Handbook Section 3a Flashcards
Common skin lesions, cancers
Basal Cell Carcinoma - pearly pink bump/flat area
Squamous Cell Carcinoma - red scaly occasionally tender plaque
Melanoma - Irregular multicolored flat area
Common skin lesions, benign
Benign Mole - single colored demarcated brown area
Seborrhoeic Keratosis - Stuck on mole
Neurofibromatosis, general definition
Usually diagnosed in childhood, it is a genetic condition characterised by the growth of usually benign neurofibromas
A common sign is ‘café au lait’ spots with vision problems.
Types of neurofibromatosis
Neurofibromatosis type 1 (NF1) — the most common form, caused by a change in a gene on chromosome 17, presents with more than 6 cafe au lait spots
Neurofibromatosis type 2 (NF2) — a very rare form, caused by a change in a gene on chromosome 22, found in ears, brain, spinal cord
Schwannomatosis — similar to NF2, but not associated with inner ear tumours and hearing loss, initially presents with random localized pain
Reactive arthritis (Reiter syndrome) triad
conjunctivitis, urethritis, arthritis
Cranial nerves (OOOTTA FAG VAH)
- Olfactory - smell
- Optic - Visual acuity
- Oculomotor - all eye movement (except SO4, LR6)
- Trochlear - SO eye movement (down medial)
- Trigeminal - Facial sensation, chewing
- Abducens - LR eye movement
- Facial - facial muscles (except chewing)
- Auditory - hearing and balance
- Glossopharyngeal - taste on posterior tongue
- Vagus - swallowing
- Accessory - shoulder shrug
- Hypoglossal - Tongue movement
Common causes of postoperative fever
Lung (aspiration, atelectasis)
Infection
Embolism
Drugs
Ulcer types
Neuropathic ulcers are painless ulcers over areas of abnormal pressure, often secondary to joint deformity in diabetics
Venous ulcers are shallow ulcers with a granulated base, often with other clinical features of venous insufficiency present
Arterial ulcers are found at distal sites, often with well-defined borders and other evidence of arterial insufficiency
Acute primary angle closure glaucoma, presentation
Risk factors
1. Asian
2. Hypermetropia (far sighted)
3. medications that affects the eye
Signs and Symptoms
1. blurred vision
2. haloes
3. eye/brow pain
4. headache
5. red eye
6. nausea and vomiting
Acute primary angle closure glaucoma, examination results
- IOP usually >35mmHg
- Corneal oedema
- Mid-dilated, poorly reactive pupil
- Shallow central and peripheral anterior chamber (AC) in the affected/both eyes
- Closed angle on gonioscopy
- Anterior chamber inflammation
- Signs of previous angle-closure attacks; e.g. peripheral anterior synechiae,
segmental iris atrophy, glaukomflecken, posterior synechiae or irregular pupil
Acute Primary Angle Closure Glaucoma, Management
After history and examination, discuss with specialist if still with doubt
- Acetazolamide - carbonic anhydrase inhibitor (WOF renal)
- Pilocarpine - muscarinic cholinergic (dry)
- Brimonidine - alpha adrenergic (dry)
- Timolol - beta blocker
- Prednisolone - instant corticosteroids
- Mannitol - diuretic
- Laser PI
Follow up 1 week or earlier
Brain death confirmation requirements
REQUIREMENTS MUST BE SUFFICIENT:
1. severe brain injury.
2. condition is not due to sedatives
3. No other reversible cause of the condition
Two senior doctors must perform separate tests to check if the cranial nerves are working
They also check to see if the person:
1. response to pain
2. response when a light is shone in the pupil of each eye
3. blinks or moves when each eye is touched
4. responds to ice cold water put into the ear canal
5. has a cough or gag (swallowing) reaction
6. can breathe when disconnected from the ventilator
For a person to be certified brain dead, they must show no response to every one of these tests.
Wernicke encephalopathy, overview
Risk factor - alcoholic, Vit B1 (thiamine) deficiency
Complication - Wernicke - Korsakoff syndrome (alcohol related dementia)
Presentation:
1. Eyes (drooping, jerking, double vision)
2. Balance (difficulty standing)
3. Movement (difficulty walking)
4. Consciousness (drowsy/confused, disoriented)
3 major nerves in the arm
Front arm
- thumb side (medial nerve)
- pinky side (ulnar nerve)
Back arm (radial nerve)
Cushing’s triad (Increased ICP)
- bradycardia
- irregular respirations
- hypertension
Common fractures - artery/vein and nerve injuries
(TORSO and PELVIS)
TORSO
Vertebra - Spinal cord, nerve root
Clavicle - Subclavian artery, Brachial plexus
PELVIS
Sacroiliac - Sacral plexus, lumbosacral plexus
Acetabulum - Sciatic
Common fractures - artery and nerve injuries
(UPPER EXTREMITIES)
- Proximal Humerus - Axillary and brachial artery; Axillary and Suprascapular nerve
- Humerus shaft - Brachial artery; Radial, Median and Ulnar nerve
- Supracondylar (humerus) - Brachial artery; Median, Anterior interosseous, Radial and Ulnar nerve
- Radius/Ulna - Brachial, Axillary and Ulnar artery; Median and Ulnar nerve
- Scaphoid - Median nerve (Acute carpal tunnel)
Common fractures - artery and nerve injuries
(LOWER EXTREMITY)
- Femur - Femoral artery; Femoral nerve
- Tibia - Popliteal, Anterior tibial and Posterior tibial artery; Tibial, Superficial peroneal and deep peroneal artery
- Fibular head and neck - Peroneal nerve
Stenosing Tenosynovitis (Trigger finger), presentation
The first indication of the condition may be slight stiffness or even “clicking” when flexing the finger/thumb especially in the morning, due to an increasing blockage in the finger “pulley” that facilitates movement.
