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Last Build Date: Sun, 28 May 2017 08:42:19 GMT

 



Chlorpromazine

Fri, 26 May 2017 07:36:51 GMT

up date on dose

← Older revision Revision as of 07:36, 26 May 2017
Line 14: Line 14:
*Initially 25mg three times a day (or 75mg at night)
*Initially 25mg three times a day (or 75mg at night)
*Usual maintenance dose - 75-300mg/day
*Usual maintenance dose - 75-300mg/day
-
*Maximum dose - 1000mg/day
+
*Maximum dose - 1000mg/day (There is no trial evidence for benefit over 400mg/day in adults)
*Use 1/3 -1/2 dose in the elderly
*Use 1/3 -1/2 dose in the elderly



Retigabine

Fri, 26 May 2017 07:34:29 GMT

withdrawal

← Older revision Revision as of 07:34, 26 May 2017
Line 2: Line 2:
[[Category:medicines]]
[[Category:medicines]]
==Introduction==
==Introduction==
-
In development for [[epilepsy]] (refractory partial-onset epilepsy)
+
Used for [[epilepsy]] (refractory partial-onset epilepsy) its low use resulted in it being withdrawn worldwide in [[2017]]
==Clinical Use==
==Clinical Use==
===Indications===
===Indications===



Finasteride

Fri, 26 May 2017 07:31:28 GMT

SE

← Older revision Revision as of 07:31, 26 May 2017
Line 18: Line 18:
*Blockage sex hormones
*Blockage sex hormones
*Orthostatic hypotension
*Orthostatic hypotension
 +
*Depression and suicidal thoughts
May be used concurrently with [[:Category:Alphablockers|alphablockers]]
May be used concurrently with [[:Category:Alphablockers|alphablockers]]
{{refsec}}
{{refsec}}
[[Category:5alpha-reductase inhibitors]]
[[Category:5alpha-reductase inhibitors]]



Rolapitant

Fri, 26 May 2017 07:29:23 GMT

anti nausea

New page

{{PharmacologyBox||Varuby®, rolapitant hydrochloride monohydrate|[[image:{{PAGENAME}}Molecule.png|thumb|{{PAGENAME}} Molecule]]|[[image:{{PAGENAME}}.png|center]]|||}}
[[Category:medicines]]
==Introduction==
Rolapitant is metabolised by [[CYP3A4]] to form a major active metabolite, M19 (C4-pyrrolidine-hydroxylated rolapitant). This blocks brain [[substance-P|substance-P]]/NK1 receptors
==Clinical Use==
===Indications===
*Chemotherapy-induced nausea and vomiting (CINV)
===Administration===
''Oral'' 90mg to 180mg .
==Clinical Issues==
===Contra-indications===
===Cautions and Interactions===
===Side effects===
===Special advice===
==Pharmacology==
Selective antagonist of [[Substance-P|human substance P]]/neurokinin 1 (NK1) receptors
[[Category:antiemetics]][[Category: Substance P antagonists]][[Category:Neurokinin 1-receptor antagonists]]



Auer bodies

Fri, 26 May 2017 07:18:15 GMT

APL if lots of them

← Older revision Revision as of 07:18, 26 May 2017
Line 1: Line 1:
{{SubjectBox}}
{{SubjectBox}}
-
'''Auer bodies''' (Auer rods) are azurophilic granules within lysosomes as found in [[myeloblast]]s. They were described by John Auer in leukaemia cells in [[1906]]. Auer rods are found in multiple myeloid neoplasms but never in benign conditions.
+
'''Auer bodies''' (Auer rods) are azurophilic granules within lysosomes as found in [[myeloblast]]s. They were described by John Auer in leukaemia cells in [[1906]]. Auer rods are found in multiple myeloid neoplasms but never in benign conditions. Abundant Auer bodies are suggestive of [[acute promyelocytic leukaemia]].
[[Category:Histology]]
[[Category:Histology]]



