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Cases For PACES > Station 5 > Flashcards

Station 5 Flashcards

1
Q

Ix of Sickle cell disease/ crisis?

A
  • Blood tests: low Hb; high WCC and CRP; renal impairment; sickling on blood film
  • CXR: linear atelectasis in a chest crisis; cardiomegaly: cardiac size proportional to degree of longstanding anaemia
  • Urinalysis: microscopic haematuria if renal involvement in crisis
  • Arterial blood gas: type I respiratory failure
  • Echocardiogram: dilated right ventricle with impaired systolic function; raised peak
    tricuspid regurgitant velocity: abnormal range for sickle cell patients is lower than other populations; i.e. >2.7 m/s abnormal
  • Computed tomography pulmonary angiography: linear atelectasis with patchy
    consolidation ± acute pulmonary embolism
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2
Q

Acute Treatment of sickle cell crisis?

A
  • Oxygen ± continuous positive airways pressure
  • Intravenous fluids
  • Analgesia
  • Antibiotics if evidence of infection
  • Blood transfusion/exchange transfusion depending on degree of anaemia and severity of crisis
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3
Q

Long term chronic management of sickle cell disease?

A
  • Hydroxycarbamide or exchange transfusion programme if frequent crises or other features suggestive of a poor prognosis
  • Long‐term treatment with folic acid and penicillin as patient will have features of hyposplenism
  • May need further investigation of possible pulmonary hypertension if raised peak tricuspid regurgitant velocity, including right heart catheterization, after the acute event
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4
Q

Prognosis of sickle cell disease?

A
  • HbSS ≈40–50 years old
  • Worse prognosis with frequent chest crises or following development of pulmonary hypertension
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5
Q

Examination findings of sickle cell patient +/- crisis?

A
  • Fever
  • Dyspnoeic
  • Jaundice
  • Pale conjunctiva
  • Raised JVP, pansystolic murmur loudest at left sternal edge (tricuspid regurgitation 2’ PH)
  • Reduced chest expansion due to pain with coarse expiratory crackles
  • Small, crusted ulcers on lower third of legs
  • abdo scar suggesting splenectomy, splenomegaly
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6
Q

Features of Addisons disease?

A
  • Fatigue, muscle weakness, low mood, loss of appetite, weight loss, thirst (dehydration) * Darkened skin (Addison’s disease)
  • Fainting or cramps
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7
Q

Causes of Addison’s disease (cortisol insufficiency)?

A
  • TB/ mets to adrenal
  • Primary autoimmune Addison’s disease (may be assoc hypothyroidism/ T1DM/ vitiligo)

DDx secondary adrenal insufficiency: pituitary adenoma or sudden discontinuation of steroid

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8
Q

Examination findings of patient with known Addison’s disease?

A
  • Medic alert bracelet
  • Hyper‐pigmentation: palmar creases, scars, nipples and buccal mucosa
  • Postural hypotension
  • Visual fields: bitemporal hemianopia (pituitary adenoma)

cause: signs of other associated autoimmune diseases/ TB/ malignancy

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9
Q

What is Addison’s disease?

A

Primary adrenal insufficiency

  • Pigmentation due to a lack of feedback inhibition by cortisol on the pituitary, leading to raised ACTH and melanocyte‐stimulating hormone
  • 80%: autoimmune process. Other causes include adrenal metastases, adrenal tuberculosis, amyloidosis, adrenalectomy and Waterhouse–Friederichsen syndrome (meningococcal sepsis and adrenal infarction)
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10
Q

Ix of suspected Addison’s disease?

A
  • 8 am cortisol: likely low (unreliable)
  • Short Synacthen test
    -> Exclude addison’s disease if cortisol rises to adequate levels
  • long Synacthen test
    -> Diagnose addison’s disease if cortisol does not rise to adequate levels
  • adrenal imaging (primary) and/or pituitary imaging (secondary) with MRI or CT

Others:
Blood tests: eosinophilia, ↓ Na+ (kidney loss), ↑ K+, ↑ urea (dehydration), ↓ glucose, adrenal autoantibodies (if autoimmune cause), thyroid function tests (hypothyroidism)
CXR: malignancy/TB

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11
Q

Tx of acute adrenal crisis?

A
  • 0.9% saline IV rehydration +++ and glucose
  • Hydrocortisone
  • Treatment may unmask diabetes insipidus (cortisol is required to excrete a water load)
  • Anti‐TB treatment increases the clearance of steroid, therefore higher doses required
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12
Q

Prognosis of addisons disease?

A

normal life expectancy

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13
Q

Chronic tx of addison’s disease?

A
  • Education: compliance, increase steroid dose if ‘ill’, steroid card, medic alert bracelet * Titrate maintenance hydrocortisone (and fludrocortisone) dose to levels/response
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14
Q

Examination findings of patient with Cushing’s syndrome?

A
  • face: moon‐shaped, hirsute, with acne
  • Skin: bruised, thin, with purple striae
  • Back: ‘buffalo hump’
  • abdomen: centripetal obesity
  • legs: wasting (‘lemon on sticks’ body shape) and oedema
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15
Q

common complications of Cushing’s syndrome?

A
  • Hypertension (BP)
  • Diabetes mellitus (random blood glucose) * osteoporosis (kyphosis)
  • Cellulitis
  • proximal myopathy (stand from sitting)
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16
Q

examination findings which can suggest underlying cause of cushings syndrome?

A
  • Exogenous steroids: signs of chronic condition (e.g. RA, COPD) requiring steroids * Endogenous: bitemporal hemianopia and hyperpigmentation (if ACTH ↑)
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17
Q

Cushing’s disease vs Cushings syndrome?

A

Cushing’s disease: glucocorticoid excess due to ACTH secreting pituitary adenoma

Cushing’s syndrome: the physical signs of glucocorticoid excess

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18
Q

Ix of suspected Cushings?

A

1. Confirm high cortisol
* 24‐hour urinary collection
* Low dose (for 48 hours) or overnight dexamethasone suppression test
> Suppressed cortisol: alcohol/depression/obesity (‘pseudo‐Cushing’s’)

**2. if elevated cortisol confirmed, then identify cause: **
* ACTH level
-> High: ectopic ACTH secreting tumour or pituitary adenoma
-> low: adrenal adenoma/carcinoma
* MRI pituitary fossa ± adrenal CT ± whole body CT to locate lesion
* Bilateral inferior petrosal sinus vein sampling (best test to confirm pituitary vs
ectopic origin; may also lateralise pituitary adenoma)
* High‐dose dexamethasone suppression test may help >50% suppressed
cortisol: Cushing’s disease

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19
Q

Prognosis of untreated Cushings syndrome?

A

Untreated Cushing’s syndrome: 50% mortality at 5 years (usually due to accelerated ischaemic heart disease secondary to diabetes and hypertension)

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20
Q

Causes of proximal myopathy?

A
  • inherited:
    ⚬ Myotonic dystrophy
    ⚬ Muscular dystrophy
  • Endocrine:
    ⚬ Cushing’s syndrome
    ⚬ Hyperparathyroidism
    ⚬ Thyrotoxicosis
    ⚬ Diabetic amyotrophy
  • inflammatory:
    ⚬ Polymyositis
    ⚬ Rheumatoid arthritis
  • metabolic:
    ⚬ Osteomalacia (Low Vit D)
  • malignancy:
    ⚬ Paraneoplastic
    ⚬ Lambert–Eaton myasthenic syndrome
  • Drugs:
    ⚬ Alcohol
    ⚬ Steroids
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21
Q

Treatment of Cushings syndrome?

A

Surgical: Trans‐sphenoidal approach to remove pituitary tumours. Adrenalectomy for adrenal tumours

pituitary irradiation
medical: Metyrapone

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22
Q

What is Nelsons sydrome?

A

bilateral adrenalectomy (scars) to treat Cushing’s disease, causing massive production of ACTH (and melanocyte‐stimulating hormone), due to lack of feedback inhibition, leading to hyper‐pigmentation and pituitary overgrowth

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23
Q

Causes of macroglossia?

