Medicine A Flashcards

1
Q

What are the differentials for a cutaneous horn?

A

Differentials include viral wart, seborrhoeic keratosis, actinic keratosis (pre cancerous lesion which often occur with background sun damage), Bowen’s disease (the cutaneous horn has a red rim and often become SCC) and squamous cell carcinoma which have a fleshy red component beneath which is suspicious. SCCs produce keratin whereas BCCs do not. SCC will need excision.

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2
Q

What are the differentials for a red scaly plaque?

A

Differentials include inflammatory conditions (psoriasis and discoid eczema) or neoplastic (Bowen’s and superficial basal cell carcinoma). BCC is usually pertly, nodular with a rolled edge or central depression and ulceration, scab or even telangiectasia (wide venules with threadlike red lines or patterns on the skin).

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3
Q

How is Bowen’s disease diagnosed and treated?

A

Bowen’s disease is confirmed clinically or with a biopsy. It is treated with Effudix (5-flurouracil) which is a chemotherapy cream.

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4
Q

How should BCCs be treated?

A

BCC should be treated with imiquimod which is an immune response modifier or with complete excision.

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5
Q

How should psoriasis be treated?

A

The main treatment for psoriasis are emollients, vitamin D analogues, steroids, tar and dithranol. Vitamin D analogues should generally be used as first line treatment. For severe localised psoriasis should be treated with potent topical steroids. Scalp psoriasis may need tar shampoo or topical steroids. Some diffuse psoriasis can be given phototherapy.

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6
Q

How is eczema treated?

A

The main topical treatments of eczema include emollient for dryness and as a soap substitute. Anti-inflammatory drugs such as steroids and calcinerurin inhibitors.
Emollients need to chosen carefully because of the degree of greasiness and length of effect. There is no frequency limit.

Topical steroids are used in a ladder. Hydrocortisone is first choice followed by Eumovate. Bentovate and elocon are the step up with dermovate used last as it is very potent.

Calcineurin inhibitors can be tacrlinus (protopic) or elidel and should be used on delicate sites such as around the eyes. Eczema which has lichenification requires higher potency to treat and should be taken very seriously. Golden crusting may imply infection, never use fusibet as a maintenance treatment because resistance develops very quickly.

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7
Q

How does rosacea present?

A

Rosacea presents with erythema and pustules. They may also have a history of flushing. This can be treated with topical metronidazole, azeliac acid or oral tetracyclines. Rosacea does not itch but often feels like it is burning.

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8
Q

What are the dermatological symptoms of SLE?

A

SLE presents with redness over the cheeks and nose like the wolf pattern and looks indurated. There will be no papules and you should ask about other SLE symptoms and ask about photosensitivity.

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9
Q

How does seborrhoeic eczema present?

A

Seborrhoeic dermatitis is distributed around the nasal folds but can extend onto the cheeks and central forehead. Check the scalp as it may be greasy and yellowish. This is treated with antifungals as it is linked with the overgrowth of pityrosporum ovale. Also hydrocortisone.

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10
Q

How does atopic eczema present on the face?

A

Atopic eczema on the face usually occurs with pruritus and causes eyelid oedema. This can be treated with hydrocortisone. Allergic contact dermatitis can cause swelling of the eyes and is treated with avoidance and topic steroids. Acute contact dermatitis does not have as much scaling as chronic cases.

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11
Q

How does cellulitis present?

A

Cellulitis (Erysipelas) also presents with swelling but clear margins to the erythema. The skin will look stretched and is almost always unilateral. Unilateral localised erythema with less swelling may also be cellulitis and both should be given flucoxicillin or other antibiotics which the swab reveals are effective.

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12
Q

How does gravitational eczema present?

A

Bilateral lightly erythematous legs may be gravitational eczema (otherwise known as stasis eczema, venous or varicose eczema). This is caused by impaired venous drainage or chronic venous insufficiency and will often present with other signs such as oedema and pigmentation. Cellulitis should not itch whereas eczema itches.

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13
Q

How does lipodermatosclerosis present?

A

Bilateral dark erythema which is asymmetrical and is slowly spreading may be lipodermatosclerosis. The skin may feel thick, bound down and sclerotic. This is often seen in overweight people and is difficult to treat. Compression may have some effect.

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14
Q

How does erythema nodosum present?

A

Erythematous blotchy patches which are very tender is caused by erythema nodosum. It tends to be bilateral.

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15
Q

How should acne be treated?

