Showing posts from May, 2010


Laceration ABRASION - superficial skin layer is removed Contusion Avulsion puncture wounds crush injury thermal or chemical wounds

De Quervains Tendosynovitis


Heberden's and Bouchard's nodes

Heberden's and Bouchard's nodes Bony bumps on the finger joint closest to the fingernail are called Heberden's nodes. Bony bumps on the middle joint of the finger are known as Bouchard's nodes. Bony bumps are also common at the base of the thumb. These bumps do not have a nickname, but the joint is called the CMC or carpometacarpal joint. The name comes from the bone of the wrist (carpal) and the bone of the thumb (metacarpal).

dermatofibroma, Neurofibroma

Dermatofibroma Dermatofibroma  - A slowly-growing, benign skin papule, nodule or tumor that usually has overlying hyperpigmentation.  Dermatofibromas clinically exhibit the " dimple sign ," and are the most common growth below the knee in young adults. The true etiology of a dermatofibroma is unknown, but the lesions are thought to arise at sites of prior trauma or as a late histiocytic reaction to an arthropod bite. Microscopic appearance shows a cellular proliferation of spindled cells in the dermis which has an irregular outline and at the periphery, entraps and surrounds the (normal) thickened (“keloidal”) dermal collagen bundles. The cells may appear as fibrocytes, lipid laden histiocytes, and multinucleate histiocytes sometimes containing hemosiderin pigment. These benign dermal proliferations can induce overlying epidermal proliferation. The basal epidermal layer is classically hyperpigmented. It is also known as a fibrous histiocytoma. Clinical: dermatofibroma  

Nevus, lentigo, Seborrheic Keratosis, Pyogenic granuloma

Nevus (pl. Nevi) Nevus (pl. Nevi)  - Umbrella term for a group of benign, circumscribed overgrowth of cells composed of tissue elements normally present in the skin.  The most well known of the group is the melanocytic nevus (“mole”), composed of an increased proliferation of melanocytes, but multiple other types of nevi exist, such as vascular nevi, epidermal nevi, connective tissue nevi. Melanocytic Nevus  - These can be congenital, but most are acquired after birth.  They vary greatly in appearance.  They can be flat, elevated, smooth, rough, polyp-like, or sessile.  Nevi often come in a shade of brown, but some may be skin colored or occasionally blue in color. It is important to distinguish a melanocytic nevus from  malignant melanoma .  A symmetric shape, regular border, uniform color, small size (diameter <6 mm) are features that help distinguish the former from the latter.  Change in color, shape, or size, bleeding, pruritus, or other symptoms may be signs of suspicious l

MRSA - Methicillin-Resistant Staphyloccocus Aureus (MRSA)

Heparin Induced Thrombocytopenia (HIT)

Heparin Induced Thrombocytopenia (HIT): Happening more and more frequently - as we use heparin more and more. Heparin is produced from the intestines of Pigs and Buffalo 50% reduction in platelets while on Heparin within 5 to 15 days of beginning to use Heparin. If previously used Heparin you can get this in a few hours. Pathophysiology: Immune mediated IgG - Ab recognises a complex of Heparin and platelet factor 4 (PF4) leading to platelet activation via platelet Fc receptor and activation of coagulation system - causing thrombocytopenia SE: Non-hemorragic side effects Increase in Aminotransferase - this is not liver dysfunction Increase K levels - hyperkalemia hemorragic side effects thrombosis is detected in 50% of patients: Venous or Arterial 50% decrease in platelets Do an ELISA test to detect the heparin Ab's BLEEDING COMPLICATIONS ARE UNCOMMON Venous thrombosis: DVT and PE Arterial thrombosis: MI, Stroke, limb and mesenteric arteries, adrenal gland involvem

Heparin Induced Trombocytopenia

Happens more frequently as we use more Heparin (HIT) Heparin is produced from the intestines in Pigs and Buffalo In patients using Heparin they get increased Aminotrasferase - (this is not liver dysfunction) HyperKalemia (Potassium level goes up) Platelet count drops to upto 50% Immune mediated,  Ab recognizes the a complex of heparin and platelet factor 4 (PF4) leading to platelet activation via platelet Fc receptor and activation of the coagulation system Pathophysiology:

von Willwbrands Disease - Most Important Points

Most common congenital bleeding disorder, affecting 1-2 percent of the population. vWF - is synthesized by the vascular endothelium, and a cofactor for platelet adhesion and a co factor for factor VIII Forms the clot for the vascular injury site - and attaches 3 types- I,II,III mild quantitative, 90 % present - most common - less serious  quantitative defect - less vWF - more serious Absent - vWF is almost absent - most serious Clinical features: Bleeding particularly in children Mild -  asymptomatic  Mucosal or cutaneoous bleeding - easy bruising, gingival bleeding, epistaxis, menorrhagia Moderate to severe Soft-tissue hematomas, petechiae (rare), GI Bleed and hemarthroses Investigations: Coagulation profile - increased bleeding time and PTT low factor VIII (5 to 50%) (PT and factor VIII is normal - also blood group O has 30% less vWF) platelet count normal reduced ristocetin cofactor activity (normally causes vWF to bind platelets tightly) analysis of vWF multi