A

• acromegaly
• Amyloidosis
• Hypothyroidism
• Down’s syndrome

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24
Q

Complications of Acromegaly to look out for?

A

acanthosis nigricans
Bp ↑*
Carpal tunnel syndrome
Diabetes mellitus*
Enlarged organs
field defect*: bitemporal hemianopia goitre, gastrointestinal malignancy
Heart failure, hirsute, hypopituitary
iGF‐1 ↑
Joint arthropathy
kyphosis
lactation (galactorrhoea)
myopathy (proximal)

(*Signs of active disease)

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25
Q

Examination findings in acromegaly?

A

• Hands: large ‘spade like’, tight rings, coarse skin and sweaty

• face: prominent supra‐orbital ridges, prognathism, widely spaced teeth and
macroglossia

  • features of OA/ DM
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26
Q

Ix for diagnosis of acromegaly?

A

• non‐suppression of GH after an oral glucose tolerance test
• Raised plasma igf‐1
• CT/MRI pituitary fossa: pituitary adenoma
• Also assess other pituitary functions

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27
Q

Ix for complications of acromegaly?

A

• CXR: cardiomegaly
• ECG: ischaemia (DM and hypertension)
• pituitary function tests: T4, ACTH, prolactin and testosterone
• glucose/ HbA1c: DM
• visual perimetry: bitemporal hemianopia
• sleep study for obstructive sleep apnoea (in 50%): due to macroglossia

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28
Q

Ix for complications of acromegaly?

A

• CXR: cardiomegaly
• ECG: ischaemia (DM and hypertension)
• pituitary function tests: T4, ACTH, prolactin and testosterone
• glucose/ HbA1c: DM
• visual perimetry: bitemporal hemianopia
• sleep study for obstructive sleep apnoea (in 50%): due to macroglossia

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29
Q

Management of acromegaly?

A

Aim is to normalize GH and IGF‐1 levels

  1. Surgery: trans‐sphenoidal approach Medical post‐op complications:
    • Meningitis
    • Diabetes insipidus
    • Panhypopituitarism
  2. medical therapy: somatostatin analogues (Octreotide), dopamine agonists (Cabergoline) and growth hormone receptor antagonists (Pegvisomant)
  3. Radiotherapy in non‐surgical candidates
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30
Q

Long term follow up of acromegaly?

A

Annual GH, PRL, ECG, visual fields and CXR ± CT head

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31
Q

Conditions associated with acanthosis nigricans

A

Associations:
⚬ Obesity
⚬ Type II diabetes mellitus
⚬ acromegaly
⚬ Cushing’s syndrome
⚬ Ethnicity: Indian subcontinent
⚬ Malignancy, e.g. gastric carcinoma and lymphoma

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32
Q

Men1?

A

• parathyroid hyperplasia (Ca2+ ↑)
• pituitary tumours
• pancreatic tumours (gastrinomas)

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33
Q

Important drug history in suspected hypothyroidism?

A

Amiodarone, lithium and anti‐thyroid drugs

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34
Q

Associated illnesses to elicit in suspected hypothyroidism?

A

• Previously treated thyroid disease
• Autoimmune: Addison’s disease, vitiligo and type I diabetes mellitus
• Hypercholesterolaemia
• History of ischaemic heart disease: treatment with thyroxine may precipitate angina

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35
Q

Examination findings in hypothyroidism?

A

• Hands:
⚬ Slow pulse
⚬ Dry skin
⚬ Cool peripheries

• Head/face/neck:
⚬ ‘Peaches and cream’ complexion (anaemia and carotenaemia)
⚬ Eyes: peri‐orbital oedema, loss of eyebrows and xanthelasma
⚬ Thinning hair
⚬ Goitre or thyroidectomy scar

• legs:
⚬ Slow relaxing ankle jerk (tested with patient kneeling on a chair)

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36
Q

Examination findings of complications associated with hypothyroidism

A

• Cardiac: pericardial effusion (rub), congestive cardiac failure (oedema)

• neurological: carpel tunnel syndrome (Phalen’s/Tinel’s test), proximal myopathy (stand from sitting) and ataxia

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37
Q

Ix of hypothyroidism?

A

• Blood: TSH (↑ in thyroid failure, ↓ in pituitary failure), T4 ↓, autoantibodies Associations: hyponatraemia, hypercholesterolaemia, macrocytic anaemia, consider short Synacthen test (exclude Addison’s)
• ECG: pericardial effusion and ischaemia
• CXR: pericardial effusion and CCF

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38
Q

Management of hypothyroidism?

A

• Thyroxine titrated to TSH suppression and clinical response

NB. 1. Can precipitate angina
2. Can unmask Addison’s disease → crisis

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39
Q

Causes of hypothyroidism?

A

• autoimmune: Hashimoto’s thyroiditis (+ goitre) and atrophic hypothyroidism
• iatrogenic: Post‐thyroidectomy or I131, amiodarone, lithium and anti‐thyroid drugs
• iodine deficiency: dietary (‘Derbyshire neck’)
• Dyshormonogenesis
• genetic: Pendred’s syndrome (with deafness)

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40
Q

History to enquire about in hyperthyroidism?

A

Enquire about: sleep and energy levels, heat intolerance and sweating, agitation, stress and tremor, appetite and weight loss and palpitations
Periods

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41
Q

Examination findings in hyperthyroidism/ Graves’ disease?

A
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42
Q

Ix of hyperthyroidism?

A

• Thyroid function tests: TSH and T3/T4
• Thyroid autoantibodies
• Radioisotope scanning: increased uptake of I131 in Graves’ disease, reduced in thyroiditis

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43
Q

Tx of hyperthyroidism?

A

• β‐Blocker, e.g. propranolol
• Carbimazole or propylthiouracil (both thionamides)
⚬ Block and replace with thyroxine
⚬ titrate dose and monitor endogenous thyroxine
Stop at 18 months and assess for return of thyrotoxicosis. One‐third of patients will remain euthyroid

If thyrotoxicosis returns, the options are
⚬ A repeat course of a thionamide
⚬ Radioiodine (I131): hypothyroidism common
⚬ Subtotal thyroidectomy

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44
Q

Management of graves eye disease?

A

Severe ophthalmopathy may require high‐dose steroids, orbital irradiation or surgical decompression to prevent visual loss

*stop smoking!

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45
Q

mnemonic for the progression of eye signs in Graves’ disease?

A

NOSPECS

  • no signs or symptoms
  • only lid lag/retraction
  • Soft tissue involvement
  • proptosis
  • Extraocular muscle involvement
  • Chemosis
  • Sight loss due to optic nerve compression and atrophy
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46
Q

History to elicit in diabetic retinopathy?

A

• Ask the patient to detail their problem: duration and nature of visual disturbance
• Establish any underlying medical diagnoses: especially presence or absence of diabetes
• Previous eye problems or treatment
• If they are diabetic: do they have regular retinal screening?

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47
Q

Examination of diabetic retinopathy?

A

• Look around for clues: a white stick, braille book or glucometer
• Fundoscopy: check for red reflex (absent if cataract or vitreous haemorrhage)
Tip: find the disc (inferonasally) then follow each of the four main vessels out to the periphery of the quadrants and finish by examining the macular ‘look at the light’
• Check for coexisting hypertensive changes (they always ask!)

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48
Q

Features of background diabetic retinopathy?

A

1 Hard exudates
2 Blot haemorrhages
3 Microaneurysms

-> Routine referral to eye clinic.

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49
Q

Features of pre proliferative diabetic retinopathy?

A

Background changes plus:
4 Cotton wool spots
5 Flame haemorrhages

Also venous beading and loops and IRMAs (intraretinal microvascular abnormalities)

Urgent referral to ophthalmology.

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50
Q

Features of proliferative diabetic retinopathy?

A

Pre-proliferative changes plus

6 Neovascularization of the disc (NVD) and elsewhere
7 Panretinal photocoagulation scars (treatment)

Urgent referral to ophthalmology.

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51
Q

Features of diabetic maculopathy

A

Macular oedema or hard exudates within one disc space of the fovea.

