C.

PHYSICAL EXAMINATION
PALLOR

Definition
Paleness of skin and mucous membranes.
Sites of Examination
1. Conjunctiva (Fig. 2C.1)
2. Tongue
3. Oral mucosa
4. Palmar crease (Fig. 2C.2)
5. Nail bed (Hb <8 g/dL).

hands.
Demonstration of pallor in
2C.2:
Fig.

demonstration of pallor
Fig. 2C.1: Method of
Over conjunctiva.

Grading of Pallor

Moderate
Severe
Mild one of the hum.
Clinically visible plus Fig. 2C.3: Demonstration of cervical venous
Cannot be Clinically following features
detected visible
1 .Palmar crease

clinically disappearance Conditions Causing Pallor without Anemia

venous hum
2. Cervical
(suggestive of chronic Hypopituitarism
compensation) Hypothyroidism
Hypogonadism
2C.3) Shock
Method of Elicitation
of Cervical Venous Hum (Fig. Left heart failure.
root of the
neck o n the right side with
.Auscultate the
or sitting
with patient in standing Definition of Anemia
bell of stethoscope,
position.
murmur will be heard. Anemia is detined as decrease in circulating red blood
A continuous
cell
The cervical
venous hum was first described by Pontain (RBC) mass. lt is
characterized by decrease of
called Pontain's
murmur.
concenuration (Hb)/RBC hemoglobin
and hence
venous hum indicates chronic count/hematocrit (packed-cell
volume (PCV)| below normal
. T h e presence ofa cervical for the
patient's age, sex, and
c o m p e n s a t e d severe anemia. altitude of residence.
 Normal adult
/dL in males andhemoglobin
level is in the range of 13-17
12-15 g/dL in females. Per
Peripheral smear Microcytic hypochromic
(thalassemia)
.Microspherocytes (hereditzry
lues for Etiology of Anemia spherocytosis)
Sickle cells
Reticulocytosis
Iron deficiency anemia Hemoglobin electrophoresis
Specific symptoms Pica, dysphagia, restless leg Other specific
Coombs test, sickling test, and
syndrome, and melena investigation
osmotic fragility
Specific signs Bald tongue (Fig. 2C.4) Aplastic anemia
Koilonychia (Fig. 2C.5) Recurrent infections
Blue sclera (Fig. 2C.6) Specific symptoms
Bleeding manifestations
Peripheral smear Microcytic hypochromic red cells
Signs of pancytopenia
Iron studies. BM staining for iron, Specific signs
Other specific No organomegaly
stool/urine for occult blood, and
investigation Peripheral smear Pancytopenia
endoscopy Other specific Bone marrow examination
Megaloblastic anemia Cytogenetics
numbnesS investigation
Specific symptoms Tingling and
Sensory ataxia

Specific signs Glossitis, knuckle pigmentation

(Fig. 2C.7),absent deep tendon
reflexes (DTRs), sensory loss, and
positive Romberg's test

Peripheral smear Macrocytic RBC's, hypersegmented

neutrophils, and pancytopenia
Serum vitamin B,, levels, red
Other specific
cell folate levels. bone marrow
investigation
examination, and Schillings test

Anemia of chronic disease

Specific symptoms Symptoms of chronic kidney, liver

disease, and connective tissue
disorders
Hypertension, arteriovenous (AV)
Specific sign fistula-chronic kidney disease

(CKD)
failure-chronic
Signs ofliver cell
liver disease (CLD) Fig. 2C.4: Bald tongue.
Signs of rheumatoid arthritis,
systemic lupus erythematosus
(SLE), etc.
Normocytic normochromic anemia
Peripheral smear
pancytopenia
Renal function test, liver function
Other specific
investigation tests, autoantibodies, and raised
serum ferritin

Hemolytic anemia
Specific symptoms History of associated jaundice,
developmental delay, family
history positivity, recurrent blood
transfusions, and gallstones

Specific signs .Triad of anemia +jaundice+

splenomegaly
Hemolytic (Chipmunk) facies
(Fig. 2C.8) Cia 2 C AL
 Hyperpigmentation
of palm
Fig. 2C.6: Blue sclera. Fig 2C.9:

ICTERUS

Definition
m u c o u s membranes, sclera,
Yellowish discoloration ofskin,
to increased bilirubin (bile
and blood vessels secondary
have for elastin tissue).
affinity
pigments

