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
Name secondary causes of clubbing
``` 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 ``` 2. 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 ``` 4. Malignancy - thyroid Ca - thymus Ca - Hodgkin's - disseminated CML 5. Skin - pachydermoperiostosis - Bureau-Barriere-Thomas syndrome - Fischer syndrome - palmaplantar keratoderma - volavsek syndrome 6. Misc - acromegaly - thyroid acropachy - pregnancy - sickle cell disease - hypoxemia
26
What is POEMS syndrome?
``` Polyneuropathy Organomegaly Endocrinopathy Monoclonal gammopathy Skin changes ```
27
What is acropachy associated with?
Grave's disease
28
What are the 5 steps of developing clubbing?
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
How can you grade clubbing?
Grade 1: Nail bed fluctuation. Grade 2: Obliteration of the Lovibond angle Grade 3: Parrot beaking Grade 4: Hypertrophic osteoarthropathy (HOA)
30
What do you call Filbert/watch glass nails? What is preserved?
Pseudoclubbing | Lovibond angle preserved
31
What are causes of pseudoclubbing?
Congenital | Hyperkeratosis (palms/soles)
32
What is the pathophysiology of clubbing?
Distal digital vasodilation -> hypervascularization! Increased interstitial oedema followed by incr vascular connective tissue and change in vascular connective tissue Terminal phalanx spurs
33
What are the proposed mediators of vasodilation in clubbing?
1. Circulating/local vasodilator 2. Neural mechanism 3. Response to hypoxemia 4. Platelet GF 5. Genetic predisposition 6. Combination
34
Explain the vasodilator theory of clubbing
``` Vasodilators bypass inactivation in lungs - ferritin - prostaglandins - bradykinin - adenine nucleotides - 5-hydroxytryptamine\ Issue: not always assoc with lungs ```
35
Explain the neural mechanism theory of clubbing
Vagally innervated organ pathology - regression after vaotomy Issue: still found in other organ pathologies
36
Explain the hypoxia theory of clubbing
Hypoxia -> local vasodilator stimulation -> incr blood flow to digits Issue: rest of conditions no hypoxia
37
Explain the platelet-derived growth factor theory of clubbing
Fragments of platelet clumps/megakaryocytes -> lodge in nail bed -> release platelet-derived GF -> incr capillary permeability + connective tissue hypertrophy