Treated with focal photocoagulation.

Urgent referral to ophthalmology.

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52
Q

Treatment of diabetic retinopathy

A

tight glycaemic control
• Improved glycaemic control is associated with less retinopathy
• There may be a transient worsening of the retinopathy initially

treat other risk factors
• Hypertension; hypercholesterolaemia; smoking cessation
• Accelerated deterioration occurs in poor diabetic control, hypertension and
pregnancy

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53
Q

Indications for photocoagulation in diabetic retinopathy?

A

• Maculopathy
• Proliferative and pre‐proliferative diabetic retinopathy

Pan‐retinal photocoagulation prevents the ischaemic retinal cells secreting angiogenesis factors causing neovascularization.
Focal photocoagulation targets problem vessels at risk of bleeding.

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54
Q

Complications of proliferative diabetic retinopathy?

A

• Vitreous haemorrhage (may require vitrectomy)
• Traction retinal detachment
• Neovascular glaucoma due to rubeosis iridis

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55
Q

Clinical signs of cataracts

A

• Loss of the red reflex
• Cloudy lens
• May have relative afferent pupillary defect (with normal fundi if visible)
• Associations: dystrophia myotonica (bilateral ptosis)

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56
Q

Causes of cataracts?

A

• Congenital (pre‐senile): rubella, Turner’s syndrome
• Acquired: age (usually bilateral), diabetes, drugs (steroids), radiation exposure, trauma
and storage disorders

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57
Q

Management of cataracts?

A

Surgery (outpatient):
⚬ Phacoemulsification with prosthetic lense implantation
⚬ Yttrium aluminium garnet (YAG) laser capsulotomy

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58
Q

Causes of tophaceous gout?

A

• Diet and alcohol: xanthine‐rich foods (meat/seafood)
• Drugs: diuretics
• Other conditions: chronic renal failure

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59
Q

Examination findings to look for in patient with gout?

A

• Asymmetrical swelling of the small joints of the hands and feet (commonly first MTPJ)
• Gouty tophi (chalky white deposits) seen around the joints, ear and tendons
• Reduced movement and function

Associations:
• Obesity
• Hypertension
• Urate stones/nephropathy: nephrectomy scars
• Chronic renal failure: fistulae
• Lymphoproliferative disorders: lymphadenopathy

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60
Q

Ix of gout

A

• Uric acid levels (diagnostically unreliable)
• Synovial fluid: needle‐shaped, negatively birefringent crystals
• Radiograph features: ‘punched out’ periarticular changes

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61
Q

Acute mx of gout flare

A

⚬ Treat the cause
⚬ Increase hydration
⚬ High‐dose NSAIDs
⚬ Colchicine and high fluid intake

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62
Q

Prevention of gout

A

⚬ Avoid precipitants
⚬ Allopurinol (xanthine oxidase inhibitor)

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63
Q

Treatment for Osteoarthritis

A

• Simple analgesia
• Weight reduction (if OA affects weight‐bearing joint)
• Physiotherapy and occupational therapy
• Joint replacement

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64
Q

Examination findings of osteoarthritis

A

• Asymmetrical distal interphalangeal joint deformity with Heberden’s nodes (and sometimes Bouchard’s nodes at the proximal interphalangeal joint)

• Disuse atrophy of hand muscles
• Crepitation, reduced movement and function
• Carpal tunnel syndrome or scars
• Other joint involvement and joint‐replacement scars

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65
Q

X-RAY features of osteoarthritis

A

• Loss of joint space
• Osteophytes
• Peri‐articular sclerosis and cysts

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66
Q

What to ask about in history in patient with osteoarthritis?

A

Symptoms of OA: stiffness, disuse weakness
Functional aspect: mobility aids, ADLs, work
Treatments: previous joint replacement, side effects of analgesia eg stomach ulcer from NSAIDs

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67
Q

History in Pagets Disease?

A

Symptoms
• Usually asymptomatic
• Bone pain and tenderness (2%)

Assoc Conditions
• Entrapment neuropathy: carpal tunnel syndrome, visual problems, deafness
• CCF: breathlessness

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68
Q

Examination findings of Paget’s disease?

A

• Bony enlargement: skull and long bones (sabre tibia)
• Deafness (conductive): hearing‐aid
• Pathological fractures: scars

Cardiac
• High‐output heart failure: elevated JVP, SOA, shortness of breath

Neuro
• Entrapment neuropathies: carpal tunnel syndrome

Fundi
• Optic atrophy and angioid streaks

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69
Q

Ix of Pagets Disease

A

• Grossly elevated alkaline phosphatase, normal calcium/phosphate
• Radiology:
⚬ ‘Moth‐eaten’ on plain films: osteoporosis circumscripta
⚬ Increase uptake on bone scan

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70
Q

Tx of Paget’s disease

A

• Symptomatic: analgesia and hearing‐aid
• Bisphosphonates

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71
Q

Causes of sabre tibia

A

• paget’s
• Osteomalacia
• Syphilis

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72
Q

Associations of angioid streaks?

Angioid streaks are visible irregular crack-like dehiscences in Bruch’s membrane
A

• paget’s
• Pseudoxanthoma elasticum
• Ehlers–Danlos

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73
Q

Complications of Paget’s disease

A

• Osteogenic sarcoma (1%)
• Basilar invagination (cord compression)
• Kidney stones (usually high calcium from bone breakdown)

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74
Q

Complications of Paget’s disease

A

• Osteogenic sarcoma (1%)
• Basilar invagination (cord compression)
• Kidney stones (usually high calcium from bone breakdown)

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75
Q

Examination findings in Marfans Syndrome?

A

General (Spot diagnosis)
• tall with long extremities (arm span > height)

Hands
• arachnodactyly: can encircle their wrist with thumb and little finger
• Hyperextensible joints: thumb able to touch ipsilateral wrist and adduct over the palm with its tip visible at the ulnar border

Face
• High arched palate with crowded teeth • Iridodonesis (with upward lens dislocation)

Respi
• Pectus carinatum (‘pigeon’) or excavatum
• Scoliosis
• Scars from cardiac surgery or chest drains (pneumothorax)

Cardiac
• Aortic incompetence: collapsing pulse
• Mitral valve prolapse
• Coarctation

Abdo
• Inguinal herniae and scars

CnS
• Normal IQ

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76
Q
A

High arched palate

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77
Q

What is Iridodonesis

A

condition in which the iris (coloured part of the eye) vibrates during eye movements.
Usually due to lens subluxation

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78
Q

Genetics of marfans syndrome

A

• Autosomal dominant and chromosome 15
• Defect in fibrillin protein (connective tissue)

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79
Q

Management of patients with Marfans Syndrome?

A

• Surveillance: monitoring of aortic root size with annual transthoracic echo
• treatment: β‐blockers and angiotensin receptor blocker to slow aortic root dilatation and pre‐emptive aortic root surgery to prevent dissection and aortic rupture
• Screen family members

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80
Q

Ddx for Marfans?

A

• Homocystinuria
⚬ Mental retardation and downward lens dislocation

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81
Q

History of ankylosing spondylitis?

A

Explore back symptoms
Psychosocial impact
• Work, driving, ADLs, etc.

Assoc problems
• Eye problems: anterior uveitis
• Pneumonia
• Syncope: CHB

Drugs and treatment

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82
Q

Examination findings in ankylosing spondylitis

A

• ‘?’ caused by fixed kyphoscoliosis and loss of lumbar lordosis with extension of cervical spine
• Protuberant abdomen due to diaphragmatic breathing as there is reduced chest expansion (<5 cm increase in girth)
• Increased occiput–wall distance (>5 cm)
• Reduced range of movement throughout entire spine
• Schöber’s test: Two points marked 15 cm apart on the dorsal spine expand by less than 5 cm on maximum forward flexion

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83
Q

Complications of ankylosing spondylitis?

