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Clinical 1 Flashcards

1
Q

Prolonged PR on ECG is associated with:

A

Endocardial cushion defects (e.g. AVSD, ASD - or cardiac surgery in this area)
Ebstein’s
Acute rheumatic fever (carditis)
Congenital heart block (e.g. maternal lupus)

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2
Q

What are the biochemical abnormalities causing prolonged QRS?

A

Hyperkalemia
Hypothyroidism
Digoxin

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3
Q

What are the main medical things to think about with management of DMD?

A
  • Medical treatment - STEROIDS

Surveillance and management of complications:
- mood and behaviour
- Cognitive impairment slightly more common - Wisckott score to identify areas requiring assistance and strengths, individualised learning plan for appropriate assistance with educational and physical needs
- CVS: cardiomyopathy - regular echo, treat if failure
- Resp: nocturnal failue - PSG + BiPAP. Don’t smoke, treat infections aggressively
- Ortho: Contractures/scoliosis - passive and active exercises, PT assisted programmes
OT for assisted supports, equipment, suitable home environment
Orthotist for orthotics, ortho for surgery
- Nutrition: diet/exercise
- Many will transition to adult services (get to 20s)

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4
Q

What are the social issues that are common in management of DMD?

A

Family support:

  • end of life and palliative (life limiting illness) support from MDA for coping grief and loss
  • Steroid side effects - behaviour - handling
  • Avoid patronising and overprotective
  • Workbridge - vocation planning
  • Resources: Parent Project muscular dystrophy (int) or nzord.org.nz (NZ)
  • Support with long-term goals (dating, work, etc)
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5
Q

What are the syndromes associated with dextrocardia?

A

Situs solitus or inversus (midline liver indicates situs ambiguous or heterotaxy)
Primary ciliary dyskinesia (Kartagener syndrome)
Heterotaxy: asplenia (Ivemarks) and polysplenia syndrome

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6
Q

What investigations do you want for dextrocardia and why?

A

ECG to review atria and ventricle orientation - needs to be reverse positions!

  • normal lead placement leads to no R waves
  • p axis and SA node in RA position
  • q waves in V1/2 if L-TGA
  • D-TGA associated with arrhythmia

Echo to review IVC and great vessels

AXR to determine situs

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7
Q

What are the corticosteroid side effects?

A

CUSHINGOID MAP

Cataract/cushingoid face – moon face/interscapular adiposity
Ulcer
Striae/skin thinning
Hypertension
Infection – thrush
Necrosis of bone (avascular)
Growth - short stature
Osteoporosis/obesity
Intracerebral pressure elevation (pseudotumour cerebri)
Diabetes mellitus - glucose intolerance
Myopathy(proximal)/moon face/mood
Adipose tissue hypertrophy/acne
Pancreatitis/psychosis – behavioural problems
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8
Q

What are the (non-cardiac) causes of hypertension?

A

MONSTER

Medications
Obesity (steroids/Cushing syndrome/phaeo)
Neonatal history
Symptoms / signs / syndromes (collagen, neurofibromatosis, tuberous sclerosis, SLE)
Trends in family (idiopathic)
Endocrine
Renal

White coat HTN

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9
Q

What causes isolated splenomegaly?

A

Remember “HIP”

Haematological

  • Hereditary spherocytosis (autosomal dominant)
  • G6PD deficiency (X-linked recessive)

Infective

  • Typhoid
  • Subacute bacterial endocarditis

Portal hypertension

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10
Q

What are the complications of splenomegaly?

A

Hypersplenism – thrombocytopenia
Functional asplenism – immunodeficiency and infection by encapsulated organisms
Splenic infarction
Early satiety (mass effect) causing poor growth

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11
Q

What is chorea caused by and what part of the brain is affected?

A

Occurs secondary to pathology affecting corpus striatum
Rapid movements: Occurs in: cerebral palsy, Sydenham’s Chorea, Wilson’s Disease, SLE, Moyamoya disease.
Also degenerative conditions such as: Ataxia telangiectasia, Huntington’s Chorea, Lesch Nyhan syndrome, PKU

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12
Q

What is athetosis caused by and what part of the brain is affected?

A

Athetosis (slow writhing movements, proximal extremeities)

Occurs secondary to pathology affecting the outer putamen

Can accompany chorea in dyskinetic CP, Wilson’s disease, Lesch-Nyhan, ataxia telangiectasia

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13
Q

What are the causes of dystonia?

A

Drugs (tardive dystonia), degenerative disorders such as Wilson’s, Hallervorden–Spatz diseases and hemiplegia

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14
Q

What are the causes of myoclonus?

A

Seizure disorder (infantile spasms, benign juvenile myoclonic epilepsy), degenerative conditions (neurocutaneous syndromes, Menkes, TaySachs, Wilson’s), structural brain anomalies (Aicardi syndrome, porencephaly), CVA, infections, and metabolic disorders

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15
Q

What is hemiballismus?

A

Unilateral random gross throwing movements of the proximal portion of the limb. Caused by contralateral subthalamic pathology

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16
Q

What are the causes of static tremor?