Sturge-Weber syndrome

Thu, 25 May 2017 07:46:36 GMT

categorise

New page

{{GeneticsBox}}
[[Category:Epilepsy]]
[[Category:Genetic syndromes]]
Sturge-Weber syndrome (SWS) is a congenital neurocutaneous disorder with[https://www.ncbi.nlm.nih.gov/sites/entrez?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=28384923 Chhabria BA, Subramanium PB, Nampoothiri R, Bhalla A, Varma S. Sturge-Weber Syndrome. Journal of clinical and diagnostic research : JCDR. 2017 Feb; 11(2):OJ05-OJ06.](Print-Electronic) ([http://dx.doi.org/10.7860/jcdr/2017/22731.9378 Link to article] – subscription may be required.):
*Intracranial leptomeningeal vascular malformations (leptomeningeal angiomatosis, cerebral pial angioma)
*Retinal angioma
*Facial portwine stain (nevus flaemmus, facial naevus)
The clinical hallmark of nevus flaemmus is absent in some which poses a diagnostic challenge.

The genetics are complex but include mutations of the [[GNAQ]] gene[https://www.ncbi.nlm.nih.gov/sites/entrez?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=28454448 Huang Z, Li Y, Zhao Z, Hu J, Tong X, Chen X, Liu S, Xu X, Tao Y, Wang T, Cheng X, Dai Y, Gui Y, Wu J. GNAQ mutation R183Q as a potential cause of familial Sturge-Weber syndrome: A case report. Oncology letters. 2017 Apr; 13(4):2665-2669.](Print-Electronic) ([http://dx.doi.org/10.3892/ol.2017.5791 Link to article] – subscription may be required.)[https://www.ncbi.nlm.nih.gov/sites/entrez?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=25374402 Nakashima M, Miyajima M, Sugano H, Iimura Y, Kato M, Tsurusaki Y, Miyake N, Saitsu H, Arai H, Matsumoto N. The somatic GNAQ mutation c.548G>A (p.R183Q) is consistently found in Sturge-Weber syndrome. Journal of human genetics. 2014 Dec; 59(12):691-693.](Print-Electronic) ([http://dx.doi.org/10.1038/jhg.2014.95 Link to article] – subscription may be required.)[https://www.ncbi.nlm.nih.gov/sites/entrez?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=23656586 Shirley MD, Tang H, Gallione CJ, Baugher JD, Frelin LP, Cohen B, North PE, Marchuk DA, Comi AM, Pevsner J. Sturge-Weber syndrome and port-wine stains caused by somatic mutation in GNAQ. The New England journal of medicine. 2013 May; 368(21):1971-1979.](Print-Electronic) ([http://dx.doi.org/10.1056/nejmoa1213507 Link to article] – subscription may be required.).
==Complications==
Refractory epilepsy is common (bilateral facial port-wine stain and cerebral developmental venous anomalies increase the risk)[https://www.ncbi.nlm.nih.gov/sites/entrez?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=27637568 Kaseka ML, Bitton JY, Décarie JC, Major P. Predictive Factors for Epilepsy in Pediatric Patients With Sturge-Weber Syndrome. Pediatric neurology. 2016 Nov; 64:52-58.](Print-Electronic) ([http://dx.doi.org/10.1016/j.pediatrneurol.2016.08.009 Link to article] – subscription may be required.). Stroke presentations with venous thrombosis is known and more rarely intracranial haemorrhage. Glaucoma and intellectual disability are also described.
{{refsec}}