A

• anterior uveitis (commonest 30%)
• apical lung fibrosis
• aortic regurgitation (4%): midline sternotomy
• atrio‐ventricular nodal heart block (10%): pacemaker
• arthritis (may be psoriatic arthropathy)

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84
Q

Treatment of ankylosing spondylitis

A

• Physiotherapy
• Analgesia
• Anti‐TNF eg infliximab

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85
Q

Genetics of ankylosing spondylitis

A

90% association with HLA B27

86
Q

History taking in systemic sclerosis?

A

Hands
• Raynaud’s phenomenon
Colour change order: white (vasoconstriction) → blue (cyanosis) → red (hyperaemia)
• Ask about function: how does the condition affect ADLs/work, etc.

• Hypertension or heart problems
• Lung problems
• Swallowing problems or indigestion

87
Q

Examination findings in Systemic Sclerosis

A

Hands
• Sclerodactyly: ‘prayer sign’
• Calcinosis (may ulcerate)
• Assess function: holding a cup or pen

Face
• Tight skin
• Beaked nose
• Microstomia
• Peri‐oral furrowing
• Telangiectasia
• Alopecia

Other skin lesions
• Morphoea: focal/generalized patches of sclerotic skin
• En coup de sabre (scar down central forehead)

Blood pressure
• Hypertension

Respiratory
• Interstitial fibrosis (fine and bibasal crackles)

Cardiac
• Pulmonary hypertension (RV heave, loud P2 and TR)
• Evidence of failure
• Pericarditis (rub)

88
Q

Limited vs diffuse systemic sclerosis?

A

Limited

• Distribution limited to below elbows and knees and face
- slow progression (years)

Diffuse

• Widespread cutaneous and early visceral involvement
• Rapid progression (months)

89
Q

CREST in systemic sclerosis

A

CRESt:
⚬ Calcinosis
⚬ Raynaud’s phenomenon
⚬ Esophageal dysmotility
⚬ Sclerodactyly
⚬ telangiectasia

90
Q

Ix in systemic sclerosis?

A

• autoantibodies:
⚬ ANA positive (in 90%)
⚬ Anti‐centromere antibody = limited (in 80%)
⚬ Scl‐70 antibody = diffuse (in 70%)

• Hand radiographs: calcinosis

• pulmonary disease: lower lobe fibrosis and aspiration pneumonia:
⚬ CXR, high‐resolution CT scan and pulmonary function tests

• gastrointestinal disease: dysmotility and malabsorption
⚬ Contrast scans, FBC and B12/folate

• Renal disease: glomerulonephritis
⚬ U&E, urinalysis, urine microscopy (casts) and consider renal biopsy

• Cardiac disease: myocardial fibrosis and arrhythmias
⚬ ECG and echo

91
Q

Tx of systemic sclerosis?

A

Symptomatic treatment only:
• Camouflage creams
• Raynaud’s therapy:
⚬ Gloves, hand‐warmers, etc.
⚬ Calcium‐channel blockers
⚬ ACE‐Is
⚬ Prostacyclin infusion (severe)

• Renal:
⚬ ACE‐Is: prevent hypertensive crisis and reduce the mortality from renal failure

• gastrointestinal:
⚬ Proton‐pump inhibitor for oesophageal reflux

92
Q

Prognosis of systemic sclerosis

A

Diffuse systemic sclerosis: 50% survival to 5 years (most deaths are due to respiratory failure)

93
Q

History taking in pt with SLE?

A

Rash:
* Location, appearance, other areas affected
* Photosensitivity

Associations
* Cold hands: Raynaud’s phenomenon
* Dry eyes/mucous membranes: Sjögren’s syndrome

Psychosocial impact
* Particularly important in young women
* Confidence, relationships, work
* Depression
* Family planning: infertility/teratogenicity from treatment

Systemic effects of SLE/treatment
* Renal: hypertension, haematuria, frothy urine/oedema (proteinuria)
* Immunosuppression: skin changes/infections

94
Q

Examination findings of SLE pt?

A

Face
* Malar ‘butterfly’ rash
* Discoid rash ± scarring (discoid lupus)
* Oral ulceration
* Scarring alopecia

Hands
* Vasculitic lesions (nail‐fold infarcts)
* Jaccoud’s arthropathy (mimics rheumatoid arthritis but due to tendon contractures not
joint destruction)

Systemic effects of SLE
* Respiratory: percussion and auscultation
⚬ Pleural effusion, Pleural rub, Fibrosing alveolitis

  • Neurological: finger‐nose‐finger and/or pronator drift
    ⚬ Focal neurology
    ⚬ Chorea
    ⚬ Ataxia
  • Renal: Hypertension
95
Q

ix of SLE?

A

Diagnosis: Serum autoantibodies (ANA, anti dsDNA)

Disease activity:
- elevated ESR but normal CRP
- elevate Immunoglobulins
- reduced C3/C4
- Renal panel, urine microscopy for casts (Glomerulonephritis)

96
Q

Diagnostic criteria for SLE?

A

4/11 of American College of Rheumatology Criteria:

  • Malar rash
  • Discoid rash
  • Photosensitivity
  • Oral ulcers
  • Arthritis
  • Serositis (pleuritis or pericarditis)
  • Renal involvement (proteinuria or cellular casts)
  • Neurological disorder (seizures or psychosis)
  • Haematological disorder (autoimmune haemolytic anaemia or pancytopenia)
  • Immunological disorders (positive anti‐dsDNA or anti‐Sm antibodies)
  • Elevated ANA titre
97
Q

Treatment of mild SLE disease (cutaneous/ joint involvement only)?

A

Topical corticosteroids
Hydroxychloroquine

98
Q

treatment of moderate SLE disease (+organ involvement)?

A

Prednisolone
Azathioprine

99
Q

Treatment of severe SLE disease (+ severe inflammatory involvement of vital organs)?

A

Methylprednisolone
MMF (Lupus nephritis)
Cyclophosphamide
Azathioprine

100
Q

Cyclophosphamide side effects?

A
  • Haematological and haemorrhagic cystitis * infertility
  • teratogenicity
101
Q

Prognosis of SLE?

A

Good: 90% survival at 10 years

102
Q

History to take for RA patient?

A

Symptoms
* Joints involved, pain, function

Disability
* Occupation and ADLs

Drugs
* Will help assess disease activity

Systemic effects of disease and treatment
- lungs, eyes, neuropathies, haematological (Anaemia), cardiac, renal

103
Q

Examination of Rheumatoid Arthritis patient?

A

examine hands
assess disease activity
assess function
treatment side effects
systemic manifestations of rheumatoid arthritis

104
Q

Hand examination of Rheumatoid Arthritis patient?

A
  • Symmetrical and deforming polyarthropathy
  • Volar subluxation and ulnar deviation at the MCPJs
  • Subluxation at the wrist
  • Swan‐neck deformity (hyperextension of the PIPJ and flexion of the DIPJ)
  • Boutonnière’s deformity (flexion of the PIPJ and hyperextension of the DIPJ)
  • ‘Z’ thumbs
  • Muscle wasting (disuse atrophy)
  • Surgical scars:
    ⚬ Carpal tunnel release (wrist)
    ⚬ Joint replacement (especially thumb)
    ⚬ Tendon transfer (dorsum of hand)
  • Rheumatoid nodules (elbows)
105
Q

examination findings in rheumatoid arthritis that reflect disease activity?

A
  • Red, swollen, hot, painful hands imply active disease
106
Q

examination to assess function in rheumatoid arthritis?

A
  • power grip: ‘squeeze my fingers’
  • precision grip: ‘pick up a coin’ or ‘do up your buttons’
  • key grip: ‘pretend to use this key’
  • Remember the wheelchair, walking aids and splints
107
Q
A
108
Q

examination to look for treatment effects in rheumatoid arthritis?

A
  • Steroids: Cushingoid
  • C‐spine stabilization scars
109
Q

systemic manifestations of rheumatoid arthritis?