Sites to Look for Jaundice

1. Sclera (Fig. 2C.10)

2. Sublingual mucosa
3. Oral cavity
4. Palms and soles
5. Skin.
Fig. 2C.7: Knuckle pigmentation

Scleral icterus is a term

commonly used but from a
histopathologic perspective, it is a misnomer. Bilirubin has
a high
affinity for elastin, which is an abundant protein in
the conjunctivae as well as the
superficial, fibrovascular
episclerae, but not the sclerae proper. One actually is
observing icterus of the bulbar conjunctiva
against the white
background provided by sclera. Conjunctival icterus is often
the first sign of
the use of term
hyperbilirubinemia. Hence we recommended
icterus"
"conjunctival icterus" instead of "scleral

Why unexposed
When the sclera/conjunctiva seen
sclera/conjunctiva
bilirubin gets converted to its
is exposed to
sunlight,
soluble form and hence
exposed part of conjunctiva may not reveal mild jaundice.
Yellowish discoloration can be
parts of normally seen in the
exposed
Fig. 2C.8: Chipmunk facies. sclera/conjunctiva
conjunctiva.
which is called as muddy sclera/
 Fig. 2C.10: Demonstration of icterus. Fig. 2C.11: Dark yellow icterus.

Serum Bilirubin Levels and Jaundice

Examination
0.3-1.2 mg/dL Normal Bradycardia
1.2-2.5 mg/dL Latent jaundice (generally not Pallor Present Absent Absent
appreciated on clinical examination) Jaundice Mild Moderate Severe
>2.5 mg/dL Clinically appreciated Splenomegaly Present Variable Absent
Yellowish discoloration without jaundice: Palpable ++

1. gallbladder
Hypercarotenemia (here sclera is not affected) Features of
2. Hypothyroidism (due to decreased metabolism of
Absent +(early (late feature)
liver cell failure feature)
carotene)
3. Excessive exposure to
phenols/nitric acid Laboratony data
4. Quinacrine intake. Serum bilirubin UCB UCB+ CB
CB
Grading Serum enzymes LDH AST 1 ALP
No standard grading system is available; however, few ALT
examiners prefer the following: Urine bilirubin
Mild jaundice Only sclera becomes yellow Urine
Moderate jaundice Skin also becomes yellow urobilinogen
Examples
Differentiating Type of Jaundice Based on Sderal Color Examples Thalassemia Hepatitis CBD stones
Sickle cell (viral/ Helminths in
Lemon yellow Most likely
hemolytic jaundice anemia alcoholic/ the CBD
Dark yellow (Fig. 2C.11) Obstructive jaundice Sphero- drug Carcinoma
Greenish dark yellow Longstanding obstructive cytosis induced) -head of
jaundice due to oxidation of Malaria Infiltrative pancreas
bilirubin to biliverdin Immune disorders Primary biliary
hemolytic Ischemic cirrhosis
anemias hepatitis Primary
Differentiating Jaundice Based on Clinical and
Sclerosing
Laboratory Findings cholangitis
Posthepatic (AST: aspartate aminotransferase; ALP: alkaline phosphatase
Prehepatic (obstructivel CB; conjugated bilirubin; CBD: common bile duct; LDH: lactate
Hepatic dehydrogenase; UCB: unconjugated bilirubin)
(hemolytic) Surgical)
History CYANOSIS
Urine Normal Yellow Yellow
Definition
Stools Normal Normal Pale clay like
Bluish color of skin and mucous membranes resulting8
Pruritis from an increased quantity of reduced hemoglobin
deoxygenated) or hemoglobin derivatves (methemoglobin 2. Pseudocyanosis
or sulfhemoglobin) in the small vessels of those tissues
.Metals:
Gold
Criteria Siver
Deoxy Hb >5g% or abnormal Hb (metHb or sulfHb) + SaO, Mercury
Arsenic.
<85%.
Drugs
Minocycline
Classification Chloroquine
Amiodarone.
1. True cyanosis:
a. Cenural cyanosis Atypical presentation
of cyanosis
Example
b. Peripheral cyanosis Description
PDA with
c. Mixed cyanosis. Cyanosis is
seen in
eisenmengerization
Differential
2. Pseudocyanosis. only lower limbs
cyanosis PDA with
in
Cyanosis is
seen
eisenmengerization
Reverse
Etiology of Cyanosis differential
only upper limbs
a n d transposition

