tag:blogger.com,1999:blog-23034740077206037212024-03-06T01:24:54.897+00:00MRCP revision on the go...One busy junior doctor's battle with the MRCP exam/retaining her sanity.Marie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comBlogger389125tag:blogger.com,1999:blog-2303474007720603721.post-38242575169142851662010-11-22T11:34:00.000+00:002010-11-22T11:34:55.793+00:00MRCP revision battle 57.1: Stroke thrombolysisNow we're at utterly last minute topics... <br />
<br />
MRCP revision battle 57.1: Stroke thrombolysis<br />
MRCP revision battle 57.2: Cardiac tamponade<br />
MRCP revision battle 57.3: Systemic sclerosis<br />
MRCP revision battle 57.4: Tapeworms<br />
MRCP revision battle 57.5: Brown-Sequard Syndrome<br />
MRCP revision battle 57.6: Trigeminal neuralgia<br />
<br />
<span style="font-size: large;"><b><br />
</b></span><br />
<span style="font-size: large;"><b>MRCP revision battle 57.1: Stroke thrombolysis</b></span><br />
<br />
Contraindications to stroke thrombolysis:<br />
<ul><li>evidence of intracranial haemorrhage on CT/MRI</li>
<li>minor neurological defect</li>
<li>symptoms rapidly improving</li>
<li>seizures at onset of stroke</li>
<li>any prior history of stroke and diabetes</li>
<li>stroke within 3 months</li>
<li>systolic BP >185 or diastolic BP >110</li>
<li>hyperglycaemia >25mmol</li>
<li>weight >15 stones</li>
<li>platelets <100</li>
<li><br />
</li>
</ul>Marie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comtag:blogger.com,1999:blog-2303474007720603721.post-76308493645287669932010-11-22T11:33:00.003+00:002010-11-22T11:35:07.403+00:00MRCP revision battle 57.2: Cardiac tamponadeCardiac tamponade occurs when pericardial fluid collects to a degree that prevents the heart pumping.<br />
<br />
On echo you see RA+/- RV collapse during diastle.<br />
<br />
<br />
The classic triad is Becks:<br />
<ul><li>falling BP</li>
<li>rising JVP</li>
<li>muffled heart sounds</li>
</ul><br />
Other possible signs include:<br />
<ul><li>Kussmauls = rising JVP on inspiration</li>
<li>pulsus paradoxus</li>
<li>JVP - loss of y descent, x descent prominant </li>
</ul><br />
<br />
ECG may show electrical alternanas <br />
<br />
<br />
Treatment is ugern pericardiocentesisMarie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comtag:blogger.com,1999:blog-2303474007720603721.post-67308886158087288462010-11-22T11:32:00.000+00:002010-11-22T11:35:19.361+00:00MRCP revision battle 57.3: Systemic sclerosisSystemic sclerosis is a connective tissue disease characterised by thickening and fibrosis of skin (scleroderma) and involvement of internal organs.<br />
<br />
<br />
Female: male 4:1<br />
<br />
Commonest in 5th/6th decades<br />
<br />
<br />
Limited systemic sclerosis = skin involvement is limited to face, hands and feet.<br />
Associated with anti-centromere antibodies in 70-80%<br />
<br />
Diffuse systemic sclerosis = more skin involvement<br />
Anti Scl 70 in 40%<br />
<br />
<br />
Features of sclerosis:<br />
<ul><li>Raynaulds - 1st presentation in 70% of cases</li>
<li>arthralgia</li>
<li>renal failure</li>
<li>scleroderma</li>
<li>GI problems</li>
<li>classical skin presentation:</li>
<ul><li>telangiectasia</li>
<li>peri-oral puckering</li>
<li>smooth shiny skin</li>
<li>livedo reticularis</li>
</ul><li>pulmonary fibrosis/hypertension</li>
</ul><br />
ESR/CRP are raised<br />
<br />
<br />
CREST is a type of limited systemic sclerosis:<br />
- calcinosis, raynaulds, eosophageal dysmotility, sclerodalyl, telangectasia<br />
- renal crsis is rare but pulmonary hypertension is common<br />
<br />
<br />
Linear scleroderma = coup de sabre<br />
<br />
Treatment:<br />
<ul><li>supportive</li>
<li>d-penicillamine</li>
<li>steroids if lung disease</li>
<li>ACE-i to help kidneys</li>
</ul>Marie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comtag:blogger.com,1999:blog-2303474007720603721.post-41925935878048770032010-11-22T10:53:00.004+00:002011-08-26T16:10:10.714+01:00MRCP revision battle 57.4: TapewormsCysticercosis:<br />
<ul><li>taenia solum - found in pork</li>
<li>taenia saginata - found in beef</li>
