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Showing posts with label general examination. Show all posts
Showing posts with label general examination. Show all posts

Radiofemoral delay

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Examination of pulse

How to examine the Pulse ?

What are the variations in pulse rate?

Bradycardia and its causes

Relative bradycardia and relative tachycardia

What is pulse deficit?

What is pulse volume and what are its alterations?

High volume pulse and its causes

What are the causes of low volume pulse?

What is water-hammer pulse ?

 What is Hyperkinetic Pulse?

High volume jerky pulse (Spike and Dome Pulse)

What is anacrotic pulse?

What is Dicrotic pulse

What is catacrotic pulse?

What is pulsus alternans ?

Pulses bigeminus

Pulses paradoxus or Kussmaul's pulse

What is pulsus bisferiens ?

Describe the pulse in complete heart block (CHB)

How to assess the condition of the arterial wall?

What is the cause of radioradial and radiofemoral delay?

What are the basic bedside features of coarctation of aorta ?

Different cardiac rhythms
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Temperature recording and fever

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Examination of nail

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Examination of hair

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Examination of skin

What are the functions of the Skin ?

Alterations in colour of skin

Primary and secondary skin lesions

Causes of cutaneous hyperpigmentation

What is melasma or chloasma ?

Cardinal features of addisons disease

What are the cardinal manifestations of hemochromatosis?

Hypopigmentation of skin

Skin lesions that give clue to the underlying diagnosis

What are Neurocutaneous diseases?

What is Cafe au lait spot?

What are the cutaneous signs of internal malignancy?

Cutaneous manifestations of chronic kidney disease

Skin in Hematological Diseases

What are the cutaneous manifestation of Diabetes mellitus?

Cutaneous manifesation of gastrointestinal disease

Cutaneous manifestations of Cardiovascular Diseases

What are the cutaneous markers in Collagen Vascular disease?

Skin in Hematological Diseases

What are the systemic diseases with Pruritus?


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Clinical assessment of clubbing

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Clinical assessment of jaundice

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Clinical assessment of anemia

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Assessment of emaciation and obesity

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Assessment of tall stature

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Assessment of shortstature

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Abnormalities of fingers

Polydactyly 
It is the presence of supernumerary fingers
Causes
  • Congenital
  • Familial
  • Associated with VSD
  • Laurence-Moon-Biedl syndrome
  • Turner's syndrome.
Syndactyly
 It is the presence of webbed fingers. May occur in normal individuals or in those with, certain congenital abnormalities. It is seen in Poland's syndrome (absent unilateral pectoralis major muscle with TOF).
Arachnodactyly
It is the presence of Spider fingers. These are long and thin fingers.
Causes
  • Marfan's syndrome
  • Hypogonadism
  • Hypopituitarism
  • Homocystinuria
  • Normal individuals.
Absence of digits
Absence of one or more fingers may be congenital. Thumb may be absent in Fanconi's congenital aplastic anemia.
Sausage fingers
Thick and fleshy fingers seen in
  • Acromegaly
  • Myxoedema
  • Psoriatic arthropathy.


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Significance of posture of the patient

The position or attitude that is constantly assumed by a patient at rest or in motion is referred to as posture. The posture of a patient, when viewed from the side, may be characteristic enough to suggest an underlying diagnosis.

