓：乙型腎上腺素性受體阻斷作用

錐體外毒性症狀：多巴胺受體阻斷作用口乾及尿液滯留：毒蕈素性受體阻斷作用

ANS D

Ras point mutations are the single most common abnormality of human proto-oncogenes.^[

Goodpasture’s syndrome (also known as Goodpasture’s disease and anti-glomerular basement antibody disease) is a rare disease characterized by glomerulonephritis and hemorrhaging of the lungs.^[1] Although many diseases can present with these symptoms, the name Goodpasture’s syndrome is usually reserved for the autoimmune disease triggered when the patient’s immune system attacks Goodpasture antigen (a type II hypersensitivity reaction^[2]), which is found in the kidney and lung, and in time, causing damage to these organs. The disease bears the name of the American pathologist Dr. Ernest Goodpasture of Vanderbilt University, whose 1919 description is regarded as the first report on the existence of the condition.^[3][4]

The GBM antigen responsible for this disease is a component of the non-collagenous domain (NC1) of the alpha-3 chain of collagen type IV.

Malakoplakia

From Wikipedia, the free encyclopedia

Malakoplakia
Classification and external resources
Micrograph showing the characteristic finding of malakoplakia (Michaelis-Gutmann bodies). H&E stain.
DiseasesDB	29128
eMedicine	derm/872
MeSH	D008287

Malakoplakia is a rare inflammatory condition which makes its presence known as a papule, plaque or ulceration that usually affects thegenitourinary tract.^[1]:274 However, it may also be associated with other bodily organs. It was initially described in the early 1900s as soft yellowish plaques found on the mucosa of the urinary bladder. Microscopically it is characterized by the presence of foamy histiocyteswith basophilic inclusions called Michaelis-Gutmann bodies.

It usually involves gram negative bacteria.^[2]

[edit]Causes

Malakoplakia is thought to result from the insufficient killing of bacteria by macrophages. Therefore, the partially digested bacteria accumulate in macrophages and leads to a deposition of iron and calcium. The impairment of bactericidal activity manifests itself as the formation of an ulcer, plaque or papule.

Malakoplakia is associated with patients with a history of immunosuppression due to lymphoma, diabetes mellitus, renal transplantation, or because of long-term therapy with systemic corticosteroids.