A

Topical treatments: Benzoyl peroxide, retinoid and antibiotics

Oral treatments: Antibiotics, COCP and retinoid

Tetracyclines and lymecyclines are the main oral antibiotics whereas erythromycin or clarithromycin are used topically. Retinoids are vitamin A derivatives. The oral contraceptive pill can be used for patients with acne. Retinoids are the last resort and have considerable side effects but are extremely effective. Always beware of pregnancy and offering treatments.

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16
Q

What does the ‘A’ in the ABCDE approach to X-rays represent?

A

Projection (is it AP or PA as AP will have a larger heart shadow). Take note of the rotation and the inspiratory effort by counting ribs, at least 6 should be visible.

Look for the trachea and assess whether it is central as pleural effusion, pneumothorax and lobar collapse or lobotomy will change the way it lines. The left and right bronchi should also be visible.

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17
Q

What does the ‘B’ in the ABCDE approach to X-rays represent?

A

Compare the lung zones on both sides. Increased density implies consolidation, interstitial change, masses, collapse and effusions. Reduced density is seen in pneumothorax. The lower lobes extend below the diaphragm and there may be pathology in this area. Look for hyperinflation seen in COPD.

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18
Q

What does the ‘C’ in the ABCDE approach to X-rays represent?

A

Assess the heart size. It should be less than 50% of the chest diameter. The cardiothoracic ratio can be used to determine cardiomegaly. Follow the cardiac contours and check for any loss of normal contours. If the retrocardiac region has an increased density which is known as the sail sign it suggests lower lobe collapse.

Check the mediastinal contours for mediastinal widening which is seen in lymphadenopathy, make note of the aorta-pulmonary window which is the dip between the aortic knuckle and the pulmonary trunk. Abnormalities may also indicate lymphadenopathy. Also check the hilae.

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19
Q

What does the ‘D’ in the ABCDE approach to X-rays represent?

A

There may be loss of normal contours in consolidation or collapse of the diaphragm. Under the diaphragm there may be gas. Assess for an NG tube entering the stomach, foreign objects, gallstones, pancreatic calcification and lumbar vertebrae.

Also assess the pleural spaces. Look for the fluid level/meniscus at the costophrenic angle. Look for Kerley B lines (interstitial fluid) around the CP angle. Pneumothorac has apical lucency and visible lung edge.

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20
Q

What does the ‘E’ in the ABCDE approach to X-rays represent?

A

Look for any bubbly lucency which may suggest subcutaneous emphysema. Look for pick lines. Look at the bones to check for fractures.

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21
Q

What are the features of Torsades de pointes?

A

Torsades de pointes is known as twisting of the peaks which is QTc prolongation which can be fatal. Check for drug-induced prolonged QT interval. Drugs which can cause this include antiarrythmics (Disopyramide, procainamide, quinidine and sotalol) but also macrolides, fluroquinolones, antifungals, antipsychotics, antiemetics, opioids and antidepressants such as Citalopram and Escitalopram. Beware of cocaine.

Risk factors include bradycardia, congestive heart failure with poor LV function, previous MI, female gender, over 65, chronic renal impairment, hyperkalaemia and diuretic treatment.

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22
Q

What are the causes of wide complex tachycardias?

A

The QRS widens as the normal ventricular depolarisation through the His-purkinje system is either impaired or bypassed, and the ventricles rely on the myocyte-myocyte currents for depolarisation which is much slower.
The common causes of Wide complex tachycardia include ventricular tachycardia, supra ventricular tachycardia with aberrant conduction and pre-excitation tachycardia which is seen in people with Wolfe Parkinson White Syndrome.
Aberrant conductions include bundle branch blocks, hyperkalaemia and sodium channel blocking drugs.

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23
Q

Describe ventricular tachycardia

A

A ventricular tachycardia on ECG will have very broad complexes (>160), extreme axis deviation, AV dissociation, capture beats, fusion beats, positive or negative concordance through the chest leads and brugada algorithm. A capture beat is when the SA node transiently captures the ventricles in the midst of AV dissociation and fusion beats are when the sinus and ventricular beats coincide.

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24
Q

How should wide complex tachycardia be treated?

A

Acute management depends on the hemodynamic stability of the patient. If they are unstable the patient will need immediate electrical synchronised DC cardioversion. Wide complex tachycardia can be caused by hyperkalaemia which requires emergency treatment with calcium and sodium bicarbonate.