The various postures seen in clinical practice are the following :
1. Postures seen when the patient is standing / sitting.
  • Vertical line seen in standing posture, when the patient is viewed from the side, is a good posture.
  • Standing posture, when it assumes a S-shaped curve, when viewed from the side of the patient , is a poor posture.
  • Asthenic posture : The normal curves of the spine are exaggerated in asthenic posture. Seen in debility, wasting and insenility.
  • Parkinsonian posture : Universally flexed posture.
  • Lordotic posture : There is an exaggerated lumbar lordosis.This is seen in muscular dystrophy, due to proximal muscle weakness.Lordotic posture is also seen in bilateral hip problems.
  • Cerebellar posture : In lesions of the cerebellum or its connections, the patient stands with his feet wide apart, and is unable to maintain a upright steady posture when standing with both his or her feet placed close together. Patient is ataxic on standing (truncal ataxia) when the cerebellar vermis of is involved.
  • Posture in ankylosing spondylitis : There is loss of the lumbar lordosis, and an exaggeration of the upper thoracic kyphosis.
  • Catatonic posture : It is seen in schizophrenia. In this the patient maintains particular posture of the body and limb for hours together. 
2. Postures seen when the patient is lying down:
  • Decerebrate posture : There is extension of elbows and wrists, with pronation of the arms is seen. This posture suggests that the lesion is at the brainstem level, disconnecting the cerebral hemispheres from the brainstem.
  • Decorticate posture : There is flexion of elbows and wrists, with supination of the arms is seen. It suggests severe bilateral hemispherical damage above the midbrain.
  • Hemiplegic posture : The patient lies on his back,with the cheek on the affected side blowing out with each time the patient expires. The affected upper limb lies flaccidly by his side, and the affected lower limb is externally rotated. This picture is seen immediately after the onset of hemiplegia. In long standing hemiplegia, there may be loss of naso labial fold of the face on the side of the paresis, with the affected upper limb in a flexed posture and the affected lower limb in an extended posture.
  • Opisthotonus : In this posture the patient is arched up like a bow, with his or her heel and occiput in contact with the bed. This posture is seen in patients affected with tetanus and strychnine poisoning.
  • The lateral decubitus posture with curled up limbs to minimise the stretching of the meninges, is seen patients with meningitis or meningism.
  • Patient lying up with a back rest or cardiac rest (propped up posture )suggests a possibility of the patient having CCF or COPD.
  • Patient sitting up and holding on to a support before him, in order to fix his shoulders, and the patient is dypneic suggests a diagnosis of bronchial asthma.
3. Patient lying down still and
  • Clutching his chest-suggest anginal chest pain
  • Shallow breathing, with minimal or no movement of the anterior abdominal wall is seen in peritonitis.
4. Patient rolling about in the bed from side to side and
  • Clutching his chest is observed in Myocardial infarction.
  • Holding his upper abdomen is seen in Biliary colic.
5. Patient sitting up and bending forwards, may be seen in
  • Pericarditis
  • Pancreatitis
The patient assumes this posture because the pain caused by both these conditions is relieved by assuming this posture.
Prone posture : Patient preferring to lie in the prone position than in the supine position may be due to the presence of an abdominal aortic aneurysm which may erode on the vertebra in the supine posture and this may cause back pain. On lying prone as the  the aorta falls forward from the vertebra and the back pain subsides.
Pleuritic pain and pleural effusion patient may be seen lying on the affected side for relief of pain and dyspnea.
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Clinical diagnosis based on body habitus

First impression of a patient's appearance will  give certain clue that lead to diagnosis, but one should substantiate tha diagnosis by seeking for other signs on proper examination-these may be labelled as spotters.
Endocrine illness

  • Acromegaly-there is characteristic facies with acral enlargement
  • Gigantism-tall stature, bilateral acral enlargement and prognathism
  • Thyrotoxicosis-anxious look, bilateral proptosis, restlessness, thin built bodv ,tremor of hands
  • Myxedema-characteristic facies, dull expression and edema of legs
  • Cretinism-characteristic facies, dwarfism and protruding tongue
  • Addison's disease-hyperpigmentation, asthenia and thinning of body
  • Cushing's syndrome-moon face, plethoric face, striae, obesity-truncal obesity and buffalo hump
  • Pseudohypoparathyroidism-short stature,moon face and brachydactyly
  • Rickets-frontoparietal bossing, bowing of legs, delayed dentition

Auto immune disease

  • SLE characteristic facies-butterfly rash
  • PSS - characteristic facies-vitiligo-pepper and salt appearance, sclerodactyly, hyperpimentation, digits-telangiectasia, ulcers,pitted scars
  • Ankylosing spondylitis- posture of patient affected due to spine involvement, loss of lumbar lordosis, increased dorsal kyphosis and forward stoop of neck, flexion of hip and knee joints, limitation of spine movement

Neurological illness

  • Dystrophia myotonica-baldness with characteristic facies
  • Abnormal movement-chorea, athetosis, dyskinesia, tics,hemifacial spasm
  • Charcot marie tooth disease-peroneal muscular atrophy, inverted champagne bottle appearance of legs.


Syndromes with tall stature

  • Klinefelters syndrome-tall stature, absence secondary sexual characters, alopecia ± gynaecomastia
  • Marfan syndrome-tall stature, long thin extremities and arachnodactyly
  • Acromegaly
  • Gigantism


Syndrome with short stature

  • Turners syndrome-short stature, cubitus valgus webbing of neck and widely spaced nipple,shield like chest.
  • Achondroplasia-dwarfism, normal trunk short limbs especially proximal parts, macrocephaly, saddle nose, increased lumbar lordosis
  • Pseudohypoparathyroidism-short stature,moon face and brachydactyly


Other diseases
Mongolism -characteristic facies, mongoloid slant of eyes, protruded tongue with open mouth  hypotonic muscles, single transverse crease of hand
Mucopolysaccharoidosis-short stature, chraracteristic facies, joint stiffness, kyphoscoliosis

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What are the characteristic facies in clinical medicine?

