2008年12月29日 星期一

phrase

discharge:
按時依照醫囑服藥.
定期門診追蹤治療.

2008年12月28日 星期日

AEIOU tips

Mental:
AEIOU TIPS
A - alcohol, anoxia
E - epilepsy
I - insulin (diabetes)
O - overdose
U - uremia, underdose

T- trauma
I - infection
P - psychiatric
S - stroke (cardiovascular)

Alcohol
Epilepsy
Insulin
Overdose
Uremia (and other metabolic causes)

Trauma
Infection
Psychiatric
Stroke


Altered Mental Status
"AEIOU TIPS"
Alcohol/drugsEndocrineInsulinOpiatesUremia

Toxins/traumaInfectionsPsych/porhyriaSAH, shock, stroke, seizure, space occupying lesion

DM treatment


Sulfonylureas are time-honored insulin secretagogues (ie, oral hypoglycemic agents) and probably have the greatest efficacy for glycemic lowering of any of the oral agents. The UKPDS confirmed their safety after years of suspicion from the University Group Diabetes Program (UGDP).
Glipizide (Glucotrol, Glucotrol XL)
Second-generation Sulfonylureas. More potent and exhibits fewer drug interactions than first-generation agents. May cause more physiologic insulin release with less risk for hypoglycemia and weight gain than other sulfonylureas.
Considerable debate exists regarding the best initial oral therapy for patients with type 2 diabetes mellitus. Based on the results of the UKPDS and safety record, patients who are obese (120% ideal body weight) should be started on metformin initially, titrated to at least 2000 mg/d administered in divided doses (during or after meals to reduce gastrointestinal side effects). Patients who are markedly symptomatic may be treated with an insulin secretagogue initially to rapidly alleviate symptoms and then perhaps switched to other agents. Patients with near-normal weight may be treated with sulfonylureas or metformin initially. Short-acting insulin secretagogues (eg, repaglinide, nateglinide) can be used in patients unusually predisposed to hypoglycemia.

Failure of initial therapy usually should result in addition of another class of drug rather than substitution (reserve substitution for intolerance to a drug due to adverse effects). Considerable debate exists regarding second agents added to (or used initially in conjunction with) metformin. The time-honored approach is to add an insulin secretagogue (usually titrated to no more than the half-maximal approved dose to reduce risk for hypoglycemia). However, some experts recommend a glitazone because of the positive effects of these drugs on inflammation and the vasculature. If this strategy is used, a moderate dose of glitazone (as opposed to the highest approved dose) should be used. A therapeutic scheme utilized by the author is listed in Image 11.

The author usually only uses glitazones in cases of metformin intolerance or contraindication because of the side effects of weight gain and edema seen not infrequently with glitazones. Exceptions to the practice might include patients with marked insulin resistance of relatively normal weight, such as patients of Asian heritage. If an insulin secretagogue is being taken by the patient prior to adding a second agent, the patient should be warned about the possibility of inducing hypoglycemia when another agent is added. In such cases, the insulin secretagogue, not the newly added agent, should be reduced.



From: http://emedicine.medscape.com/article/117853-treatment
Emedicine: Diabetes Mellitus, Type 2: Treatment & Medication

2008年12月26日 星期五

High P LOW Ca

A potential complication of calcium therapy is that absorption of some of the administered calcium may promote the development of coronary arterial calcification, which is postulated to be associated with coronary atherosclerosis [34,35]. To help decrease this possibility, the working group for the K/DOQI guidelines suggest that the total dose of elemental calcium (including dietary sources) should not exceed 2000 mg/day [21]. In addition, with the recommended upper limit of plasma calcium of 9.5 mg/dL (2.35 mmol/L), the amount of elemental calcium is usually also reduced to no more than 1500 mg/day. Even these doses of calcium result in positive calcium balance in the setting of vitamin D therapy, which may have untoward long-term consequences. (See "Active vitamin D analogs and calcimimetics to control hyperparathyroidism in chronic kidney disease" and see "Vascular calcification in chronic kidney disease").

2008年12月22日 星期一

cva artery

GCS:http://en.wikipedia.org/wiki/Glasgow_Coma_Scale

NE: http://medinfo.ufl.edu/other/opeta/neuro/NE_main.html
http://www.stroke.org.tw/guideline/guideline_index.asp

ml=widht1(cm) * width2(cm) * cut number / 2
mca=butterfly wings lateral, aca=mercedes anterior(supraventricle more), pca=mercedes 2 legs


When blood pressure control is necessary, the use of vasodilators such as nitroprusside or nitroglycerin should be avoided because of their propensity to increase cerebral blood volume and therefore intracranial pressure. Labetalol is preferred.
Nimodipine — The calcium channel blocker nimodipine was initially used in patients with SAH to prevent vasospasm. (See "Prevention of vasospasm" below). However, despite the vasodilatory effects of nimodipine on cerebral vessels, there is no convincing evidence that nimodipine affects the incidence of either angiographic or symptomatic vasospasm.