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25
Q

What are the complications of uncontrolled hypertension

A

LV hypertrophy, heart failure, CKD, stroke, vascular dementia and retinopathy

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26
Q

Why is microalbuminaemia important?

A

Microalbuminuria is vital as it can alert the physician to vascular disease at other sites of the body in addition to the kidney. It is the earliest detectable sign of diabetic nephropathy and at this stage it is potentially reversible. It is a risk factor for other cardiovascular events as well and antihypertensive treatments can be vital in renal protection, especially ACE inhibitors as they effect the RAAS system.

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27
Q

What is the Vaughan Williams classification?

A

Class 1: Sodium channel blockers (can be subdivided into 1a, b and c depending on the effect they have on the action potential)

Class 2: B-blockers

Class 3: Potassium channel blockers

Class 4: Slow (L-type) calcium channel blockers

Class 1a includes Quinidine, Procainamide and Disopyramide

Class 1b includes Lidocaine, Mexiletine and Phenytoin

Class 1c includes Flecainide, propafenone and ethmozine

28
Q

What is Brugada syndrome?

A

Brugada syndrome is a mutation in the cardiac sodium channel. It is familial and autosomal dominant in inheritance. There will be transient ECG changes and can be masked by fever, ischaemia and hypokalaemia.

Brugada is a concern because it is associated with life threatening ventricular arrhythmias and sudden death. Class 1 anti-arrhythmic drugs such as flecianide can be used to diagnose Brugada because they are able to block sodium channels and induce the brugada syndrome.

29
Q

What are the three potential mechanisms of SVT?

A
  1. Re-entry - two pathways of differing electro physical properties (conduction velocity and refractory period)
  2. Increased automaticity (from a group of cells with changes in resting potential)
  3. Triggered activity (extra depolarisation following cellular repolarisation such as digoxin toxicity)
30
Q

Describe WPW syndrome

A

The most common accessory pathway is the bundle of Kent which is the cause of Wolff Parkinson White Syndrome. WPW will have slurring of the delta wave causing an upstroke which is indicative of WPW. The accessory pathway means the AV node can be bypassed so there is a shortened PR interval. There will be initial slurring of the delta wave at the start of the QRS complex. These cannot be seen during the SVT.

This should be suspected in young patients with irregularly irregular broad complex tachycardias. AV node blockers should be avoided in atrial fibrillation with WPW as this can lead to ventricular arrhythmias.

31
Q

How should SVTs be treated?

A

Adenosine acts on the AV node to activate potassium channels and cause potassium to leave the cell, inhibits calcium influx and thus inhibits conduction.

32
Q

Describe the importance of extreme axis deviation

A

Extreme axis deviation is seen in emphysema, hyperkalaemia, lead transposition, ventricular pacing and ventricular arrhythmia.

33
Q

Describe the importance of left axis deviation

A

Left axis deviation is seen post inferior MI, left anterior fascicular block, ventricular pacing, emphysema, hyperkalaemia, WPW, tricuspid atresia and atrial septal defects.

34
Q

Describe the importance of right axis deviation

A

Right axis deviation is seen in children (normal finding), left ventricular hypertrophy, COPD, post anterolateral MI, PE, WPW, ASD and VSD.

35
Q

Describe a hypertensive emergency

A

A raise in blood pressure which can cause organ damage such as brain (headache, confusion, stoke, agitation and seizures), eyes (papilloedema), heart (chest pain and SOB) and kidneys (urinalysis and renal function). 75% of people with sustained hypertensive emergency will have microscopic haematuria.

36
Q

How should hypertensive emergencies be treated?

A

Blood pressure should be gradually dropped over 24 hours with 10% reduction in the first hour. Exceptions are acute phase of an ischaemic stroke, haemorrhagic stroke or acute aortic dissection. Suddenly dropping the blood pressure can cause a rebound ischaemic episode which causes stroke or cardiovascular event. Acute hypertensive nephrosclerosis should also be treated faster.

The treatment options for hypertensive emergency is with sodium nitroprusside IV infusion which is a potent vasodilator acting very quickly which can cause a significant BP drop. Labetalol IV infusion is a combined beta-adrenergic and alpha adrenergic blocker. It is also rapid but is safer for patients with active coronary heart disease because it does not increase the heart rate. It is unsafe in asthma, however.

37
Q

What is SIADH?

A

SIADH (Syndrome of inappropriate antidiuretic hormone secretion) is a condition in which the body makes too much antidiuretic hormone and so too much water is retained and sodium levels drop.

