This document discusses various aspects of assessing the cardiovascular system. It defines tachycardia, pathological tachycardia, pulse deficit, rhythm, sinus arrhythmia and its mechanism. It also describes irregular pulses, volume of pulse, pulsus alternans, paradoxus, parvus and bigemini. Character of pulse including pulsustardus, bisferiens, dicrotic and jerky are explained. Other assessments covered include radiofemoral delay, vessel wall thickness, blood pressure measurement techniques, normal ranges, respiratory assessment including rate, rhythm, type and temperature measurement.
Brief Presentation on clinical examination of Cardio Vascular System with Report of Normal case
references:
macleod's clinical examination 13th edition
hutchinson clinical methods
The jugular venous pressure (JVP, sometimes referred to as jugular venous pulse) is the indirectly observed pressure over the venous system via visualization of the internal jugular vein. It can be useful in the differentiation of different forms of heart and lung disease.
Brief Presentation on clinical examination of Cardio Vascular System with Report of Normal case
references:
macleod's clinical examination 13th edition
hutchinson clinical methods
The jugular venous pressure (JVP, sometimes referred to as jugular venous pulse) is the indirectly observed pressure over the venous system via visualization of the internal jugular vein. It can be useful in the differentiation of different forms of heart and lung disease.
Each examining system can be described using four elements;
- looking/inspection
- feeling/palpation
- tapping/percussion
- listening/auscultation
- assessment of function
Each examining system can be described using four elements;
- looking/inspection
- feeling/palpation
- tapping/percussion
- listening/auscultation
- assessment of function
In this presentation students will have the opportunity to learn all definitions and acronyms related to patient assessment. We have links to YouTube videos to further demonstrate various assessments.
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Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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2 Case Reports of Gastric Ultrasound
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
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neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
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10. Pathological tachycardia
• Shock
• High out put states Fever , anemia ,
hyperthyroidism , beriberi
• Tachy arrythmias SVT
• Drugs Thyroxine , nifedipine , atropine ,
catacholamines like adrenaline
11. Pulse deficit
• PR and HR are counted simultaneously for 1
minute
• In AF and ectopics
12. Rhythm
• It is the regularity with which one beat follows
other
• Assessed by palpating radial artery
• MC cause in child is sinus arrythmia
acceleration during inspiration and
deceleration during expiration
13. Sinus arrhythmia
• Increase in PR with inspiration and decrease in
PR during expiration
• Common in childresn ,athletes
• Sinus arrhythmia may be absent inCCF and
autonomic nueropathy
14. • Respiratory sinus arrhythmia (RSA) is a
naturally occurring variation in heart rate that
occurs during a breathing cycle. RSA is also a
measure of parasympathetic nervous system
activity
15. Mechanism of Sinus arrhythmia
• Primarily due to fluctuations in
parasympathetic output to heart
• Inspiration stretch receptors in lungs
vagus inhibits the Cardio inhibitory area in
the medulla
• The tonic vagal discharge that keeps the heart
rate slow decreases and HR increases
16. Regularly irregular
• Ventricular bigemini/pulsus bigemini bi -2,
gemini – twins , digitalis toxicity
• Ectopic beat occuring so frequently that there
is one ectopy after each sinus beat
• Alternating strong(sinus) and weak (ectopic)
pulse with compensatory pause
• Other causes ectopics/extrasystoles , 2nd
degree heart block /any atrial arrhythmia with
fixed block
19. Volume of pulse
• It is the amplitude of movement of arterial
wall against the palpating fingers
• It is the degree of movement of arterial wall
against the palpating fingers
• It depends on stroke volume of the LV and
distensibility of the vessel wall
• It depends on Pulse pressure
20. High volume pulse
• Bounding pulse
• Anxiety
• After exercise
• Fever
• Anaemia
• Hyperthyroidism
• AV fistula
• Higher SBP +/_ lower DBP
21. • PDA
• AR
• Early septic shock warm shock due to
peripheral Vasodilatation ( here there is fall in
Diastolic BP and hence wider PP )
• Status asthmaticus as CO2 retenstion VD
wide PP bounding
22. Low volume (Pulsus Parvus )
• Parvus = small
• When PP is narrow
• CCF
• Shock
• Severe AS
• Coarctation of aorta
• Severe MS
23. Difference in Pulse volume
• Coarctation of aorta if distal to subclavian
artery volume will be different between
upper and lower limbs
• If proximal to Left subclavian artery
diminished Left upper limb pulse
24. Pulsus alternans
• Alternate volume of pulse beats
• Method By light palpation of the femoral
artery , with breath held in mid expiration(to
avoid respiratory variation )
• It is exaggerated by standing up (by reducing
the venous return )
25. • Can be detected by taking BP
• Korotkoff’s sound doubles as the pressure falls
• It is a rare but valuable sign of advanced LVF
• It is due to varying force of LV contraction
26. Pulsus Paradoxus
• Normally SBP falls during inpiration around 3 –
10 mm Hg
• PP is present when SBP falls by more than 10
mm Hg quiet inspiration
• Using BP apparatus
• Korotkoff’s sounds during inspiration and
expiration
• When difference become >20 it will be
palpable
30. • Patient’s forearm is gripped using examiner’s
left palm with sufficient pressure so that the
pulse is just palpable
• Arm is lifted using examiner’s right hand
• When a thud will be felt if the pulse is water
hammer
31. it is toy of sealed
glass tube
containing water
and vacuum
On inversion water
drops through
vacuum to give a
thud
32. Character of pulse
Pulsus tardus /anacrotic pulse
Pulsus bisferiens
Dicrotic pulse
Jerky pulse
Catacrotic pulse
33. • It describes the pulse wave form
• Best assessed over carotids
• Because it is closest to the heart
• Wave form is not dampened by multiple
branching
• Pulse wave if faster(5m/s) than actual
movement of blood along the arterial tree(50
cm / sec)
34. Normal character
• Will have 2 positive waves in systole
1. Percussion wave due to rapid upstroke
2. Tidal wave –due to reflected waves from aortic
bifurcation
3. The end of systole is indicated by a sharp notch
dicrotic notch
4. Which is followed by a positive wave Dicrotic
wave
• Dicrotic notch correponds to closure of Aortic
valve
35.