Cannabidiol

Thu, 25 May 2017 07:25:20 GMT

← Older revision Revision as of 07:25, 25 May 2017 (One intermediate revision not shown)Line 1: Line 1: {{PharmacologyBox||CBD, 2-[(1R,6R)-6-isopropenyl-3-methylcyclohex-2-en-1-yl]-5-pentylbenzene-1,3-diol}} {{PharmacologyBox||CBD, 2-[(1R,6R)-6-isopropenyl-3-methylcyclohex-2-en-1-yl]-5-pentylbenzene-1,3-diol}}  +==Introduction==  +Cannabidiol is the major phytocannabinoid in [[cannabis]] and has minimal psychoactive properties. It may prove useful in refractory epilepsy[http://www.ncbi.nlm.nih.gov/sites/entrez?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=26352816  Friedman D, Devinsky O. Cannabinoids in the Treatment of Epilepsy. The New England journal of medicine. 2015 Sep 10; 373(11):1048-58.]([http://dx.doi.org/10.1056/NEJMra1407304 Link to article] – subscription may be required.), or dyskinesia. Its neuroprotective, antispasmodic, anti-inflammatory and anti‑anxiety properties also may have therapeutic potential. There is limited evidence of effectiveness in [[Dravet syndrome]] and [[Sturge-Weber syndrome]][https://www.ncbi.nlm.nih.gov/sites/entrez?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=28454984  Kaplan EH, Offermann EA, Sievers JW, Comi AM. Cannabidiol Treatment for Refractory Seizures in Sturge-Weber Syndrome. Pediatric neurology. 2017 Feb.](Print-Electronic) ([http://dx.doi.org/10.1016/j.pediatrneurol.2017.02.009 Link to article] – subscription may be required.). The pure compound has been tried in a wide range of conditions such as Crohns disease[https://www.ncbi.nlm.nih.gov/sites/entrez?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=28349233  Naftali T, Mechulam R, Marii A, Gabay G, Stein A, Bronshtain M, Laish I, Benjaminov F, Konikoff FM. Low-Dose Cannabidiol Is Safe but Not Effective in the Treatment for Crohn's Disease, a Randomized Controlled Trial. Digestive diseases and sciences. 2017 Jun; 62(6):1615-1620.](Print-Electronic) ([http://dx.doi.org/10.1007/s10620-017-4540-z Link to article] – subscription may be required.) without marked net benefit and has been brought to market as one constituent of delta-9-tetrahydrocannabinol/cannabidiol (Sativex®) oromucosal spray for [[multiple sclerosis]] related spasticity. -Cannabidiol is the major phytocannabinoid in [[cannabis]] and has minimal psychoactive properties. It may prove useful in refractory epilepsy[http://www.ncbi.nlm.nih.gov/sites/entrez?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=26352816  Friedman D, Devinsky O. Cannabinoids in the Treatment of Epilepsy. The New England journal of medicine. 2015 Sep 10; 373(11):1048-58.]([http://dx.doi.org/10.1056/NEJMra1407304 Link to article] – subscription may be required.), or dyskinesia. Its neuroprotective, antispasmodic, anti-inflammatory and anti‑anxiety properties also may have therapeutic potential. However there is a lack of RCT evidence of effectiveness.+   +===Side effects===  +*[[Diarrhoea]]  +*Vomiting  +*Fatigue  +*Pyrexia  +*Somnolence  +*Dizziness  +===Special advice===  +==Pharmacology==   [[Category:Cannabinoids]] [[Category:Cannabinoids]] {{refsec}} {{refsec}} [...]