<li>treatment:albendazole</li>
</ul><br />
Hydatid disease<br />
:<br />
<ul><li>caused by echinococcus</li>
<li>treatment: albendazole</li>
</ul>Marie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comtag:blogger.com,1999:blog-2303474007720603721.post-6378965780999238152010-11-22T10:00:00.000+00:002010-11-22T11:33:40.532+00:00MRCP revision battle 57.5: Brown-Sequard SyndromeBrown-Sequard Syndrome is caused by a lesion in one half of the cord.<br />
<br />
Commonest cause = MS<br />
Other causes:<br />
<ul><li>trauma</li>
<li>tumour</li>
<li>degenerative disease</li>
</ul><br />
Result is:<br />
<ul><li>ipsilateral UMN weakness below</li>
<ul><li>increased reflexes</li>
<li>spastic paralysis</li>
</ul><li>ipsilateral dorsal column loss</li>
<ul><li>loss of proprioception and vibration</li>
</ul><li>contralateral spinothalmic loss</li>
<ul><li>loss of pain and temperature sensation</li>
</ul></ul>Marie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comtag:blogger.com,1999:blog-2303474007720603721.post-24880523699109568712010-11-22T09:00:00.000+00:002010-11-22T11:33:53.004+00:00MRCP revision battle 57.6: Trigeminal neuralgiaTrigeminal neuralgia is intense stabbing pain in the trigeminal root distribution.<br />
<br />
It is unilateral and tends to affect the mandibular or maxillary divisions<br />
<br />
Most common in females over 50.<br />
<br />
<br />
Over 1 in 10 cases will be secondary (to aneuysm, tumour) so ?MRI<br />
<br />
<br />
Treatment is carbamazepineMarie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comtag:blogger.com,1999:blog-2303474007720603721.post-90814475162625547072010-11-21T11:06:00.000+00:002010-11-22T11:06:58.982+00:00MRCP revision battle 56.1: Amyloidosis7 non-waffling battles <br />
<br />
<br />
MRCP revision battle 56.1: Amyloidosis<br />
MRCP revision battle 56.2: Plasma exchange <br />
MRCP revision battle 56.3: P450 inducers and inhibitors <br />
MRCP revision battle 56.4: Therapeutic drug monitoring <br />
MRCP revision battle 56.5: Vaccines<br />
MRCP revision battle 56.6: Acute lymphoid leukaemia<br />
MRCP revision battle 56.7: Nematodes = roundworms<br />
<br />
<br />
<br />
<span style="font-size: large;"><b>MRCP revision battle 56.1: Amyloidosis </b></span><br />
<br />
Amyloidosis is a pathological process characterised by extracellular accumulation of fibrils of insoluble protein.<br />
<br />
<br />
Inherited forms of amyloidosis are rare but amyloid deposition is central to many diseases including Alzheimers and type 2 diabetes.<br />
<br />
<br />
Types of amyloid:<br />
<br />
1: AL = light chains<br />
<ul><li>secreted by plasma B cells</li>
<li>occurs in 15% of myeloma patients</li>
<li>also occurs in:</li>
<ul><li>Waldenstroms</li>
<li>MGUS</li>
</ul><li>features:</li>
<ul><li>cardiac deposition = 'sparkling' appearence on echo</li>
<li>GI </li>
<li>macroglossia</li>
<li>peri orbital</li>
</ul><li>median survival is 12 months</li>
<li>treatment is to treat the underlying condition, ?prednisolone</li>
</ul><br />
2: AA = serum amylase A<br />
<ul><li>this is secondary amyloidosis, with the amyloid derived from serum amylase A which is an acute phase protein</li>
<li>seen in:</li>
<ul><li>RA</li>
<li>TB</li>
<li>bronchiectasis</li>
<li>familial med fever</li>
<li>IBD</li>
</ul><li>commonest organ involved = kidney (congo red stain -->red-green birefrigence under polarised light)</li>
<li>median survival is 24 months</li>
</ul><br />
3:Marie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comtag:blogger.com,1999:blog-2303474007720603721.post-59944345923889702112010-11-21T10:27:00.000+00:002010-11-22T11:06:34.339+00:00MRCP revision battle 56.2: Plasma exchangeA summary of the indications for plasma exchange:<br />
<ul><li>GBS</li>
<li>myathesnia gravis</li>
<li>Goodpastures</li>
<li>ANCA + vasculitis</li>
<li>TTP/HUS</li>
<li>cryoglobulinaemia</li>
<li>some hyperviscosity eg myeloma </li>
</ul>Marie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comtag:blogger.com,1999:blog-2303474007720603721.post-6037894387233307742010-11-21T10:20:00.000+00:002010-11-22T11:06:24.556+00:00MRCP revision battle 56.3: P450 inducers and inhibitorsP450 inducers include:<br />
