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MBChB IV Paediatrics > Cardiac examination > Flashcards

Cardiac examination Flashcards

1
Q

What murmurs can you hear in the URSB and what is the potential origin?

A

Ejection systolic - aortic stenosis

Continuous - right BT shunt, venous hum

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2
Q

How can you increase the venous hum?

A

Turn child’s head to the left

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3
Q

What is a BT shunt?

A

Blalock Taussig shunt in CHD

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4
Q

What murmurs can you hear in the ULSB and what is the potential origin?

A

Ejection systolic - pulmonary stenosis, ASD, innocent murmur

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5
Q

How can you check if a murmur is innocent?

A

It will not radiate to the back

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6
Q

What murmurs can you hear in the LLSB and what is the potential origin?

A

Pansystolic - tricuspid regurg, VSD

Diastolic - tricuspid stenosis, aortic regurg, Still’s murmur

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7
Q

What is a Still’s murmur?

A

A benign flow murmur across the aortic valve from high cardiac output and/or increased contractility

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8
Q

What murmurs can you hear in the apex and what is the potential origin?

A

Pansystolic - mitral regurg, VSD
Late systolic - mitral prolapse
Ejection systolic - aortic stenosis
Mid-diastolic - mitral stenosis

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9
Q

Which structures form the right heart border?

A

SVC

RA

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10
Q

Which structures form the left heart border?

A

Aorta knuckle
PA knuckle
LA appendage
LV

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11
Q

Which structures form the anterior heart border?

A

RV

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12
Q

Which structures form the posterior heart border?

A

Descending aorta

LA

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13
Q

What are clinical signs of RV enlargement?

A

LPS

Epigastric heave

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14
Q

What are clinical signs of pulmonary hypertension?

A

Palpable P2
LPS
Epigastric heave

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15
Q

What are clinical signs of aortic stenosis?

A 
Displaced apex (LVH)
Suprasternal thrill
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16
Q

Name causes of central cyanosis

A
  1. Inadequate ventilation
    - pneumonia
    - airway obstruction
    - lung changes
    - CNS depression
    - - inadequate ventilatory drive
    - weak resp mm
  2. Desaturated blood bypassing lungs
    - cyanotic HD
    - pulmonary AVMs
    - PPHN
  3. Methaemoglobinaemia
    - congenital
    - toxin
  4. Poisoning
    - carbon monoxide
17
Q

Discuss your approach to oedema

A

Low protein

  1. Decr intake
    - PEM
  2. Decr production
    - liver failure
  3. Incr loss
    - nephrotic syndrome
    - PLE

Capillary leak

  • CCF
  • cor pulmonale
  • sepsis
  • anaphylaxis
18
Q

What are the features of PEM to look out for in approach to oedema?

A

Skin lesions
Hepatomegaly
Plot growth
Deficiency (vitamins, iron ca)

19
Q

What are the features of liver failure to look out for in approach to oedema?

A 
Decr LOC
Decr albumin
Decr glucose
Incr NH3
Incr INR
20
Q

What are the features of nephrotic syndrome to look out for in approach to oedema?

A 
Anasarca
Urine dipstix
Albuminuria
Prot:creat
TP normal
Decr albumin
Decr C3, C4
Incr chol
21
Q

What are the features of PLE to look out for in approach to oedema?

A

Diarrhoea
Decr TP
Decr albumin
Decr globulin

22
Q

What are the features of CCF to look out for in approach to oedema?

A 
Cardiomegaly
Hepatomegaly
Tachycardia
Tachypnoea
CXR
ECG
Sonar
Bloods
23
Q

Define digital clubbing

A

Bulbuous uniform swelling of soft tissue of terminal phalanx with loss of normal angle between nail and nail bed

24
Q

Name primary causes of clubbing

A 
Idiopathic
Inherited
- pachydermoperiostosis
- hypertrophic osteoarthropathy
- familial
25
Q

Name secondary causes of clubbing

A 
1. Pulmonary
Malignancy
- lung carcinoma
- pleural mesothelioma
- lung mets
CLD
- bronchiectasis
- cystic fibrosis
- interstitial lung disease
- idiopathic pulmonary fibrosis
- sarcoidosis
- pulmonary TB
Suppurative 
- empyema
- lung abscess
Other
- lipoid pneumonia
- cryptogenic fibrosing avleolitis
- PHT
  1. Cardiac
    - CCHD
    - R to L shunt
    - IE
    - PHT
    - atrial myxoma
    - limb vascular anomalies
3. GIT
Inflammatory
- UC
- Chron's
- proctitis
- peptic ulcer
- primary biliary cirrhosis
- hepatic cirrhosis
Other
- malabsorption
- achalasia
- esophageal leiomyoma
  1. Malignancy
    - thyroid Ca
    - thymus Ca
    - Hodgkin’s
    - disseminated CML
  2. Skin
    - pachydermoperiostosis
    - Bureau-Barriere-Thomas syndrome
    - Fischer syndrome
    - palmaplantar keratoderma
    - volavsek syndrome
  3. Misc
    - acromegaly
    - thyroid acropachy
    - pregnancy
    - sickle cell disease
    - hypoxemia
26
Q

What is POEMS syndrome?

A 
Polyneuropathy
Organomegaly
Endocrinopathy
Monoclonal gammopathy
Skin changes
27
Q

What is acropachy associated with?

A

Grave’s disease

28
Q

What are the 5 steps of developing clubbing?

A
  1. Fluctuation + softening of nail bed
  2. Loss of lovibond angle
  3. Increased nail fold convexity
  4. Thickening of distal finger
  5. Shiny aspect and striation of nail + skin
29
Q

How can you grade clubbing?

A

Grade 1: Nail bed fluctuation.
Grade 2: Obliteration of the Lovibond angle
Grade 3: Parrot beaking
Grade 4: Hypertrophic osteoarthropathy (HOA)

30
Q

What do you call Filbert/watch glass nails? What is preserved?

A

Pseudoclubbing

Lovibond angle preserved

31
Q

What are causes of pseudoclubbing?

A

Congenital

Hyperkeratosis (palms/soles)

32
Q

What is the pathophysiology of clubbing?

A

Distal digital vasodilation -> hypervascularization!
Increased interstitial oedema followed by incr vascular connective tissue and change in vascular connective tissue
Terminal phalanx spurs

33
Q

What are the proposed mediators of vasodilation in clubbing?

A
  1. Circulating/local vasodilator
  2. Neural mechanism
  3. Response to hypoxemia
  4. Platelet GF
  5. Genetic predisposition
  6. Combination
34
Q

Explain the vasodilator theory of clubbing

A 
Vasodilators bypass inactivation in lungs 
- ferritin
- prostaglandins
- bradykinin
- adenine nucleotides
- 5-hydroxytryptamine\
Issue: not always assoc with lungs
35
Q

Explain the neural mechanism theory of clubbing

A

Vagally innervated organ pathology - regression after vaotomy
Issue: still found in other organ pathologies

36
Q

Explain the hypoxia theory of clubbing

A

Hypoxia -> local vasodilator stimulation -> incr blood flow to digits
Issue: rest of conditions no hypoxia

37
Q

Explain the platelet-derived growth factor theory of clubbing

A

Fragments of platelet clumps/megakaryocytes -> lodge in nail bed -> release platelet-derived GF -> incr capillary permeability + connective tissue hypertrophy

MBChB IV Paediatrics (81 decks)

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