Angiotensin

Wed, 24 May 2017 07:41:22 GMT

typos ← Older revision Revision as of 07:41, 24 May 2017 (2 intermediate revisions not shown)Line 3: Line 3: [[Image:AngiotensinII.png|thumb|Angiotensin II]][[Image:AngiotensinIIMolecule.png|thumb|Angiotensin II minimum energy conformation]] [[Image:AngiotensinII.png|thumb|Angiotensin II]][[Image:AngiotensinIIMolecule.png|thumb|Angiotensin II minimum energy conformation]] '''Angiotensin''' is the group name for polypeptides with significantly different active properties which have: '''Angiotensin''' is the group name for polypeptides with significantly different active properties which have: -#Key regulatory functions for blood pressure and fluid homeostasis both on a classic endocrine basis acutely but possibly more importantly chronically intracellularly in various tissues[[Pubmed:7614502|Stock P, Liefeldt L, Paul M, Ganten D. Local renin-angiotensin systems in cardiovascular tissues: localization and functional role. Cardiology 1995;86 Suppl 1:2-8.]].+#Key regulatory functions for blood pressure and fluid homeostasis both on a classic endocrine basis acutely but possibly more importantly chronically intracellularly in various tissues[[Pubmed:7614502|Stock P, Liefeldt L, Paul M, Ganten D. Local renin-angiotensin systems in cardiovascular tissues: localization and  +  functional role. Cardiology 1995;86 Suppl 1:2-8.]]. #Further paracrine properties such as with  Angiotensin II increasing hematopoietic progenitor cell proliferation[[Pubmed:15488662|Oztürk MA, Güven GS, Haznedaroglu IC. How hematopoietic stem cells know and act in cardiac microenvironment for stem cell plasticity? Impact of local renin-angiotensin systems. Medical hypotheses 2004;63(5):866-74.]] ([http://dx.doi.org/10.1016/j.mehy.2004.04.011 Direct link] – subscription may be required.) #Further paracrine properties such as with  Angiotensin II increasing hematopoietic progenitor cell proliferation[[Pubmed:15488662|Oztürk MA, Güven GS, Haznedaroglu IC. How hematopoietic stem cells know and act in cardiac microenvironment for stem cell plasticity? Impact of local renin-angiotensin systems. Medical hypotheses 2004;63(5):866-74.]] ([http://dx.doi.org/10.1016/j.mehy.2004.04.011 Direct link] – subscription may be required.) #Feedback properties as with angiotensin-(1-7) to the Mas G protein-coupled receptor #Feedback properties as with angiotensin-(1-7) to the Mas G protein-coupled receptor Line 20: Line 21: **↓ [[Urine]] flow **↓ [[Urine]] flow **↑ Urine [[osmolality]] **↑ Urine [[osmolality]] -**Proinflamatory (activates [[nuclear factor-kappaB]](NF-kappaB)) [[Pubmed:15831814|Esteban V, Ruperez M, Sánchez-López E, Rodríguez-Vita J, Lorenzo O, Demaegdt H, et al. Angiotensin IV activates the nuclear transcription factor-kappaB and related proinflammatory genes in vascular smooth muscle cells. Circulation research 2005;96(9):965-73.]] ([http://dx.doi.org/10.1161/01.RES.0000166326.91395.74 Direct link] – subscription may be required.)+**Proinflamatory (activates [[nuclear factor-kappaB]](NF-kappaB)) [[Pubmed:15831814|Esteban V, Ruperez M, Sánchez-López E, Rodríguez-Vita J, Lorenzo O, Demaegdt H, et al. Angiotensin IV activates the nuclear transcription factor-kappaB and related  +  proinflammatory genes in vascular smooth muscle cells. Circulation research 2005;96(9):965-73.]] ([http://dx.doi.org/10.1161/01.RES.0000166326.91395.74 Direct link] – subscription may be required.)  +**'''Continuous iv infusion in those presenting with vasodilatory shock refractory to vasopressors inc[...]