<ul><li>rifampicin</li>
<li>antiepileptics except sodium valproate</li>
<li>griseofulvin</li>
<li>smoking</li>
<li>st johns wort</li>
<li>barbituates</li>
<li>chronic alcohol</li>
</ul><br />
P450 inhibitors include:<br />
<ul><li>anti-infection meds</li>
<ul><li>ciprofloxacin</li>
<li>erythromycin</li>
<li>ketoconazole</li>
<li>isoniazid</li>
</ul><li>Anti reflux </li>
<ul><li>cimetidine</li>
<li>omeprazole</li>
</ul><li>Pysch meds</li>
<ul><li>SSRIs</li>
<li>antipyschotics</li>
<li>TCA</li>
</ul><li> sodium valproate</li>
<li>acute alcohol</li>
<li>class IV antiarrhymics</li>
<ul><li>diltiazen</li>
<li>verapamil</li>
</ul></ul>Marie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comtag:blogger.com,1999:blog-2303474007720603721.post-14139714960942054942010-11-21T10:15:00.000+00:002010-11-22T11:06:12.047+00:00MRCP revision battle 56.4: Therapeutic drug monitoringWhen to take the sample, that is the question....<br />
<br />
Lithium: 12 hrs post dose<br />
<br />
Digoxin: at least 6 hours post dose<br />
<br />
Ciclosporin and pheytoin: immediately post-doseMarie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comtag:blogger.com,1999:blog-2303474007720603721.post-7037876968055805062010-11-21T10:10:00.000+00:002010-11-22T11:05:59.071+00:00MRCP revision battle 56.5: VaccinesLive attenuated vaccines:<br />
<ul><li>BCG</li>
<li>MMR</li>
<li>polio</li>
<li>yellow fever</li>
<li>oral typhoid</li>
</ul><br />
Whole killed:<br />
<ul><li>rabies</li>
<li>petussis</li>
<li>influenza</li>
</ul><br />
Fragment:<br />
<ul><li>tetanus</li>
<li>diptheria</li>
<li>meningococcus</li>
<li>pneumococcus</li>
</ul>Marie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comtag:blogger.com,1999:blog-2303474007720603721.post-18840090837642912972010-11-21T10:05:00.000+00:002010-11-22T11:05:43.974+00:00MRCP revision battle 56.6: Acute lymphoid leukaemiaALL is commonest in children.<br />
<br />
There is >60% cure<br />
<br />
Treatment is by non-myelosupressive chemo.<br />
<br />
Prognosis is worse if:<br />
<ul><li><1yr or >10yrs</li>
<li>higher WCC</li>
<li>male</li>
<li>philidelphia chromosome +</li>
</ul><br />
Better if >47 chromosomesMarie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comtag:blogger.com,1999:blog-2303474007720603721.post-77237363036331222682010-11-21T10:00:00.001+00:002010-11-22T11:05:30.525+00:00MRCP revision battle 56.7: Nematodes = roundworms2 main groups to consider for MRCP:<br />
<br />
<br />
1. Strongyloides stercoralis<br />
<ul><li>AKA threadworm</li>
<li>acquired percutaneously</li>
<li>causes migratory urticaria = larva currens</li>
<li>presents with itching</li>
<li>if it reaches lungs -->pneumonitis</li>
<li>treatment: mebendazole</li>
</ul><br />
2. Toxocara canis <br />
<ul><li>caused by ingesting eggs from soil contaminated with dog poo</li>
<li>treatmet: mebendazole</li>
</ul>Marie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comtag:blogger.com,1999:blog-2303474007720603721.post-42450651523912540102010-11-20T19:37:00.000+00:002010-11-20T19:37:21.471+00:00MRCP revision battle 55.1: TrypanosomiasisMore randomness... <br />
<br />
<br />
MRCP revision battle 55.1: Trypanosomiasis<br />
<a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-552-hypokalaemia.html">MRCP revision battle 55.2: Hypokalaemia</a><br />
<a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-553-cryoglobulins.html">MRCP revision battle 55.3: Cryoglobulins</a><br />
<a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-554-cold.html">MRCP revision battle 55.4: Cold agglutinins</a><br />
<a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-555-lateral.html">MRCP revision battle 55.5: Lateral medullary syndrome</a><br />
<a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-556-purtscher.html">MRCP revision battle 55.6: Purtscher retinopathy</a><br />
<a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-557-optic-atrophy.html">MRCP revision battle 55.7: Optic atrophy </a><br />