Peculiar facies can be seen associated with various disease 

 Facies in endocrine disease
  • Acromegalic facies: In acromegaly there is prominent lower jaw, coarse features, large nose, lips, ears, prominent forehead and check bones and widespread teeth
  • Cushing's syndrome patients have rounded 'moon face' with excessive hair growth and facial plethora.
  • Hypothyroid face is characterised by puffy face with a dull expression with swollen eyelids and loss of hair over eyebrows.
  • Hyperthyroid face: In hyperthyroidism patients has anxious look with widely opened eyes with the upper and lower limbus visible this is associated with infrequent blinking and absence of wrinkling of the forehead.
  • Cretinoid face: Face is pale and has a stupid and dull look. Nose is broad and flattened. Lips are thick and separated by a large and fissured protruding tongue. Hair on eyebrows, eyelashes and scalp are very scanty. Prominent medial epicanthal folds and low set ears are noticed
Facies  in autoimmune disease
  • Face in scleroderma: Scleroderma patients has the following characteristic facies.Skin over the face is taut and shiny. Patient finds it difficult to in open his mouth or to smile (microstomia).
  • Face in SLE: SLE is a disease predominantly in women. There is butterfly rash seen over the face affecting the upper cheeks and the nasal bridge.Photosensitivity may be present that is erythema may be seen over the rash on exposure to sunlight.
  • Face in Sjogren's syndrome: There is enlargement of the lacrimal gland on both sides along with enlargement of the parotid and submandibular glands on both sides.
Facies in neurological disease
  • Myasthenic facies: There is bilateral ptosis with outward deviation of the eyes, wrinkling of the forehead and partially opened mouth.
  • Myotonic dystrophy:Is characterised by bilateral ptosis with absence of wrinkling of the forehead, frontal baldness with absent sternomastoids and bilateral cataract.This is characterised by the transverse smile .
  • Parkinsonian face:Patients have immobile, fixed and expressionless face with infrequent blinking of the eyes.Normal rate of eye blinking is about 20 per minute.In Parkinsonism, the rate of blinking is reduced to less than 10 per minute. Blepharoclonus that is on closing the eyes fluttering of the eyelids is seen In postencephalitic parkinsonism, oculogyric crisis is observed.This is characterised by tonic upward deviation or the eyes. A jaw tremor may also be seen.
  • Bell's palsy:There is absence of wrinkling of forehead on the side of the lesion, and the patient is unable to close the eyes, and on attempting to do so the eyeball is seen to move upwards and outwards It is called as Bell'sphenomenon. There is also loss of the nasolabial fold on the side of lesion and deviation of the angle of the mouth to the opposite healthy side on smiling. However in long standing case of Bell's palsy, when contractures of the facial muscles develop,there is prominent nasolabial grooves may be seen on the affected side, creating confusion as to the side of lesion.
Facies in various infections
  • Tabetic facies: Partial ptosis with wrinkling of forehead and unequal.small and irregular pupils.
  • Hippocratic facies-sunken eyes and cheeks,dry lips, looks severely ill.
  • Tetanus-there is characteristic risus sardonicus  blepharospasm and spasm of facial muscle;
  • Leonine facies: Seen in leprosy, there is thickening of the skin and ear lobes with a flattened nasal bridge and there is madarosis rhat is loss of hair over the lateral aspect of eyebrows and eyelashes
Facies in cardiovascular disease
  • Elfin facies: This is seen in supravalvular aortic stenosis, or pulmonary artery stenosis (William's syndrome). There is a presence of a wide mouth with large lips (pouting effect), teeths are widely spaced with broad forehead, pointed chin, protruding ears and hypertelorism(eyes set wide apart).
  • Congenital pulmonary stenosis:Patients have a broad face with eyes set wide apart (moon face).
Facies in respiratory disease
  • Face in pneumonia: In lobar pneumonia, the alae nasi are over active, eyes are bright and shiny.There may be herpes labialis that is herpetic lesions may be present over the angle of the mouth.
  •  Face in COPD: COPD patients have anxious look with bluish discoloration of lips, tip of the nose, ear lobes and breathing out through pursed lips.
Facies in other conditions
  • Cirrhotic facies there is sunken cheeks and eyes with malar prominence and presence ot bilaterally enlarged parotid glands especially in alcoholic cirrhosis 
  • Chip munk facies-characterised by frontomaxillary prominence due to marrow expansion-hemolytic facies in hemolytic anemias
  • Mucopolysaccharidosis (Hurler's)-Patients have coarse features of face, hypertrichosis, large tongue and corneal haziness
  • Face in nephrotic/nephritic syndrome: Face is puffy with periorbital edema and pallor.


