HRT & progesterone

If you're prescribing HRT to someone, you should also be prescribing progesterone at the same time in the same way that you give laxatives to people on morphine.

(I don't know why - work this out at some stage)

Tutorial - Basic and Applied Anatomy of the Eye

This site has a great tutorial about opthal stuff. Appears there's a few other things there as well, but I haven't sussed out anything apart from the eye stuff yet.

Hmmm...maybe not

I just did a Medical Speciality aptitude test that a friend sent me the link for. My results:

1. Nuclear Medicine - wtf I don't even know the first thing about this!
2. Infectious diseases - like I know anything about that either!
3. Plastic Surgery - one of my favourite rotations so far.
   
4. Emergency - likewise, another favourite.
   

Some reflection

I've just completed the second essay I had to write for this silly portfolio we have to hand in tomorrow. The first essay was infinitely painful - writing up a case report on an ethical issue we had witnessed this year - and I've spent the past few evenings struggle to get that one done.

The second essay I wrote tonight - a reflection of my personal and professional development over this year. It was actually quite cathartic; writing this essay actually felt quite similar to writing a blog entry, so I'm cheating and using it as both. Here goes!!

Third year has been an interesting year; it’s a vastly difference experience to second year. It’s been busier than ever, but despite the busyness it has somehow managed to be less stressful, something I am immensely thankful for, because I am not sure if I could cope with the stress of second year and its barrier exam again. The third year barrier exam that looms in a mere months time somehow does not seem such a daunting task after having been through one before and passed out the other end, and after having successfully made my way through the Long Case exam that was the major stress-inducing object to deal with this year. I’m unsure of whether my reduced stress is due to improved coping, lower motivation to be able to induce stress, or heightened perspective of where I’ve been, where I’m going and what I need to do to get there. Either way, for my sanity’s sake, I am glad.

That’s not to say this year has been a walk in the park. Yes, it’s been very busy, and compared to the last two years, the busyness is less focused and frustrating, because it seems less outcome driven. The year had barely started; our first few days at a new hospital (in Orange) and already we were being bombarded with EBM, PPD and CDT presentations to prepare. Where was the time to study? And what did our lectures have to do with our PBL topics for the week? And what about our ICAs – when were we supposed to learn anything relating to them? And what about the ICAs we never got allocated – will I never learn anything about Respiratory or Neurology?

This year was filled with many unknowns and unanswered questions. I kept waiting for a mystical ah-hah moment, when everything would suddenly snap together and make sense. I continue to wait.

But comparing myself now to where I was at the start of the year, things have changed -just as previous third years, when imparting their wisdom to us - told us they would. Somehow this crazy and confusing system I’ve had to muddle through for the last 7 months has worked. Sure I’m still no pharmacist, but I know a lot more about many more medications than I did this time last year. Flipping through most patients’ medication charts I can make reasonable sense of what their main medical issues are, instead of the bewilderment I felt last year. And sure, I still stammer and give stupid answers whilst in the middle of an operation getting grilled about anatomy by surgeons, but now I welcome it, not dread it, because it’s a great way to learn.

One area I thought I would feel more confident about by this stage is procedural skills. Unfortunately they are something that I continue to feel that if I don’t do them with regularity, then I need to learn again. The only thing I feel vaguely confident in at this stage is venepuncture. Cannulation, ABGs and suturing are still stress inducing experiences for me. I have discussed this with my supervisors, who say don’t get caught up with these things now, that by the time pre-internship arises I’ll be bored with cannulating ten patients a day, that now is the time to be on the wards talking to patients and practicing history-taking and performing physical exams. Taking this advice on board is something I have tried to do, with varying success at times, and is something I am still aware of.

As third year draws to a close, I am stunned by how quickly it has come and gone. I am filled with awe about everything I have learnt this year, and disgust at all that I knew last year but have now forgotten. I’m also starting to think about next year, and all the new experiences that will bring with anticipation. Not to mention the year after.

Anyway, I'm glad that's over and done with. I'm going to go have a glass of wine now, and celebrate its completion, as well as the fact that instead of having a 7:15am vascular tutorial tomorrow morning, we're having it at 2pm instead. I get a sleep-in yay. Much more civilised!! I'm even going to try and go to the gym beforehand as well!

Microalbumuria

Screening for microalbumuria in non-diabetics is a good way to screen for CV risks. The microalbumuria is caused by endothelial dysfunction.

SAAB drugs for use in acute coronary syndrome

• Statin
• Ace inhibitor
• Aspirin
• Beta blocker

Electrolyte imbalances that occur in diabetes

• Hypocalcaemia - kidney doesn't activate vitamin D -> decreased GIT absorption of Ca
  
• Hyponatraemia
• Hyperphosphataemia - it can't be excreted. Treatment is by giving a phosphate binder e.g. mylanta.

Treatment of endocarditis

Endocarditis requires 6 weeks of IV antibiotic treatment. This length of time is required because it is difficult for antibiotics to penetrate to the valve cusps which are relatively avascular.

Calcium channel blockers

Mechanism of action

Calcium channel blockers have a negative inotropic effect - they decrease the force of contraction of the myocardium.

They block L-type voltage gated calcium channels in the heart and blood vessels. This prevents calcium levels from increasing as much in the cells when stimulated, leading to less contraction.

They also decrease total peripheral resistance by dilating the blood vessels, and decreasing cardiac output by lowering the force of contraction. Because resistance and output drop, so does blood pressure. With low blood pressure, the heart does not have to work as hard; this can ease problems with cardiomyopathy and coronary disease.

Unlike with beta-blockers, the heart is still responsive to sympathetic nervous system stimulation, so blood pressure can be maintained more effectively.

Many calcium channel blockers also slow down the conduction of electrical activity within the heart by blocking the calcium channel during the plateau phase of the action potential of the heart. This causes a lowering of the heart rate and may cause heart blocks (negative chronotropic effect) of calcium channel blockers.

Classes

There are 2 classes of CCBs:

1. Dihydropyridines
   
   
   • Used to reduce systemic vascular resistance and arterial pressure, but are not used to treat angina because the vasodilation and hypotension can lead to reflex tachycardia.
     
   • This CCB class is easily identified by the suffix "-pine" e.g. Amlodepine, Felodipine.


2. Non-dihydropyridines
   
   
   
   • Relatively selective for myocardium, reduce myocardial oxygen demand and reverse coronary vasospasm, and are often used to treat angina.
     
   • They have minimal vasodilatory effects compared with dihydropyridines.
     
   • Action is intracellular.
   • E.g. verapamil.
     

Indications

• Atrial fibrillation or flutter - to control heart rate via negative chronotropic effect.