36.
37. Pulsus tardus
• Tardus slow
• Slow rising pulse
• AS
because LV takes a much longer time to push
the blood through the stenosed valve
47. • When sounds not audible open and close
the fist
• LL BP prone position
• SBP >10
• DBP same
• Postural hypotension
• Flush method ???
48. BP cuff size
• The length of the inflatable bladder should
encircle the arm without over lapping
• The width of the bladder should cover atleast
2/3rd of the length of arm
• Small cuff “super” BP
49. Recommended bladder size
• Newborns 3 cm
• Infants 5 cm
• Child 7 cm
• Adult 12.5 cm
• The inflatable bag of the cuff is to be 20%
wider than the diameter of the limb on which
it is used
50. Normal BP
• Newborn 90
• Infants 100
• Preschool 110
• School age 110+2mm for each year above 6
years (till 120)
• Hypertension >95th centile
• High BP between 90 – 95th centile
• Normal 90th centile
51. Hypotension
• Less than the 5th percentile of normal age
• <60 mm Hg in term neonates
• <70 mm Hg in infants
• <70 + 2x mm of Hg (up to 10 years )
• <90 mm Hg in children more than 10 years
52. Respiration
• Inspiration is an active process by the
diaphragm and intercostals
• Expiration is a passive process by the elastic
recoiling of lungs
• Accessory muscles of inspiration scaleni
,Pectoralis , trapezius
• Accessory muscles of expiration Abdominal
muscles and latissimus
60. Cheyne stokes breathing
• Periodic breathing in which periods of apnoea
alternate regularly with periods of
hyperpnoea
• Severe LVF
• Raised ICT
• Narcotic drug poisoning
• Renal failure
66. Temperature
• Normal 36.8 +/- 0.4 degree C
• 98.2 +/- 0.7 degree F
• Rectal > Oral > Axillary by 0.5 degree C
• Normal Diurnal variation is 1 degree F
67. • If placed under tongue 1 min
• If placed under axilla 3 min
• Axilla need to be dry
• Rectal temperature is needed only in rare
cases sever PEM rectal thermometer
with a rounded bulb
71. Intermittent
• Quotidian if it occurs daily ( JRA)
• Tertian alternate days
P.falciparum/ovale/vivax
• Quartan fever every 3rd day plasmodium
malaria
• Elevated temperature touches the base line
72. Relapsing fever
• Febrile episodes are seperated by afebrile
episodes of more than one day
• Eg quartan
• Pel ebstein fever HL
• Fall by crisis pneumococcal pneumonia
• Fall gradually lysis typhoid
73. • With each degree rise in F , PR rises by 10 and
RR by 4
• Fever with relative bradycardia Typhoid
fever , also meningitis (raised ICT )
• Viral fever (myocardial involvement )
74. Hyperpyrexia
• Temperature above 41 degree C
1. Heat stroke
2. Pontine haemorrhage
3. Malaria
4. Septicemia / Meningitis
5. Malingnant hyperthermia that may occur
in myopathy patients when halothane
anaesthetic is used
75. Pallor
• Lower palpebral conjunctiva
• Tongue
• Oral mucosa
• Hard palate
• Nail beds
• Palm
• Sole
76. • Pallor / paleness, is waxy appearance of skin
and mucous membrane
• It depends on thickness of the skin and
quantity and quality of blood in capillaries
• Thus pallor and anemia are not interchangable
words
77. Icterus
• Examine in good sunlight
• Upper sclera
• Under aspect of tongue
• Palms
• Nails
• Skin
78. • It is the yellowish discolouration of skin and
mucous membrane due to excess amount of
Brn in blood
• Normal 0.3 – 1 mg%
• Clinical jaundice when s.brn crosses 3mg%
79. • Why upper border of bulbar conjunctiva??
• Sclera contains lot of elastin
• Brn has strong affinity for elastic tissue
• A white background is formed by sclera
80. d/d for jaundice
• Carotenemia skin will be yellow , sclera and
mucous membrane are unaffected
• Diffuse xanthamatosis
• Muddy sclera
• Atabrine toxicity
81. Cyanosis
• It is defined as bluish discolouration of skin
and mucous membrane due to the presence
of increased amount of reduced haemoglobin
• >5g%
• Kyanos dark blue colour
• Osis condition
84. Peripheral cyanosis
• Arterial PaO2 is normal
• Oxygen unsaturation at the venous end of
capillary
• Reduced cardiac output
• Peripheral vasoconstriction
• Slow speed of circulation in the peripheries
85. Causes
• Exposure to cold air/water
• CCF
• Frost bite
• Raynaud’s phenomenon
• Shock / Peripheral circulatory failure due to
any cause
• Venous obstruction – produces local cyanosis (
eg SVC syndrome )
86. • Hyperviscosity syndorome Multiple
myeloma , Polycythemia , macroglobinemia
• Mitral stenosis lips , tip of nose and cheeks
may be cyanosed in mitral facies
• Septicemia (especially Gram neg organism)
87. Sites for peripheral C
• Tip of nose
• Ear lobule
• Outer aspect of lips , chin and cheek
• Tips of fingers and toes
• Nail bed of fingers and toes
• Palms and soles
88. • Tongue remains unaffected in peripheral
cyanosis
• Mechanism of peripheral cyanosis stagnant
hypoxia , over utilisation hypoxia
89. Central cyanosis
• Arterial PaO2 is reduced
• Due to imperfect oxygenation of blood
• Oxygen saturation will go below 80 – 85%
90. Sites
• Tongue mainly margins as well as
undersurface
• Inner aspect of lips
• Mucous membrane of gum , palate and cheek
• Plus Peripheral areas
• Mechanism hypoxic hypoxia
93. Enterogenous / Pigment cyanosis
• Cyanosis due to excessive meth Hb or sulph Hb in
blood
• Causes
1. Hereditary Hb M disease
2. Posioning by anilline dyes
3. Drugs like nitrates , nitrites , phenacetin ,
sulphonamides , dapsone ,
4. Carboxy haemoglobinemia
• Diagnosis can be confirmed by spectroscopic
examination of blood
94. d/d of bluish discolouration of body
• Cyanosis
• Carbon monoxide poisoning cherry red
flush
• Argyria silver poisoning
• Osteogenesis imperfecta
• Drugs like Amiodarone produces bluish hue in
the skin ( ceruloderma)
95. Mixed cyanosis
• CCF due to left sided heart failure
• Acute MI with Acute LVF
• Rarely polycythemia
96. Differential cyanosis
• Hand red and feet blue PDA with
Eisenmenger’s syndrome
• VV Coarctaion of aorta , transposition of