of great arteries
cyanosis
1. True cyanosis When the patent
lower
a. Central cyanosis Three by four In addition to ductus opens
limbs, the left
Cardiac Cyanotic heart diseases cyanosis proximal to the
upper limb may
Truncus arteriosus origin of left
also be cyanosed
Transposition of great arteries subcdavian artery
Total anomalous pulmonary venous Seen in Ebstein's
connection (TAPVC) Intermittent
Tetralogy of Fallot
anomaly
cyanosis
Bilateral choanal
Tricuspid atresia Cyclical atresia
Ebstein's anomaly
Eisenmengerization (tardive cyanosis) cyanosis
Orthocyanosis Development of Seen in pulmonary
arteriovenous
Pulmonary Asthma cyanosis only in
disease
Chronic obstructive pulmonary upright position
malfomation

(COPD) due to hypoxia

Cor pulmonale occuming in erect
cause like pneumonia,
Respiratory failure of any posture
massive pleural effusion,
tension pneumothorax,
edema
In severe anemia
and acute pulmonary Cyanosis
carbon monoxide
absent despite
Others .High altitude of sufficient poisonin9
Polycythemia reduced
cyanosis
Enterogenous or pigment
(replacement cyanosis) hemoglobin
(>1.5 g/dL)
Methemoglobinemia
Differences between Central and Peripheral Cyanosis
-

Sulfhemoglobinemia (>0.5 g/dL)

Carboxyhemoglobin (produces
cherry red
discoloration) Central cyanosis Peripheral cyanosis
b. Peripheral cyanosis Due to inadequate Due to sluggish peripheral
oxygenation of systemic circulation
Low cardiac output circulation
(cold, frostbite, and Raynaud's
vasoconstriction
Local
.
It is a hypoxic hypoxia It is a stagnant hypaxia
phenomenon)

Arterial obstruction Site of examination: Site of examination:

Venous obstruction
conditions (multiple myeloma and
Tongue (Fig. 2C.12) Tip of nose
Hyperviscosity Oral mucosa (Fig. 2C.13) Ear lobule
polycythemia)
Outer lips
Finger tips
Cryoglobulinemia

c. Mixed cyanosis
central and peripheral cyanosis)
Nail bed
failure (has both Extremities
Left ventricular
 An

vs Pulmonary
Cyanosis)
Hyperoxia Test (Cardiac
Extremities are cold
for 10 minutes, repeat arterial
a
Extremities a r e warm
100% oxygen then
rewarming After giving is <150 m m Hg
done and if PaO,
Improves on
Do not improve on rewarming blood gas (ABG) is to >200 mm
cardiac and if
the PaO, improves
PaO, <85% PaO,>85 thec a u s e is
Does not improve with respiratory.
Improves on oxygenation Hg, the c a u s e is
oxygenation
Usually absent Versus Iron Deplete Cyanosis
Dyspnea and high volume Iron Replete Cyanosis
pulse seen Iron deplete cyanosis
Exercise may improve Iron replete cyanosis
Exercise may worsen It is d e c o m p e n s a t e d

It is compensated which fails to

with erythrocytosis
May be associated erythrocytosis which establish equilibrium with
clubbing and polycythemia establishes equilibrium with
unstable, rising hematocrit
a r e a s of the body,
Note: Cyanosis is best appreciated in hematocrit
cells are less
the blood vessel Iron deplete
where the overlying epidermis is thin and cells are
(nose Iron replete deformable
such as the lips, malar prominences
supply abundant, membranes (buccal and deformable Hyperviscosity symptoms
ears, and oral
mucous
and cheeks), fluorescent lighting. Hyperviscosity symptoms
appreciated in are frequent
sublingual); it is better
are rare

Theories of Cyanosis
Secondary to shunts
Admixture cyanosis
of shunt
Due to reversal
Tardive cyanosis (eisenmengerization)

type 1 respiratory failure

Due to
Hypoxic cyanosis
hemoglobins
Due to abnormal
Replacement cyanosis
Venous of blood
pooling
Distributive cyanosis

CLUBBING(HIPPOCRATES FINGERS)