A
  • pulmonary:
    ⚬ Pleural effusions
    ⚬ Fibrosing alveolitis
    ⚬ Obliterative bronchiolitis
    ⚬ Caplan’s nodules
  • Eyes:
    ⚬ Dry (secondary Sjögren’s)
    ⚬ Scleritis
  • neurological:
    ⚬ Carpal tunnel syndrome (commonest)
    ⚬ Atlanto‐axial subluxation: quadriplegia
    ⚬ Peripheral neuropathy
  • Haematological:
    ⚬ Felty’s syndrome: RA + splenomegaly + neutropaenia
    ⚬ Anaemia (all types!)
  • Cardiac:
    ⚬ Pericarditis
  • Renal:
    ⚬ Nephrotic syndrome (secondary amyloidosis or membraneous glomerulonephritis, e.g. due to penicillamine)
110
Q

main differential diagnosis of rhuematoid arthritis?

A

Psoriatic arthropathy:
⚬ Nail changes
⚬ Psoriasis: elbows, behind ears and scalp

111
Q

ix of rheumatoid arthritis?

A
  • Elevated inflammatory markers
  • Radiological changes:
    ⚬ Soft tissue swelling
    ⚬ Loss of joint space
    ⚬ Articular erosions
    ⚬ Periarticular osteoporosis
  • Positive rheumatoid factor in 80%
112
Q

Prognosis for rheumatoid arthritis

A

5 years – 1/3 unable to work;
10 years – 1/2 significant disability

112
Q

diagnosis of rheumatoid arthritis?

A

Diagnosis: 4/7 of American college of Rheumatology Criteria

  • Morning stiffness
  • Arthritis in 3+ joint areas
  • Arthritis of hands
  • Symmetrical arthritis
  • Rheumatoid nodules
  • Positive rheumatoid factor
  • Erosions on joint radiographs
113
Q

management of rheumatoid arthritis?

A

medical
* Symptomatic relief: NSAIDs and COX‐2 inhibitors
* Early introduction of disease‐modifying anti‐rheumatoid drugs (DMARDs) to suppress disease activity

Ongoing disease activity may require immunomodulation therapy:
* anti‐tnf therapy: Infliximab/Etanercept/Adalimumab
* B cell depletion therapy: Rituximab (anti‐CD20 mAb)

Supportive
⚬ Explanation and education
⚬ Exercise and physiotherapy
⚬ Occupational therapy and social support

Surgery
⚬ Joint replacement, tendon transfer, etc.

114
Q

side effects of anti-TNF therapy?

A

rash, opportunistic infection (exclude TB: Heaf test and CXR)

115
Q

what DMARDs are used in Rheumatoid arthritis to suppress disease activity?

A
116
Q

what history to take in patient with pseudoxanthoma elasticum?

A

Explore skin problems
* Hereditary: chronic

other problems
* Hyperextensible joints
* Reduced visual acuity
* Hypertension
* MI or CVA
* Gastric bleed

family history

117
Q

pseudoxanthoma elasticum

what examination findings?

A

Skin
* ‘Plucked chicken skin’ appearance: loose skin folds especially at the neck and axillae, with yellow pseudoxanthomatous plaques

Eyes
* Blue sclerae
* Retinal angioid streaks (cracks in Bruch’s membrane) and macular degeneration

Cardiovascular
* Blood pressure: 50% are hypertensive
* Mitral valve prolapse: EC and PSM

118
Q

pseudoxanthoma elasticum

inheritance pattern?

A

80% autosomal recessive (ABCC6 gene, chromosome 16)

119
Q

pathophysiology of pseudoxanthoma elasticum?

A

Degenerative elastic fibres in skin, blood vessels and eye

premature coronary artery disease

120
Q

main differential for elastic skin apart from pseudoxanthoma elasticum?

A

Ehlers Danlos

121
Q

Examination findings of ehlers danlos

A

Skin and joints
• Fragile skin: multiple ecchymoses, scarring – ‘fish‐mouth’ scars especially on the knees
• Hyperextensible skin: able to tent up skin when pulled (avoid doing this)
• Joint hypermobility and dislocation (scar from joint repair/replacement)

Cardiac
• Mitral valve prolapse

abdominal
• Scars:
⚬ Aneurysmal rupture and dissection
⚬ Bowel perforation and bleeding

122
Q

Features/ pathophysiology of ehlers danlos

A

• Inheritance: autosomal dominant (family history more apparent)
• Defect in collagen causing increased skin elasticity
• No premature coronary artery disease

123
Q

History taking for skin lump suspected malignancy?

A

Symptoms
• Location and rapidity of growth
• Recent changes or bleeding

Risk factors
• Sun exposure
• Occupation: exposure to dust/chemicals, outdoor work
• Family or past medical history of skin cancer

Associations
• Solid organ transplant: immunosuppression

Complications
• Local invasion or metastasis: bone pain, neurological or abdominal problems

124
Q

Usual findings in basal cell carcinoma

A

• Usually on face/trunk: sun‐exposed areas
• Pearly nodule with rolled edge
• Superficial telangiectasia
• Ulceration in advanced lesions

• Slowly grow over a few months
• Local invasion only, rarely metastasize

125
Q

Treatment of basal cell carcinoma

A

• Curettage/cryotherapy if superficial
• Surgical excision ± radiotherapy

126
Q

Bowens disease?

A

Squamous cell carcinoma in situ

127
Q

Bowens disease?

A

Squamous cell carcinoma in situ

128
Q

Examination of pt with squamous cell carcinoma?

A

• Sun‐exposed areas (+ lips + mouth)
• Actinic keratoses: pre‐malignant (red and scaly patches)

• Varied appearance
⚬ Keratotic nodule
⚬ Polypoid mass
⚬ Cutaneous ulcer

• Other lesions/previous scars
• Metastases (draining lymph nodes/hepatomegaly/bone tenderness)

129
Q

Treatment of squamous cell carcinoma?

A

• Surgery ± radiotherapy
• 5% metastasize

130
Q

Examination findings of malignant melanoma

A

• Patient’s appearance: mention risks
⚬ Fair skin with freckles
⚬ Light hair
⚬ Blue eyes

• Appearance of lesion
asymmetrical
Border irregularity
Colour (black: often irregular pigmentation, may be colourless) Diameter >6 mm
Enlarging

• Other lesions/previous scars
• Metastases (draining lymph nodes/hepatomegaly/bone tenderness)

131
Q

Diagnosis and treatment of malignant melanoma?

A

• Excision
• Staged on Breslow thickness (maximal depth of tumour invasion into dermis):
⚬ <1.5 mm = 90% 5‐year survival
⚬ >3.5 mm = 40% 5‐year survival

Beware the man with a glass eye and ascites: ocular melanoma!

132
Q

History of henoch schonlein purpura

A

Triad
• Purpuric rash: usually on buttocks and legs
• Arthritis
• Abdominal pain

Precipitant
• Infections: streptococci, HSV, parvovirus B19, etc.
• Drugs: antibiotics

Complications
• Renal involvement (IgA nephropathy): visible or non‐visible haematuria, proteinuria
• Hypertension

133
Q

Examination of henoch schonlein purpura?

A

Rash
• Purpuric rash: usually on buttocks and legs

Joints
• Arthritis

Other
• Blood pressure
• Urine dipstick

134
Q

pathophysiology of henoch schonlein purpura?

A
  • Small‐vessel vasculitis: IgA and C3 deposition
  • Normal or raised platelet count (distinguishes from other forms of purpura)
  • Children more than adults, males > females
135
Q

prognosis of henoch schonlein purpura

A

90% full recovery although can recur

136
Q

treatment of henoch schonlein purpura

A

most spontaneously recover without treatment although steroids may help
recovery and treat painful arthralgia

137
Q

history in erythema nodosum

A

Skin
* Tender, red, smooth, shiny nodules on the shins

Causes
* Sarcoidosis
* Streptococcal throat infection
* Streptomycin, sulphonamides
* Oral contraceptive pill
* Pregnancy
* TB
* Inflammatory bowel disease
* Lymphoma
* Idiopathic

138
Q

examination findings of erythema nodosum?