great vessels
97. Orthocyanosis
• It is the development of cyanosis only ion the
upright position due o hypoxia occuring in
erect posture as a result of associated
pulmonary AV malformations
98. Clubbing
• Defined as the bulbous enlargement of the
distal segments of fingers and toes due to the
proliferation of soft tissue especially on their
dorsal surface
99. Grades of clubbing
• Grade 1 Fluctuation of nail bed
• Grade 2 Obliteration of nail– nail fold angle
• Grade 3 Drum stick or parrot beak
appearance
• Grade 4 Hypertrophic Pulmonary
Osteoarthropathy
100. Methods of eliciting
• Lovibond’s angle the non dominent finger
is inspected from the side
• Normal angle 172+/- 8
• Clubbing angle > 180
101. • Digital index method Dermographic method
• Dital phalangeal distance/Interphalangeal
distance
• Most sensitive measure of clubbing
• Forefinger of the non dominant hand is used
• Outline of the finger is drawn
• Transverse distance at the level of Distal Inter
phalangeal joint (IPD) & at the base of the nail
(DPD) is measured
102. • DPD/IPD
• Normal ratio < 0.825
• Clubbing when ratio exceeds 1
• Ratio of all the ten fingers added together if
exceeding 10 is very suggestive
103. Schamroth sign
• The tip and distal phalanx of both the thumb
when approximated enclose a rhomboid
space normally
• In clubbing this space is obliterated
105. HPOA
• Triad of Clubbing , Joint pain and sub
periosteal new bone formation
• Technetium Bone Scintigraphy is the best
method of assessing HPOA
• Causes SCC, Benign Mesothelioma ,
suppurative lung disease
106. Theories of clubbing
• Neural disease in lungs –vagu stimulation --
VD
• Humoral substances produced by diseased
lungs gets deposited
• Toxic toxic substance gets deposited
• Shunt theory
107. Shunt theory of clubbing
• Normally Megakaryocytes are converted into
platelets in the lungs
• In lung pathology they bypass the lungs
(shunt) and gets deposited in the small AV
connections in the finger tips and produce
PDGF which causes fibroblast proliferation and
tissue fibrosis
108. Causes
• Cardiac Cyanotic Heart disease , Infective
endocarditis , Eisenmenger syndrome
• Pulmonary Bronchiectasis , Lung Abscess,
Empyema
• GIT IBD, cirrhosis
• Hereditary clubbing familial , usually not
present at birth , appears later
• Unidigital local insults
113. Lymphadenopathy
• Patient in sitting position cervical and axillary
nodes
• In supine position for abdominal and inguinal
nodes
114. Note
• Site
• Number
• Size
• Consistency
• Tenderness
• Mobility
• Matted / discrete
• Fixity to skin
• Condition of overlying skin
• Condition of area of drainage
115. Cervical nodes
• Stand behind the patient
• Keep the neck slightly flexed forward and
sideways toward the side of examination
• Palpate submental , submandibular ,
preauricular , jugulodigastric , supraclavicular ,
deep cervical
116. • Scalene nodes dipping the palpating finger
behind the clavicle through the clavicular
insertion of SCM from behind
Or
• Standing in front palpating the node behind
the clavicular head of SCM with thumb and
index finger
117. • Now stand in front to examine
• Posterior auricular and occipital nodes
• Epitrochlear lift the arm , flex the elbow to
the right angle. Palpate the nodes with the flat
of the thumb of the opposite hand
118. Axillary nodes
• Pectoral group
• Brachial group
• Subscapular group
• Central group
• Apical group
119. Pectoral group
• Examined from front
• Situated just behind the Anterior axillary fold
• Patients’s arm is elevated and using the right
hand for the left side the fingers are insinuate
behind the pectoralis major
120. Brachial group
• Lie on the lateral wall of axilla in relation to the
axillary vein
• Left hand is used for left side
• This group is felt with the palm directed laterally
against the upper end of humerus
121. Subscapular group
• This lies on the posterior axillary fold
• Examined from behind
• Standing behind the patient the examiner
palpates the antero internal surface of the
posterior fold while with the other hand the
patient’s arm is semi lifted
122. Central group
• Group of left side is examined with right
• Patient’s arm is slightly abducted and pass the
extended fingers right upto the apex of axilla
directing the parm towards the lateral thoracic
wall
• Other hand in the shoulder to stabilise
124. • Abdominal nodes can be looked for by deep
palpation of the abdomen
• Inguinal nodes patient supine with thigh
flexed at 10 degree
• Palpate the horizontal and vertical group
• Popliteal nodes are palpated deep in the
popliteal fossa with knee flexed
125. • Widening of dullness in the upper
mediastinum on light percussion of chest may
indicate the presence of enlarged mediastinal
nodes
• As a general statement LN of more than 1 cm
is considered as relevent
126. Edema
• Patient supine / left lateral position
• Inspect the lower extrimities and pre sacral
areas
• Skin will be stretched and shiny and normal
wrinkles will be obliterated
• Apply gentle pressure with the flat of the
thumb 30 seconds over the bony area
• And look for pitting
131. Microcephaly
• 2/3 SD below normal
• One SD = 2.5% of the expected
A. Primary Microcephaly
I. Asymptomatic
II. Symptomatic
B. Secondary Microcephaly
132. Primary Microcephaly
• Brain is small
• Because of genetic , chromosomal ,idiopathic,
familial reasons
• Brain inherently had very poor potential for
growth
• It can be asymptomatic – usually familial
/when followed up will be normal
133. • Primary Microcephaly with symptoms like
seizures
• Includes genetic, chromosomal , or
dysmorphic syndromes and some cases of
microcephaly with Mendelian inheritance
• It can be AD/AR/X linked
• Features receding forehead tapering off
towards the vertex and flat occiput– usually in
AR transmitted PSFMi.