Nimodipine is marketed as a cerebral selective drug
































































Artery involvedSyndromePathophysiology
Anterior cerebral artery

Motor and/or sensory deficit (foot >> face, arm)




Grasp, sucking reflexes




Abulia, paratonic rigidity, gait apraxia

Embolic > atherothrombotic
Middle cerebral artery

Dominant hemisphere: aphasia, motor
and sensory deficit (face, arm >leg >foot), may be complete
hemiplegia if internal capsule involved, homonymous hemianopia.




Non-dominant hemisphere: neglect, anosognosia, motor and sensory deficit (face, arm > leg>foot), homonymous hemianopia.

Embolic > atherothrombotic
Posterior cerebral arteryHomonymous hemianopia; alexia without agraphia (dominant
hemisphere); visual hallucinations, visual perseverations (calcarine
cortex); sensory loss, choreoathetosis, spontaneous pain (thalamus);
III nerve palsy, paresis of vertical eye movement, motor deficit
(cerebral peduncle, midbrain).
Embolic > atherothrombotic
Penetrating vessels

Pure motor hemiparesis (classic lacunar syndromes)




Pure sensory deficit




Pure sensory-motor deficit




Hemiparesis, homolateral ataxia




Dysarthria/clumsy hand

Small artery (lacunar) infarct
Vertebrobasilar

Cranial nerve palsies




Crossed sensory deficits




Diplopia, dizziness, nausea, vomiting, dysarthria, dysphagia, hiccup




Limp and gait ataxia




Motory deficit




Coma




Bilateral signs suggest basilar artery disease.

Embolic = atherothrombotic
Internal carotid arteryProgressive or stuttering onset of MCA syndrome, occasionally ACA syndrome as well if insufficient collateral flow.Atherothrombotic > embolic

2008年12月8日 星期一

Cancer Pain

Step-Up of analgesics by WHO
First step: Acetaminophen
Second step: NSAID (careful), or Temgesic (sublingual tablet)
Third step: Codeine, Tramal, Durogesic patch (Fentanyl patch)
Fourth step: oral morphine solution
Fifth step: IV morphine. Auxillary medication: anti-depressant, anxielytics

Chills or Fever Management

1. Never use NSAID in thrombocytopenia patients
2. First line: Acetaminophen
3. Second line: Vena, Hydrocortisone (Solucortef)
4. Third line: Morphine or Demerol (血壓低病患不宜)
5. Fever 應視情況給予antipyretics 例如1: Past history of febrile convulsion (child), 2:Cardiac or pulmonary insufficiency patients, 3 Pregnancy patients, 4: High metabolism 會惡化thrombocytopenia ,6. Fever or chills 是cytokine reaction 臨床無法分別tumor fever or infection, (不管是feverpattern or temperature) 排除infection 之後才能當成tumor fever, Myeloid Leukemia 基本上不會tumor fever, 應視為infection 處理, Hodgkin disease, Lymphoma(AILD like, T cell, NKcell) tumor fever 比較常見。
FNHTR: (Febrile Non-hemolysis transfusion reaction) 基本上是血品內WBC 釋出的cytokine 會引起fever and chills, 即使使用filter 還是會發生,
Pack RBC 可換成Washed RBC 來避免
Platelet 可用prestorage-leukocyte depleted PLT 來避免
FFP則無法避免),可以使用Panadol or steroid 預防

電血:使血品中的lymphocyte ”inactivation”,將來無法再複製分裂(transfusion-related GVHD) 何時該電血?
Immunocompromised pt, ex. Post-allo-HSCT(一日BMT,終身電血),
ALC<1000 (Absolute lymphocyte count)
需要近親輸血時
(因HLA 可能相當接近,電血可以避免transfusion GVHD)
哪些血液製品要電血? RBC & PLT 製品要irradiation (FFP, cryopricipitate 不必電血)

Pack RBC: A, B, O type 要 match
1. Kept Hb > 6 g/dL for chronic anemia (non-malignant)
2. Kept Hb > 8 g/dL for acute leukemia & lymphoma
3. Kept Hb >10 g/dL for cardiopulmonary disease OR receiving radiotherapy
4. 若病人有症狀,亦需給予治療, keep Hb > 9~10 g/dL

Platelet: 盡量配合A, B, O type,但若無ABO matched 其他血型也可輸,
以single donor,WBC depleted platelet 為佳
若有anti-platelet 抗體可輸HLA matched 血小板 (需知道HLA-ABC 的結果)
1. Kept Plt > 10K active bleeding(-), aspirin(-)
2. Kept Plt > 20K aspirin(+), active bleeding(-)
3. Kept Plt > 50K if active bleeding(+), including DIC, APL patient, menstrual bleeding
4. Check anti-platelet antibody for refractory thrombocytopenia
5. Give Premarin 1 amp q6-8h and platelet supplement for menstrual bleeding

2008年12月7日 星期日

Ca/Cr clearance ratio, hyperparathyroidism

Ca/Cr clearance ratio = [Urine Ca x plasma Cr] ÷ [Plasma Ca x Urine Cr]

Diagnosis of primary hyperparathyroidism

Intubation