<br />
<br />
<br />
<br />
<b><span style="font-size: large;">MRCP revision battle 55.1: Trypanosomiasis </span></b><br />
<br />
<b>Trypanosomiasis </b>= diseases causes by <b>parasitic protozoa trypanosoma.</b><br />
<br />
<br />
2 main divisions:<br />
<br />
<span style="font-size: large;"><b><br />
</b></span><br />
<span style="font-size: large;"><b>1. African = sleeping sickness</b></span><br />
<ul><li>spread by<b> tsetse fly</b></li>
<li> caused by</li>
<ul><li><b>t. rhodesiense </b>- east africa - quicker</li>
<li><b>t.gambiense </b>- west africa - slower</li>
</ul><li>classical presentation </li>
<ul><li>fever, rigors, headache, hepatosplenomegaly, lymphadenopathy </li>
<li>sleepy during day, awake at night</li>
<li> meningoencephalitis</li>
</ul><li>look for chancre and <b>posterior cervical nodes</b> (=<b>Winterbottom's sign</b>)</li>
<li>diagnosis is by <b>microscopy</b></li>
<li>treatment:</li>
<ul><li><b>IV pentamide</b></li>
<li><b>IV melarsoprol</b></li>
</ul></ul>Below is an image of t.gambiense: <br />
<div class="separator" style="clear: both; text-align: center;"><a href="http://upload.wikimedia.org/wikipedia/commons/6/67/Afric_tryp_1a_DPDxi.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="162" src="http://upload.wikimedia.org/wikipedia/commons/6/67/Afric_tryp_1a_DPDxi.jpg" width="320" /></a></div><br />
<br />
<br />
<span style="font-size: large;"><b>2. American - Chagas disease</b></span><br />
<ul><li>carried by<b> triatomine bugs</b></li>
<li>caused by<b> t. cruzi</b></li>
<li>classical presentation</li>
<ul><li>fever, rash, hepatosplenomegaly, lymphadenopathy </li>
<li>myocarditis</li>
<li>meningoencephalitis</li>
<li><b>megaoesophagus/megacolon</b></li>
</ul><li>look for:</li>
<ul><li><b>chagoma</b> (=indurated, erythamatous nodule at site of infection)</li>
<li><b>periorbital oedema</b> (=<b>Romana's sign</b>)</li>
</ul><li> diagnosis is by <b>blood culture</b></li>
<li>treatment:<b> benznidazole</b></li>
</ul><br />
<br />
Now for some <a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-552-hypokalaemia.html">low potassium.... </a>Marie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comtag:blogger.com,1999:blog-2303474007720603721.post-34974758284689880432010-11-20T19:36:00.000+00:002010-11-20T19:36:34.597+00:00MRCP revision battle 55.2: Hypokalaemia<b>Hypokalaemia</b> is defined as K <3.5mmol; if <2.5mmol it is severe.<br />
<b><br />
</b><br />
<b>Symptoms/signs include:</b><br />
<ul><li><b>muscle weakness</b></li>
<li><b>hypotonia</b></li>
<li>cramps</li>
<li><b>tetany</b></li>
<li>worsening of dig toxicity</li>
<li>cardiac arrhythmias</li>
</ul><br />
ECG may show:<br />
<ul><li><b>small/inverted T waves</b></li>
<li><b>U waves</b></li>
<li><b>long PR</b></li>
<li><b>depressed ST</b></li>
</ul><br />
<span style="font-size: large;"><b>Causes of hypokalaemia</b></span><br />
<b><br />
</b><br />
<b>Low K with hypertension</b><br />
<ul><li>raised plasma renin</li>
<ul><li>Cushings</li>
<li>renin-secreting tumour</li>
</ul><li>low plasma renin</li>
<ul><li>Conns</li>
<li>liquorice</li>
<li><a href="http://mrcpandme.blogspot.com/2010/10/mrcp-revision-battle-299-liddles.html">Liddles</a></li>
</ul></ul><br />
<b>Low K without hypertension</b><br />
<ul><li>diuretics</li>
<li>GI loss</li>
<li>CRF</li>
<li><a href="http://mrcpandme.blogspot.com/2010/10/mrcp-revision-battle-297-bartters.html">Bartters</a></li>
<li><a href="http://mrcpandme.blogspot.com/2010/10/mrcp-revision-battle-298-gitelman.html">Gitelmans</a></li>
<li>secondary hyperaldosteronism</li>
</ul><br />
<br />
On to <a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-553-cryoglobulins.html">cryoglobulins... </a><br />
<ul></ul>Marie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comtag:blogger.com,1999:blog-2303474007720603721.post-41537755875835717862010-11-20T19:35:00.000+00:002010-11-20T19:35:45.192+00:00MRCP revision battle 55.3: Cryoglobulins<b>Cryoglobulins</b> are <b>immunoglobulins </b>that undergo <b>reversible precipitation at 4c </b>and <b>dissolve</b> when warmed to<b> 37c.</b><br />