135. Rubinstein Taybi syndrome
• Rubinstein–Taybi syndrome (RTS), also known as
broad thumb- hallux syndrome or Rubinstein
syndrome, is a condition characterized by short
stature, moderate to severe learning difficulties,
distinctive facial features, and broad thumbs and first
toes. Other features of the disorder vary among
affected individuals. People with this condition have an
increased risk of developing noncancerous and
cancerous tumors, leukemia, and lymphoma. This
condition is sometimes inherited as an autosomal
dominant pattern and is uncommon, many times it
occurs as a de novo (not inherited) occurrence, it
occurs in an estimated 1 in 125,000-300,000 births.
136. Secondary Microcephaly
• Due to insults in brain that had normal
potential for growth
1. Intrauterine infections – CMV , Rubella ,
Toxoplasma
2. Intrauterine Toxins – Foetal Alcohol
syndrome , foetal hydantoin syndrome ,
maternal PKU
137. 3. Perinatal and Post natal insults to brain
Meningitis ,encephalitis , Intracranial
haemorrhage , HIE,
4. Craniostenosis –it is a primary disorder
premature fusion of cranial sutures even
though brain is growing normally
skull may be odd shaped ,with palpable riging
of suture lines
138. • Microcephaly in Rett’s syndrome is supposed
to be acquired , the child grows normally till
about one year after which the arrest of brain
growth occurs
• See for other evidence of squint , cataract ,
Choreoretinitis
139. Rett’s syndrome
• Rett syndrome, originally termed as cerebroatrophic
hyperammonemia is a rare genetic postnatal neurological disorder
of the grey matterof the brainthat almost exclusively affects
females but has also been found in male patients. The clinical
features include small hands and feet and a deceleration of the rate
of head growth (including microcephaly in some). Repetitive
stereotyped hand movements, such as wringing and/or repeatedly
putting hands into the mouth, are also noted.People with Rett
syndrome are prone to gastrointestinal disorders and up to 80%
have seizures.They typically have no verbal skills, and about 50% of
individuals affected do not walk. Scoliosis, growth failure, and
constipation are very common and can be problematic.
• The signs of this disorder are most easily confused with those of
Angelman syndrome, cerebral palsy and autism. Rett syndrome
occurs in approximately 1:10,000 live female births in all
geographies, and across all races and ethnicities.
140. Macrocephaly
• 2 SD above normal
• Causes
1. Familial
2. Hydrocephalus(congenital /Acquired )
3. Achondroplasia (partly due to ventricular
dilatation and partly due to megalencephaly )
4. Cerebral gigantism / Sotos syndrome
5. Fragile X syndrome
6. Mucopolysaccharidosis
141. Achondroplasia
• Achondroplasia is a common cause of dwarfism. It occurs as a
sporadic mutation in approximately 80% of cases (associated with
advanced paternal age) or may be inherited as an autosomal
dominant genetic disorder.
• People with achondroplasia have short stature, with an average
adult height of 131 centimeters (52 inches) for males and 123
centimeters (48 inches) for females. Achondroplastic adults are
known to be as short as 62.8 cm (24.7 in). The disorder is caused by
a change in the gene for fibroblast growth factor receptor 3
(FGFR3), which causes an abnormality of cartilage formation. If
both parents of a child have achondroplasia, and both parents pass
on the mutant gene, then it is very unlikely that the homozygous
child will live past a few months of its life. The prevalence is
approximately 1 in 25,000.[1]
142. Sotos sydrome
• Sotos syndrome (cerebral gigantism) is a rare genetic disorder
characterized by excessive physical growth during the first 2 to 3
years of life. The disorder may be accompanied by autism, mild
mental retardation, delayed motor, cognitive, and social
development, hypotonia (low muscle tone), and speech
impairments. Children with Sotos syndrome tend to be large at
birth and are often taller, heavier, and have relatively large skulls
(macrocephaly) than is normal for their age. Signs of the disorder,
which vary among individuals, include a disproportionately large
skull with a slightly protrusive forehead, large hands and feet, large
mandible, hypertelorism (an abnormally increased distance
between the eyes)(large inter-pupillary distance), and downslanting
eyes. Clumsiness, an awkward gait, and unusual aggressiveness or
irritability may also occur. Although most cases of Sotos syndrome
occur sporadically, familial cases have also been reported. It is
similar to Weaver syndrome.
143. Fragile x syndrome
• Fragile X syndrome (FXS), also known as Martin–Bell
syndrome, or Escalante's syndrome (more commonly
used in South American countries), is a genetic
syndrome that is the most widespread single-gene
cause of autism and inherited cause of intellectual
disability especially among boys. It results in a
spectrum of intellectual disabilities ranging from mild
to severe as well as physical characteristics such as an
elongated face, large or protruding ears, and large
testes (macroorchidism), and behavioral characteristics
such as stereotypic movements (e.g. hand-flapping),
and social anxiety.
144. 7. Neurocutaneous syndromes like Tuberous
sclerosis , Neurofibromatosis
8. Certain white matter degenerative diseases –
Alexander and Canavan Disease
9. Macrocephaly due to thickening of widening
of skull - Rickets , Thalassemia
10. Pseudohydrocephalus when compared
with dwarfed face and body Russel silver
syndrome
145. Alexander ds
• Alexander disease, also known as fibrinoid leukodystrophy, is a slowly
progressing and fatal neurodegenerative disease. It is a very rare disorder
which results from a genetic mutation and mostly affects infants and
children, causing developmental delay and changes in physical
characteristics.
• Alexander disease is a genetic disorder affecting the central nervous
system (midbrain and cerebellum). It is caused by mutations in the gene
for glial fibrillary acidic protein (GFAP)that maps to chromosome 17q21. It
is inherited in an autosomal dominant manner, such that the child of a
parent with the disease has a 50/50 chance of inheriting the condition, if
the parent is heterozygotic. However, most cases arise de novo as the
result of sporadic mutations.