A

Skin
* Tender, red, smooth, shiny nodules commonly found on the shins (although anywhere with subcutaneous fat)
* Older lesions leave a bruise

Joints
* Tenderness and swelling

Cause
* Red, sore throat (streptococcal infection)
* Parotid swelling (sarcoidosis)

139
Q

pathology of erythema nodosum?

A

inflammation of subcutaneous fat (panniculitis)

140
Q

skin manifestations of sarcoidosis

A
  • erythema nodosum
  • nodules and papules: red/brown seen particularly around the face, nose, ears and neck. Demonstrates Koebner’s phenomenon
  • lupus pernio: diffuse bluish/brown plaque with central small papules commonly affecting the nose
141
Q

diabetes and skin rash?

A

necrobiosis lipoidica diabeticorum

142
Q

history to take in diabetes patient with new rash

A

diabetic history/care
* Duration
* Insulin administration and glucose control: rotation of injection sites
* Foot care: podiatry

Microvascular complications of diabetes
* Neuropathy
* Retinopathy

Psychosocial
* Impact on ability to work, form relationships, body image

143
Q

Rashes in diabetic patients? differentials

A

necrobiosis lipoidica diabeticorum
diabetic dermopathy, granuloma annulare, leg ulcers, eruptive xanthomata, vitiligo, candidiasis

144
Q

examination findings in necrobiosis lipoidica diabeticorum?

A

Shins
* Necrobiosis lipoidica diabeticorum:
⚬ Well‐demarcated plaques with waxy‐yellow centre and red–brown edges
⚬ Early: may resemble a bruise
⚬ Prominent skin blood vessels
⚬ Female preponderance (90%)
* Diabetic dermopathy: Red/brown, atrophic lesions

Feet/legs
* Ulcers: arterial or neuropathic
* Eruptive xanthomata:
⚬ Yellow papules on buttocks and knees (also elbows)
⚬ Caused by hyperlipidaemia
* Granuloma annulare: flesh‐coloured papules in annular configurations on the dorsum feet (and more commonly fingers)

injection sites
* Lipoatrophy
* Fat hypertrophy

cutaneous infections
* Cellulitis
* Candidiasis (intertrigo): in skin creases

others
* Vitiligo (and other autoimmune diseases)
* PVD: pulses

145
Q

Treatment for necrobiosis lipoidica diabeticorum?

A
  • Topical steroid and support bandaging
  • Tight glycaemic control does not help
146
Q

examination findings in patient with xanthomata?

A
  • Hypercholesterolaemia: tendon xanthomata, xanthelasma and corneal arcus
  • Hypertriglyceridaemia: eruptive xanthomata and lipaemia retinalis
  • other causes of secondary hyperlipidaemia:
    ⚬ Hypothyroidism
    ⚬ Nephrotic syndrome
    ⚬ Alcohol
    ⚬ Cholestasis
147
Q

History taking for patient with leg ulcer?

A

Symptoms
• Pain: arterial (venous and neuropathic are painless)
• Location

Associated diseases
• Venous: DVT, chronic venous insufficiency, varicose veins, CCF
• Arterial: PVD
• Neuropathic: sensory neuropathy, diabetes

Complications
• Systemic signs of infection

148
Q

Examination of leg ulcer?

A

Venous
• Gaiter area of lower leg
• Stigmata of venous hypertension: varicose veins or scars from vein stripping, oedema, lipodermatosclerosis, varicose eczema, atrophie blanche
• pelvic/abdominal mass

Arterial
• Distal extremities and pressure points
• Trophic changes: hairless and paper‐thin shiny skin
• Cold with poor capillary refill
• absent distal pulses

neuropathic
• Pressure areas, e.g. under the metatarsal heads
• peripheral neuropathy
• Charcot’s joints

Complications
• infection: temperature, pus and cellulitis
• malignant change: Marjolin’s ulcer (squamous cell carcinoma)

149
Q

Other causes of leg ulcer apart from the usual venous/arterial/ neuropathic?

A

• Vasculitic, e.g. rheumatoid arthritis
• Neoplastic, e.g. squamous cell carcinoma
• Infectious, e.g. syphilis
• Haematological, e.g. sickle cell anaemia
• Tropical, e.g. cutaneous leishmaniasis

150
Q

Ix leg ulcer

A

• Doppler ultrasound
• Ankle–brachial pressure index (0.8–1.2 is normal, <0.8 implies arterial insufficiency)
• Arteriography

151
Q

Treatment of venous ulcers

A

• Four‐layer compression bandaging (if no PVD)
• Varicose vein surgery

152
Q

Tx of arterial ulcers

A

Angioplasty or vascular reconstruction/amputation

153
Q

Causes of neuropathic ulcers

A

• Diabetes mellitus
• Tabes dorsalis
• Syringomyelia

154
Q

History taking in psoriasis

A

Describe the rash
• Location, appearance, pruritis

Psychosocial impact
• Particularly important in young women • Confidence, relationships, work
• Depression

Exacerbating factors
• Stress, alcohol, cigarettes, drugs (β‐blockers), trauma

treatment
• PUVA: risk of melanoma (fair skin, family history)
• Immunosuppression: intercurrent infections
• Systemic side‐effects: steroids
• Pregnancy? Some treatments are teratogenic

155
Q

Examination findings in psoriasis?

A

Skin
• Chronic plaque (classical) type: multiple, well‐demarcated, ‘salmon‐pink’, scaly plaques on extensor surface
• Check behind ears, scalp and umbilicus
• Koebner phenomenon: plaques at sites of trauma
• Skin staining from treatment

Nails
• Pitting, onycholysis, hyperkeratosis, discoloration

Joints
• psoriatic arthropathy (10%), five forms:
⚬ DIPJ involvement (similar to OA)
⚬ Large joint mono/oligoarthritis
⚬ Seronegative (similar to RA)
⚬ Sacroilitis (similar to ankylosing spondylitis)
⚬ Arthritis mutilans

156
Q

Treatment options of psoriasis?

A

Topicals:
Emollients, topical steroids, calcitriol, coal tar

Phototherapy: • UVB
• Psoralen + UVA (PUVA)

Systemics
• Cytotoxics (methotrexate and ciclosporin)
• anti‐tnfα (adalimumab: Humira) and other immunological
• Retinoids (Acitretin): teratogenic

157
Q

Complications of psoriasis

A

Pustular psoriasis
GED

158
Q

Causes of nail pitting

A

• psoriasis
• Lichen planus
• Alopecia areata
• Fungal infections

159
Q

Koebner phenomenon assoc w

A

• psoriasis
• Lichen planus
• Viral warts
• Vitiligo
• Sarcoid

160
Q

History taking in eczema

A

Rash
• Location, appearance, pruritis

psychosocial impact
• Particularly important in young women • Confidence, relationships, work
• Depression

atopic (Endogenous)
• Asthma, hay fever and allergy

Environmental (Exogenous)
• Primary irritant dermatitis: may just affect hands
• What is their job?
• Triggers?

161
Q

Examination in eczema

A

Rash
• Erythematous and lichenified patches of skin
• Predominantly flexor aspects of joints
• Fissures (painful), especially hands and feet
• Excoriations
• Secondary bacterial infection

associated atopy
• Respiratory: polyphonic wheeze (asthma)

Systemic treatment Effects
• Steroids: e.g. blood pressure

162
Q

Ix in eczema?

A

• Patch testing for allergies

163
Q

Treatment options for eczema

A

• Avoid precipitants

• Topical:
⚬ Emollients
⚬ Steroids
⚬ Tacrolimus (protopic): small increased risk of Bowen’s disease

• Anti‐histamines for pruritis
• Antibiotics for secondary infection
• UV light therapy
• Systemic therapy (prednisolone) in severe cases
Or even azathioprine/ ciclosporin/ MTX
Immunologics: dupilumab, baricitinib, abrocitinib

164
Q

History in young hypertensive patient with headache?