<br />
Cryoglobulins may be IgG, IgM or IgA.<br />
<br />
One third of cases are idiopathic.<br />
<br />
<u><b><br />
</b></u><br />
<u><b>Type 1 cryoglobulinaemia</b></u><br />
<ul><li><b>monoclonal </b></li>
<li>high titres, usually >5mg/ml</li>
<li>associated with:</li>
<ul><li><b>myeloma</b></li>
<li><b>Waldenstroms</b></li>
</ul><li>features include vasculitis, ulceration and Raynaud's</li>
</ul><br />
<u><b>Type 2 cryoglobulinaemia</b></u><br />
<ul><li><b>mixed mono and polyclonal </b></li>
<li>titres usually >1mg/ml</li>
<li>associated with:</li>
<ul><li>RA</li>
<li>sjogrens</li>
<li>lympoma</li>
<li>CLL</li>
<li>hep C</li>
<li>HIV</li>
</ul><li>features include vasculitis, mesangiocapillary GN</li>
</ul><br />
<br />
<u><b>Type 3 cryoglobulinaemia</b></u><br />
<ul><li><b>mixed polyclonal</b></li>
<li>associated with:</li>
<ul><li>RA</li>
<li>sjogrens</li>
<li>SLE</li>
</ul><li>features include purpura, GN, arthritis </li>
</ul><br />
<br />
Now on to a similar but <a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-554-cold.html">distinct topic... </a>Marie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comtag:blogger.com,1999:blog-2303474007720603721.post-50907179585797905482010-11-20T19:34:00.000+00:002010-11-20T19:34:33.126+00:00MRCP revision battle 55.4: Cold agglutininsCold agglutinins are molecules, usually IgM, which act against red cells agglutinising and haemolysing them at low temperatures.<br />
<br />
Symptoms of cold agglutinins include:<br />
<ul><li>Raynauds</li>
<li>acrocyanosis</li>
<li>mild haemolytic anaemia</li>
</ul><br />
Causes of cold agglutinins include:<br />
<ul><li>idiopathic</li>
<li>CLL</li>
<li>lymphoma</li>
<li>mycoplasma</li>
<li>coxsachie</li>
<li>mononucleosis </li>
<li>HIV</li>
</ul><br />
Management is to avoid cold weather. <br />
<br />
<br />
<br />
Now to diversify to <a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-555-lateral.html">neurology....</a>Marie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comtag:blogger.com,1999:blog-2303474007720603721.post-20327396074716822042010-11-20T19:33:00.000+00:002010-11-20T19:33:45.796+00:00MRCP revision battle 55.5: Lateral medullary syndrome<b>Lateral medullary syndrome</b> is a condition in which a patient has a set of <b>symptoms </b>as a result of <b>insult to the medulla.</b><br />
<br />
Lateral medullary syndrome is usually due to <b>PICA or vertebral artery occlusion.</b><br />
<br />
<br />
Features include:<br />
<ul><li><b>cerebellar signs</b></li>
<li><b>contralateral pain and temperature sensation loss</b></li>
<li><b>ipsilateral Horners</b></li>
<li><b>ipsilateral loss of pain and temperature sensation on face</b></li>
<li><b>ipsilateral paralysis of palate, pharynx and cords</b></li>
</ul><br />
<br />
On to some <a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-556-purtscher.html">vision loss... </a>Marie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comtag:blogger.com,1999:blog-2303474007720603721.post-78736158087865518032010-11-20T19:32:00.000+00:002010-11-20T19:32:45.396+00:00MRCP revision battle 55.6: Purtscher retinopathy<b>Purtscher's retinopathy</b> is characterised by <b>cotton wool spots</b> on fundoscopy with<b> sudden detioration in vision.</b><br />
<br />
<br />
It is classically associated with<b> head trauma </b>or <b>chest trauma.</b><br />
<br />
Other associations include:<br />
<ul><li><b>pancreatitis</b></li>
<li><b>fat embolism</b></li>
<li><b>amniotic fluid embolism</b></li>
<li><b>vascular diseases</b></li>
</ul><br />
There is no treatment. <br />
<br />
<br />
Finally - <a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-557-optic-atrophy.html">optic atrophy...</a>Marie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comtag:blogger.com,1999:blog-2303474007720603721.post-58472368244909845332010-11-20T19:31:00.000+00:002010-11-20T19:31:47.479+00:00MRCP revision battle 55.7: Optic atrophy<b>Optic atrophy</b> is<b> loss of fibres of the optic disc.</b> It is characterised by <b>decreased vision </b>(particulary loss of colour vision) and a <b>pale disc</b> on fundoscopy.<br />