HyperKalemia - Potassium increase - Causes, level, diagnosis and Rx:

Hyperkalemia - increase in the level of potassium Causes, level, diagnosis and Rx: s-K> 5.5mmol/l requires emergency management: ECG, repeat bloods,  stop exogenous potassium and potassium retaining medications Assess potential causes of transcellular shift estimate the GFR Drugs: ACE inhibitors, Potassium sparing drugs, digitalis toxicity (blocks the Na/K ATPase, Succinylcholine, B-Blockers Potassium Supliments - Potassium Chloride suppliments or KCl IVI PEN G - antibioltics Breakup of cells: Rhabdomyolysis, tumour lysis syndrome, Hemolysis - the intracellular K leaks out to the extracellular space - increasing potassium in the blood Metabolic Acidosis (except for keto and lactic acidosis) and Insulin deficiency  - DKA - both acidosis and insulin deficiency Potassium can not be  excreated decreased GFR renal failure decreased effective circulating volume NSAID in renal insufficiency HYPOALDOSTERONISM Causes of Hyerkalemia with Normal GFR Low renin and low

Facial Pain

Facial Pain Sinusitis Dental Disease Tic Douloureux (Trigeminal Neuralgia) Trigeminal Neuropathic Pain (secondary to trigeminal nerveinjury or Disease) Glossopharyngeal Neuralgia Postherpetic neuralgia Atypical facial pain Multiple Sclerosis


P ulse rate >120bpm Main differential diagnoses and typical outline evidence Fever Suggested by: warm skin, erythema, sweats, temperature >38°C. Confirmed by: temperature chart, fever pattern and pulse rate↑. Haemorrhage Suggested by: signs of blood loss, pallor, sweats, low BP, poor peripheral perfusion. Confirmed by: low Hb (can be normal in initial stages), low central venous pressure. Hypoxia Suggested by: cyanosis, respiratory distress. Confirmed by: ↓ P a O 2 . Thyrotoxicosis Suggested by: sweating, fine tremor, weight loss, lid lag, frequent bowel movements, sweats. Confirmed by: ↑ FT4 , ± ↑ FT3 and ↓ TSH . Management: Severe anaemia Suggested by: subconjunctival and nail-bed pallor. Confirmed by: ↓ Hb (and indices). Heart failure (LVF, RHF, CCF) associated with ischaemic heart disease, myocarditis etc. Suggested by: 3 rd heart sound, fine crackles at bases, raised JVP. Confirmed by: CX

Paralysis or Paresis

Stroke Tumour Multiple Sclerosis Mysenthenia Gravis Gullian - Barre Syndrome Amyotropic Lateral Sclerosis Myopathies


Stroke This is a sudden onset of a neurological deficit. Some differential diagnoses and typical outline evidence Cerebral infarction Suggested by: onset over minutes to hours of hemiaparesis or major neurological defect that lasts >24 hours. Confirmed by: CT scan appearing after days. Management: Transient cerebral ischaemic attack due to carotid artery stenosis etc. (see below) Suggested by: onset over seconds to minutes of a neurological deficit that is improving already. Confirmed by: deficit resolving within 24 hours. Management: Cerebral embolus due to atheroma, atrial fibrillation, myocardial infarction Suggested by: onset over seconds of hemiaparesis or other neurological defect that lasts >24 hours. Confirmed by: CT scan and lumbar puncture showing little change originally. Evidence of a potential source for an embolus. Management: Cerebral haemorrhage due to atheromatous degeneration, cerebral tumour Suggested by: on