• Delays in development of some physical, psychological and behavioral
skills, progressive enlargement of the head (macrocephaly), seizures,
spasticity in some cases also hydrocephalus, idiopathic intracranial
hypertension (IIH), dementia.
146. Canavan’s ds
• Canavan disease, also called Canavan-Van Bogaert-
Bertrand disease is an
autosomalrecessivedegenerative disorder that causes
progressive damage to nerve cells in the brain, and is
one of the most common degenerative cerebral
diseases of infancy. It is caused by a deficiency of the
enzyme aminoacylase 2 deficiency, and is one of a
group of genetic diseases referred to as a
leukodystrophies. It is characterized by degeneration of
myelin in the phospholipid layer insulating the axon of
a neuron and is associated with a gene located on
human chromosome 17.
147. Russell silver syndrome
• Russell-Silver syndrome is a growth disorder characterized by slow growth before
and after birth. Babies with this condition have a low birth weight and often fail to
grow and gain weight at the expected rate (failure to thrive). Head growth is
normal, however, so the head may appear unusually large compared to the rest of
the body. Affected children are thin and have poor appetites, and some develop
low blood sugar (hypoglycemia) as a result of feeding difficulties. Adults with
Russell-Silver syndrome are short; the average height for affected males is about
151 centimeters (4 feet, 11 inches) and the average height for affected females is
about 140 centimeters (4 feet, 7 inches).
• Many children with Russell-Silver syndrome have a small, triangular face with
distinctive facial features including a prominent forehead, a narrow chin, a small
jaw, and down-turned corners of the mouth. Other features of this disorder can
include an unusual curving of the fifth finger (clinodactyly), asymmetric or uneven
growth of some parts of the body, and digestive system abnormalities. Russell-
Silver syndrome is also associated with an increased risk of delayed development
and learning disabilities.
148. Other associated findings
• Full fontanel
• Seperation of sutures
• Cracked pot sound (in older children with sutures closed)
• Brisk lower limb reflexes
• Papilloedema
• Spine – spina bifida tuft of hair
• Cranial bruit Vein of Galen Malformation
• Always measure Parents head circumference
• Dysmorphism ( Mucopolysaccharidosis)
• Ask for blood transfusion history hemolytic anemia ,
osteoporosis
149. Fontanales
• There are 6 fontanales
• Only 2 palpable
• AF – 2.5 *2.5 cm
• Can be 4 cm in the AP direction
• Size of AF “increases” after birth
• Normally slightly depressed from the surface
150. • PF is normally <1 cm , barely admits tip of
little finger
• PF closes by 2 months
• AF closes by 9 – 18 months
• Pulsation of AF is normal
• Significant depression dehydration
• Bulging normal pulsation also decreases
155. Bulging Fontanel
1.Raised ICT Maningitis , SDH , IC bleed ,
ICSOL ,
As the ICT raises AF pulsation decrease and
ultimately vanish
Note that absent AF pulsation can be normal
but in that case it will not be bulging
156. • 2. Hydrocephalus AF may be bulging and
non pulsatile or pulsation may reduce from
what was there previously
• Scalp veins appear prominent
3. Crying child
4. Benign Intracranial Hypertension
161. Brachycephaly
• Premature fusion of coronal suture
• Transverse diameter is more
• Occiput may be flat as in Brachycephaly of
Down’s syndrome
162. Plagiocephaly
• Head shape is assymmetric due to premature
fusion of sutures unilaterally
• Eg:- Premature unilateral fusion of coronal or
lamdoid suture or both
164. Turricephaly
• Skull is high , narrow and tower shaped
• Head is tower shaped with short AP diameter ,
high forehead and flat occiput
• Due to premature fusion of many sutures (
usually 4 or more )
• It is found in Apert syndrome
165. Apert syndrome
• Apert syndrome is a form of acrocephalosyndactyly, a
congenital disorder characterized by malformations of the
skull, face, hands and feet. It is classified as a branchial arch
syndrome, affecting the first branchial (or pharyngeal) arch,
the precursor of the maxilla and mandible. Disturbances in
the development of the branchial arches in fetal
development create lasting and widespread effects.
• In 1906, Eugène Apert, a French physician, described nine
people sharing similar attributes and
characteristics.Linguistically, "acro" is Greek for "peak",
referring to the "peaked" head that is common in the
syndrome. "Cephalo", also from Greek, is a combining form
meaning "head". "Syndactyly" refers to webbing of fingers
and toes.
168. Cephalhematoma
• Sub periosteal collection of blood
• Due to elevation of periosteum
• Does not cross the suture line s
• Reaches maximum size by 3rd day
• Usually the parietal bone is most commonly
affected
• When B/L it may be associated with skull #
• Disappears by 3-6 weeks /calcified /and then
remodels
169. Caput succedaneum
• Diffuse , soft , boggy , swelling of the scalp
• Seen at time of birth
• Crosses suture lines
• Disappears by 1- 2 days
170. Cranial bossing
• It is the prominence of central part of parietal
and frontal bones
• When frontal bone alone is involved it is called
frontal bossing
171. Causes
• Rounded prominence in the centre of the parietal
and frontal bones may be an early manifestation
of rickets
• Hydrocephalus
• Congenital syphilis
• Thalassaemia
• Cleidocranial dysostosis
• Hurler’s syndrome
• Achondroplasia
172. Hurler syndrome
• Hurler syndrome, also known as
mucopolysaccharidosis type I (MPS I), Hurler's
disease, also gargoylism, is a genetic disorder
that results in the buildup of glycosaminoglycans
(formerly known as mucopolysaccharides) due to
a deficiency of alpha-L iduronidase, an enzyme
responsible for the degradation of
mucopolysaccharides in lysosomes. Without this
enzyme, a buildup of heparan sulfate and
dermatan sulfate occurs in the body. Symptoms
appear during childhood and early death can
occur due to organ damage.
173. Head tilt / Torticollis
• Local painful conditions /sternomastoid
“tumour”
• Compensation of visual defect /strabismus
• Herniation of cerebellar tonsils
• Klippel Feil deformity
• Dystonic reaction to drugs
•
174. Klippel Feil syndrome
• Klippel – Feil syndrome is a rare disease, initially
reported in 1912 by Maurice Klippel and André
Feil from France , characterized by the congenital
fusion of any 2 of the 7 cervical vertebrae. The
syndrome occurs in a heterogeneous group of
patients unified only by the presence of a
congenital defect in the formation or
segmentation of the cervical spine. Klippel–Feil
syndrome can be identified by shortness of the
neck. Those with the syndrome have a very low
hairline and the ability of the neck to move is
limited.