This is seen in some patients with small cell lung cancer

38
Q

How should adenocarcinomas of the lung be treated?

A

Adenocarcinomas can be treated with surgery, radiation, chemotherapy, targeted therapies, angiogenesis inhibitors and immunotherapy. Targeted therapies include tyrosine kinase inhibitors are used in metastatic adenocarcinomas but resistance to these can develop.

39
Q

What are the causes of respiratory acidosis?

A

COPD exacerbation and very severe pneumonia

40
Q

What are the causes of respiratory alkalosis?

A

PE, hyperventilation or salicylate toxicity

41
Q

What are the causes of metabolic acidosis?

A

DKA, AKI and rhabdomyolysis

42
Q

What are the causes of metabolic alkalosis?

A

recurrent vomiting or diuretics

43
Q

What is a pleural effusion?

A

A pleural effusion is an abnormal collection of fluid within the pleural space which can be transudates or exudates on the basis of their protein content. There can also be blood, pus or lymphatic fluid in these effusions. These are often secondary to malignancy.

44
Q

What are the transudate causes of pleural effusion?

A

Transudative causes include congestive heart failure, cirrhosis with hepatic hydrothorax, nephrotic syndrome, peritoneal dialysis, hypo-proteinemia, glomerulonephritis and superior vena cava obstruction.

45
Q

What are the exudate causes of pleural effusion?

A

Exudative causes include malignancy, pneumonia, TB, PE, post cardiac bypass or injury, hypothyroidism, asbestosis and intra abdominal abscesses.

46
Q

What are the symptoms of pleural effusion?

A

Symptoms inclide SOB on exertion, cough, pleuritic chest pain and possibly signs of cancer. The patient will have an increased respiratory rate, deviated trachea away from the side of the effusion, decreased expansion and stony dullness. Pleural friction rub is also possible.

Clubbing, lymphadenopathy, elevated JVP, ascites, stigmata and signs of hypothyroidism are also possible signs of causative disease.

47
Q

What are the investigations for pleural effusion?

A

Investigations are with a CXR, CT and aspiration. ABGs should always be done. Treatment is to address the underlying cause. Chest drains are important but carries risks of infection, bleeding, subcutaneous emphysema and drain falling out.

48
Q

How should acute coronary syndrome be investigated?

A

IV access, serial ECGs, serial troponin, CXR and pulse oximetry

49
Q

Describe the enzymes that are tested for in acute coronary syndrome

A

Troponin I or T rises in 3-12 hours after chest pain, peaks at 24-48 and is baseline at 5-14 days so do at presentation and 10-12 hours after start of chest pain - amount relative to size of MI - other enzyme biomarkers not as sensitive - myoglobin rises first, creatinine kinase in about 3 hours, also WCC can rise, ESR and CRP can rise and B-Natriuretic Peptide (BNP) may rise

50
Q

What is the initial management for NSTEMI and unstable angina?

A

Oxygen 

Nitrates for ischaemic pain relief - 1st sublingual glyceryl trinitrate, 2nd IV glyceryl trinitrate, 3rd diamorphine/morphine IV + antiemetic (eg metoclopramide)

Aspirin and clopidogrel (prasugrel alternative for clopidogrel in pts undergoing percutaneous coronary intervention) 

Heparin (unfractionated) or low molecular weight heparin 

Patients w/o contraindications have beta-blockers - continued indefinitely 

51
Q

What is the long term management for STEMI and unstable angina?

A

Aspirin + clopidogrel (prasugrel or ticagrelor alternatives, warfarin can also be considered) 

Low dose rivaroxaban, in combination with aspirin and clopidogrel is licensed to prevention of atherothrombotic events following a STEMI

Beta-blockers (diltiazem or verapamil can be considered if contra-indicated) 

ACE inhibitor (or ARB for patients with HF) 

Nitrates for angina 

Statins may be given for prevention of recurring cardiovascular events 

52
Q

What is the initial management for STEMI?

A

Oxygen 

Diamorphine hydrochloride or morphine for pain relief + IV antiemetic (eg metoclopramide) (if poor LV function - cyclizine)

Aspirin + clopidogrel (prasugrel for alternative in percutaneous coronary intervention) 

Patency of occluded artery can be restored by percutaneous coronary intervention (give heparin prior) or by giving a thrombolytic drug

A glycolprotein IIb/III inhibitor used to reduce the risk of immediate vascular occlusion in intermediate- and high-risk patients

Nitrates given to relieve ischaemic pain - 1st sublingual glyceryl trinitrate, 2nd IV glyceryl trinitrate

Early administration of beta-blockers + ACE inhibitors (if not ARBs) benefit

Monitor closely for hyperglycaemia - especially in DM (give insulin if required)

53
Q

What is erythema multiforme?

