|
Yoracle
|
Tachyarrhythmias |
|
|
|
Contributed by randeep
|
|
Wednesday, 12 December 2007 |
|
Untitled Document
HR > 100 bpm)
Broad Complex
- ECG findings:
- Rate > 100 bpm
- QRS complex > 120ms/3 small squares
- Differentials include VT, or SVT with aberrant conduction (LBBB or RBBB). Should always think VT first as this is immediately life threatening and much more common. Irregular rhythms caused by, Torsades de pointes and AF or atrial flutter with variable block.
On ECG VT will show left axis deviation, AV dissociation, fusions/capture beats, QRS concordance in chest leads
- Connect to cardiac monitor and gain IV access
- Have defibrillator close by
- 100% oxygen
- Ix – bloods, ECG, ABG, CXR
- Correct biochem abnormalities
- Amiodarone – 300mg IV over 20-60mins then 900mg over 24hr
- OR lidocaine – 50mg IV over 2min then repeated every 5min until 200mg given
- IF VT starts >24hrs after MI then give IV lidocaine & oral amiodarone
Check the BLS algorithm early on to plan your management!
Effects of adenosine:
- Tachycardia terminates = SVT (AVNRT, AVRT)
- Ventricular rate slows unmasking atrial activity = AF, atrial flutter
- No effect = VT
- Patient feels like they are being kicked in the chest!
Narrow Complex
- Originate above the Bundle of His in either the atria or conduction system.
- EGC findings:
- Rate > 100 bpm
- QRS complex < 120ms/3 small squares
- Irregular with NO p waves either AF or atrial flutter with variable block
- Irregular + >3 p waves = multifocal atrial tachycardia
- Regular with flutter waves, seen most often in V1 raises possibility of atrial flutter, rate of 150 = 2:1 block, rate of 100 = 3:1 block and so on
- Differentials include sinus tachycardia, SVT (absent p wave), AF (absent p wave with irregular rate), atrial tachycardia, junctional tachycardia (AVNRT, AVRT).
- Management:
- Connect to monitor and get IV access
- 100% oxygen
- IF rhythm is regular then perform vagal manoeveres (carotid sinus massage, valsalva) to unmask atrial rhythm. If this fails use adenosine 6mg fast IV dose, then 12mg
- IF there are adverse signs (BP<90, HF, reduced conscious level, chest pain, cardiac failure), sedate and synchronised DC cardiovert, then amiodarone infusion
- IF irregular rhythm with likely AF and no adverse signs then give digoxin or IV metoprolol to reduce rate.
- Heparin to reduce risk of thromboembolism in patients with AF
|
|
Last Updated ( Wednesday, 12 December 2007 )
|
|
|
Dermatological Manifestations of Cancer |
|
|
|
Contributed by Rachel Blears
|
|
Thursday, 06 December 2007 |
|
Untitled Document
1.
Acanthosis nigricans
Brown-grey papillomatous/keratotic skin lesions on flexor surface, neck and axillae
Rare paraneoplastic syndrome assoc with highly malignant internal carcinoma
Most commonly secondary to gastric malignancy
2. Erythema gyratum repens
Concentric erythematous/exfoliant arcs and rings spread across skin at 1cm/day
Commonly associated with internal malignancy including lung (most common), breast, bladder and stomach
Extensive screen for occult malignancy required at least 5-10 yrs after disappearance of rash
3. Necrolytic migratory erythema
Rare psoriasiform skin disorder affecting the genital and anal region, buttocks, groin and lower legs
Fluctuates in severity; ring shaped erythema → blistering and crusting; painful and itchy
Possible association with Glucagonoma – slow growing tumour of α-cells of pancreas (affects over 50’s)
4. Heliotrope rash (dermatomyositis)
Patchy violet heliotrope rash on face, neck, upper chest, elbows, knees, knuckles and back
Gottron’s lesions – erythematous scaly lesions on elbow and knees
Periocular oedema seen
Adult onset form is associated with several malignancies including stomach and breast
5. Superficial Thrombophlebitis
Widespread/recurrent forms associated with carcinoma of the tail of the pancreas
Redness, swelling and tenderness along the course of a vein (eg long saphenous vein)
|
|
Last Updated ( Thursday, 06 December 2007 )
|
|
|
Dermatology Definitions |
|
|
|
Contributed by Rachel Blears
|
|
Thursday, 06 December 2007 |
|
Untitled Document
Below are some commonly used dermatological words with a brief definition followed by typical examples:
- ABSCESS – pus filled lesion, erythematous, tender, fluctuant, painful, may discharge
- Typically results from staphylococcal infection
- Incision and drainage; swab if oozing, antibiotics only if septic
- BLISTERS – vesicles <5mm, bullae >5mm; intra-epidermal vs sub-epidermal (intra are easily ruptured)
- Burns, scalds, friction, viruses (varicella zoster, herpes zoster, herpes simplex), impetigo, insect bites, papular urticaria, scabies, photosensitivity, drugs (barbiturate OD)
- Swab and culture if infection suspected
- CRUSTING – dried exudate (pus, blood, serum),
- Blepharitis – may be staphylococcal, contact dermatitis, seborrhoeic (incl scalp, brows and ears)
- Infection → Lid hygiene, topical AB’s (fusidic acid gel)
- Allergic → Avoid allergen, short course mild steroid cream
- Seborrhoeic → Meticulous daily cleaning of affected areas, remove scales daily from lids
- CYSTS – epithelial lined cavity containing viscous/semi-solid epithelial degradation products
- Epidermal/pilar (hair follicles), ganglion (joint synovium/tendon sheaths)
- Infected epidermal → incision, drainage, culture, antibiotics
- Uninfected epidermal → remove under LA; ensure all remnants are removed as frequently recur
- Pilar cysts → excision
- Ganglion → spontaneous resolution, aspiration, steroid injection if recurs
- ERYTHEMA – red skin due to vasodilation, should blanch on pressure
- Slapped cheek disease (human erythrovirus B19), erythema multiforme, erythema nodosum, multiple causes
- ERYTHRODERMA – generalised redness of >90% of body SA.