175. Head tilt
• Both occiput and chin are
deviated to same side
Torticollis
• Occiput is tilted to one side
and chin is shifted to other
side
176. Scalp hair
• Colour and texture
• White hair Albinism
• Malnutrition sparse , straight , thin ,easily
pluckable , lack luster , grey or red shcked , or
alternatively depigmented and pigmented
called flag sign
• Flag sign in kwashiorkor , where there is
alternating periods of abnormal and normal
nutrition
179. Alopecia
• Congenital ectodermal dysplasia
• Chemotherapy and radiation
• Localised area of hair loss Alopecia aerata,
over scars, fungal infections , also
psychological (trichotillomania )
181. Low hair line
• Extending below the spine of C4
• Turner’s sundrome
• Low hairline in front Hypothyroidism
• Hair is coarse and sparse in hypothyroidism
• Low hairline in back can be a feature of
short neck Klippel Feil syndrome
• Excess projection of hair into the cheek is seen
in Treacher Collins syndrome
182. Treacher Collins syndrome
• Treacher Collins syndrome (TCS), also known as
Treacher Collins–Franceschetti syndrome, or
mandibulofacial dysostosis, is a rare autosomal
dominant congenital disorder characterized by
craniofacial deformities, such as absent
cheekbones. Treacher Collins syndrome is found
in about one in 50,000 births. The typical physical
features include downward-slanting eyes,
micrognathia (a small lower jaw), conductive
hearing loss, underdeveloped zygoma, drooping
part of the lateral lower eyelids, and malformed
or absent ears.
185. Menkes kinky hair syndrome
• Menkes disease (MNK), also called Menkes
syndrome, copper transport disease, steely hair
disease, kinky hair disease, or Menkes kinky hair
syndrome, is a disorder that affects copper levels
in the body] leading to copper deficiency. It is an
x-linked recessive disorder, and is therefore
considerably more common in males: females
require two defective alleles to develop the
disease.
• The disorder was originally described by John
Hans Menkes (1928–2008) et al. in 1962.
186. Craniotabes
• Thin, parchment like , soft , mushy areas of
skin that indents like ping pong ball
• Physiological upto 3 months
• Should be elicited away from the suture lines ,
as it may be normally elicitable near the
suture lines
193. William’s syndrome
• Williams syndrome (WS), also known as Williams–Beuren
syndrome (WBS), is a rare neurodevelopmental disorder
characterized by: a distinctive, "elfin" facial appearance,
along with a low nasal bridge; an unusually cheerful
demeanor and ease with strangers; developmental delay
coupled with strong language skills; and cardiovascular
problems, such as supravalvular aortic stenosis and
transient hypercalcaemia.
• It is caused by a deletion of about 26 genes from the long
arm of chromosome 7 . The syndrome was first identified in
1961 by New Zealander J.C.P. Williams and has an
estimated prevalence of 1 in 7,500 to 1 in 20,000 births.
194. Mask like facies
• Face is expression less
• Wilson’s disease and other diseases affecting
EPS
• Tranquilizer overdose
• Mobius syndrome (neuroparalysis)
• Infantile botulsim (neuroparalysis)
• Depression
• Myotonic dystrophy
195. Mobius syndrome
• Möbius syndrome (also spelled Moebius) is an
extremely rare congenital neurological disorder which
is characterized by facial paralysis and the inability to
move the eyes from side to side. Most people with
Möbius syndrome are born with complete facial
paralysis and cannot close their eyes or form facial
expressions. Limb and chest wall abnormalities
sometimes occur with the syndrome. People with
Möbius syndrome have normal intelligence, although
their lack of facial expression is sometimes incorrectly
taken to be due to dullness or unfriendliness. It is
named for Paul Julius Möbius, a neurologist who first
described the syndrome in 1888
197. Hemolytic facies
• Typically in Beta thalassemia
• Frontal bossing
• Depressed bridge of nose
• Maxillary prominence
• Prominent malar eminence
• Protruding malaligned teeth
198. Adenoid facies
• Protruding perioral area
• With partially open mouth
• No changes over maxilla or frontal bones
199. Absent DAOM
• Depressor anguli oris muscle
• Its congenital absence produces assymetric
lowering of lower lip during crying
• Can be seen in normal children
• Has association with heart disease
200. Depressed nasal bridge
• Normal in certain races
• Down’s syndrome
• Congenital syphilis (called saddle nose)
• Late stage of leprosy
201. Short columella
• Short columella pulls down the nasal tip and
distorts the nose and gives flat appearance to
the nose
202. Hypoplasia of ala nasi
• Gives a pinched appearance and produces
beak nose
205. Micrognathia
• Pierre Robin syndrome
• Treacher collins syndrome
• Sequle of long standing juvenile RA
• Cri du chat syndrome
• Di George syndrome
• Foetal alcohol syndrome
• Rubinstein Taybi syndrome
• Russel silver syndrome
207. Eyes
• Eye ball tension
• Palpate with index finger with eye closed
• Increased in glaucoma
• And reduced in dehydration
208. Lip edema
• Part of generalised edema ( Nephritis , NS ,
cardiac failure, kwashiorkor)
• Severe cough and excessive crying
• Local causes conjunctivitis , stye
• Angioedema
• Dermatomyositis
• Hypothyroidism
• IMN (occassionally)
209. Microphthalmos
• Reduction in size of all ocular structures
• Congenital infections CMV , Rubella ,
Toxoplasmosis
• Goldenhar syndrome
• CHARGE syndrome
• Microphthalmia with colobomata is usualy an
AD inheritance
210. Eye lid colobomas
• Eyelid defects
• Lower eyelid Tracher collins syndrome
• Upper eyelid Goldenhar’s syndrome
• CHARGE