A

Wilson’s, Parkinson’s, Huntington’s, and Hallervorden-Spatz (pantothenate kinase disorder)

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17
Q

What are the causes of postural tremor?

A

Postural: most notable when arms outstretched in front of the body
Causes: thyrotoxicosis, phaeo, familial tremor, physiological tremor, Wilson’s

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18
Q

What are the causes of intention tremor?

A

Marked at the end points of movement. Causes include cerebellar pathology (and Wilson’s disease)
Hemiballismus

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19
Q

What are the causes of unilateral facial palsy?

A
  • Pontine lesion - tumour/CVA/infection
  • Posterior fossa - tumour/meningitis
  • Peripheral nerve – GBS, Bell’s palsy, Ramsay Hunt, parotid gland tumour, petrous temporal fracture
  • Ramsay Hunt – check ears for vesicles
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20
Q

What are the causes of bilateral facial palsy?

A

Moebius (absent CN VII +/- CN VI, can be unilateral, associated with Poland syndrome, intellectual disability, hypogonads)
Cerebral palsy
Neuromuscular junction (Myasthenia gravis, infant botulism (ptosis + opthalmoplegia)
Dystrophy - myotonic dystrophy (ptosis, distal weakness, myotonia > 5 years, myopathic facies, cataracts), facial-scapular-humeral dystrophy

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21
Q

What investigations might you ask for if a child has bilateral facial palsy?

A

If you suspect NMJ - ACh receptor antibodies for myasthena gravis, ANA, TFT, EMG
If you suspect dystrophy - CK, DNA for triplet repeat expansions, TFT, BSL

SMA may not show facial weakness (classically ‘bright’ child)

22
Q

What does lid lag suggest?

A

Thyrotoxicosis

23
Q

What does fatiguability on upward gaze suggest and what else might you see?

A

Myasthenia gravis – particularly if bilateral ptosis or myopathic facies

24
Q

What findings suggest Horner’s syndrome?

A 
Ptosis
Smaller pupil on affected side
Lack of sweating on the forehead
Light reflex is maintained
Impaired sympathetic pathway
Heterochromia if early onset
25
Q

What other areas would you like to examine (aside from face/eyes) if a child has Horner’s syndrome?

A

Horner’s syndrome can result from a lesion anywhere along the pathway from the posterior hypothalamus, down to the brain stem, lateral column of the spinal cord to C8/ T1 and with the internal carotid artery to the cavernous sinus.
Neck, heart and lungs

26
Q

What are the possible causes of Horner’s?

A

Disrupted sympathetic nervous system anywhere from hypothalamus to eye

Brachial plexus, neuroblastoma, tumours/ injuries affecting superior cervical chain or carotid artery
Commonest = post-cardiac surgery

Brain stem (lateral medullary syndrome)

Vascular
Tumour
Syringobulbia/myelia - can result in bilateral Horner’s
Neck

Thyroid mass
Trauma
Carotid

Carotid aneurysm
Carotid dissection
Lung - lung mass

27
Q

What are the causes of bilateral ptosis?

A

Myopathy is more likely than myasthenia in the younger age group.

Myopathies: nemaline rod myopathy, centronuclear myopathy, congenital myotonic dystrophy.

28
Q

What are the causes of unilateral ptosis?

A

Horner’s syndrome – associated with constriction of the pupil. Most likely congenital due to shoulder traction at birth damaging sympathetic chain – may have hypochromia of affected iris also if congenital. Differential diagnosis - neoplastic lesions along sympathetic chain/apical lung.

CN III nerve lesions – pupil dilated and paralytic squint. Pupil dilatation happens FIRST before ptosis

Facial nerve palsy

29
Q

What clinical signs should you look for if a child has bilateral ptosis?

A

Myopathic facies - restricted eye movement, long thin face, drooping mouth, lack of expression, breathlessness.

30
Q

What would cause binocular diplopia?

A

Binocular diplopia: Palsies of CN III, IV or VI; ptosis, pupil changes or abnormal eye movements
Thyroid ophthalmopathy causes – proptosis, lid lag, chemosis
Trauma to orbit

31
Q

What causes a ‘down and out’ eye?

A

Complete CN III palsy:

Pupils rest down and out.
Paralysis of most eye movement except the lateral rectus and superior abduction (abduction-nerve VI and depression-nerve IV) with a dilated pupil.
Cause: tumour, vascular lesions, arteritis, demyelination.

32
Q

If you see a head tilt what cranial nerve may be affected?

A

CN IV lesion:

Paralysis of the superior oblique= diplopia on adducting and looking down.
Head tilt is OPPOSITE. Asking them to tilt their head the other way causes worsening of the diplopia.

33
Q

What cranial nerve might cause horizontal diplopia?

A

CN VI:

Failure of abduction.
Covering the eye on the AFFECTED/SAME side causes the outer image to disappear.

Cause: Duane syndrome (limited abduction of the affected eye with retraction of the eyeball into the socket on adduction, which causes eye closure - affects one eye in 80%), tumour, vascular lesions, mononeuritis multiplex.