Definition
digits of
enlargement of distal
segment
ctive bulbous
nail and
elecive between the
2C.12:
Demonstration of central cyanosis. (In
this patient
with subsequent loss of normal angle
Fig. be clearly demarcated,
and lingual veins can nail bed.
mucosa is pink
which is normal).
Theories of Clubbing
The megakaryocytes preferably
PDGF (role of platelet) and
lodge in the tips of the digits
derived
locally release platelet
vascular
growth factor (PDGF) and
endothelial growth factor (VEGF).
These growth factors along with
endothelial
other mediators increase
cause
permeability and activate and
proliferation of connective tissue

cells (e.g. fibroblasts)

Persistent vagal stimulation
Neurogenic
causes vasodilation and clubbing
(e.g. lung carcinoma)
Hypoxic Causes opening of deep arterio-
venous fistula in fingers (e.g.
2C.13: Bluish discoloration
of tongue and oral mucosa
tetralogy of Fallot)
Fig.
suggestive of central cyanosis.
Ferritin
Circulating vasodilators, which
Prostaglandins are
usually inactivated as blood
Bradykinin passes through the lungs, bypass
Adenine the inactivation
nucleotides process in the
patients with right to left shunts
5-hydroxytryptamine
Grades of clubbing (Figs. 2C.14 to 2C.19)
Grade 1 Increased fluctuation of nail bed
Grade 2 Loss of Lovibond
(normal is <180°)
angle/onychonychial angle
Profile sign
Schamroth sign
Grade 3 Parrot beaking
Drumstick fingers (seen in severe cyanotic
clubbing.
heart disease, bronchiectasis, and empyema) Demonstration
of grade 1
2C.14:
Pain along the distal ends of long bone due to
Fig.
Grade 4
subperiosteal new bone formation
Condition seen generally seen with
bronchogenic carcinoma
Grade 5 Glossy changes in nails and adjacent skin with
longitudinal striations (as proposed by Lung India)

Causes of clubbing
Respiratory causes

Bronchogenic carcinoma
Malignancies
Mesothelioma

Suppurative diseases Bronchiectasis

Lung abscess
Empyema
Interstitial lung disease (ILD)
Seen in 30% cases as a
Tuberculosis
sequelae to complications

Can be seen
Sarcoidosis
Fig. 2C.15: Demonstration of profile sign.
Cardiac causes

S u b a c u t e bacterial endocarditis

Atrial myxoma
Cyanotic heart disease
Eisenmengerization
Acyanotic heart disease with
Gastrointestinal causes

Inflammatory bowel disease

Ulcerative colitis
Crohn's disease
Primary biliary cirrhosis
Hepatocellular carcinoma

Neurological causes

Syringomyelia
Median nerve injury
Hemiplegia
Miscellaneous
Pachydermoperiostosis (pan digital hereditary clubbing)
Touraine-Solente-Gole syndrome
Note: Chronic obstructive pulmonary disease (COPD) never
causes clubbing. Fig. 2C.16: Demonstration of Schamroth's sign.
 Atypical presentation of clubbing
Acute clubbing .Subacute bacterial endocarditis
Lung abscess
Empyema
Unilateral clubbing Hemiplegia
Aneurysm of subclavian artery
Pancoast tumor
Pseudoclubbing Leprosy
Leukemic infiltration
Hyperparathyroidism
Thyroid acropachy
Sclerodactyly
Exposure to vinyl chloride
Subungual tumors or cysts
Painful clubbing Bronchogenic carcinoma
Fig. 2C.17: Demonstration of Subacute bacterial endocarditis
grade 3 ciubbing. Lung abscess

Reversible clubbing Lung abscess

Empyema
Unidigital clubbing Median nerve injuryY
Trauma
Clubbing with Cyanotic congenital heart diseases
cyanosis ILD
Differential clubbing: Patent ductus arteriosus (PDA) with
Upper limb (N) reversal of shunt
Lower limb (clubbing)
Reverse differential PDA+ transposition of the great
clubbing: arteries (TGA) + reversal of shunt
Upper limb (clubbing)
Lower limb (N)

Phalangeal Depth Ratio (Fig. 2C.20)

Fig. 2C.18: Demonstration of grade 4 clubbing. .Ratio

of distal phalangeal depth (DPD) with inter
phalangeal depth (IPD).
. < l is normal, >1 is suggestive
1800 160° of clubbing.