Contraindications

• Avoided (or used with caution) in individuals with cardiomyopathy due to negative inotropic effect.
• Non-dihydropyridine CCBs should not be combined with beta-blockers because they are both negative inotropes and affect the AV node.
  

References:

• Wikpedia, http://en.wikipedia.org/wiki/Calcium_channel_blocker
  

Boils, furuncles and impetigo

Boils (furuncles) are localised, subcutaneous pyogenic infections, most frequently by Staphylococcus aureus, originating deep in a hair follicle.

Impetigo is a contagious superficial pyoderma, caused by Staphylococcus aureus and/or group A streptococci, that begins with a superficial flaccid vesicle that ruptures and forms a thick yellowish crust.



References:

• Stedman's Electronic Medical Dictionary, v5.0
• Image from http://www.clinical-virology.org/gallery/images/non_viral/impetigo-1.jpg
  

Wound swabs

Contamination = the presence of organisms in a wound that are not multiplying.

Colonisation = the presence of organisms in a wound that are multiplying but causing negligible host reaction. Colonisation can have a detrimental effect on wound healing, but as the ‘classic’ signs of infection do not accompany it, is often not identified.

Infection = the presence of organisms in a wound that are multiplying and causing a host reaction.

Signs of infection

• delayed healing
• purulent discharge from the wound
• Green, yellow or brown wound exudate or increased amount of wound exudate
• Offensive odour
• Inflammation and erythema of the wound and surrounding tissue – may include cellulitis
• Hypergranulation tissue
• Systemic signs: fever, malaise/lethargy
• Increased or unusual pain (Note: persons with diabetes may not experience this)
• Confusion
• Elevated BSL in diabetics
• Leucocytosis
  

Indications for Wound Swabbing

• An obvious wound exists and the surface can be sampled
• Clinical signs of infection
• Viable tissue exists - not slough or necrotic tissue (although these need to be removed via debridement)
  

References:

• Templeton S., Royal District Nursing Service of SA, http://www.rdns.org.au/research_unit/Newsletters/11_Wound_Sep02.pdf
  

Chest Imaging tutorial

Another great radiology resource - this time a tutorial on reading CXRs.

Popliteal fossa

Boundaries

• superior and medial: semitendinosus (semimembranosus is medial to the semitendinosus)
• superior and lateral: biceps femoris
• inferior and medial: medial head of gastrocnemius
• inferior and lateral: lateral head of the gastrocnemius

Contents

• popliteal artery (continuation of the femoral artery)
• popliteal vein
• tibial nerve
• common peroneal nerve
• popliteal lymph nodes embedded in the fat

References

• http://en.wikipedia.org/wiki/Popliteal_fossa
• Posterior Compartment of the Thigh, http://mywebpages.comcast.net/wnor/postthigh.htm
  

MedPix™

MedPix™ is a great radiology resource.

Focal neurological symptoms

A focal neurologic symptom is a problem that affects either:

• A specific location - such as the left face, right farm or even just a small area such as the tongue
• A specific function - for example, speech may be affected, but not the ability to write

The problem occurs in the brain or nervous system. The type, location, and severity of the change can indicate the area of the brain or nervous system that is affected.

In contrast, a non-focal problem is NOT specific - such as a general loss of consciousness.


References:

• MedLine Plus Medical Encyclopedia, http://www.nlm.nih.gov/medlineplus/ency/article/003191.htm
  

Asthma Hx

Things you need to ask someone with asthma:

• Sx: wheeze, dyspnoea, cough, disturbed sleep
• Exercise - quantify distance to breathlessness
• Days per week off work or school
  
• Diurnal variation
• Triggers - RTIs, cold, exercise, pets, emotions, drugs
  
• How & when they monitor their asthma e.g. peak flow meter
• Use of preventers and inhalers. Has there been any changes?
• For elderly people, ask if they've had Fluvax and Pneumovax vaccines (major RF for infective exacerbation)
• Any other atopic diseases like eczema, hay fever, allergy
• Previous attacks or hospitalisations
• Family history of asthma

References:

• http://www.aippg.net/forum/viewtopic.php?p=55254
  

T4 during infection

Metabolism of thyroid hormones is accelerated during acute infection in man and in experimental animals. The mechanisms for this is uncertain, but activated leukocytes of the infected host have been implicated as potentially important sites of hormone degradation.

Apparently T4 can go up in infection similar to an acute pahse reactant - but I couldn't find anything on the net really backing this up!!


References:

• DeRubertis, Accelerated host metabolism of L-thyroxine during acute infection, Journal of Clinical Endocrinology & Metabolism, Vol 40, 589-600
  

Nilstat

Actions

Anti-fungal.

Indications

Treatment of candida.

References:

• AMH
  

Lipodermatosclerosis (LDS)

• LDS literally means "scarring of the skin and fat" and is a slow process that occurs over a number of years.
• Occurs in patients with long-standing venous disease resulting in chronic venous insufficiency.
• Affects the skin just above the ankle, usually on the inside surface.
  
• Over time the skin becomes brown, smooth, tight and often painful.
  
• The precise mechanism of LDS is not fully understood, but we do know that it is caused by an excessively high venous pressure in the subcutaneous veins in the lower leg.

References:

• http://www.simondodds.com/Venous/LDS.htm
• http://www.bu.edu/woundbiotech/wounds/UncommonWounds%20Gallery/pages/19..htm
  

Chronic Venous Insufficiency (CVI)

Symptoms

• Varicose veins
• Ulceration or skin breakdown
• Lipodermatosclerosis
  
• Reddened or discolored skin on the leg
• Oedema

Risk factors

• Heredity
• Obesity
• Pregnancy
• Sedentary lifestyle
• Smoking
• Jobs requiring long periods of standing or sitting in one place
• Age and sex (women in their 50s are more prone to developing CVI)
• Incompetent valves
• previous DVT

Pathophysiology

• Increased venous pressure transcends the venules to the capillaries, impeding flow.
  

• Low-flow states within the capillaries cause leukocyte trapping.

• Trapped leukocytes release proteolytic enzymes and oxygen free radicals, which damage capillary basement membranes.

• Plasma proteins,such as fibrinogen, leak into the surrounding tissues, forming a fibrin cuff.
  

• Interstitial fibrin and resultant oedema decrease oxygen delivery to the tissues, resulting in local hypoxia.
  

• Inflammation and tissue loss result. Ulceration may occur.
  

Management

• Leg elevation
  
• Elastic compression therapy - especially with older patients you need to ensure they are actually able to put the compression stockings on for themselves.
  