- Psoriasis, eczema, urticaria
- Treat systemically, can result in high output cardiac failure so IV access and fluids are essential
- EXCORIATION – superficial loss of substance, such as skin due to scratching
- GRANULOMA – a discrete region of granulomatous inflammation (defined by histology)
- Infection (tuberculosis, leprosy, syphilis, brucellosis, Schistosomiasis, Cryptococcus neoformans)
- Inorganic material (silica, beryllium, asbestos, pneumoconiosis, talc, zirconium)
- Systemic diseases (sarcoidosis, rheumatoid arthritis, Wegener's granulomatosis, Crohn's disease)
- Caseating = dead tissue = TB, non-caseating = no necrosis = sarcoidosis, Crohns etc
- KERATINISATION – disruption of keratinisation causes several common disorders.
- Corns/callosities (due to pressure), keratosis pilaris (grey, hard follicular plugs and red papules on outer aspect of upper arms and thighs – common in adolescence)
- LICHENIFICATION - chronic thickening of the epidermis with prominence of the normal skin markings
- Chronic scratching/rubbing, common in eczema
- MACULE - flat - ie non palpable - area of altered skin colour or texture < 1cm
- NODULE - raised solid lesion, larger than 0.5 cm both width and depth, may be inspected or palpated
- PAPILLOMA - benign tumour caused by overgrowth of all elements of the skin; pedunculated, smooth, soft, solid and of any shape, < 1cm, common on face and neck, common in elderly
- PAPULE - small, superficial elevation < 0.5 cm in diameter
- PETECHIAE - purpura < 1 cm diameter
- Thrombocytopenia (viruses, marrow infiltration, alcohol, megaloblastic anaemia, SLE, heparin induced, DIC, thrombotic thrombocytopaenic purpura, haemolytic uraemic syndrome)
- Platelet dysfunction (myelodysplasia, dysproteinaemia, uraemia, liver disease, hypoglycaemia, cardiopulmonary bypass, anti-platelet antibodies, DIC, drugs e.g. aspirin)
- Small vessel disease (septicaemia, endocarditis, Cushings, steroid abuse, vasculitis)
- PLAQUE - elevated, disc-like lesion, > 2 cm, no substantial depth
- PURPURIC RASH - skin lesions < 2 mm diameter (leakage of blood into the skin) Non-blanching, typical rash of meningococcal septicaemia
- PUSTULE – pus filled lesion < 1cm diameter
- Folliculitis, acne vulgaris, rosacea, pustular psoriasis, halogen eruptions, infected eczema, fungal infections
- WEAL - elevated, oedematous, evanescent area surrounded by a zone of erythema
Feel free to send us more dermatology definitions and we will continue to add them to this page
|
|
Last Updated ( Thursday, 06 December 2007 )
|
|
|
Hepatitis - General |
|
|
|
Contributed by Sadia
|
|
Monday, 03 December 2007 |
|
Untitled Document
Liver disease- with any condition affecting the liver (Viral hepatitis, autoimmune hepatitis, alcoholic liver disease, paracetamol overdose, Haemochromatosis, wilson’s disease or alpha-1 antitrypsin defieciency), you can get a spectrum of presentations. These are: Acute liver disease, fulminant hepatic failure and chronic liver disease. The most important aspects of each of these are highlighted below.
Acute liver disease
- Short-term liver inflammation which is self-limiting
- Jaundice, nausea, anorexia, RUQ pain, fever and fatigue
- Causes are: Viral hepatitis, Autoimmune hepatitis, wilson’s disease, Haemochromatosis, alcohol
Fulminant hepatic failure (is kind of like acute liver failure)
- Progression from normal liver to liver failure within 8 weeks
- Clinical features are encephalopathy, jaundice and haemorrhage
- Management- resuscitate, broad spectrum antibiotics and transplantation
Chronic liver failure
- Can be divided into compensated and decompensated. Compensated implies a relatively well patient, whereas those with decompensation have substantial symptoms and/or signs
- This progresses to liver fibrosis and cirrhosis (due to long term liver damage)
- Cause portal hypertension and GI bleed, ascites, encephalopathy
- Treatment: Varices (as for GI bleed), ascites (spiranolactone and salt restriction) and encephalopathy (lactulose-to reduce nitrogenous waste)
With all three of the above also need to treat the underlying condition!