IPD DPD

Curth's modified profile sign

Lovibond's 'profile sign

Schamroth's
window PD DPD

Nomal Clubbing

Schamroth's sign Fig. 2C.20: Picture depicting the phalangeal depth at

depicting profile sign and
Schamroth's sign. proximal and distal interphalangeal joints.
Fig. 2C.19: Image
Digital Index
Sum of
A digital
phalangeal depth ratios of 10 In bed ridden
supirie Sacrum
index of 10.2 or fingers patient B a c k over the s c a p a

Although, a phalangeal higher is

indicative of clubbing.
depth ratio of 1.0 or greater To check for abdominat Pinch the skin over te

any finger is
suggestive of clubbing, digital index is in
specific for clubbing.
wall edema abdomen
more

Other Nail Changes Technique (Fig. 2C.21)

Press the skin and subcutaneous tissue
for at least 15-20
for abdominal
Nail changes Causes seconds against a bony prominence (except
and subcutaneous tissue).
Koilonychia Iron wal edema where we pinch the skin
deficiency anemia (IDA)
Beaus lines Hemochromatosis
Measles Grading of Pitting Edema (Fig. 20.22)
Pneumonia 2-mm depression, immediate
rebound
1+
Plummer nails
Pulmonary infarction to rebound
Seen in hyperthyroidism 2 4-mm deeppit, a few seconds
Red nails 6-mm deep pit, 10-12 seconds to
rebound
Congestive cardiac failure (CCF) 3+
Blue nails Copper or silver deposit >20 seconds to rebound
8-mm deep pit,
Black nails
Peutz-Jegher's syndrome
.Cushing'sdisease
Addison's disease
White nails Anemia
Hypoalbuminemia
Diabetes mellitus (DM)
CCF
Rheumatoid arthritis
EDEMA

Definition
Abnormal accumulation of fluid in interstitium.

Sites of Examination of Edema

In mobile patient Legs 2-3 cm above the
medial malleolus Fig. 2C.21: Method of eliciting pedal edema.

1+ 2+ 3+ 4+

E E E
2 mm 4mm mm 8 mm

Fig. 2C.22: Grading of pitting edema.

 Edema Nonpitting (Brawny edemaj
Pitting
in few s e c o n d s
Rapid recovery Slow recovery
Does not pit orrecover
Recovers in <40 seconds Recovery takes >40 seconds Nontender

Skin shows hyperkeratosis

Mechanism: Lymphedema

Mechanism: 1oncotic pressure Mechanism: thydrostatic pressure Lymphatic obstruction

Low serum protein (N) serum protein Causes:

M y x e d e m a (Fig. 2 C . 2 4 ) - h y p o t h y r o i d i s m

Causes: Causes: Pretibial myxedema-Graves's disease

Systemic venous hypertension
Increased protein loss
Burns (HTN) failure (CHF) Upper limb
Congestive heart Breast cancer
Nephrotic syndrome (Fig. 2C.23)
Bowel disease Radiation induced
Pericarditis Lower limb
Decreased intake or Tricuspid valve diseases
synthesis Local venous HTN Aplasia cutis tarda, milroy's disease, and
Kwashiorkor thrombosis (DVT) .Congenital (praecox,
venous
Deep Meigs disease)
Malabsorption cava syndrome
Inferior vena Filariasis (Fig. 2C.25)
Liver disease Recurred streptococcal infection

Malignancies
(Quincke's edema)
syndrome. and angioedema
nephrotic
hypothyroidism, allergies,
Faclal edema: Trichinosis, (NSAIDs), and insulin
to autonomic dysfunction anti-inflammatory drugs
Neurogenic edema: Secondary corticosteroids, estrogen, nonsteroidal left iliac vein by the right common
Drug-induced edema:
Nifedipine, edema due to
compression ofthe
syndrome-chronic,
unilateral, pitting
May-Thurner
lumbar spine
iliac artery against the
e d e m a - c h r o n i c , bilateral, and pitting
ldiopathic
more during
menstrual cycles.
In females <50 age,

seen in
Fig. 2C.23: Pitting type of pedal edema
congestive cardiac failure.