• Sclerotherapy - chemically scarring the veins from the inside out so that they can then no longer fill with blood. Blood that would normally return to the heart through these veins returns to the heart through others. The body eventually absorbs the veins that received the injection.
• Vein stripping
• Deep vein surgery - note that surgical treatment is reserved for those with discomfort or ulcers refractory to medical management.
• Valve repair

Great resource on hands

Handworld - the name says it all huh? :)

Ankle-Brachial Index

The Ankle – Brachial Index (ABI) is a ratio of the systolic blood pressure measured simultaneously in the leg and arm. This test is done to screen for peripheral arterial disease (PAD) of the legs.

What the values mean:

• An ABI ratio less than 0.8 implies significant arterial obstruction.
• A ratio of 0.5 or less implies critical obstruction.
• A ratio of < 0.3 implies impending gangrene.
  

Patients with PAD should not wear compression stockings due to high risk of ischaemia.

References:

• Ankle-brachial index test, WebMD
  
• Facts about Intermittent Claudication, North Suburban Cardiology Group

Management of adult cardiorespiratory arresst

Geris tutorial with the Prof

The acute geriatric admission

Principle 1 - Atypical presentation

Geriatric giants:

• Confusion
• Falls
• Incontinence
• Failure to cope

The reasons that the geriatric syndrome exists and that older people don't present with simple complaints the way younger people would is due to a combination of their underlying medical conditions as well as decreased reserve from multi-system failure and inability to compensate.

Principle 2 - Comorbidity

• Multiple Dxes and complex issues in Dx and management plan.
• Drugs and bugs - common precipitants of acute hospitalisation.

Principle 3 - Complications of immobility

Seven sins of immobilisation:

1. pressure sores
2. constipation and urosepsis
3. deconditioning
4. depression
5. malnutrition
6. venous thrombosis
7. bronchopneumonia
   

Prinicple 4 - Function

• Level of function and independence.
• Discharge planning on admission.

Rules of prescribing

• Rule of halves (impaired drug clearance, increased adverse effects)
• Rule of fives (polypharmacy)
• Medication untrial (adverse drug reactions)
• Medication trial (careful medical management)

Falls

• Syncope (Stokes Adams, postural hypotension, aortic stenosis, cerebrovascular disease, epilepsy, diabetic hypoglycaemia SPACED)
• Acute - drugs and bugs etc
• Chronic - 4 causes: drugs and disorders of eyes, cognition and gait

Incontinence

• Post void residual for retention (obstruction or neurological disorder)
• 5 causes: drugs, UTI, atrophic vaginitis, faecal impaction, prostate

Delirium

• Acute and fluctuating, inattention, altered LOC
• Reversible causes (drugs and bugs etc)

Giant cell arteritis (GCA)

Giant cell arteritis is a vasculitis of large and medium size vessels. Although it can affect arteries in the neck, upper body and arms, it occurs most often in the arteries in the temples. For this reason, giant cell arteritis is sometimes called temporal arteritis or cranial arteritis.

Giant cell arteritis is also known as granulomatous arteritis — a reference to a particular type of inflammation it causes.

Epidemiology & Aetiology

• Adults older than age 50 are at greatest risk of giant cell arteritis.
• Women and caucasians are most commonly affected.
• The exact cause isn't known, but researchers believe that genetic, viral and environmental factors may play roles in the inflammation.

Clinical presentation

Giant cell arteritis frequently causes headaches, jaw pain, and blurred or double vision, but the most serious potential complications are blindness and, less often, stroke. These problems occur when swelling in the arteries impairs blood flow to the eyes or brain.

The onset of the symptoms tends to be gradual and includes low grade fever, fatigue, weakness and weight loss.

• A new headache, mild or severe, occurs in at least two-thirds of patients with the pain tending to be located over the sides of the head in front of the ears but may be frontal or other located.
• Nearly one-half of patients suffer from jaw claudication after chewing.
• Impaired vision is often an early manifestation of the disease.
• Permanent partial or complete loss of vision in one or both eyes has been observed in 15-20 % of patients. It is rare for patients to become completely blind in both eyes.
• Polymyalgia rheumatica, which is characterized by pain in the shoulders and hips, is closely linked to GCA, occurring in about 40-50 % of patients.
  

Investigations

• ESR – elevated in most patients with GCA.
• Temporal artery biopsy

Suggested in all cases of suspected GCA even if the diagnosis may appear "classic".

The biopsy is of low risk, causes very little pain, and often leaves little or no scar.

After the use of a topical numbing medication (the same one used by a dentist), a small part of the temporal artery from under the scalp is removed.

• Other ways to diagnose GCA include: ultrasonography, angiographic examination, CT scanning and MR angiography, high resolution MRI and position emission tomography (PET).

Management

• Although there's no cure for giant cell arteritis, immediate treatment with corticosteroid medications usually relieves symptoms and prevents loss of vision.
• Glucocorticoid treatment should be instituted immediately once the diagnosis of GCA is established.
• Daily dosing is more effective than alternate day dosing. The response usually occurs within two to four weeks after the institution of therapy.
• The diagnosis should be reevaluated in patients who are resistant to adequate steroid therapy.
• Steroid withdrawal can begin once clinical remission has been induced.
• Relapses are seen more frequently in the first year or two of the disease.
• Relapses often necessitate increased dosage or prolonged steroid treatment. Some researchers have suggested that the addition of methotrexate may be steroid-sparing while others have not demonstrated any benefit. However the routine addition of methotrexate to glucocorticoid therapy for GCA is not recommended. The efficacy of other cytotoxic drugs, dapsone, antimalarials, etanercept, and penicillamine has not been studied adequately although they have been reported to be helpful in some case reports.
• The finding of an increased risk of visual loss in patients with GCA and thrombocytosis (increase of the number of platelets in the blood), has led some to suggest the addition of drugs like aspirin for patients with high platelet counts, but there is not a lot of data to prove that this may reduce brain/skull problems.

References:

• “Giant cell arteritis”, mayoclinic.com, http://www.mayoclinic.com/health/giant-cell-arteritis/DS00440
• “Giant Cell Arteritis (Temporal Arteritis)”, Vasculitis Foundation, http://www.vasculitisfoundation.org/giantcellarteritis

Relationship between pulmonary embolism (PE) and atrial fibrillation (AF)

If PE and AF occur together it is most likely that the PE is the cause of the AF.

The mechanism of the AF is said to be acute right ventricular dilatation with "strain" due to the embolus in the pulmonary circulation creating backpressure into the right ventricle.

If a patient presents with unexplained AF, look for an accompanying PE as the cause.

It is postulated that AF can cause PE if a clot originates in the right atrium rather than the left, but this is less common than clots originating from the right ventricle and more studies need to be done in this area.

