Posts filed under ‘MISCELLANEOUS’
LDH
LDH 5 type
LDH-1 (4H) – in the heart and RBCs
LDH-2 (3H1M) – in the reticuloendothelial system
LDH-3 (2H2M) – in the lungs
LDH-4 (1H3M) – in the kidneys, placenta, and pancreas
LDH-5 (4M) – in the liver and striated muscle[1]
Treatment of Metabolic alkalosis
Treatment of Metabolic alkalosis
1. Volume depletion patient
-Rx Volume replacement
-if cause from diuretic induce -> Rx K sparing Spironolactone, amiloride,triamterene
2. Volume repletion patient
-Cause from mineralocorticoid excess
-Rx Spironolactone
3.Miscellaneous cause
-Post hypercapnic metabolic alkalosis
1.Acteazolamide (CAI) ตรง intercalated cell inh secretion of H+
Aceatazolamide 500 mg reduce serum HCO3 6mmol/L
Beware K loss becase inh H+/K+
2.NH4Cl and arginine ห้ามให้ใน liver disease because induce hepatic enceph
3.Acid infusion 100-200 mEq/L of HCL via central line
Beware of tissue necrosis and acid induce hemolysis
4.Hemodialysis with Low HCO3 dialysate
Narrow PP in sever AR
Pathophysiology of chronic aortic regurgitation
All forms of aortic regurgitation produce a similar hemodynamic abnormality. The inability of the aortic valve leaflets to remain closed or coapted during diastole results in a portion of the left ventricular stroke volume leaking back from the aorta into the left ventricle. The added volume of regurgitant blood produces an increase in left ventricular end-diastolic volume; according to Laplace’s law, the increase in left ventricular end-diastolic volume causes an elevation in wall stress. The heart responds with compensatory myocardial hypertrophy, which returns wall stress toward normal.
The combination of hypertrophy and chamber enlargement raises the total stroke volume. The net effect is that forward stroke volume and hence cardiac output are maintained despite the regurgitant lesion. Although left ventricular volume is increased, end-diastolic pressure is normal due to an increase in ventricular compliance. Thus, the heart initially adapts well to chronic aortic regurgitation, functioning as a very efficient and compliant high output pump.
In very severe regurgitation with ventricular decompensation, the murmur may become soft or even absent. This change in character reflects the near equivalence of aortic diastolic and left ventricular end-diastolic pressures which markedly diminishes regurgitant flow. A similar situation can occur when aortic regurgitation is acute and the left ventricular end-diastolic pressure is very high.
สรุปเอาเองว่า ช่วงแรก LV compensateได้ complianceยังดี LVEDV increaseแต่LVEDPไม่เพิ่ม–>murmurดัง, pulse pressureกว้าง–>–>decompensated state, LVEDPสูงขึ้นเรื่อยๆ murmurเลยเงียบ, pulse pressureลดลงเพราะgradient across LVต่ำลง
Coagulation effect
W/U hypercoagulable state
After heparin or LMWH therapy is begun, remember that it affects antithrombin, as well as protein C, protein S, and activated protein C resistance. Warfarin affects protein C, protein S, and antithrombin. Neither drug affects anticardiolipin antibodies, factor V Leiden, the prothrombin mutation, lipoprotein(a) or homocysteine levels. (จากemedicineจ้า)
Risk factor of Asbestosis
High risk jobs of asbestos exposure
insulators=อุตสาหกรรมฉนวนกันความร้อนจากasbestos
ship building (มักใช้asbestosเป็นฉนวนหุ้มรอบboiler และstream pipe ,dockของอาจารย์น่าจะหมายถึงชานชาลาสำหรับขนถ่ายสินค้าซึ่งน่าจะใช้asbestosเป็นฉนวนกันความร้อน?)
refinery=โรงกลั่น(น้ำตาล,น้ำมัน)
plumber=ช่างประปา
textile industry=อุตสาหกรรมสิ่งทอ
minings of talc/vermiculite
auto mechanics=อุตสาหกรรมผ้าเบรค, รองเท้า
Doxapram
Doxapram “possible” benefit in post op
a respiratory stimulant. Administered intravenously, doxapram stimulates an increase in tidal volume, and respiratory rate.
stimulates chemoreceptors in the carotid arteries, which in turn, stimulates the respiratory centre in the brain stem.