<br />
<br />
Causes include:<br />
<b><br />
</b><br />
<b>Congenital:</b><br />
<ul><li>Friedrichs ataxia (<a href="http://mrcpandme.blogspot.com/2010/10/mrcp-revision-battle-306-friedreichs.html">battle 30.6</a>)</li>
<li>Lebers optic atrophy (<a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-463-mitochondrial.html">battle 46.3</a>)</li>
<li>DMOAD (=diabetes mellitus, optic atrophy and deafness)</li>
<li>retinitis pigmentosa (<a href="http://mrcpandme.blogspot.com/2010/10/mrcp-revision-battle-301-retinitis.html">battle 30.1</a>)</li>
</ul><br />
<b>Acquired:</b><br />
<ul><li>MS</li>
<li>papilloedema</li>
<li>glaucoma</li>
<li>ischaemia</li>
<li>B6, B12, folate deficieny</li>
<li>lead poisoning</li>
<li>arsenic poisoning</li>
<li>methanol</li>
<li>ethambutol</li>
<li>isoniazid</li>
<li>chloramphenicol</li>
</ul>Marie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comtag:blogger.com,1999:blog-2303474007720603721.post-56747579347987346712010-11-19T19:58:00.000+00:002010-11-19T19:58:48.562+00:00MRCP revision battle 54.1: Primary sclerosing cholangitisToday is in pairs: a pair of gastro battles, a pair of cardiology battles, a pair of haematology battles then a strange inherted disorder to finish on....<b> </b><br />
<br />
<br />
MRCP revision battle 54.1: Primary sclerosing cholangitis <br />
<a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-542-jaundice.html">MRCP revision battle 54.2: Jaundice</a><br />
<a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-543-patent-ductus.html">MRCP revision battle 54.3: Patent ductus arteriosus</a><br />
<a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-544-cardiac-axis.html">MRCP revision battle 54.4: Cardiac axis</a><br />
<a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-545-haemolysis.html">MRCP revision battle 54.5: Haemolysis</a><br />
<a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-546.html">MRCP revision battle 54.6: Leukoerythroblastic change</a><br />
<a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-547-gauchers.html">MRCP revision battle 54.7: Gaucher's disease</a><b><br />
</b><br />
<br />
<br />
<b><span style="font-size: large;">MRCP revision battle 54.1: Primary sclerosing cholangitis </span></b><br />
<br />
<b>Primary sclerosing cholangitis </b>is a condition of unknown aetiology in which there is <b>inflammation and fibrosis of bile ducts.</b><br />
<br />
<br />
Presentation:<br />
<ul><li>patients may be asymptomatic with an incidental finding of <b>raised ALP</b></li>
<li>may present as:</li>
<ul><li><b>jaundice</b></li>
<li><b>pruritus</b></li>
<li><b>abdo pain</b></li>
<li><b>fatigue</b></li>
</ul></ul><br />
Diseases associated with primary sclerosing cholangitis include:<br />
<ul><li>IBD (<b>UC</b>>crohns; 70% of patients with PSC have UC but only 5% of patients with UC have PSC)</li>
<li><b>HIV</b></li>
<li><b>HLA A1, B8, DR3</b></li>
</ul><br />
Males are more frequently affected than females.<br />
<br />
<br />
Diagnosis is by:<br />
<ul><li><b>ERCP</b> - shows <b>strictures</b> of the biliary tree and a <b>'beaded' appearence</b></li>
<li>liver biopsy - fibrous, obliterative cholangitis</li>
<li><b>ANA, SMA</b> and <b>ANCA</b> may be positive </li>
</ul><br />
Treatment is:<br />
<ul><li><b>colestyramine</b> for pruritis</li>
<li><b>ursodeoxycholic acid</b> to improve cholestatis</li>
<li>?stenting of strictures </li>
<li>?liver transplant </li>
</ul><br />
Complications include:<br />
<ul><li>decreased absorption of fat-soluble vitamins A,D,E and K</li>
<ul><li>clotting abnormalities and easy bruising</li>
<li>osteoporosis</li>
</ul><li><b>cholangiocarcinoma (10-30%)</b></li>
<li>bacterial cholangitis</li>
<li><b>liver cirrhosis</b></li>
<ul><li>portal hypertension</li>
</ul></ul><br />
Survival tends to be around 10 yrs<br />
<br />
<br />
As an aside, the other 2 conditions associated with cholangiocarcinoma are:<br />
<ul><li>liver flukes</li>
<li>Caroli's disease = dilation of hepatic ducts</li>
</ul><br />
<br />