Fig. 2C.25: Nonpitting type of pedal edema seen in filanass

LYMPHADENOPATHY

Definitions
Generalized Lymphadenopathy
Generalized involvemen
Fig. 2C.24: Nonpiting type of pedal
lymphadenopathy is defined
of 22 noncontiguous lymph node groups and is typ
as
icall

edema teen in myzedema.

indicative of systemnic disease.
Significant Lympnadenopatny (0ased on Size, Fixity and
Size 2 cm in Consistency)
Size 1 cm in Inguinal region
Any size Extrainguinal region
Supraclavicular
Epitrochlear
Popliteal draining are
Any lymph node with a lesion in the
Based on fixity
Fixed to each other (matting)
Fixed to underlying tissues
Fixed to skin
Based on consistency Hard/firm lymph nodes
( m n e m o n i c

Persistent Generalized Lymphadenopathy

m o n t h s

m o r e

or

It is defined as lymph nodes of more than 1 cm in size, in 2 or more areas persist m e (HIV/AIDS).

1-2-3). Seen in human immunodeficiencyvirus/acquired immune deficiency syna

lymphadenopathy
Causes of generalized
Disseminated TBB
Infections Bacterial
Secondary syphilis
HIV
Viral Infectious mononucleosis

Toxoplasmosis
Parasitic
Histoplasmosis
Fungal Coccidioidomycosis

P a r a c o c c i d i o i d o m y c o s i s

Lymphomas
Malignancy Acute leukemiaas (CLL)
leukemia
lymphocytic
(CML) (in blast crisis)
Chronic
leukemia
C h r o n i c myeloid

erythematosus (SLE)
Systemic lupus
Immunological Adult-onset Still's disease
J u v e n i l e rheumatoid
arthritiss (JRA)
Sjogren's syndrome
Kawasaki disease p h e n o m e n o n - e x c e s s of antibody)
sickness (postzone
Serum

.Sarcoidosis
G r a n u l o m a t o u s
Amyloidosis
Histiocytosis X
Hyperthyroidism

Endocrine
.Phenytoin (pseudolymphoma)
.Primidone
Drugs Carbamazepine

Allopurinol
Captopril
Cotrimoxazole

Sulindac (NSAIDs)
Hydralazine
Beta-blockers

Kikuchi-Fujimoto disease
Castleman's disease
S y n d r o m i c l y m p h a d e n o p a t h y

Kimura disease
.Rosai-Dorfman syndrome
Familial Mediterranean fever
Niemann-Pick disease
M i s c e l l a n e o u s
 4. Consistency

5. Overlying skin

Describing a Lymph Node 6. Mobility

1. Size (signiicant or not) 7. Tenderness

8. Draining area.

2. Site
3. Number

Normal consistency

Consistency
Malignancy
Soft Hodgkin's l y m p h o m a

Hard
Syphilis
Indian rubber Lymphogranuloma venereum
Shotty lymph node periadenitis)
(due to
central necrosis)
Tuberculosis

Hyperplastic t u b e r c u l o s i s l y m p h a d e n o p a t h y
Bubo (largge node with
Matted
tuberculosis
nodes in
Hard lymph

Nodes (Fig. 2C26)

Different Group of Lymph

Cervical
Pre-auricular

Upper cervical
Cervical Median or lower cervical
Posterior
Supraclavicular
cervical

Mediastinal Axillary
Paratacheal
Hilar
Retrocrura

O-

Mesenteric
Epitrochlear Celiac
Splenic hilar

Portal

Para-aortic-

Common ihac
Extenal diac
Inguinal
Femoral

OPalpable nodes
O Nonpalpable nodes

Popliteal

Fig. 2C.26: Image showing different groups of lymph nodes.

 39
E x a m i n a t i o n

General

Capter 2:

Cervical Lymph Nodes

Divided into:
Superficial or deep (based on wlhether above or below
deep cervical fascia)
Vertical or horizontal

Superficial Cervical Lymph Nodes

.They are superticial to deep cervical fascia
They include:
External Waldeyer ring
»Submental

Submandibular bilateral
» Preauricular bilateral submandibular

» Postauricular bilateral examining

of
»Occipital lymph nodes. ig.
20.28:
Method
lymph nodes.

Pretracheal
Paratracheal

Posterior triangle lymph nodes

Nodes
Deep Cervical Lymph
.Horizontal: Supraclavicular lymph
nodes

Vertical: Jugulodigastric and jugulo-omohyoid lymph

nodes.