A
  • Duration of symptoms, nature of headache
  • Past history of hypertension: previous blood pressure readings (e.g. employment
    medical, with prescription of oral contraceptive pill, during pregnancy)
  • Other medical history (e.g. renal disease), cardiovascular risk factors (smoking, diabetes, known ischaemic heart disease)
  • Drug history (prescribed and illicit), alcohol consumption
  • Visual disturbance (in accelerated phase hypertension)
  • Paroxysomal symptoms (phaeochromocytoma)
  • Check if pregnant!
165
Q

Examination in young hypertensive patient with headaches?

A
  • Body habitus: obese, Cushingoid, acromegalic
  • Radial pulse (SR/AF), radio‐radial and radio‐femoral delay (coarctation)
  • Check the blood pressure yourself, with a manual sphygmomanometer, in both arms
  • Evidence of cardiac failure
  • Underlying renal cause: renal bruit(s), polycystic kidney disease, current renal replacement therapy, ask to dip urine
  • fundoscopy: hypertensive retinopathy
166
Q

Fundoscopy in hypertensive retinopathy?

A

⚬ Grade 1: silver wiring (increased reflectance from thickened arterioles)
⚬ Grade 2: plus arteriovenous nipping (narrowing of veins as arterioles cross them)
⚬ Grade 3: plus cotton wool spots and flame haemorrhages
⚬ Grade 4: plus papilloedema

There may also be hard exudates (macular star)

167
Q

causes of hypertension?

A
  • Essential (94%: associated with age, obesity, salt and alcohol)
  • Renal (4%: underlying chronic kidney disease secondary to glomerulonephritis, ADPKD, renovascular disease)
  • Endocrine (1%: Conn’s, Cushing’s, acromegaly or phaeochromocytoma)
  • Aortic coarctation
  • Pre‐eclampsia: pregnancy
168
Q

Ix of young hypertension?

A
  • Evidence of end‐organ damage: fundoscopy, LVH on ECG, renal impairment, cardiac failure on CXR, echocardiography
  • Exclude underlying cause:
    ⚬ Urine pregnancy test (where appropriate!)
    ⚬ Urinalysis (and urine ACR)
    ⚬ U&Es
    ⚬ Consider secondary screen: renin/aldosterone levels, plasma and/or urinary metanephrines
169
Q

Diagnosis of hypertension?

A

Current (2011) British Hypertension Society guidelines:
⚬ Clinic BP >140/90 mm Hg: use 24h ABPM to confirm diagnosis (average of daytime
values)

Definitions;
⚬ Stage 1 hypertension: clinic BP ≥140/90 mm Hg or ABPM daytime average ≥135/85 mm Hg
⚬ Stage 2 hypertension: clinic BP ≥160/100 mm Hg or ABPM daytime average ≥150/95 mm Hg
⚬ Severe hypertension: clinic SBP ≥180 mm Hg or DBP ≥110 mm Hg

170
Q

When to treat hypertension?

A

⚬ Treat if stage 1 hypertension and evidence of end‐organ damage, ischaemic heart
disease, diabetes, CKD or 10‐year cardiovascular risk ≥20%
⚬ Treat all with stage 2 hypertension
* Arrange same‐day admission if severe hypertension and grade 3 or 4 retinopathy (or other concerns; e.g. new renal impairment)

171
Q

Management of hypertension

A
  • Lifestyle modification (lose weight, increase exercise, stop smoking)
  • Initial treatment:
    ⚬ ACE‐I or ARB
  • Aged >55 years or Afro‐Caribbean ethnicity: CCB or thiazide‐like diuretic
    ⚬ Titrate dose to maximum tolerated
  • Then add 2nd agent: CCB or thiazide‐like diuretic
  • Then ACE‐I/ARB + CCB + thiazide‐like diuretic
  • Consider adding spironolactone, β‐blocker, α‐blocker or seeking specialist opinion
  • Consider other cardiovascular risk modification: aspirin, statin
172
Q

Management of malignant hypertension with Grade III and IV retinopathy

A

Bed rest, oral anti‐hypertensives (long‐acting CCB) and non‐invasive blood pressure monitoring: aiming for gradual reduction in blood pressure

173
Q

Management of HTN Plus encephalopathy/stroke/myocardial infarction/left ventricular failure.

A

⚬ Parenteral venodilators and invasive blood pressure monitoring.
⚬ Over rapid fall in blood pressure can lead to ‘watershed’ cerebral and retinal infarction.

174
Q

what is papilloedema?

A

Blurring of disc margins/elevation of disc/loss of venous pulsation/venous engorgement

175
Q

causes of papilloedema?

A
  • Raised intracranial pressure: space‐occupying lesion, benign intracranial hypertension and cavernous sinus thrombosis
  • Accelerated phase hypertension
  • Central retinal vein occlusion
176
Q

History taking in inflammatory bowel disease?

A
  • Gastrointestinal symptoms
    ⚬ Duration
    ⚬ Precipitants (travel, antibiotics, infectious contacts, foods, sexual history)
    ⚬ Stool frequency and consistency (Bristol stool scale)
    ⚬ Blood: fresh PR/mixed with stools
    ⚬ Mucus/slime
    ⚬ Urgency, incontinence, tenesmus
    ⚬ Abdominal pain, bloating: and association with eating, defecation
  • Systemic symptoms
    ⚬ Fever
    ⚬ Anorexia
    ⚬ Weight loss
    ⚬ Rash, arthralgia, aphthous ulcers
  • Family history
177
Q

Examination findings of IBD?

A
  • General
    ⚬ Pallor/anaemia
    ⚬ Nutritional status
    ⚬ Pulse and BP
    ⚬ Oral ulceration
  • Abdomen
    ⚬ Surgical scars, including current/past stoma sites
    ⚬ Tenderness
    ⚬ Palpable masses (e.g. right iliac fossa mass in Crohn’s disease or colonic tumour
    in UC)
    ⚬ Ask to examine for perianal disease
  • Evidence of treatment
    ⚬ Steroid side effects
    ⚬ Ciclosporin (gum hypertrophy and hypertension)
    ⚬ Hickman lines/scars
178
Q

Ix in suspected IBD?

A

⚬ Stool microscopy and culture: exclude infective cause of diarrhoea
⚬ FBC and inflammatory markers: monitor disease activity
⚬ AXR: exclude toxic dilatation in UC and small bowel obstruction due to strictures in
Crohn’s
⚬ Sigmoidoscopy/colonoscopy and biopsy: histological confirmation
⚬ Bowel contrast studies: strictures and fistulae in Crohn’s disease
⚬ Further imaging: white cell scan and CT scan

179
Q

Cause of IBD?

A

Genetic, environmental and other factors combine to produce an exaggerated,
sustained and mucosal inflammatory response

180
Q

Differentials for IBD?

A

⚬ Crohn’s: Yersinia, tuberculosis, lymphoma (and UC)
⚬ UC: infection (e.g. campylobacter), ischaemia, drugs and radiation (and Crohn’s)

181
Q

Extra intestinal manifestations of IBD?

A

Mouth: Apthous ulcers*

Skin: Erythema nodosum*
Pyoderma gangrenosum*
Finger clubbing*

Joint:
Large joint arthritis*
Seronegative arthritides

Eye: Uveitis, episcleritis and iritis*

Liver: Primary sclerosing cholangitis (UC)

Systemic amyloidosis

*related to disease activity

182
Q

Complications of Crohns Disease?

A

Malabsorption
Anaemia
Abscess
Fistula
Intestinal obstruction

183
Q

Complications of Ulcerative Colitis?

A

Anaemia
Toxic dilatation
Perforation
Colonic carcinoma

184
Q

Which UC patients are at higher risk of developing Colon Ca?

A

Higher risk in patients with pancolitis (5–10% at 15–20 years), and in those with PSC

185
Q

Recommended surveillance for colon ca in UC?

A

Surveillance: 3‐yearly colonoscopy for patients with pancolitis >10 years, increasing in frequency with every decade from diagnosis (2‐yearly 20–30 years, annually >30
years)

186
Q

Overall treatment strategies for IBD?

A

Medical therapies: steroids/ 5-ASA etc

Antibiotics (metronidazole): in Crohn’s with perianal infection, fistulae or small bowel bacterial overgrowth

Nutritional support: high fibre, elemental and low residue diets

Psychological support

Surgery

187
Q

what nutrition / diet is recommended in IBD?