References:

• Flegel K., When atrial fibrillation occurs with pulmonary embolism, is it the chicken or the egg?, CMAJ 1999;160:1181-2

Tests for hearing loss

Rinne test

Normal hearing = POSITIVE. Air conduction is louder than bone conduction.
Conductive hearing loss = NEGATIVE. Bone conduction is better than air conduction.
Sensorineural hearing loss = POSITIVE because both bone air and bone conduction are equally reduced (NB: may need to mask normal ear to avoid a false negative from the opposite side).

Weber test

Normal hearing = sound comes from middle of forehead.
Unilateral conductive hearing loss = sound is loudest in AFFECTED ear because the ambient noise is picked up by the normal ear, masking the sound of the tuning fork on that side.
Unilateral sensorineural hearing loss = sound is loudest in UNAFFECTED (normal) ear.

References

• http://en.wikipedia.org/wiki/Weber_test
• "C:\Tam's docs\uni\Admin\year2\OSCE\Clinical skills summaries\ProcSkills\Procedural Skills.doc"
  

Sequestra

A sequestrum is a piece of dead bone that has become separated from normal/sound bone during the process of necrosis . It is a complication (sequelae) of osteomyelitis.

Pathological process of development of sequestra:

• infection in the bone -> inflammatory exudate -> increase in intramedullary pressure
• periosteum becomes stripped from the osteum -> vascular thrombosis
• lack of blood supply -> bone necrosis
• sequestra are formed

Due to the avascular nature of sequestra, antibiotics which travel to sites of infection via the bloodstream, poorly penetrate these tissues. Hence the difficulty in treating chronic osteomyelitis.

At the same time as sequestra are developing, new bone is forming (known as involcrum). Openings in the involcrum allow debris and exudates (including pus) to pass from the sequestrum via sinus tracts to the skin.

References:

• http://en.wikipedia.org/wiki/Sequestrum

• Image from http://www.steinergraphics.com/surgical/006_19.3.html

Stigmata of infective endocarditis

• Fever (often spiking)
• Continuous presence of micro-organisms in the bloodstream in serial collection of blood cultures
• Vegetations on valves on echocardiography, which sometimes can cause a new or changing heart murmur, particularly murmurs suggestive of valvular regurgitation
• Vascular phenomena:

Septic emboli - mitral regurg -> LA dilatation -> ectopic foci -> stasis in LA -> formation of thrombi -> circulatory problems such as stroke or gangrene of fingers

Janeway lesions (painless hemorrhagic cutaneous lesions on the palms and soles)

hemorrhage: intracranial hemorrhage, conjunctival hemorrhage, splinter hemorrhages

• Immunologic phenomena: Glomerulonephritis, Osler's nodes (painful subcutaneous lesions in the distal fingers), Roth's spots on the retina, positive serum rheumatoid factor

References:

• http://en.wikipedia.org/wiki/Endocarditis
  

Peroneus tendons

Remember that ligaments are
structures that connect bone to bone wheras tendons are structures that muscle to bone.

The peroneus tendons are often involved in inversion sprains of the ankle if they are overstretched.

The peroneus longus muscle arises from the head and lateral/superior shaft of the fibula. It follows a path down the lateral side of the leg passing behind the lateral malleolus and goes under the lateral aspect of the foot to attach on the plantar surface (bottom) of the foot on the medial cuneiform and the base of the first metatarsal. It performs ankle plantarflexion and eversion.

The peroneus brevis muscle arises from the shaft of the fibular, but more distally on the shaft than peroneus longus. It also passes down the lateral aspect of the lower leg and behind the lateral malleolus to insert on the lateral tubercle of metatarsal V. Unlike peroneus longus, it does not go under the foot. It also performs plantar flexion and eversion of the ankle.

References:

• http://www.dubinchiro.com/features/PDF/16ankle.pdf
• http://www.courses.vcu.edu/DANC291-003/unit_8.htm
  

Management of AF

References:

• http://www.aafp.org/afp/20020715/249.html
  

Difference between a twitch and a tremor

A twitch is a jerky or spasmodic movement.

A tremor is an involuntary, rhythmical, alternating movement.

Pars defect

Spondylolysis is a condition in which the there is a defect in a portion of the spine called the pars interarticularis (a small segment of bone joining the facet joints in the back of the spine). The pars interarticularis defect can be on one side of the spine only (unilateral) or both sides (bilateral). The most common level it is found is at L5-S1, although spondylolisthesis can occur at L4-5 and rarely at a higher level.

Spondylolysis is the most common cause of isthmic spondylolisthesis, in which one vertebral body is slipped forward over another.

References:

• http://www.spine-health.com/topics/cd/spondy/spondy01.html
• http://www.chirogeek.com/005_Spondylo-Slide-Show.htm
  

Ottawa ankle rules

Online resources

• Wikipedia has a nice, short summary of these rules.
• An online version of these rules in also available.

References

• http://www.mdcalc.com/anklekneerules
  

S1Q3T3

What it is

The S1Q3T3 is the ECG manifestation of acute pressure and volume overload of the right ventricle.

It is characterised by:

• Lead I - an S wave signifying a complete or more often incomplete RBBB.
• Lead III - a Q wave, slight ST elevation, and an inverted T wave. These findings are due to the pressure and volume overload over the right ventricle which causes repolarization abnormalities.

Causes

Any cause of acute cor pulmonale can cause the S1Q3T3 finding on the ECG. This includes PE, acute bronchospasm, pneumothorax, and other acute lung disorders. In addition, transient LPFB may cause this finding as well.

What this means for Dx'ing PE

The ECG is often abnormal in PE, but findings are not sensitive & not specific. S1Q3T3 pattern is present in only in 20% of cases of PE.

The ECG is a poor diagnostic tool for PE. The greatest utility of the ECG in the patient with suspected PE is ruling out other potential life-threatening diagnoses such as MI.


References:

• http://medicine.ucsf.edu/housestaff/Chiefs_cover_sheets/ecg_pe.pdf
• http://www.ispub.com/ostia/index.php?xmlFilePath=journals/ijem/vol3n1/cor.xml
  

Ileus

Ileus is a partial or complete non-mechanical blockage of the small and/or large intestine. It causes colic, vomiting, and constipation.

Ileus occurs because peristalsis stops. Causes of ileus include:

• peritonitis
• disruption or reduction of the blood supply to the abdomen e.g. post-operatively
• kidney diseases, especially when potassium levels are decreased
• gallstone ileus - obstruction of the large intestine by a gallstone that has blocked the intestinal opening.

References:

• http://www.answers.com/topic/ileus
• http://www.answers.com/gallstone%20ileus
  

Pneumoperitoneum

Pneumoperitoneum is air or gas in the abdominal (peritoneal) cavity.