Shaking or Tremor of the Hands

Fine tremor of hands Elicited by asking patient to hold arms out straight in front and placing sheet of paper to rest on them (to amplify fine tremor). Some differential diagnoses and typical outline evidence Thyrotoxicosis Suggested by: fine tremor, anxiety, tachycardia, sweating, weight loss, goitre, increased reflexes. Confirmed by: ↑ FT4 or FT3 and ↓↓ TSH. Management: Anxiety state Suggested by: fine tremor, anxiety, tachycardia, sweating, weight loss, goitre, increased reflexes. Confirmed by: normal thyroid function tests. Improvement with sedation, psychotherapy etc. Alcohol withdrawal Suggested by: fine or coarse tremor, history of high alcohol intake and recent withdrawal, anxiety. Confirmed by: improvement with sedation, etc. Management: Sympathomimetic drugs Suggested by: fine tremor, drug history. Confirmed by: improvement with withdrawal of drug. Benign essential tremor Suggested by: usually coarse tremor, long hi


acute, new onset -  Onset over seconds to hours. Meningitis viral or bacterial Suggested by: photophobia, fever, neck stiffness, vomiting, Kernig's sign. Petechial or purpuric rash (in meningococcal meningitis). Confirmed by: CT brain if neurological signs present, Lumbar puncture —Viral meningitis: CSF clear, ↑lymphocytes, ↑protein, normal glucose). Bacterial meningitis: CSF with ↑neutrophils, ↑protein, ↓glucose ± visible bacteria on gram stain. Management: Low CSF pressure Suggested by: worsening or recurrence of headache after lumbar puncture (usually for suspected meningitis) made worse by sitting up. Confirmed by: spontaneous resolution after few days. Management: Subarachnoid haemorrhage Suggested by: sudden occipital headache (often described as ‘like a blow to the head’), variable degree of consciousness, ± neck stiffness, subhyaloid haemorrhage, ± focal neurological signs. Confirmed by: CT or MRI brain scan. Lumbar punc

One joint affected by pain, swelling, overlying redness, stiffness and local heat

Monoarthritis One joint affected by pain, swelling, overlying redness, stiffness and local heat (±fever). Acute septic arthritis Suggested by: extremely painful, hot red joint, high fever. Confirmed by: increased  WBC . Joint aspiration: synovial fluid turbid. Culture growing staphylococcus or streptococcus or pseudomonas or gonococci or TB, etc. Gout Suggested by: one acutely inflamed joint (usually small esp. big toe) at a time, but other joints in hands, arms, legs, and feet deformed. Tophi on ears and tendon sheaths. Confirmed by: serum urate Increase ( not always). Urate crystals (negatively birefringent in plane-polarised light) present on joint aspiration . Pseudogout (Ca 2+ pyrophosphate arthropathy/ chondrocalcinosis) Suggested by: one painful joint (usually knee) especially in elderly or history of hyperparathyroidism or myxoedema or osteoarthritis or haemochro-matosis or acromegaly. Confirmed by: joint aspiration: synovi

Joint symptoms

Muscle stiffness or pain Usually worse in the early morning often with pain and stiffness. Your GP will consider the following differential diagnoses: Normal response to strenuous exercise Suggested by: fit healthy, unaccustomed exercise 1 to 2 days before. Confirmed by: spontaneous resolution. Polymyalgia rheumatica Suggested by: onset over weeks or months, stiff, painful, and tender proximal muscles. Fatigue, fever in elderly person. Confirmed by:  elevated  ESR . Rheumatoid factor -ve, prompt response to prednisolone, no other cause (e.g. infection on follow-up). Management: See your GP Rheumatoid arthritis Suggested by: early morning stiffness. Fingers showing swan neck or boutonnireâ deformities. Thumbs show Z-deformities. MCP joints and wrists are sublux giving ulnar deviation. Knees: valgus or varus deformity and popliteal Baker's cysts. Feet: subluxation of meta-tarsal heads with hallux valgus, clawed toes. Confirmed by: rheumatoid

Fatigue its causes and fixes

I found this following presentation on fatigue fantastic and thought I must share this with you - author unknown Fatigue Cause No. 1: Not Enough Sleep It may seem obvious but you could be getting too little sleep. That can negatively affect your concentration and health. Adults should get seven to eight hours every night. Fix:   Make sleep a priority and keep a regular schedule. Ban laptops, cell phones, and PDAs from your bedroom. Still having trouble? Seek help from a doctor. You may have a sleep disorder. Fatigue Cause No. 2: Sleep Apnea Some people think they're sleeping enough, but sleep apnea gets in the way. It briefly stops your breathing throughout the night. Each interruption wakes you for a moment, but you may not be aware of it. The result: you're sleep-deprived despite spending eight hours in bed. Fix:   Lose weight if you're overweight, quit smoking, and sleep with a CPAP device to help keep airway passages open at night. Fatigue Cause No. 3: Not Enough Fuel