Into the <a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-542-jaundice.html">yellow...</a>Marie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comtag:blogger.com,1999:blog-2303474007720603721.post-74807176229407524012010-11-19T19:56:00.000+00:002010-11-19T19:56:06.619+00:00MRCP revision battle 54.2: Jaundice<b>Jaundice</b> is y<b>ellow pigmentation</b> of the skin caused by<b> raised bilirubin.</b><br />
<br />
It is generally clinically <b>visible above 35micromol/l.</b><br />
<br />
<br />
The 'story' of bilirubin is illustrated in the diaphragm below:<br />
<ul><li>phagocytes break haemoglobin down into unconjugated (=insoluble) bilirubin</li>
<li>unconjugated bilirubin is joined with glucoronic acid in the liver, making it conjugated (=soluble)</li>
<li>conjugatde bilirubin passes into the gallbladder and on to the small intestine, where it is converted into urobilinogen and excreted in urine by the kidneys or to stercobilinogen and excreted in faeces</li>
</ul><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhVQR3EHydvbgjp8XmRG3MPQ80ghMSep1pcaSTHW6GuXMotdn-g5YLq8S0hz1F8dp1O_C3Rl5WaxpYpNcfrFSOB-6hlGfBwhuDEPsoaky9QFrMw1uBPqfQXnXinqvI79THMzsvFSjGHJmg/s1600/Screen+shot+2010-11-19+at+16.57.42.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="340" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhVQR3EHydvbgjp8XmRG3MPQ80ghMSep1pcaSTHW6GuXMotdn-g5YLq8S0hz1F8dp1O_C3Rl5WaxpYpNcfrFSOB-6hlGfBwhuDEPsoaky9QFrMw1uBPqfQXnXinqvI79THMzsvFSjGHJmg/s400/Screen+shot+2010-11-19+at+16.57.42.png" width="400" /></a></div><br />
<br />
<br />
The types of jaundice are:<br />
<br />
<span style="font-size: large;"><b>1. Pre-hepatic = unconjugated</b></span><br />
<ul><li>caused by:</li>
<ul><li><b>haemolysis</b></li>
<li><b>lack of UDP: Gilberts, Crigler Najjar</b></li>
</ul><li>urine/faeces colours <b>normal</b></li>
</ul><br />
<span style="font-size: large;"><b>2. Hepatic = both conjugated and unconjugated</b></span><br />
<ul><li>caused by:</li>
<ul><li>infection: HBV, HCV, EBV</li>
<li>Wilsons</li>
<li>Budd-Chiari</li>
<li>Dubin-Johnson/Rotor syndromes</li>
<li><b>cirrhosis</b></li>
<li>drugs:</li>
<ul><li>anti-TB meds</li>
<li>statins</li>
<li>sodium valproate</li>
<li>MAOIs</li>
<li>halothane</li>
<li>paracetamol OD</li>
</ul></ul><li><b>urine dark, faeces normal</b></li>
</ul><br />
<span style="font-size: large;"><b>3. Post-hepatic = conjugated = obstructive/cholestatic</b></span><br />
<ul><li>gallstones</li>
<li>pancreatic cancer</li>
<li>cholangiocarcinoma </li>
<li>primary bilary sclerosis</li>
<li>sclerosing cholangitis</li>
<li><b>Mirrizi's syndrome</b> = obstructive jaundice secondary to compression of the common hepatic duct by a gallstone impacted in the cystic duct</li>
<li>Drugs</li>
<ul><li>antibiotics - co-amoxiclav, nitrofurantoin, flucloxacillin</li>
<li>OCP</li>
<li>chlorperazine</li>
<li>sulphonylureas</li>
<li>anabolic steroids</li>
</ul><li><b>urine pale and faeces pale </b></li>
</ul><br />
<br />
Now for something different... <a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-543-patent-ductus.html">PDA...</a>Marie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comtag:blogger.com,1999:blog-2303474007720603721.post-29921694878902836322010-11-19T19:55:00.000+00:002010-11-19T19:55:33.863+00:00MRCP revision battle 54.3: Patent ductus arteriosusThe <b>ductus arteriosus</b> is a <b>connection</b> between the<b> pulmonary trunk and the descending aortic arch </b>allowing blood flow in the fetus to avoid the fluid-filled lungs.<br />
<br />
It should <b>close shortly after birth</b>, being mostly closed within 48 hrs and fully closed within 3 weeks, leaving the<b> ligamentum arteriosum</b> in its place.<br />
<br />
<br />
Closure is due to 2 mechanisms:<br />
<ol><li>exposure of infants lungs to oxygen promotes <b>bradykinin</b> production which promotes PDA closure</li>
<li><b>loss of maternal prostaglandins</b> encourages closure</li>
</ol><br />
Closure is more likely to fail (=patent ductus arteriosus) in:<br />
<ul><li><b>premature </b>infants</li>
<li>infants exposed to <b>rubella in 1st trimester</b></li>