A pneumoperitoneum is deliberately created by the surgical team in order to perform laparoscopic surgery. This is achieved by insufflating the abdomen with carbon dioxide.

Aetiology

The most common cause is a perforated abdominal viscus, generally a perforated ulcer, although any part of the bowel may perforate from a benign ulcer, tumor or trauma.

A perforated appendix seldom causes a pneumoperitoneum.

Diagnosis

It is often seen on x-ray, but small amounts are often missed and CT is nowadays regarded as the gold standard in the assessment because CT can visualize as small as 5 cm cubic air.

Complications

Increased intrathoracic pressure -> decreased venous return. This means that DVT prophylaxis is required!!

References:

• http://en.wikipedia.org/wiki/Pneumoperitoneum

Reactive arthritis

Reactive arthritis aka Reiter's syndrome aka Reiter's disease aka arthritis urethritica, venereal arthritis, seronegative spondyloarthropathy, polyarteritis enterica.

Reactive arthritis is a RF-seronegative, HLA-B27-linked spondyloarthropathy with symptoms similar to arthritis or rheumatism. It is caused by genitourinary or gastrointestinal infections, and is thus "reactive", i.e. dependent on the other condition.

Reactive arthritis is the combination of three seemingly unlinked symptoms:

1. an inflammatory arthritis of large joints
2. inflammation of the eyes (conjunctivitis and uveitis), and
3. urethritis.

Epidemiology

• Most commonly strikes individuals aged 20-40.
• More common in men than in women.
• More common in white men than in black men due to white individuals being more likely to have tissue type HLA-B27 than black individuals.
  
• People with HIV have an increased risk of developing reactive arthritis.

History

Reactive arthritis was first described by Hans Reiter, a German military physician, who in 1916 described the disease in a World War I soldier who had recovered from a bout of diarrhea.

The term Reiter's syndrome is being phased out, partly due to a move in the field of medicine to give descriptive names, rather than personal names, to conditions, and partly due to Dr. Reiter's experiments in Nazi concentration camps.

Causes

• Reactive arthritis is set off by a preceding infection, the most common of which would be a genital infection with Chlamydia trachomatis.
• Other bacteria known to cause reactive arthritis are Neisseria gonorrhoeae, Ureaplasma urealyticum, Salmonella spp., Shigella spp., Yersinia spp., and Campylobacter spp..
• A bout of food poisoning or a gastrointestinal infection may also trigger the disease.
• Reactive arthritis usually manifests about 1-3 weeks after a known infection.

Pathophysiology

The mechanism of interaction between the infecting organism and the host is unknown.

Synovial fluid cultures are negative, suggesting that RA is caused either by an over-excited autoimmune response or by bacterial antigens which have somehow become deposited in the joints.

Signs and symptoms

• Symptoms generally appear within 1-3 weeks but can range from 4-35 days from the onset of the inciting episode of the disease.
• The classical presentation is that the first symptom experienced is a urinary symptom such as burning pain on urination (dysuria) or an increased need to urinate (polyuria or frequency).
• Other urogenital problems may arise such as prostatitis in men, and cervicitis, salpingitis and/or vulvovaginitis in women.
• The arthritis that follows usually affects the large joints such as the knees causing pain and swelling with relative sparing of small joints such as the wrist and hand.
• Eye involvement occurs in about 50% of men with urogenital reactive arthritis and about 75% of men with enteric reactive arthritis. Conjunctivitis and uveitis can cause redness of the eyes, eye pain and irritation, and blurred vision.
• Roughly 20 to 40 percent of men with reactive arthritis develop penile lesions called balanitis circinata (circinate balanitis) on the end of the penis. A small percentage of men and women develop small hard nodules called keratoderma blennorrhagica on the soles of the feet, and less often on the palms of the hands or elsewhere. In addition, some people develop mouth ulcers that come and go. In some cases, these ulcers are painless and go unnoticed.
• About 10 percent of people with Reactive Arthritis, especially those with prolonged disease, will develop cardiac manifestations including aortic regurgitation and pericarditis.

Commonly remembered with the mnemonic "Can't See, Can't Pee, Can't Climb a Tree"

Diagnosis

There are countless clinical symptoms, but the clinical picture is dominated by polyarthritis. There is pain, swelling, redness, and heat in the joints. MRI's are effective for diagnosis.

The urethra, cervix and throat may be swabbed in an attempt to culture the causative organisms. Cultures may be carried out on urine and stool samples.

Synovial fluid from an affected knee may be aspirated to look at the fluid under the microscope and for culture.

A blood test for the gene HLA-B27 may be given to determine if the patient has the gene. About 75 percent of all patients with Reiter's Syndrome have the gene.

Treatment

• The main goal of treatment is to identify and eradicate the underlying infectious source with the appropriate antibiotics.
• Treatment is symptomatic for each problem. Steroids and analgesics may be given for severe joint inflammation.
  
• Immunosuppressants may be needed for patients with severe reactive arthritis who do not respond to any other treatment.

Prognosis

• Reactive arthritis may be self limiting, frequently recurring or develop continually.
• Most patients have severe symptoms lasting a few weeks to six months.
• Approximately 15 to 50 percent of cases have recurrent bouts of arthritis.
• Chronic arthritis or sacroiliitis occurs in 15-30 percent of cases.
• Repeated attacks over many years is common, and more than 40 percent of the patients end up with chronic and disabling arthritis, heart disease or impaired vision.
• However, most people with reactive arthritis can expect to live normal life spans and maintain a near-normal lifestyle with modest adaptations to protect the involved joints.

References:

• http://en.wikipedia.org/wiki/Reiter%27s_disease

Molar pregnancies

Molar pregnancy aka Hydatidiform mole aka mola hydatidiforma is a common complication of pregnancy, occurring once in every 1000 pregnancies in the US, with much higher rates in Asia (e.g. up to one in 100 pregnancies in Indonesia).

It consists of a nonviable embryo which implants and proliferates within the uterus.

Clinical presentation

Molar pregnancies usually present with painless vaginal bleeding in the fourth to fifth month of preganancy.

Diagnosis

• Ultrasound makes the definitive Dx - the uterus may be larger than expected, or the ovaries may be enlarged.
• There may also be hyperemesis (more vomiting than would be expected).
• Sometimes there is an increase in BP along with proteinuria.
• Blood tests will show very high levels of hCG.
• Sometimes symptoms of hyperthyroidism are seen, due to the extremely high levels of hCG, which can mimick the normal TSH.

Pathophysiology

• A mole is characterized by a conceptus of hyperplastic trophoblastic tissue attached to the placenta. The conceptus does not contain the inner cell mass (the mass of cells inside the primordial embryo that will eventually give rise to the fetus).
• The hydatidiform mole can be of two types: a complete mole, in which the abnormal embryonic tissue is derived from the father only; and a partial mole, in which the abnormal tissue is derived from both parents.