A

This is an acute skin condition caused by herpes simplex or rarely TB.

It is a reactive eruption on acral sites, there can be mucosal involvement, target lesions, blistering lesions and resolves after two weeks.

54
Q

What is granuloma annulare? (necrobiotic papulosis)

A

These are annular plaques with no scale. (TInea has a scaly edge)

These are usually asymptomatic and can be associated with diabetes.

55
Q

What is necrobiosis lipoidica?

A

This is a rare granulomatous skin disorder which can affect the shin, usually in insulin dependent diabetics.

These usually occur bilaterally and can be asymptomatic or tender. There will be elements of telangiectasia

56
Q

What is acanthosis nigricans?

A

This is a velvety thickening and hyperpigmentation in flexures. This can be paraneoplastic to gastric cancer or associated with diabetes.

57
Q

What is dermatomyositis?

A

Peri-ocular heliotrope rash 

Gottron’s papules over knuckles

Nail-fold inflammation 

Photosensitivity 

Myositis causing muscle weakness 

Paraneoplastic in adults 

58
Q

What is pyoderma gangrenosum?

A

Initial acute onset of painful expanding ulcer(s) with undermined, violaceous borders 

Mostly occurs on legs 

Associations - myeloproliferative disease, IBD, autoimmune disease, DM, cocaine use

59
Q

What is dermatitis herpetiformis?

A

Intensely itchy vesicles which quickly become excoriated 

Especially affects extensor surfaces 

Implies underlying coeliac disease

60
Q

How should cutaneous vasculitis be investigated?

A

BP, urinalysis, FBCs, U+Es, LFTs, inflammatory markers, ANA, ANCA, ASOT, hepatitis serology, throat swab, possible biopsy

61
Q

How should cutaneous vasculitis be managed?

A

If asymptomatic - no need to treat

If symptomatic - give initial short course of prednisolone 

62
Q

How should chronic spontaneous urticaria be treated?

A

Increased dose of non-sedating antihistamines, prednisolone rarely required, omalizumab and immunosuppression second line, diet probably not related 

63
Q

How should toxic epidermal necrolysis be treated?

A

Stop all non-essential drugs 

Analgesia 

Fluid resuscitation

Grease

NG feeds 

Dressings (preferably on burns unit)

Urgent referral to dermatology, ophthalmology, gynaecology 

Mortality 30% 

64
Q

Describe the clinical features of Toxic Epidermal necrolysis

A

SJS/TEN usually develops within the first week of antibiotic therapy but up to 2 months after starting an anticonvulsant

Before rash - prodromal phase of fever >39, sore throat, coryzal symptoms, conjunctivitis, general malaise 

Skins lesions may be macules or purpura, diffuse erythema, targetoid and/or blisters (flaccid)

The blisters then merge to form sheets of skin detachment, exposing red, oozing dermis

65
Q

What are the complications of toxic epidermal necrolysis?

A

Dehydration and acute malnutrition

Infection of skin, mucous membranes, lungs (pneumonia), septicaemia (blood poisoning)

Acute respiratory distress syndrome

Gastrointestinal ulceration, perforation and intussusception

Shock and multiple organ failure including kidney failure

Thromboembolism and disseminated intravascular coagulopathy

66
Q

What is erythroderma?

A

Skin Conditions Causes of Erythroderma 

Drug eruption

Dermatitis - especially atopic 

Psoriasis - especially after withdrawal from systemic steroids

Pityriasis rubra pilares 

Blistering diseases - pemphigus and bullous pemphigoid 

Sezary syndrome (the erythrodermic form of cutaneous T-cell lymphoma)

Clinical Features 

By definition, generalised erythema and oedema or papulation affect 90% or more of the skin surface

Warm skin, pruritus leading to lichenification, eyelid ectropion, scaling, hair loss, diffuse keratoma, oncholysis, generalised lymphadenopathy

67
Q

How is erythroderma treated?

A

Discontinue all unnecessary medications

Monitor fluid balance and body temperature

Maintain skin moisture with wet wraps, other types of wet dressings, emollients and mild topical steroids 

Prescribe antibiotics for bacterial infection

Antihistamines may be helpful for itch

Then treat the underlying cause