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Koilonychia and its causes

Koilonychia is the spoon-shaped deformity of the nail ,it is usually found in chronic iron deficiency anaemia.
Koilonychia develops due to the retarded growth of the nail plate. Koilos' means hollow and onych' means nail.
How will you examine for koilonychia ?
To examine for koilonychias first keep the patients finger at your eye level and look tangentially, you can observe as well as palpate the nail plate for spooning or flattening
What are the stages of koilonychia ?
There are three stages of koilonychia
First stage is characterised by brittle and rough nail
Second stage is charecterised by flattening of nail without longitudinal ridges and the nail is flat
Third stage the nail is spoon shaped and is concave.
What are the causes of koilonychia?
Causes of koilonychias are the following

  • Iron deficiency anaemia
  • Haemochromatosis
  • Raynaud's syndrome
  • Porphyria
  • Occupational

              Motor mechanics
              Rickshaw pullers

  • Ischaemic heart disease
  • Syphilis
  • Inherited—autosomal dominant.
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What are the causes of clubbing?

Cardiovascular cause of clubbing 
  • Infective endocarditis
  • Cyanotic CHD
  • Myxoma of atria
  • Aneurism of major vessels such as aorta and  subclavian artery
Gastrointestinal causes of clubbing 
  • Malabsorption
  • IBD - Crohn's, ulcerative colitis
  • Cirrhosis of liver particularly biliary cirrhosis
Respiratory causes of clubbing
  • Broochiectasis.
  • Lung abscess.
  • Bronchogenic carcinoma.
  • Empyma thoracis.
  • Fibrosing alveolitis.
  • Pleural mesothelioma.
  • Pulmonary arteriovenous fistula.
  • Cystic fibrosis.
In pulmonary tuberculosis clubbing denotes
  • Post tuberculous bronchiectasis
  • Diffuse B/L lung fibrosis
  • Empyema
Others  causes of clubbing 
  • Congenital 
  • Thyrotoxicosis 
  • Acromegaly
  • Unidigital clubbing is seen in - sarcoidosis, trauma, gout.
  • Pachydermoperiostosis
  • Thyroid acropachy
What are the different types of clubbing?
Drum stick type of clubbing  is seen in
  • Congenital cyanotic heart diseases, e.g. Fallot's tetralogy.
  • Bronchiectasis.
Parrot-beak type of clubbing : Commonly seen in bronchogenic carcinoma.
What are the  causes of painful clubbing ?
  • Bronchogenic carcinoma.
  • SBE.
What are the causes of unilateral clubbing ?
  • Presubclavian coarctation of aorta (left sided clubbing).
  • Bronchogenic carcinoma.
  • Cervical rib.
  • Aneurysm of subclavian artery.
  • Ervthromelalgia.
  • Arteriovenous fistula of brachial vessels.
What are the causes of unidigital clubbing?
  • Hereditary (if bilateral).
  • Local trauma.
  • Rarely from median nerve injury' or deposition of tophi (gout).
  • Sarcoidosis.
Causes of clubbing limited to upper extremity ?
Chronic obstructive phlebitis of upper extremity as a result of chronic I.V drug addiction (eg. heroin).
Causes of clubbing limited to lower extremity ?
In infected abdominal aortic aneurysm : sometimes in PDA with reversal of shunt.
What is the cause of acute clubbing ?
Development of clubbing within 10 to 14 days of onset of illness.This is seen in lung abcess
What are the causes of pseudoclubbing?
Psuedoclubbing is seen in conditions associated with subperiosteal bone resorption of terminal phalanges. Here there is absence of soft tissue proliferation and increased curvature of nails and is seen in.
  • Scleroderma.
  • Acromegaly.
  • Hyperparathyroidism.
  • Leprosy.


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How will you examine for clubbing ?