<li>infants at <b>high altitude</b></li>
</ul><br />
Features of patent ductus arteriosus include:<br />
<ul><li><b>machinery murmur</b></li>
<li><b>wide, collapsing pusle</b></li>
<li><b>apical heave</b></li>
</ul><br />
If it does not close the infant may fail to thrive or develop heart failure.<br />
Many cases however will be asymptomatic. <br />
5% of patients with PDA go to develop pulmonary hypertension and Eisenmengers.<br />
<br />
<br />
Treatment:<br />
<ul><li><b>indomethacin</b> (a prostaglandin antagonist) causes closure in 90%</li>
<li>surgical treatment is also an option</li>
</ul><br />
In some cases (eg transposition of the great vessels) keeping the ductus arteriosus open may be beneficial to the infant, in which case IV prostaglandin E1 is given. <br />
<br />
<br />
On to the <a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-544-cardiac-axis.html">cardiac axis...</a>Marie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comtag:blogger.com,1999:blog-2303474007720603721.post-80462618291406681272010-11-19T19:54:00.000+00:002010-11-19T19:54:04.327+00:00MRCP revision battle 54.4: Cardiac axisThe <b>normal</b> cardiac axis is<b> -30 to +90 degrees.</b><br />
<br />
More negative = left axis deviation<br />
More positive = right axis deviation.<br />
<br />
<br />
Causes of<b> left axis deviation:</b><br />
<ul><li>LBBB</li>
<li>LVH</li>
<li>ASD</li>
<li>cardiomyopathies</li>
<li>aortic stenosis </li>
<li>can be normal in:</li>
<ul><li>ascites</li>
<li>pregnancy</li>
<li>obesity</li>
</ul></ul><br />
Causes of <b>right axis deviation:</b><br />
<ul><li>RBBB</li>
<li>RVH --> lung disease</li>
<li>PE</li>
<li>can be normal in:</li>
<ul><li>infancy</li>
<li>thin people</li>
</ul></ul><br />
<br />
Next: <a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-545-haemolysis.html">haemolysis </a>Marie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.comtag:blogger.com,1999:blog-2303474007720603721.post-28833393046130837122010-11-19T19:53:00.000+00:002010-11-19T19:53:39.234+00:00MRCP revision battle 54.5: HaemolysisHaemolysis (=breakdown of red blood cells) may be intravascular or extravascular.<br />
It causes a <b>microcytic anaemia </b>and<b> raised reticulocyte count.</b><br />
<br />
<br />
<span style="font-size: large;"><b>Intravascular haemolysis</b></span><br />
<br />
Intravascular haemolysis is characterised by:<br />
<ul><li><b>low haptoglobin</b> (as all used up trying to 'recycle' the broken down red cells)</li>
<li>raised free plasma haemoglobin</li>
<li>haemoglobuinuria: red-brown urine</li>
<li><b>haemosiderinuria</b>: once haptoglobin binding capacity is surpassed free Hb is filtered by the kidneys and can be detected in the urine in sloughed tubular cells using Prussian blue staining</li>
</ul><br />
Causes of intravascular haemolysis include:<br />
<ul><li>cold AIHA</li>
<li>transfusion reaction</li>
<li>G6PD (recall<a href="http://mrcpandme.blogspot.com/2010/10/mrcp-revision-battle-284-g6pd.html"> battle 28.4?</a>)</li>
<li>paroxysmal nocturnal haematuria (recall<a href="http://mrcpandme.blogspot.com/2010/10/mrcp-revision-battle-276-paroxysmal.html"> battle 27.6</a>?)</li>
<li>microangiopathic haemolytic anaemia (<a href="http://mrcpandme.blogspot.com/2010/10/mrcp-revision-battle-386.html">recall battle 38.6?</a>)</li>
<ul><li>DIC</li>
<li>TTP</li>
<li>mechanical heart valves</li>
</ul></ul><br />
<span style="font-size: large;"><b>Extravascular haemolysis</b></span><br />
<br />
Extravascular haemolysis may cause <b>splenomegaly.</b><br />
<br />
Causes of extravascular haemolysis include:<br />
<ul><li>warm AIHA (remember<a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-397-autoimmune.html"> battle 39.7</a>?)</li>
<li>cold haemagglutination disease</li>
<li>spherocytosis</li>
<li>haemoglobinopathies</li>
<li>haemolytic disease of the newborn</li>
</ul><br />
<br />
Now to the<a href="http://mrcpandme.blogspot.com/2010/11/mrcp-revision-battle-546.html"> second haem battle</a> of the day...Marie Treasurehttp://www.blogger.com/profile/13241948195128622377noreply@blogger.com