Some Examples: Click here to view an enlarged version of this table in .pdf format
|
Hepatitis A |
Hepatitis B (and D) |
Heaptitis C |
Hepatitis E |
Autoimmune |
Definition |
Liver inflammation caused by a viral infection |
Liver inflammation caused by autoantibodies |
Virus Type |
RNA virus |
DNA virus |
RNA virus |
RNA virus |
--- |
Spread/ associations |
Feacal-oral (poor sanitation, poor food hygiene, sewage workers and travel |
Sexual contact, blood and vertical transmission
Hep D co-infects |
Parenteral route- blood products, IV drug abusers, tatoos |
Feacal-oral (see A) can be very severe in pregnant women |
Other autoimmune conditions- DM, vitiligo, KCS |
Incubation period |
3-6 weeks |
3-6 months |
--- |
3-6 weeks |
--- |
Clinical features |
Prodrome- systemic features
Hepatitis- dark urine, pale stools, jaundice (for 3 weeks)
Hepatomegaly, but no stigmata of liver disease |
1-2 week prodome (systemic features + RUQ pain)
Serum sickness (arthralgia, polyarthritis and rash)
Jaundice, dark urine then develop
Stigmata of liver disease present |
Asymptomatic
Mild flu-like
Deranged LFTs
Extra-hepatic- renal dysfunction and skin rash |
Prodrome- systemic features
Hepatitis- dark urine, pale stools, jaundice (for 3 weeks)
Hepatomegaly, but no stigmata of liver disease |
Asymptomatic
Insidious onset (systemic symptoms and amenorrhoea/epistaxis)
Acute hepatitis- Serum sickness (arthralgia, polyarthritis and rash)
Jaundice, dark urine then develop
Stigmata of liver disease present, encephalopathy, ascites |
Pathogenesis |
T-cell mediated damage to hepatocytes and immune response to viral replication. Hepatocyte necrosis, followed by fibrosis and cirrhosis |
T-cell mediated autoimmune attack |
Investigations |
LFTs (AST and ALT raised more than bilirubin and ALP) in severe cases albumin and platelets reduced. Clotting screen. Also rule out other causes (Wilsons, Haemochromatosis, alcohol and alpha1 antitrypsin). Also autoantibodies for autoimmune disease. Also liver Biopsy |
Viral serology |
Anti-HAV IgM in acute pahse (3-5months)
Anti-HAV IgG recovery and long term |
Acute- HBsAg, IgM HbcAg
Chronic- IgG HbcAg and HbeAg (increased infectivity) |
Anti-HCV antibodies (IgM and IgG)
Reverse transcriptase PCR |
Anti-HEV IgM in acute phase (1-4 weeks)
Anti-HEV IgG recovery and long term |
Autoanibodies
- Type 1- ANA, Anti-smooth muscle
- Type 2- Anti-liver/kidney microsomal antibody
- Type 3- Antisoluble liver antigen
|
Management |
Bed rest and symptomatic (anti-emetics, anti-pyretics) cholestyramine for pruritis |
Prevention- blood screening and immunisation for risk groups
Medical- acute (bed rest and symptomatic) chronic (interferon-a or lamivudine) |
Prevention- blood screening, no immunisation
Medical- acute (bed rest and symptomatic) notifiable disease chronic (interferon-a +/- ribavirin) |
Bed rest and symptomatic (anti-emetics, anti-pyretics) cholestyramine for pruritis |
Immunosupression with steroids (long term maintenance) azothiaprine
Liver transplant |
Complications |
- Fulminant hepatic failure
- Post-hepatitis syndrome
|
- FHF
- HCC
- Cirrhosis
- Acute liver failure
|
- FHF
- HCC
- Cirrhosis
- Acute liver failure
|
- Fulminant hepatic failure
- Post-hepatitis syndrome
|
- FHF
- HCC
- Cirrhosis
- Portal hypertension
- Steroid side-effects
|
Prognosis |
No chronic liver disease |
20-30% develop cirrhosis |
80% progress to chronic HCV infection |
No chronic liver disease |
35% complete remission, 50% require life long maintenance. 85 % 5 year survival on treatment |
Screening |
Screen individuals regularly for HCC with liver ultrasound and AFP |
|
|
Last Updated ( Monday, 03 December 2007 )
|
|
|
Wesleyan Medical Sickness |
|
|
|
Written by Administrator
|
|
Tuesday, 20 November 2007 |
|
Wesleyan Medical Sickness |
|
Last Updated ( Sunday, 03 February 2008 )
|
|
Read more...
|
|
| | << Start < Previous 1 2 3 4 5 6 7 8 9 10 Next > End >>
| | Results 37 - 45 of 414 |
|