First step  for examination of clubbing is 
Bring the patient's lingers at examiners eye level and look tangentially.You should observe the onychodermal angle. If the angle is 180° or more, it is said that clubbing is present.
Second step for examination of clubbing 
Very early clubbing can be detected by increase in fluctuation of the nail-bed it is due to softening of the nail-bed. To elicit 'fluctuation', the patient's finger (index finger) is placed on the pulp of examiner's two thumbs and held in this position by gentle pressure with the tips of examiner’s middle fingers applied on the patient's proximal interphalangeal joint. The patient's finger is now palpated over the base of the nail by the tips of examiner's index fingers. There is always some amount of fluctuation is present in normal fingers. Clubbing is said to be present when fluctuation is obvious here the palpation of the nail-bed may give the impression that the nail is floating on its bed.
For detection of clubbing, you should first examine the onychodermal angle and then the fluctuation.
What is the most reliable  early sign of clubbing ?
Loss of normal onychodermal angle is one of the earliest sign is of clubbing  increased fluctuation of the nail-bed although occur early is not always reliable.
Which fingers are affected first in clubbing ?
Usually the index finger is affected first in clubbing
What are the points to note when clubbing is detected?
  • Unilateral or bilateral.
  • Painful or not.
  • Presence or absence of central cyanosis.
  • Presence or absence of dyspnoea.
  • The degree of clubbing.
What are the grades of clubbing?
Grade 1-Increased fluctuation of nailbed which lead to increased looseness of base of nail
Grade 2-Obliteration of nailbed angle more than or equal to 180 . It can be demonstrated by keeping the finger in profile view this is called profilesign
Grade 3-Parrot beaking—Biconvexity of nail
Grade 4-Drumstick nail-Bulbous enlargement of distal portion of fingers and toes
Grade 5-Hypertrophic osteoarthropathy-with the above mentioned features plus 
  • Thickening of periosteum
  • Distal arthropathy
  • Periosteal tenderness and heaviness of hands

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Clubbing and its pathogenesis

Clubbing is the bulbous swelling of the terminal part of the fingers and the toes with an increase in the  soft tissue mass, and increased anteroposterior as well as transverse diameter of the nails due to proliferation of subungual connective tissue.
Normal angle between the skin and the nail bed is 160 degree. It is also called as lovibond angle Obliteration of this angle is an early sign of clubbing.There is also increase in the  soft tissue of distal part of the fingers and toes.This is manifested as biconvexity of nail and the bulbous distal portion of fingers.
In normal nails when the thumb nails are placed in opposion There is a lozenge shaped gap .In clubbing this gap is obliterated called as Schamroth's window test or sign.
What is the basic mechanism of clubbing?
Arterial hypoxemia and neurohumeral stimulus produces hypervascularity and opening up of anastamotic channels in the nail bed which lead to overgrowth of soft tissue.This is the basic mechanism of clubbing
Why the pulp tissue is increased in clubbing ?
Pulp tissue is increased due to
  • Proliferation of subungual connective tissue.
  • Interstitial oedema.
  • Dilatation of arterioles and capillaries.
What is the pathogenesis of clubbing?
There are several theories to explain clubbing
Hereditary' predisposition - an autosomal gene of variable penetrance has been detected.
Vasodilators such as prostaglandins, bradykinins, 5-HT may be responsible for the development of clubbing. In bronchogenic carcinoma, vasodilator substances which are normally detoxified by lungs enters unaltered into systemic circulation
There is trapping of megakaryocytes and platelet clumps with local release of platelet-derived growth factor (PDGF) and other cytokines which increase the capillary permeability (latest and most acceptable theory). Arterial hypoxemia and neurohumeral stimulus produces hypervascularity and opening up of anastamotic channels in the nail bed which lead to overgrowth of soft tissue.
Possible mechanism of clubbing
The different hypothesis are
  • Anoxia- It is the most important theory which leads to opening up of deep arteriovenous fistula of the terminal phalanges. Fallot's tetralogy is an example
  • Toxic - Example is SBE.
  • Reflex theory- Vagotomy often improves the clubbing in bronchogenic carcinoma.
  • Metabolic causes - Example is thyrotoxicosis.
  • Humoral theory- Increased growth hormone, parathormone, bradykinin. eg. acromegaly. Pressure changes between the radial and digital arteries.
  • Reduced ferritin (may escape oxidation in lungs and leads to dilatation of  arteriovenous anastomosis by entering into systemic circulation) may play an important role (recent view).

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