Examination of Cervical Lymph Nodes

nodes is done
Examination of anterior group of lymph
the neck to relax the
behind the patientlex
by standing submental group (using a single
fascia>first feel for the submandibular
then->bilateral
and
finger) (Fig. 2C.27) preauricular (Fig.
2C.29)-
2C.28)->bilateral
(Fig. juguloomohyoid (Fig.
2C.30)>
jugulodigastric (Fig. and
2C.31)>supraclavicular
(Fig. 2C.32) (+ pre-
groups
nodes.
preauricular
lymph
paratracheal). nodes is of examining
of lymph Method
Examination of posterior group for the post Fig. 2C.29:
patient->feel
done by standing
in front ofthe 2C.34)->posterior
2 C . 3 3 ) > o c c i p i t a l (Fig.
a u r i c u l a r (Fig. 2C.35).
nodes (Fig.
of lymph
triangle group

submental
examining
Method of Fig. 2C.30: Method of examining jugulodigastric lymph nodes.
2C.27:
Fig. of lymph
node.
group
 occipital lymph nodes

Method of e x a m i n i n g
2C.34:
nodes
Fig.
jugulo-omohyoid lymph
examining
Fig. 2C.31: Method of

posterior
2C.35: Method
of examining
Fig. triangle lymph nodes.
supraclavicular
examining
2C.32: Method of
Fig. lymph nodes.
Nodes and Drainage
Supraclavicular Lymph
Leftsupraclavicular
Right supraclavicular
Left lung upper lobe
Right lung (all three lobes)
Left lung lower lobe
4 B's and Gonads:
[Link]
2. Bronchus
3. Bowel
4. Bladder, and
Gonads (testis/ovaries)
Mechanism of left supraclavicular
lymphadenopathy
Note tumor cells from the
inGl and other malignancies-reflux of or
thoracic duct into left supraclavicular
node at the junction
thoracic duct and let subclavian

Trousseau sign of tetany: Carpopedal spasms

in
Trousseaus syndrome: Migratory thrombophlebitis
malignancy
Fig. 2C.33: Method of examining Troisier's sign: Enlarged hard left supraclavicular lymphnode
postauricular lymph nodes
(Virchow's node)
 Other named lymph nodes Central and
Virchow node Left supraclavicular node Apical nodes.
The apical nodes are the final
Scalene node Sentinel node of the axillary common pathway for all
of bronchogenic lymph nodes.
(Fig. 2C.36) carcinoma Note: Pxamine the right
Relax neck hand except for humeral
axillary Iymph nodes with the lef
Palpate (deep) between the two with right hand). (lateral) group (whichis examined
heads of SCM
Winterbottom Posterior triangle lymph node Examination of Right Axillary Lymph Nodes
sign enlargement (Figs. 2C.37 to 2C.46)
Seen in early phase of
African Hyperabduct the right arm of patient
trypanosomiasis
Causes of Scalp infection Place the right forearm of patient on your left forearm
posterior triangle Measles
lymph node Rubella
enlargement Infectious mononucleosis Insinuate your left hand fingertips deep in axila of patient
Trypanosomiasis.
Node of Woods Jugulodigastric lymph node Using your right hand to apply pressure over the patient's
enlargement seen in TB when spread shoulder, feel for the apical lymph nodes using your left hand
via tonsils

Delphian node Pretracheal node Central group can be felt just below the apical group

External Waldeyer Commonly seen to be enlarged in

Anterior group can be felt on the anterior axillary fold
ring non-Hodgkin's lymphoma
Berry's node Jugulo-omohyoid lymph nodes seen the posterior axillary fold
in thyroid malignancy Posterior group can be felt on

hand by palpating
Lateral group is felt with examiner's right
Axillary Group of Lymph Nodes over the patient's humerus

There are five axillary lymph node groups

nodes:
Lymph nodes include: Drainage areas of axillary lymph
1. Chest wall with breast
Lateral (humeral), 2. Parietal pleura
Anterior (pectoral), 3. Upper limb.
Posterior (subscapular),