• Coloboma developmental defect of any
protion of eye ( MC iris)
211. Ptosis
• Transient in new born
• Congenital ptosis ( U/L or B/L )
• Oculomotor palsy
• Horner’s syndrome
• Myasthenia gravis
• Noonan syndrome
• Myotonic dystrophy
• Local eye lesions like edema of lids
213. Epicanthic fold
• It is a crescent shaped fold of skin , originating
below the eye and sweeps upwards to blend
with upper eye lid so that the inner canthus is
covered
• Tends to disappear as the bridge of nose get
elevated with the growth of child
• So flat nasal bridge gives extra skin to show up
as a fold
214. • Another reason syndromes with loose skin
• Unilateral epicanthic fold torticollis
• Classic in down syndrome
• Races but not so prominent to cover the
inner portion of both lids
215. • Seen in some normal newborns , disappears
by 1-3 months , as the bridge of the nose
grows
• Down’s syndrome , Noonan’s syndrome
,Turner’s syndrome , De lange syndrome ,
Smith- Lemli- Optiz syndrome , Ehler Danlos
syndrome , Cri du chat syndrome , William’ s
syndome , Foetal alcohol syndrome , Foetal
hydantoin syndrome
216. Mangloid slant
• Slant is upwards
• Slanting from medial to lateral
• Racial
• Down’s syndorme
• Prader Willi syndrome
217. Anti mangloid slant
• Down ward slanting of eyes
• Treacher Collins syndrome
• Noonan syndrome
• Turner’s syndorme
• Apert’s syndrome
• Edward syndrome
218. • Down ward slant under growth of maxilla
laterally
• Upward slant under growth of midline part
of anterior frontal brain
219. Hypertelorism
• Distance between the medial canthus of two
eyes is more than the width of each eyes
• Part of many syndromes
• Noonan , , Turner , Apert , Crouzen , Williams ,
Zellweger ,
• Normal variation
220. • Standard defenition
• Inerpupillary distance(orbital spacing ) is
measured in forward gaze and plotted
• > 3 SD is hypertelorsim
221. Telecanthus
• Displacement of inner canthi laterally,
eventhough the orbital spacing is normal
• There is reduction or absent visible sclera
medial to the iris along with lateral
displacement of lacrimal puncta
222. • Hypertelorism may be due to hypertrophy
of lesser wing of sphenoid
• Hypertelorism ( Canthal Index)
Distance between inner canthi divided by
distance between outer canthi >0.38
227. Heterochromia
• Assymetry of colour of iris
• Congenital horner’s syndrome
• Secondary to inflammation of the eye
• Sporadic
228. Chediac higashi syndrome
• Hypopigmentation of eyes ,
Skin and hair
• Recurrent bacterial infection
• Mild bleeding diathesis
229. Aniridia
• Absent iris , usually B/L
• Photophobia
• Impaired visual acuity
• Association with Wilm’s tumour Children
with aniridia should be checked for
Chromosome 11 deletion
• May be familial
• May be associated with hemihypertrophy
230. Blue sclera
• Normal newborn or small infants
• Osteogenesis imperfecta
• Ehler Danlos syndrome
231. White’s eye reflex or cat’s eye reflex
• Normally when light is shown through the
pupil a red flare is seen
• Here it may be absent and pupil may appear
white
• Reflex can arise from lens , uveal tract and
retina
• MC cause is cataract
• Retinoblastoma , ROP
232. Other findings …
• Cataract
• Buphthalmos(congenital glaucoma)
• Optic atrophy
• Papilloedema
• RP
• KF ring
• Strabismus
• Setting sun sign
233. Ears
Low set ears
• An imaginary line joining medial and lateral
canthi is extended towards the ear
• Normally 1/3rd of ear comes above this line
• When less than 20% is above , it is said to be
low set ears
• A line through the lateral canthus should cut
the insertion of auricle on the side of the head
234. • Small low set ears are seen in Down’s
syndrome
• Large prominent Marfan’s , Fragile X ,
• Deformed pinna treacher Collins ,
Goldenhar’s syndome
235. Low set ears
• Apert’s syndrome
• Carpenter’s syndorme
• Di George syndrome
• Noonan’s syndrome
• Potter’s syndrome
• Trisomy 13
• Trisomy 18
• Turner’s syndrome
• And many dysmorphic syndromes
236. Protuberant ear
• The normal ear makes an angle of no more
than 10 degree with the scalp
• > 15 degrees is protuberant
• > 20 degrees is Posterior rotation of pinna
238. Pre auricular tags
• Firm as it contains a bit of cartilage
• Benign condition
• Hearing assessment may be considered
• Pre auricular pits are generally benign and run
in families
• Ask about discharge / hearing loss
• U/L large ear may be positional , like Torticollis
239. • Microtia most children with microtia will
have hearing loss
• Crumpled pinna
• Tragus sign
• AOM
• Deafness
240. Nose
• Broad nasal root
I. Craniofrontonasal dysplasia
II. GM1 Gangliosidosis
• Squared nasal root Di George syndrome
241. Anteverted nose
• Acrodysostosis
• When the dorsum of nose is very short , nasal
tip is pulled upwards and this results in
anteverted nose
242. Beaked nose
• Unusually pointed prominent nose
• Or nose with poorly developed ala nasi so that
the nasal septum is seen more prominent
• Seckel syndrome
• Trisomies
• Algille syndrome
243. Mouth
• Normally mouth is constructed such that
outer edges of the lips fall on pependicular
dropped from the centre of either pupil when
eyes looking straight ahead
• When edges fall outside macrostomia
• Microstomia
244. • Large mouth Goldenhar syndrome
• Mandibular hypoplasia Pierre Robin
syndrome
• Angular stomatitis Riboflavin deficiency ,
congenital syphilis
245. Philtreum
• A long nose results in short philtrum and a
short nose results in long philtrum
• Long philtrum William’s syndrome ,
Cornelia de Lange syndrome
• Short philtrum Foetal alcohol syndrome
• Multiple frenulum Ellis van Creveld
syndrome
246. Palate