Elagolix

Wed, 24 May 2017 07:30:00 GMT

reference ← Older revision Revision as of 07:30, 24 May 2017 Line 2: Line 2: ==Introduction== ==Introduction== -[[Elagolix]], a nonpeptide gonadotropin-releasing hormone antagonist is in development for [[endometriosis]]+[[Elagolix]], a nonpeptide gonadotropin-releasing hormone antagonist is in development for [[endometriosis]][https://www.ncbi.nlm.nih.gov/sites/entrez?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=28525302  Taylor HS, Giudice LC, Lessey BA, Abrao MS, Kotarski J, Archer DF, Diamond MP, Surrey E, Johnson NP, Watts NB, Gallagher JC, Simon JA, Carr B, Dmowski WP, Leyland N, Rowan JP, Duan WR, Ng J, Schwefel B, Thomas JW, Jain RI, Chwalisz K. Treatment of Endometriosis-Associated Pain with Elagolix, an Oral GnRH Antagonist. The New England journal of medicine. 2017 May.](Print-Electronic) ([http://dx.doi.org/10.1056/nejmoa1700089 Link to article] – subscription may be required.) ==Clinical Use== ==Clinical Use== ===Indications=== ===Indications=== ===Administration=== ===Administration=== -''Oral''+''Oral'' 200 mg twice daily ==Clinical Issues== ==Clinical Issues== ===Contra-indications=== ===Contra-indications=== ===Cautions and Interactions=== ===Cautions and Interactions=== ===Side effects=== ===Side effects===  +*Hot flushes  +*[[Hyperlipidaemia]]  +*[[Osteoporosis]] ===Special advice=== ===Special advice=== ==Pharmacology==   ==Pharmacology==   Line 17: Line 20: [[Category:GnRH antagonists]] [[Category:GnRH antagonists]] [[Category:Unlicensed medicines]] [[Category:Unlicensed medicines]]  +{{refsec}} [...]



Evacetrapib

Wed, 24 May 2017 07:24:43 GMT

reference ← Older revision Revision as of 07:24, 24 May 2017 Line 1: Line 1: {{PharmacologyBox||LY2484595|||| inhibitor of [[cholesteryl ester transfer protein]]|}} {{PharmacologyBox||LY2484595|||| inhibitor of [[cholesteryl ester transfer protein]]|}} ==Introduction== ==Introduction== -A lipidprotein modulating therapy no longer in development[http://www.ncbi.nlm.nih.gov/sites/entrez?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=21957197  Cao G, Beyer TP, Zhang Y, Schmidt RJ, Chen YQ, Cockerham SL, Zimmerman KM, Karathanasis SK, Cannady EA, Fields T, Mantlo NB. Evacetrapib is a novel, potent and selective inhibitor of cholesteryl ester transfer protein that elevates high-density lipoprotein cholesterol without inducing aldosterone or increasing blood pressure. Journal of lipid research. 2011 Sep 25.](Epub ahead of print) ([http://dx.doi.org/10.1194/jlr.M018069 Link to article] – subscription may be required.)[https://www.ncbi.nlm.nih.gov/sites/entrez?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=28099220  Eyvazian VA, Frishman WH. Evacetrapib: Another CETP Inhibitor for Dyslipidemia With No Clinical Benefit. Cardiology in review. 2017 Mar/Apr; 25(2):43-52.](Print) ([http://dx.doi.org/10.1097/crd.0000000000000137 Link to article] – subscription may be required.) as the induced pleasing plasma lipoprotein profile did not mean real life benefit.  +A lipidprotein modulating therapy no longer in development[http://www.ncbi.nlm.nih.gov/sites/entrez?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=21957197  Cao G, Beyer TP, Zhang Y, Schmidt RJ, Chen YQ, Cockerham SL, Zimmerman KM, Karathanasis SK, Cannady EA, Fields T, Mantlo NB. Evacetrapib is a novel, potent and selective inhibitor of cholesteryl ester transfer protein that elevates high-density lipoprotein cholesterol without inducing aldosterone or increasing blood pressure. Journal of lipid research. 2011 Sep 25.](Epub ahead of print) ([http://dx.doi.org/10.1194/jlr.M018069 Link to article] – subscription may be required.)[https://www.ncbi.nlm.nih.gov/sites/entrez?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=28099220  Eyvazian VA, Frishman WH. Evacetrapib: Another CETP Inhibitor for Dyslipidemia With No Clinical Benefit. Cardiology in review. 2017 Mar/Apr; 25(2):43-52.](Print) ([http://dx.doi.org/10.1097/crd.0000000000000137 Link to article] – subscription may be required.) as the induced pleasing plasma lipoprotein profile did not mean real life benefit[https://www.ncbi.nlm.nih.gov/sites/entrez?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=28514624  Lincoff AM, Nicholls SJ, Riesmeyer JS, Barter PJ, Brewer HB, Fox KAA, Gibson CM, Granger C, Menon V, Montalescot G, Rader D, Tall AR, McErlean E, Wolski K, Ruotolo G, Vangerow B, Weerakkody G, Goodman SG, Conde D, McGuire DK, Nicolau JC, Leiva-Pons JL, Pesant Y, Li W, Kandath D, Kouz S, Tahirkheli N, Mason D, Nissen SE. Evacetrapib and Cardiovascular Outcomes in High-Risk Vascular Disease. The New England journal of medicine. 2017 May; 376(20):1933-1942.](Print) ([http://dx.doi.org/10.1056/nejmoa1609581 Link to article] – subscription may be required.).   ==Clinical Use== ==Clinical Use== ===Indica[...]