A

high fibre, elemental and low residue diets

188
Q

in what situation is antibiotic therapy with metronidazole indicated in crohns disease

A

Antibiotics (metronidazole): in Crohn’s with perianal infection, fistulae or small bowel bacterial overgrowth

189
Q

Surgical tx options for IBD?

A

⚬ Crohn’s: obstruction from strictures, complications from fistulae and perianal disease and failure to respond to medical therapy

⚬ UC: chronic symptomatic relief, emergency surgery for severe refractory colitis and colonic dysplasia or carcinoma

190
Q

History taking in atrial fibrillation?

A

• Symptoms of atrial fibrillation
⚬ Onset and offset, frequency and duration
⚬ Breathlessness, chest pain, palpitations, presyncope
⚬ Precipitants: alcohol, caffeine, exercise

• Associated conditions
⚬ Cardiac problems: valvular heart disease
⚬ Hypertension
⚬ Hyperthyroidism
⚬ Stroke or TIA (likely in this case)
⚬ Lung disease including PE

• Treatment consideration
⚬ Anticoagulation and risk factors for bleeding
⚬ Anti‐arrhythmic vs cardioversion vs pulmonary vein isolation

191
Q

Examination finding in atrial fibrillation?

A

• Cardiovascular examination
⚬ Pulse and BP
⚬ Auscultation: murmurs – MS or MR
⚬ Signs of CCF

• Assessment of thyroid status
⚬ Tremor
⚬ Goitre
⚬ Eye disease: lid lag, exophthalmos (Grave’s disease)

• Brief neurological examination
⚬ Pronator drift
⚬ Visual fields
⚬ CN VII weakness (facial asymmetry)
⚬ CN V and upper limb sensation
⚬ Gait

192
Q

Ix of new AF

A

⚬ Confirmation: 12‐lead ECG or 24‐hour Holter monitor
⚬ Echo: structural disease, LVH, LA size (>4.0 cm – recurrence high)
⚬ TSH

193
Q

Types of AF

A

⚬ Paroxysmal: <7 days, self terminating
⚬ Persistent: >7 days, requires chemical or electrical cardioversion
⚬ Permanent: >1 year or when no further attempts to restore sinus

194
Q

Mx of AF

A

⚬ Rhythm control: chemical or electrical cardioversion
⚬ Rate control: β‐blockers, digoxin, pacemaker and AVN ablation

195
Q

CHADVASC

A

Systemic emboli risk:

C Congestive cardiac failure = 1 Hypertension = 1
A2 Age ≥75 = 2
D Diabetes = 1
S2 Stroke/TIA/embolus = 2
V Vascular disease = 1
A Age 65–74 = 1
Sc Sex category (female) = 1

0 = Low stroke risk = no anticoagulation
1 = Medium stroke risk (1.3% per annum) = patient preference
≥2 = High risk (>2.2% per annum) = oral anticoagulation recommended

196
Q

Bleeding risk HASBLED score

A

Bleeding risk:
H A S B L E D

Hypertension = 1
Abnormal kidney or liver function = 1 for each
Stroke = 1
Bleeding = 1
Labile INR = 1
Elderly = 1
Drugs (NSAIDs) and alcohol = 1 for each

3 or more = high risk (avoid oral anticoagulation)
Patients high risk for both embolic and bleeding complications should be considered for left atrial appendage occlusion to isolate the commonest source of thrombus in AF.
• Prevalence: 8% of >80‐year‐olds have AF

197
Q

History for syncope?

A

Description of the syncopal episode:
⚬ Provocation: micturation, cough or stressful situation (vasovagal)
⚬ Prodrome: light headed, dizziness, tunnel vision (vasovagal/orthostatic), no warning
(cardiac)
⚬ Posture: sitting/lying (cardiac) or standing (orthostatic), sudden head turning
(vertebrobasilar)
⚬ Associated symptoms: palpitations and chest pain (cardiac), headache, tongue biting
and incontinence (neuro)
⚬ Duration (transient, <5 minutes) and frequency
⚬ Recovery: immediate (cardiac) or prolonged confused state and amnesia (>5 minutes)
(neuro), red/flushed face (cardiac)
⚬ Injury (neuro or cardiac)
⚬ Eyewitness account is very useful

Past medical history of syncope/presyncope, cardiac disease or neurological conditions

Medications that may cause hypotension

198
Q

Examination in syncope

A

• Brief cardiovascular exam
⚬ Pulse and blood pressure (lying and standing), postural drop: >20/10 mm Hg
difference
⚬ Auscultation: obstructive valvular pathology e.g. AS or MS or signs of a PE (loud P2 and left parasternal heave)
⚬ Pacemaker or ICD scars

• Brief neurological exam
⚬ Fundoscopy
⚬ Pronator drift
⚬ Reflexes
⚬ Parkinson’s plus tremor, rigidity, bradykinesia and orthostatic hypotension, e.g. multiple system atrophy

199
Q

Ddx syncope

A

⚬ Cardiac: brady‐ or tachycardia, obstructive cardiac lesion: AS, MS, HOCM or PE
⚬ Neurological: epilepsy, vertebrobasilar insufficiency
⚬Orthostatic (postural) hypotension: particularly in combination with vasodilator
drugs
⚬ Vasovagal (neurocardiogenic): stress, cough, micturation, defecation

200
Q

Ix in syncope

A

⚬ 12‐lead ECG, Holter monitor, implantable loop recorder, electrophysiology study, ETT
and Echo if cardiac cause suspected
⚬ Tilt table test if orthostatic hypotension suspected
⚬ EEG and/or CT MRI brain if a neurological cause is suspected

201
Q

Mx of different causes of syncope

A

⚬ Cardiac: pacemaker, ICD, revascularisation and valvular surgery
⚬ Vasovagal: education on avoidance, isotonic muscle contraction

⚬ Orthostatic hypotension: salt and water replacement, support stockings, medication review, occasionally fludrocortisone, midodrine, SSRIs and pacemaker are helpful

⚬ Neurological: antiepileptic medication

202
Q

DVLA instructions in pt w syncope?

A

⚬ Check the 3 P’s: provocation/prodrome/postural – if all present then likely benign and can continue driving.

⚬ Solitary with no clear cause – 6 month ban; clear cause that has been treated – resume driving after 4 weeks

⚬ Recurrent syncope due to seizures – must be fit free for 1 year to drive.

203
Q

Ix in suspected asthma attack

A

• Arterial blood gas:
⚬ Hypoxaemia
⚬ Normal or rising PaCO2 suggests a tiring patient requiring respiratory support (should
have a respiratory alkalosis)

• CXR in exhalation (pneumothorax)

204
Q

Tx asthma attack

A

⚬ Bronchodilators and steroids (not routine antibiotics as often viral)
⚬ Asthma specialist nurse: assess Inhaler technique
⚬ Allergy clinic

205
Q

Tx pneumothorax

A

High flow O2
⚬ Needle aspiration or chest drain
⚬ May need talc or surgical pleurodesis if it is recurrent

206
Q

examination findings of Osler Weber Rendu Syndrome aka Hereditary Haemorrhagic Telangiectasia?

A
  • Multiple telangiectasia on the face, lips and buccal mucosa
  • Anaemia: gastrointestinal bleeding
  • Cyanosis and chest bruit: pulmonary vascular abnormality/shunt
207
Q

features of Osler Weber Rendu Syndrome aka Hereditary Haemorrhagic Telangiectasia?

A
  • Autosomal dominant
  • Increased risk gastrointestinal haemorrhage, epistaxis and haemoptysis
  • Vascular malformations:
    > Pulmonary shunts
    > Intracranial aneurysms: subarachnoid haemorrhage
208
Q

Management of DVT?

A
  • Anticoagulation: 3 months if provoked, 6 months if unprovoked, lifelong if recurrent/ high risk
  • Compression stockings reduce post‐phlebitic syndrome
209
Q

TIMI risk score for MI

A

Cases For PACES (3 decks)

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