Treatment

• Hydatidiform moles should be treated by evacuating the uterus by uterine suction or by surgical curettage as soon as possible after diagnosis.
• Patients are followed up until their serum hCG titre has fallen to an undetectable level.
• Invasive or metastatic moles often respond well to methotrexate. The response to treatment is nearly 100%.
• Patients are advised not to conceive for one year after a molar pregnancy.
• The chances of having another molar pregnancy are approximately 1%.

References:

• http://en.wikipedia.org/wiki/Molar_pregnancy
  

Ring Blocks

A digital ring block (aka digital block) is the technique of blocking the nerves of the digits to achieve anesthesia of the finger(s). It is a useful procedure to facilitate minor surgery of the finger.

The nerves to be blocked are the palmar and dorsal digital nerves.

The two palmar nerves supply the anterior aspect of the fingers and are the terminal branches of the median nerve (lateral 3 1/2 fingers) and ulnar nerve (little finger and 1/2 ring finger).

The two dorsal nerves supply the posterior aspect of the fingers and arise from the radial nerve (lateral 2 1/2 to 3 1/2 fingers) and ulna nerve (medial 1 1/2 to 2 1/2 fingers).

If seen in cross section the nerves are at two, five, seven and ten o'clock positions

The procedure:

• The patient's hand and fingers are extended and fingers abducted from each other.
  
• The head of the metacarpal bone and base of the proximal phalanx is felt.
  
• The skin is cleaned.
• The needle is introduced between the fingers at the point of the interdigital fold and a skin wheal is raised. This is at the level of the head of the metacarpal bone.

• The needle is advanced along the axis of the fingers until the palmar aponeurosis is
  reached which is felt as a resistance.
  
• Before injection of local anaesthetic the needle must be aspirated to prevent intra-
  vascular injection.
  
• 1 to 2 mls of local anaesthetic is introduced as the needle is withdrawn.
  
• Subcutaneous injection around the base of the finger is then done through the same skin
  wheal to block the palmar and dorsal digital nerves.
• The procedure is repeated on the opposite side of the finger.
  
• Massaging the finger after infiltration facilitates spread and increases absorption of the
  local anaesthetic.
  

References:

• "Digital Ring Block", Dr. Mary Daniels, Department of Anaesthesia, The Chinese University of Hong Kong, http://sunzi1.lib.hku.hk/hkjo/view/23/2300620.pdf
• "Digital Nerve Block", Dr A Hazdic, New York School of Regional Anaesthesia, http://www.nysora.com/techniques/digital_block/
  

Marcain

Composition

Bupivacaine hydrochloride +/- Adrenaline

Actions

Bupivacaine is classed as a membrane stabilising agent and is a local anaesthetic of the amide type. Like all amines it causes a reversible blockade of impulse propagation along nerve fibres by preventing the inward movement of sodium ions through the nerve membrane.

Pharmacokinetics

Bupivacaine is a long acting, amide type local anaesthetic chemically related to lignocaine and mepivacaine. It is approximately four times as potent as lignocaine.

References:

• MIMS
  

Indomethacin

Drug class

NSAID

Action

Potent inhibitor of prostaglandin synthesis. Affords relief of symptoms but does not alter the progressive course of the underlying disease.

Uses

Arthritis and related inflammatory disorders; low back pain; postop bone pain; primary dysmenorrhoea, IBD.

Contraindications

NSAID sensitive asthma; active peptic ulcer, recurrent GI ulceration; pregnancy, lactation

Sold as

Athrexin

Arterial vs venous clots

Arterial clots

Arteries are thick blood vessels with fast flowing blood. Blood clots in arteries are typically triggered by underlying arteriosclerosis (roughening of the artery wall). Blood platelets get stuck to the roughened blood vessel wall and form a clot. Thus, the medication of choice in trying to prevent thrombosis in arteries are medications that act against platelets. The following medications are anti-platelet drugs:

• Aspirin (= ASA)
• Plavix (= Clopidogrel)
• Ticlid (= Ticlopidine)
• Aggrenox (= aspirin plus dipyridamole)

By interfering with platelet function, these drugs increase the patient's risk of bleeding, even though to a lesser degree than coumadin. The INR is not influenced by these drugs and vitamin K intake does not influence their effect.

Venous clots

Veins are thin blood vessels with slow flowing blood. Blood clots that form in veins (DVT, pulmonary embolism) are mainly made up of clotting proteins; platelets do not play a big role in venous clots. Warfarin is an effective anticoagulant by preventing the production of clotting factors in the liver, increasing the INR. It is therefore the drug of choice in venous thrombosis. Anti-platelet drugs do not play much of a role in preventing venous clots.

Occasionally, clots in arteries originate from one of the two left heart chambers and travel from there with the blood stream to the brain, the retina, or the extremities. This typically happens in atrial fibrillation. Such a clot is an arterial embolism that resembles the type of clots seen in veins i.e. they have little platelet participation. They are therefore best treated with warfarin, not with anti-platelet drugs, even though they are clots in arteries.

References:

• Thrombophilia Support page
  

INR & warfarin

If a patient's INR is > 3 (normal 0.8-1.2) then stop warfarin for a few days rather than reversing it with Vit K/FFPs.

Aneurysms

An aneurysm is a localized abnormal dilation of a blood vessel or the wall of the heart.

Classification of aortic aneurysms

Aneurysms can be classified by macroscopic shape and size.

• Saccular aneurysms are essentially spherical (involving only a portion of the vessel wall) and vary in size from 5 to 20 cm in diameter, often partially or completely filled by thrombus.
  
• Fusiform aneurysms involve a long segment and vary in diameter (up to 20 cm) and length; many involve the entire ascending and transverse portions of the aortic arch, whereas others may involve large segments of the abdominal aorta or even the iliacs.
  

The shape of an aneurysm is not specific for any disease or clinical manifestations.

Causes of aortic aneurysms

• atherosclerosis - causes arterial wall thinning through medial destruction secondary to plaque that originates in the intima.
• cystic degeneration of the arterial media
  
• trauma (traumatic aneurysms or arteriovenous aneurysms)
• congenital defects such as those causing berry aneurysms (in the brain)
  
• infection resulting in mycotic aneurysms,
• systemic diseases e.g. vasculitides

Abdominal aortic aneurysms

• Usually positioned below the renal arteries and above the bifurcation of the aorta.
• Saccular or fusiform, sometimes up to 15 cm in greatest diameter and of variable length (up to 25 cm).
  
