Wards Wednesday

Thursday, 18 February 2021 12:21 AM

Cardiac Murmurs and Location Best Heard

CAUSES OF CLUBBING:
The 5 Ts
- Bronchial Carcinoma - Tricuspid Atresia
- Fibrosing alveolitis - Cirrhosis - Tetralogy of Fallot
- Chronic suppurative lung diseases - IBO (Crohn's / Ulcerative colitis) - Transposition of the great
- Empyema - Coeliac disease Vessels
- Abscess - Gl lymphoma - Total Anomalous venous return
- Truncus Arteriosus
- Bronchiectasis
- Cystic fibrosis
- Mesothelioma
- Thyroid acropachy
PORV
- Familial - Pulmonary Stenosis
- Overriding aorta
- Congenital cyanotic heart diseases - R Ventricular Hypertrophy
- Endocarditis - VSD
- Axillary artery aneurysm
- Atrial myxoma
- Brachial arterio-venous malformation

What is livedo reticularis? What

Livedo reticularis refers to various conditions in which there is mottled discolouration of
the skin. It is described as being reticular (net-like, lace-like), as cyanotic discolouration is cutis marmorat
surrounds pale central skin.
The terminology of livedo reticularis may include: a?
• Cutis marmorata: physiological, variable livedo Cutis marmorata is a condition
• Cutis marmorata telangiectatica congenita: a congenital form where the skin has a pinkish blue
of persistent livedo mottled or marbled appearance
• Primary livedo reticularis: a benign form of livedo of unknown cause when subjected to cold
• Secondary livedo reticularis: association of livedo with an temperatures. Rewarming usually
underlying systemic disease restores the skin to its normal
• Livedo racemosa: a generalised and persistent form of livedo. appearance.

What causes livedo reticularis?

Livedo reticularis results from a disturbance of blood flow to the skin, causing low
blood flow and reduced oxygen tension to the skin. Cutaneous vasculature is
comprised of a series of 1–3 cm cones. The apex of each cone is located deep within
the dermis at the site of an ascending arteriole. At the margin of each cone, the density of
the arterial bed is decreased, and the superficial venous plexus is more prominent.
Any pathological or physiological process which impairs blood flow to the skin results in higher
amounts of deoxygenated haemoglobin, leading to a livid discolouration.
Physiological arteriolar vasospasm in response to cold, produces reversible skin
discolouration, such as in cutis marmorata. Prolonged

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the arterial bed is decreased, and the superficial venous plexus is more prominent.
Any pathological or physiological process which impairs blood flow to the skin results in higher
amounts of deoxygenated haemoglobin, leading to a livid discolouration.
Physiological arteriolar vasospasm in response to cold, produces reversible skin
discolouration, such as in cutis marmorata. Prolonged
vasospasm, thrombosis or hyper viscosity can cause the pathological skin changes of
livedo racemosa.
A unilateral form of livedo reticularis due to local heat injury is known as erythema ab
igne.

Who gets livedo reticularis?

Cutis marmorata causes temporary or physiological livedo in about 50% of healthy
infants and many adults, particularly young women when exposed to the cold.
Cutis marmorata telangiectatica congenita is a rare condition in which pronounced
livedo is present at birth or soon after. It often improves with age. There are several
congenital abnormalities associated with cutis marmorata telangiectatica.
Primary livedo reticularis is the idiopathic form in adults and can be persistent.
The diagnosis is usually made once other more severe causes of livedo reticularis
have been ruled out.
Secondary livedo, or livedo racemosa, is associated with a range of systemic
diseases.

Characterised by massive proteinuria of

40mg/m2/hr for 12-24 hours
Or 0.05g/kg/day in 24 hours
Acronym: HIT
Hypovolemia- ↓ albumin (↓ oncotic pressure)
Infection- ↓ Immunoglobulins (also steroid therapy predisposes)
Thrombosis- ↓ anticoagulant factors (antithrombin, protein C and S)

Diet in Nephrotic Syndrome

- Low salt
- Normal protein

Observe for Edema

- Periorbital
- Pedal
- Scrotal/ vulval

Nephrotic pt with fever and difficulty breathing?

Suspect Pleural Effusion

Hypoalbuminemia in NS can cause a decrease in oncotic pressure causing
extravasation of fluid into the interstitial space. In conditions of severe
hypoalbuminemia, fluid extravasation may cause occurrence of pleural
effusion.

Pleural Effusion on Exam:

- ↓ chest wall expansion
- Stony dullness
- Crepitations
- Tracheal deviation if massive effusion

Nephrotic pt with fever, abdominal pain and ascites?

Suspect Spontaneous Bacterial Peritonitis.

Pt will be Extremely tender on palpation and have Rebound tenderness
Nephrotic patient should be up to date on vaccinations.
Especially against pneumococcal infections since Strep pneumo can cause SBP
in children

How do you know if bacterial peritonitis is spontaneous?

The confirmed diagnosis of spontaneous bacterial peritonitis requires:
1. ascitic fluid
2. absolute polymorphonuclear leukocyte (PMN) count of at least 250
cells/mm3 (0.25 x 109/L)
3. positive ascitic fluid bacterial culture without an intraabdominal
surgically treatable source of infection.

SICKLE CELL DISEASE

Vaccines
The spleen filters and processes senescent blood cells as well as helps protect
against encapsulated micro-organisms. In sickle cell disease, patients undergo
functional asplenia (auto splenectomy) and as such should be vaccinated
against:
- S. pneumoniae (Causes community-acquired pneumonia
(CAP), bacterial meningitis, bacteraemia, and otitis media, as well as

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 (CAP), bacterial meningitis, bacteraemia, and otitis media, as well as
sinusitis, septic arthritis, osteomyelitis, peritonitis, and endocarditis)
- N. Meningitidis (causes meningitis, meningococcaemia)
- H. influenzae (causes epiglottitis, pneumonia, meningitis,
bacteraemia, cellulitis, infectious arthritis)

Sickle Cell Retinopathy:

- In Trinidad should begin screening at 7-8 years old and repeated
annually.

Complications of Sickle Cell Disease

1. Painful crises
2. Acute Chest Syndrome
3. Chest Infections (recurrent, pneumonia)
4. Avascular necrosis of the femoral head
5. Cerebral infarcts
6. Moya Moya disease
7. Gallstones
8. Osteomyelitis (salmonella typhi)
9. Adenotonsillar Hypertrophy
10. Auto splenectomy
11. Microinfarcts
12. Anaemia

STEROIDS
Consequences of Long-Term Steroid Use:
1. Central obesity
2. Purple striae, petechiae
3. Insulin resistance
4. Stunted growth
5. Skin changes
6. Baldness
7. Hypertension
8. Mood fluctuations
9. Suppressed immune system

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