History:
- common in middle aged women
- trauma/surgery
- repetitive work
- some systemic conditions (gout, arthritis,diabetes)
Dupuytren’s contracture, presentation
palmar fascia becomes thicker and tighter causing the first sign, one or more nodules on the palm. Over time these nodules get bigger which pulls your fingers towards your palm
De quervain’s tenosynovitis, definition
Affecting the extensor pollicis brevis and abductor pollicis longus, inflammation and swelling of the tendon sheaths puts pressure on the adjacent nerves and leads to pain and numbness in the thumb side of the wrist which get worse while making a fist, grasping or gripping things, or turning the wrist
Mallet finger, presentation
Caused by forceful flexion to the end of an extended finger, usually occuring in contact or ball-handling sports. The terminal extensor tendon on the dorsum of the finger at the distal interphalangeal joint (DIP) is torn, stretched or avulsed.
Assessment
- Pain, swelling (+ / bruising) on the dorsum of the DIP joint
- Flexed posture of finger tip due to inability to actively extend it
- Passive (by the examiner) extension is usually possible
Inflammatory Myopathies, presentation (Chronic Inflammatory Demyelinating Polyradiculoneuropathy)
Triggered autoimmune attack on the nervous system causing:
slow progressive weakness (legs> arms>sensation>cranial nerves)
Inflammatory Myopathies, presentation (Dermatomyositis)
inflammation causes
- skin rash (gottron’s, shawl sign, v sign, nails)
- muscle weakness (trunk going outward)
Inflammatory Myopathies, presentation (Inclusion Body Myositis)
A muscle condition that causes thin and weak muscles
Skeletal muscle weakness and wasting progresses from quadriceps (thigh) to forearm muscles.
Inflammatory Myopathies, presentation (Polymyositis)
Connective tissue disease that triggers inflammation and muscular weakness.
- Muscle weakness develops gradually over the course of a few weeks or months
- Inflammation may spread to other areas of the body including the heart
ECG rhythms, Heart blocks
1st degree
- PR interval >200ms
- benign, usually asymptomatic
2nd degree (Mobitz I - Wenckebach)
- P-R increasingly slows then a QRS is dropped
- benign, usually asymptomatic
2nd degree (Mobitz II)
- P-R is regular, sudden QRS dropped
- benign, usually asymptomatic
3rd degree
- Atria and ventricles is completely separate
- syncope, weakness
TREATMENT
- pacemaker
ECG rhythms, atrial flutter vs fibrillation
Flutter
- irregular rapid heartbeat
- sawtooth pattern
Treatment - HR, rhythm, anti emboli, ablation
Fibrillation
- irregular heartbeat, palpitations
- irregularly irregular, 0 pattern
Treatment
maintenance - digoxin, bb,ccb
stable/no HF - betablocker, calcium channel blocker
unstable - amiodarone
dying - cardioversion
ECG rhythms, supraventricular tachycardia
Supraventricular Tachycardia
- 140-200 bpm, palpitations, chestpain, syncope
- very slim sinus rhythm
Treatment
- modified valsalva
- carotid sinus massage
- adenosine (CI asthma) (safer)
- verapamil
- cardioversion
- catheter ablation
ECG rhythms, ventricular fibrillation/flutter
Ventricular flutter
- saw tooth pattern, 250-300bpm
Ventricular Fibrillation
- irregular sawtooth
Treatment
1st line - atenolol, metoprolol, diltiazem, verapamil
2nd line - digoxin, defibrillation, flecainide( only for normal hearts)
ECG rhythms, ventricular tachycardia
- fat saw tooth
Stable treatment
- procainamide
- amiodarone
Heart pathway, blood
Superior/Inferior vena cava
Right atrium
Tricuspid Valve
Right ventricle
Pulmonic valve (inside RV)
Lungs
Pulmonary vein
Left atrium
Mitral valve
Left ventricle
Aortic valve (inside LV)
High risk for ACS, features
Ongoing chest pain
Dyspnea
Syncope/presyncope
Palpitations
ACS management
Prehospital: Aspirin and sublingual GTN
Serial 12L ECG (10-15mins until pain-free)
Cardiac troponin (or other biomarkers)
Chest x-ray
MONA
morphine
oxygen
nitrates
aspirin
anti-thrombotic
Chronic stable angina, management
Goal: relieve angine, prevent cardiovascular events
RELIEF:
Betablockers
Calcium channel antagonists
Short acting nitrates
PREVENT:
Low dose aspirin
statins
Types of pneumothorax
Closed - Lungs to pleural cavity
(cavity pressure < atmosphere pressure)
Open - open passage pleural cavity to environment
(cavity pressure = environement)
Tension - one way passage environment to pleural cavity, no exit of air thus increasing tension
(cavity pressure > atmospheric pressure)
Cardiac tamponade vs Tension pneumothorax
Only cardiac tamponade and tension pneumothorax produce jugular venous distention with a chest injury. How you tell the difference is by auscultating the lungs. Tamponade will typically reveal clear, bilateral, lung sounds while a tension pneumothorax will not.
Confirming a TB diagnosis case requirement
Cases are confirmed via
1. Laboratory
- Culture (except for BCG recipients)
- Nucleic acid amplification test (NAAT) (except for prior or current TB patients)
OR
- Clinical evidence
PTB treatment
Pyrazinamide
Isoniazid
Rifampicin
Ethambutol
subject to change after culture results
Hospital acquired pneumonia, treament
Low risk for MRO (non ICU, ICU<5 days)
- Amoxycillin+clavulanate or Benzylpenicillin+gentamicin
- Pen allergic (ceftriaxone)
High risk for MRO
- piptaz + genta
- Pen allergic (cefepime + genta)