• High arched if the roof of palate is not seen
when the examiner’s eye is at the level of
upper incisor teeth and patient keeping
mouth wide open
• Prominent palatal ridging is due to poor
tongue thrusting of the baby which can be
due to neurological deficits resulting in poor
sucking
247. • Ridges make the palate look very narrow
• Cleft palate isolated anomaly , trisomy18 ,
Pierre Robin syndrome, Beckwith-Wiedemann
syndrome , Foetal hydantoin syndrome
• Look for isolated cleft lip if there is nasal
twang of voice
• Submucous cleft will have to be palpated for
248. • Bifid uvula Apert’s syndrome , Di George
syndrome , Treacher collin syndrome
• Painful ulcers HZV
• Herpangioma produces painful ulcers in
oropharynx , soft palate and uvula
249. Drooling
• Normal during teething
• Stomatitis
• Acute Epiglottitis /Diphtheria / Tonsillitis
/Herpangioma
• Pseudobulbar palsy
253. Cry
• Shrill cry in CNS insults like meningitis
• Cat like mewing cry Cri du chat syndrome
• Weak cry in Neuromuscular disorders
Werdnig Hoffman syndrome
• Crying on handling painful condtions like
arthritis , # , meningitis
• Hoarse cry hypothyroidism , laryngitis
254. Teeth
• Delayed dentition
• No teeth upto 13 month of age is considered
as delayed dentition
• Constitutional delay
• Hypothyroidism
• Hypopituitarism
• Rickets
• PEM
257. • Blue line across ridges of gum lead
poisoning
• Swollen , spongy , bleeding gums scurvy
• Neonatal teeth normal varient , Ellis van
Creveld syndrome
258. Tongue
• Macroglossia
a. Congenital hypothyroidism
b. Down’s syndrome
c. Beckwith Wiedmann syndrome
d. Local causes Cystic hygroma, hemangioma
e. Hurler’s syndrome ,GSD type 2
f. Tongue protrusion without macroglossia occur
in MR
g. Foote’s sign rhythmic protrusion of tongue in
newborn period suggest ICH , cerebral edema
260. Ulcer of the frenulum
• In severe cough , like whooping cough ( due to
mechanical injury )
261. • Smooth bald tongue without papillae may be
seen in Vitamin B12 deficiency
• Geographical tongue shows reddis areas of
desquamation
262. Neck
• Short neck
Ratio between neck length : Height
Normal 1:13
>13 short neck
Neck length distance between external
occipital protuberane and C7 spine
266. Opisthotonus
• Kernicterus
• Tetanus
• Meningitis
• Infantile Gaucher’s disease
• Part of dystonia ( metoclopramide poisoning )
• Part of decerebration
• Local causes Retropharyngeal abscess
267. Typical postures
• Epiglottitis sitting up , leaning forward,
preferred not to lie down
• Peritonitis lies quietly , does not move
much
• Meningitis Lies on one side with thighs
flexed abdomen , or opisthotonus posture
• Lordotic posture Muscular dystrophies , B/L
Hip problem
268. Chest
• Clavicle absent – cleidocraial dysostosis
• Pre sternal edema may be found in mumps
• Widely spread nipples may be seen in Turner’s
syndrome space between nipples is >25%
of the chest circumference
• Sheild shaped chest in Turner’s syndrome
• Narrow thoracic cage Ellis van Crevald
syndrome , Jeune syndrome
269. • Absecne of Pectoralis muscle Poland
syndrome
• Sprengel’s deformity High position of
scapula with lower angle turned towards the
spine
• Gynaecomastia
271. Upper limbs
• Clinodactyly absence of P2 of little finger
Down’s syndrome
• Brachydactyly Down’s syndrome ,
Achondroplasia , Prader Willi syndrome
• Camptodactyly Fixed flexion deformity of
5th finger Normal , heritable , Down’s
syndrome
272. • Hypoplasia of the 4Th metacarpal is seen in
Pseuodohypoparathyroidism
• Here the ring finger will be shorter than the
index finger
• Reverse is true in normal children
273. • Broad thumb Rubinstein –Taybi syndrome
• Bifid thumb Holt oram , Fanconi
• Arachnodactyly unduly long fingers
Marfan syndrome , Homocystinuria ,
Hypogonadism , normal
• Thumb sign Marfan’s , absent in
homocystinuria
274. • Wrist sign thumb and the fifth finger will
overlap at wrist
• Trident sign in achondroplasia thumb
and fisrt two fingers …seperated from 4th and
5th fingers
• Overriding finger’s trisomy 18
275. Polydactyly
• Post axial associated with little finger
• Pre axial associated with thumb
• Polydactyly of four limbs Ellis Van crevald
syndrome
• Laurence Moon Biedl syndrome
276. Syndactyly
• Can be complete or partial
• Apert’s syndrome
• Trisomy 13
• Smith Lemli Optiz syndrome
• MC between 2nd and 3rd digits
277. Others
• Absent digits
• Lobster hand
• Absent thumb
• Triphalangeal thumb
• Osler’s nodes transient , small , pea sized ,
tender , nodules in pulp of fingers , toes ,
thenar/hypothenar eminences (IE)
• Janeway lesions painless erythematous
patches over palms and soles
• Absent clavicle
• Phocomelia
278. Nail
• Koilonychia
• Half and half nail CRF
• White nail anemia , hypoalbumenia
• Red nail Polycythemia
• Blue lunule of nail wilson’s disease
279. • Capillary pulsations Severe AR
• Nail fold telangectesia Dermatomyositis ,
SS,SLE
• Nail – Patella syndrome
• Hypoplastic nails
• Hyper convex nail Turenr’s , Noonan syndrome
• Black nails Addisons
• Splinter haemorrhages Infective E
280. • Koilonychia soft , thin , brittile ,flattened , or
concave (spoon shaped) , nail seen in iron
defieciency
• May not be seen uniformily in all nails
• Can be inherited also
282. Lower limbs
• Valgus directed away from midline
• Cubitus valgus/varus
• Coxa varus/valgus
• Genu valgus/ varus
• Both Genu varus and valgus is physiological in
children upto 1.5 to 2 years
283. • Genu recurvatum hyperextension of the
knee joint
• Pesplanus /flat foot physiological in 1.5 to 2
years
• Pes cavus/claw foot
• Talipus equino varus foot is adducted
downwards and inwards with medial
concavity
• Hallux valgus/varus