Fig. 2C.37: Method of examining right apical group

Method of examining scalene lymph nodes
Fig. 2C.36: (axillary) lymph nodes.
Inguinal Lymph Nodes Enlarged in:
Lymphonmas
Horizontal group Vertical group Testicular malignancies
Palpated along the inguinal Palpated vertically down- Tuberculosis.
ligament wards from the midpoint of
inguinal ligament Mesenteric Lymph Nodes
Drains: Drains:
line of attachment of the
External genitalia Lower limb Examined along the mes-
Scrotum from the right
edially towardthe
iliac fossa medi
entery,
.Perineum umbilicus.
Anal canal below dentate line
Enlarged in:
HIV
Popliteal Lymphadenopathy Lymphomnas
Palpate the popliteal fossa with the knee in semiflexed Ulcerative colitis.

position
Systemic diseases associatedwith enlargement include: Mediastinal Lymph Nodes
NHL
a bronchophony/whispering
is
pect.
Disseminated TB .D'Espine sign vertebral spines (on
the back
heard over the
HIV. oriloquy bifurcation; below the fourth
below the level of tracheal

Para-aortic lymphadenopathy thoracic spine (T,) in adults. (mediastinal) lympha

tracheobronchial
It indicates
Relax abdomen. denopathy.
.With 2 hands placed over the epigastrium-one should
feel for the enlarged lymph nodes by deep palpation.
Nutritional deficiencies
Manifestation
Vitamin deficiency
Fat-soluble vitamins
keratomalacia, and Bitot's spots
Vitamin A, Retinol Night blindness,
Rickets/osteomalacia
Vitamin D, ergo/cholecalciferol costochondral beading
Bone pain,
.Proximal myopathy ataxia, muscle wasting, retinitis
Hemolysis, posterior column signs,
Vitamin E, tocopherol
pigmentosa-like changes, and night blindness
and GI bleeds
other menaquinones Bruising, purpura, nose,
Vitamin K, phylloquinone, and and vitamin C)
Water-soluble vitamin (B-complex
Wernicke/Korsakoff

B, (Thiamine) Beriberi
.Nystagmus
Sixth cranial nerve palsy
Ataxia
Acidosis
Dementia
Paraesthesiae
Neuropathy
.Cardiacfailure
Anemia
Ariboflavinosis
B, (Riboflavin) Angular stomatitis, glossitis, and magenta tongue
Pellagra
B, (Niacin) Dermatitis on sun-exposed areas
Dementia
Poor appetite, difficulty sleeping
Confusion, sore mouth
B, (Adenine)" Immune dysfunction
Aging
B, (Pantothenic acid) Nausea
Abdominal pain
Paraesthesiae, burning feet
B, (Pyridoxine)
Poor appetite
Lassitude
Oxaluria
B, (Biotin) Dermatitis,
Depression, lassitude,
Muscle pains,
Electrocardiogram abnormalities, blepharitis
B, (Inositol) Depression and other psychiatric manifestations

B, (Folic acid) Macrocytic anemia,

Thrombocytopenia and
Megaloblastic bone marrow

B, (PABA)" Free radical damage

Sun burns and skin rashes

B, (Salicylic acid) Works in tandem with vitamin B2

B, (Cobalamin) Subacute combined degeneration of spinal cord
Macrocytic anemia, icterus, knuckle pigmentation

Vitamin C (Ascorbic acid) Scurvy

Poor wound healing, fatigue, limb pain, scorbutic rosary
Difficulty sleeping, gingivitis, perifollicular purpura
Hyperkeratosis

Vitamin B4 ,8, 10, and 11 are no longer labeled as vitamins, as they do not fit the official definition of vitamin.

Minerals

Iron Koilonychia
Smooth tongue
Anemia
Esophageal web
Microcytic hypochromic anemia
Copper
.Neutropenia
Scurvy-like bone lesions, osteoporosis

Zinc Acrodermatitis enteropathica

Peristomal/perinasal/perineal
Erythema, thin hair
Diarrhea, apathy, anorexia
Growth failure
Hypoglycemia
Distorted or diminished taste (hypogeusia)
Peripheral neuropathy, hyperglycemia
Chromium
Selenium Cardiomyopathy
lodine Goiter
Others
Protein deficiency Pitting edema
Hair: Thinning, easily pluckable with dyspigmentation orflag
and change in texture to silken, sparse hair.
sign, type,
Dermatosis with desquamation of the so-called flaky-paint
with or without hyperpigmentation