• The aneurysm and the nearby aorta often contain atheromatous ulcers covered by granular mural thrombi, prime sites for the formation of atheroemboli that may lodge in the vessels of the kidneys or lower extremities.
• AAAs rarely develop before age 50 and are more common in men.
  
• There is a genetic susceptibility to AAA beyond the genetic predisposition to atherosclerosis or HT.
  

Aneurysm growth

Most aneurysms expand at a rate of 0.2 to 0.3 cm/year, but 20% expand more rapidly. The most important clinical factor affecting aneurysm growth is blood pressure.

Clinical consequences of AAAs

• Rupture into the peritoneal cavity or retroperitoneal tissues with massive, potentially fatal, hemorrhage.
• The risk of rupture is directly related to the size of the aneurysm.
• Risk varies from zero for a small AAA (less than approximately 4 cm in diameter), to 1% per year for aneurysms measuring 4.0 to 4.9 cm indiameter, 11% per year for aneurysms between 5.0 and 5.9 cm in diameter, and 25% per year for those larger than 6.0 cm.

• Obstruction of a vessel, particularly of the iliac, renal, mesenteric, or vertebral branches that supply the spinal cord leading to ischemic tissue injury
• Embolism from atheroma or mural thrombus
• Impingement on an adjacent structure, such as compression of a ureter or erosion of vertebrae
• Presentation as an abdominal mass (often palpably pulsating) that simulates a tumo

Management Large aneurysms are managed aggressively; operative mortality for unruptured aneurysms is approximately 5%, whereas emergency surgery after rupture carries a mortality rate of more than 50%.

The treatment of abdominal and thoracic aortic aneurysms is evolving toward endoluminal approaches using stent grafts (expandable wire frames covered by a cloth sleeve) rather than surgery for some patients.

Divarication

The rectus abdominis muscles should meet in the midline at the linea alba. Superior to the umbilicus, some people have a congenital defect that results in a widened linea alba. As a result, when a patient flexes the abdominal muscles the rectus muscles spread apart (divaricate).

Divarication and abdominal hernias appear very similiar. To differentiate between a divarication and a hernia clinically:

• get the patient to do a sit-up - rectus muscles spread apart in both a hernia and a divarication
• get the patient to cough - rectus muscles will only split apart if its a hernia. When coughing all abdominal muscles are used (not just the rectus), so a divarication will show a diffuse bulging, rather than locally down the midline.
  

Divarication is common in obese men. It can be surgically corrected, although such an operation would be almost entirely for cosmetic purposes and not of any functional value (unlike a hernia).

Blood flow patterns

Peripheral muscular arteries always show a triphasic pattern (forward-reverse-forward flow):

• forward - steep rise during ventricular systole
  
• reverse - brusque return to baseline with a small negative wave in early diastole caused by the high resistance of small peripheral arteries and capillaries
• forward - slow late diastolic rise due to the compliance of the peripheral arterial walls.
  

A monophasic waveform without the reverse component occurs when the volume in the artery is insufficient and extra flow is required during diastole. This is usually because stenosis or occlusion reduces the blood available to fill the reservoir during systole, but may also occur when there is a large flow to the limb caused by exercise or gross infection.

Neostigmine methylsulfate

Actions

• An anticholinesterase agent which reversibly inhibits the hydrolysis of acetylcholine by competing with acetylcholine for attachment to acetylcholinesterase. As a result, acetylcholine accumulates at cholinergic synapses and its effects are prolonged and exaggerated.
  
• Produces a generalised cholinergic response, including miosis, increased tonus of intestinal and skeletal musculature, constriction of bronchi and ureters, bradycardia and stimulation of salivary and sweat glands.
  
• Used mainly for its direct cholinomimetic effect on skeletal muscle and to a lesser extent to increase the activity of smooth muscle.
• Because of its quaternary ammonium structure, neostigmine in moderate doses, does not cross the BBB to produce CNS effects. Extremely high doses, however, produce CNS stimulation followed by CNS depression.

Indications

• Reversal of the effects of neuromuscular blocking agents (e.g. tubocurarine, pancuronium).
  
• Prophylaxis and treatment of postoperative intestinal atony and urinary retention.
  
• Treatment of myasthenia gravis during acute exacerbations, when the condition is severe, or in neonates.

Pharmacokinetics

• For IV administration the elimination half-life is 47-60 minutes.
• For IM administration the elimination half-life is 50-91 minutes.
  
• Approximately 80% of a single IM dose of neostigmine is excreted in the urine in 24 hours, about 50% as unchanged drug and the remainder as metabolites.
  
• The major site of uptake is in the liver. It is metabolised partly by the hydrolysis of the ester linkage and partly by microsomal enzymes in the liver.

Difference between purpura and ecchymoses

Moved to http://didiaskfor.freehostia.com/index.php?n=CR.AbnormalBleeding

PBL 1 - Structure of synovial joints

Common postoperative problems

Postoperative complications are common, despite good pre-op assessment, surgical technique and perioperative management.

Complications can be minimised by regular and close postoperative patient observation. Managing complications effectively requires quick diagnosis and treatment before the complication gets out of hand.

Postoperative pain

• Pain from surgical wounds should subside over the first few days, and should be controlled by planned analgesia. Some types of wounds (e.g. vertical abdominal incisions) are more painful than others.
• Postoperative pain can be reduced by:
  
  • Preoperative counselling - letting the patient know in advance what to expect after the operation in terms of wounds, IV lines, catheters, extent of pain, plans for pain relief and degree of mobility.
    
  • Peroperative measures - preemptive analgesia to ensure pain does not become established after operation e.g. long acting analgesics, local anaesthetic infiltration into the sound edges, regional nerve blocks, morphine epidurals etc.
    
  • Postoperative analgesia - better to prevent pain than to react to established pain!
    
  
  
• Patients vary in their tolerance for pain and need for analgesics. Anxiety, exhaustion and sleep deprivation all reduce pain tolerance.
  
• If the pain is not controlled by what seems to be a normal dose and frequency of analgesia, complications should be suspected.
  
  • Review dose in relation to expected severity of pain and the weight of the patient.
    
  • Consider local postoperative complications such as haematoma -> wound pain, bleeding into fascial compartment -> compartment syndrome, wound infection -> pain increasing after 48 hours.
    
  
  

Pyrexia

• Infection is not the only cause of postoperative pyrexia, however it should always be considered and investigated as a cause.
• Common postoperative infections include superficial and deep wound infections, chest infections (pneumonia), UTIs and IV cannula site infections.
• Infection is not likely to be a cause in fever developing within 2 hours of surgery - it normally takes longer to develop.
  
• Common non-infective causes of pyrexia include transfusion reactions, drug reactions, wound haematomas, DVT and pulmonary emboli.