Thrombocytosis

Wed, 24 May 2017 07:21:47 GMT

← Older revision Revision as of 07:21, 24 May 2017 (2 intermediate revisions not shown)Line 4: Line 4: **Infections **Infections **Blood loss **Blood loss  +**Malignancy Once such have been excluded and platelet count > 600x109/l on two FBCs over 1 month apart consider [[essential thrombocythemia]] Once such have been excluded and platelet count > 600x109/l on two FBCs over 1 month apart consider [[essential thrombocythemia]] }} }} Line 14: Line 15: *#The contribution of clot lysis of [[erythrocyte]]s and [[leukocyte]]s is usually negligible and to a degree this causes a true hyperkalaemia anyway  The net result is that a significant amount of potassium remains in serum but actually the plasma is in correct homeostatic balance. *#The contribution of clot lysis of [[erythrocyte]]s and [[leukocyte]]s is usually negligible and to a degree this causes a true hyperkalaemia anyway  The net result is that a significant amount of potassium remains in serum but actually the plasma is in correct homeostatic balance. *[[Hypercalcaemia]]. This has not been demonstrated to be a false hypercalcaemia as both serum and plasma  calcium is raised[http://www.ncbi.nlm.nih.gov/sites/entrez?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=10767824  Howard MR, Ashwell S, Bond LR, Holbrook I. Artefactual serum hyperkalaemia and hypercalcaemia in essential thrombocythaemia. Journal of clinical pathology. 2000 Feb; 53(2):105-9.]. *[[Hypercalcaemia]]. This has not been demonstrated to be a false hypercalcaemia as both serum and plasma  calcium is raised[http://www.ncbi.nlm.nih.gov/sites/entrez?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=10767824  Howard MR, Ashwell S, Bond LR, Holbrook I. Artefactual serum hyperkalaemia and hypercalcaemia in essential thrombocythaemia. Journal of clinical pathology. 2000 Feb; 53(2):105-9.]. -{{draft}}+*Malignancy (lung or colorectal cancer)[https://www.ncbi.nlm.nih.gov/sites/entrez?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=28533199  Bailey SE, Ukoumunne OC, Shephard EA, Hamilton W. Clinical relevance of thrombocytosis in primary care: a prospective cohort study of cancer incidence using English electronic medical records and cancer registry data. The British journal of general practice : the journal of the Royal College of General Practitioners. 2017 May.](Print-Electronic) ([http://dx.doi.org/10.3399/bjgp17x691109 Link to article] – subscription may be required.)  +**In males 40 years or more a platelet count of >400 X 109/L is associated with 11.6% risk malignancy being diagnosed in next year. In females it is 6.2%, still over three times background rate. A second raised platelet count within a few months increases risk to four times baseline. A third of such patients are asymptomatic of their malignancy at the time the blood test is done. {{refsec}} {{refsec}} [[Category:Haematology]] [[Category:Haematology]] [...]