34
Q

What are the complications of CF?

A

Respiratory

Pulmonary hypertension (six month median survival)
Pneumothorax (75% - three year mortality)
Musculoskeletal (HPOA, kyphosis in 25%)
Anaemia
Chronic disease, variceal bleed and poor clotting function, thrombocytopenia from hypersplenism, haemoptysis
Malabsorption and malnutrition (macronutrient and ADEK - unlikely to be clinically evident as most on supplements)
Intestinal obstruction
Diabetes
Chronic liver disease and portal hypertension
Delayed puberty (30%)
Mental state (modulation of affect/self harm)
Hernia (from coughing)
Rectal prolapse (usually in first few years of life)

35
Q

If a patient has a RIGHT head tilt what CN may be affected?

A

Left CN IV

36
Q

What happens to the FEF50%:FIF50% with

  • variable extra-thoracic lesions
  • variable intra-thoracic lesions
  • fixed obstruction
A
  • variable extrathoracic lesions INCREASE ratio (>1)
  • variable intrathoracic lesions DECREASE ratio (<0.2)
  • fixed obstructions (intrathoracic or extrathoracic) ratio ~1
37
Q

Pulmonary function tests in diffuse interstitial

pulmonary fibrosis typically show:

A
  • Increased FEV1/FVC %
  • FEV, FVC and TLC decrease
  • FRC increases due to air trapping
38
Q

What symptoms would you expect from someone with a flattened/rectangular inspiratory curve?

A

Extra-thoracic obstruction:

  • Bi/unilateral vocal cord paralysis (weak cry, aspiration, resp distress)
  • Tracheomalacia (cough, stridor)
  • Airway burns

Worse on inspiration because negative pressure narrows/collapses airway inwards; PEEP reduces the obstruction

39
Q

If you see someone with possible tracheomalacia what might you see on the flow-volume loop?

A

Flattened/rectangular inspiratory curve

40
Q

What are the cutoffs for respiratory failure?

A

The definition of respiratory failure is PaO2 <8

kPa (60mmHg) or PaCO2 >7 kPa (55mmHg)

41
Q

What happens to FEV1/FVC in restrictive and obstructive lung disease?

A
  • Normal in restrictive, may be increased (normal 75-80%)

- Decreased if obstructive

42
Q

Describe what happens to the flow-volume loop in restrictive and obstructive lung disease:

A
  • Restrictive - flow less affected, narrow oblong. May be smaller overall
  • Obstructive - volume less affected, concave expiratory loop
43
Q

What diseases lead to decreased FRC?

A
  • Alveolar interstitial diseases
  • Thoracic deformities
  • Restrictive lung diseases

examples: scoliosis, neuromuscular diseases

44
Q

Where are the mutations causing cystic fibrosis and what are the most common ones?

A
  • CFTR protein on Chromosome 7
- Commonest is deletion F508 (class 2, protein transport problems)
In Australia/NZ
- Gly551Asp/G551D (defective regulation of CFTR, class 3)
- Gly542X (no CFTR, class 1)
45
Q

What are the complications of CF treatments?

A

Aminoglycosides (hearing)
Ciprofloxacin (skin sensitivity, tendinopathy, arthralgia)
Steroids
Previous vascular access
Lung/liver transplantation and immunosuppression

46
Q

Ejection systolic murmur:

A

Loudest ABOVE NIPPLE LINE
With a carotid thrill = left ventricular outflow tract obstruction
Without a carotid thrill = right ventricular outflow tract obstruction

47
Q

PSM:

A

Loudest BELOW NIPPLE LINE
Mitral regurgitation
Tricuspid regurgitation
Ventricular septal defect

48
Q

Murmurs at the LEFT upper sternal edge:

A

Pulmonary area
PS: – harsh, radiates to back, systolic click (variable i.e. decreases with inspiration), soft P2, fixed widened splitting of S2
ASD: Harsh, fixed widened splitting of S2 and systolic pulmonary flow murmur
Coarctation - radiates to the back (left interscapular area); decrescendo diastolic murmur at the third left intercostal space (aortic regurgitation from a bicuspid aortic valve), thrill at the suprasternal notch, ejection click at the apex. Innocent pulmonary flow murmur

49
Q

Murmur at RIGHT upper sternal edge:

A

Valvular AS – radiates to carotids, ejection systolic click; decrescendo diastolic murmur at the third left intercostal space (aortic regurgitation from a bicuspid aortic valve or in discrete subvalvular stenosis)
Supravalvular AS - radiation to the neck/apex, right arm blood pressure is greater than the left arm blood pressure, no ejection click
Right BT shunt

50
Q

Murmur LLSE:

A

Ventricular septal defect - early systolic murmur (if muscular) or pansystolic (if perimembranous)
Still’s murmur - musical, quieter when sits up
Atrioventricular septal defect – superior axis
Hypertrophic obstructive cardiomyopathy – cardiomegaly, deep Q waves
Tricuspid regurgitation

exam prep (8 decks)

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