Tachycardia

Tachycardia can be benign or malignant.
Benign causes of postoperative tachycardia:

• pain
• anxiety

Malignant causes of postoperative tachycardia:

• infection
• circulatory disturbances
• thyrotoxicosis
• Mild tachycardia can be a sign of incipient hypovolaemic shock resulting from haemorrgahe or dehgydration.
• Cardiac failure.
• AF or flutter.
• Anastomotic leakage - after bowel surgery.
  

Week 2 eve

Well I've officially been in the OC for just over a week. It feels like a lot longer. My emotions tonight are very different to how I felt sitting here at my desk this time last week.

I'm not really nervous about tomorrow (except about getting grilled about pyloric stenosis). I'm actually looking forward to it, although I'm not looking forward to the 6:30am start. The main thing I'm worried about is mucking up my timetable and inadvertently missing a teaching session in the afternoon. I think the only session I have on is a procedural skills one, but I wouldn't bet my life on it.

I'm hoping that this week I can start working out how to come home at the end of the day and do something productive in the afternoon. The main problem so far is in working out what to do. Let's see how tomorrow goes, one day at a time!

Pyloric stenosis

Congenital hypertrophic pyloric stenosis

• Seen in infants as a disorder that affects males three to four times more often than females, occurring in 1 in 300-900 live births.
  
• Familial occurrence implicates a multifactorial pattern of inheritance; monozygotic twins have a high rate of concordance of the condition.
• May occur in association with Turner syndrome, trisomy 18, and esophageal atresia.
  
• The stenosis from hypertrophy, and possibly hyperplasia, of the muscularis propria of the pylorus. Edema and inflammatory changes in the mucosa and submucosa may aggravate the narrowing.

• Regurgitation and persistent, projectile, nonbilious vomiting usually appear in the second or third week of life.
  
• Physical examination reveals visible peristalsis and a firm, ovoid palpable mass in the region of the pylorus or distal stomach.
• Investigations include barium swallow to look for narrowing, blood tests to check for electrolyte imbalances.
  
• A pyloromyotomy - surgical muscle splitting - is curative.

• After surgery, most babies are able to return to normal feedings quickly. The baby starts feeding again 3 to 4 hours after the surgery, and the baby can return to breast-feeding or the formula that he was on prior to the surgery. Because of swelling at the surgery site, the baby may still vomit small amounts for a day or so after surgery. As long as there are no complications, most babies who have undergone pyloromyotomy can return to a normal feeding schedule and be sent home within 48 hours of the surgery.

Acquired pyloric stenosis

• Seen in adults.
• One of the long-term risks of antral gastritis or peptic ulcers close to the pylorus.
  
• Carcinomas of the pyloric region, lymphomas, or adjacent carcinomas of the pancreas are more ominous causes. In these cases, inflammatory fibrosis or malignant infiltration narrow the pyloric channel, producing pyloric outlet obstruction.
  
• In rare instances, hypertrophic pyloric stenosis is the result of prolonged pyloric spasm.

New kids on the block

I’ve got absolutely no idea where to start in describing day 1 in hospital. The morning, and indeed most of the day up until 4pm was the usual orientation stuff – getting id issued, hospital tour etc

I’m doing General Surgery for my first rotation, along with another student, who I’ll call Kate here (all names changed to protect the guilty, remember).

At around 4pm myself and Kate paged our registrar to say hello and find out what time we should turn up tomorrow. He asked if we were close by, and when I said we were in the student’s quarters across the road he asked could we meet him in the ED in 5 mins. We were free for the rest of the afternoon, so why not?

The next few hours we were thrown in the deep end taking histories and doing abdominal physical exams of patients in the ED. Although we had just done this stuff last year, I felt so ill-prepared.

Our reg is a lovely, lovely guy, more than a little crazy and I have no doubt that in the next 4 weeks we are going to learn a hell of a lot, and have fun in the process. He is not of the old-school humiliate-your-students-into-learning way of teaching, but will teach us what we are seeing on the day, and expect us to go and learn about it that night, instead of drilling the crap out of us when it’s the first time we are seeing a given case.

Things were off to an eeirily rosy start, right up until we met our consultant. This week is not a good week to get sick because the teams across the state are basically rebuilt from the ground up: brand new interns first week out of uni, new registrars etc. Chaos.

Our reg hadn’t even met his consultant right up until the consultant walked into the room where I was interviewing a patient who presented earlier that day with a palpable mass and right groin pain. Not long after the consultant walked in, our reg walked in. Not long after he walked in, Kate walked in. Our consultant had obviously had enough of people walking in the room, because he then yelled at us all to get out. The reg was mortified and apologized that we had to witness that. He’d never seen anyone act like that before.

Since then he has talked to the consultant who has calmed down and is apparently apologizing to us tomorrow morning. Talk about drama. Let’s see how this unfolds tomorrow!

New beginnings

The first two years of college are vocabulary lessons.
The second two years are spent learning who to ask and where to look it up.
--Bill Austin

Today was my second day of 3rd year.

Yesterday was spent at uni, in a lecture theatre full of our entire 200-and-something person cohort hearing all about the structure of this year - our rotations, our assessments, how to do Honours, what forms we have to have filled in and hoops we have to have jumped by the end of this year. All this information is summarised in a 70 page handbook. After 6 hours of that, it was all a bit much.

Today was spent at hospital, finding out in more detail where we are expected to be when, what rotations we will be doing, which groups we are in for the different course components, all of which was laid out in a mere 120 pages.

Talk about information overload. I still have no clue exactly what I should and will be doing next week, and I'm still petrified I'll get to the end of this year and realise that I haven't completed some important task such as witnessing an autopsy or performing a PR.

I was alarmed to hear from several speakers that this year is the toughest year of our course. In a lot of ways I feel like I only made it through last year by the skin of my teeth - both in academic terms, and in terms of motivation and sanity. I'm not sure if I have recovered even now.

It's a bit disheartening to hear that even after this year everyone still feels like they are below the curve, despite that fact that this in the year in which we develop most of the clinical skills that will take us through our career. We have been warned finishing this year with big gaps will leave us no future chance to gain the knowledge we missed this year. This is our chance and we need to work our assess off to make the most of it.

In a lot of ways I am exhausted already. I have no idea how I am going to feel next week once this caper gets going properly, let alone 6 months from now when another barrier exam starts looming large.

Today we were encouraged to spend time every day reflecting on what we have seen and learnt in the hospital, and to make a log of it if we can. To remember the patients we see as people, to see the human side of the diseases we learn about. That's how to learn and remember it, how to make it important to us.

Although this is no easy task, that’s why I'm starting this new blog. It's going to be both my log book, and my developmental portfolio.

All names and particulars will be changed to protect both the guilty and the innocent.