Wednesday, June 17, 2015

BABINSKI SIGN - - - BABINSKI LIKE SIGN

Babinski sign- Mechanism & other Babinski like responses.


The Babinski sign 

This eponym refers to the dorsiflexion of the great toe with or without fanning of the other toes and withdrawal of the leg, on plantar stimulation in patients with pyramidal tract dysfunction.


 ni_2000_48_4_314_1509_2


The characteristic response is dorsiflexion of the great toe by recruitment of extensor hallucis longus (EHL) muscle.

The art of elicitation:
The reflexogenic area for the plantar reflex is the first sacral (S1) dermatome with the receptor nerve endings being located in the skin. The afferent nerve is the tibial nerve, the spinal cord segments involved in the reflex arc being 4th and 5th lumbar and 1st and 2nd sacral.
Position 
All the leg muscles should be visible and in a relaxed state. This can be achieved by positioning the patient in a way that the knee is slightly flexed and the thigh is externally rotated. The patient should be warned that the sole is going to be scratched and ask him to try to let his limb remain as floppy as possible. The toes should not be touched at all.
Stimulation Any part of the leg can be stimulated, but the best technique is to stimulate the lateral plantar surface and the transverse arch in a single movement upto the middle metatarsophalangeal joint with a firm applicator lasting 5 to 6 seconds. Difficulties are bound to arise in certain clinical situations which makes elicitation and interpretation of plantar response inconclusive. It is imperative that one realises these problems and be aware of their solutions in order to arrive at an appropriate clinical conclusion [Table II].
ni_2000_48_4_314_1509_1
Interpretation of the response
The plantar response may be:
1. Normal flexor plantar response
2. Pathologic or abnormal extensor plantar response (Babinski’s sign)

Normal flexor plantar response
In normal people after infancy, there is a plantar flexion of the foot and toes along with adduction of the toes. The primary movement is a plantar flexion of the great toe at the metatarsophalangeal joint, even if the terminal joint appears to extend. The response is a fairly rapid one and may be accompanied at times by an associated flexion of the hip and knee on the stimulated side. 
Abnormal extensor plantar response (Babinski’s sign)
The Babinski’s sign is encountered in patients with pyramidal tract dysfunction and is characterised by a dorsiflexion or extension of the great toe with or without fanning or abduction of the other toes. The fully developed response is also accompanied by dorsiflexion of the ankle and flexion of the hip and knee joint and slight abduction of the thigh, leading to a withdrawal of the leg on plantar stimulation. 
The Babinski sign is always pathological. There is no such thing as a negative Babinski sign.
mechanism:
In most mammals the limbs are automatically retracted on painful stimulation as a defence reflex, which is more pronounced in hind limbs. Sherrington called it, the flexion reflex synergy, because activation of all muscles effected shortening of the limb; the toe extensors forming part of this shortening synergy. Confusion has arisen from the application of the term extensor plantar response to a movement which forms part of a flexion synergy of the lower limbs. The toe 'extensors' although named extensors by anatomists, are infact flexors in a physiological sense because their action is to shorten the limb and contract reflexly along with other flexor muscles.
The Babinski sign may be a normal occurrence in the first year of life. In the infant, before  myelination of the nervous system is complete and an upright stance has been achieved, the normal plantar response is extensor, due to a brisker ‘flexion synergy’as part of the withdrawal response to pain. As the nervous system matures and the pyramidal tracts gain more control over spinal motor neurons, the ‘flexion synergy’ becomes less brisk and the toe ‘extensors’ are no longer a part of it. When the child assumes an upright posture, the plantar response becomes part of the postural reflex maintaining the tones of the foot and leg. At this time, the normal response to stimulation becomes a flexor movement of the toes and the ‘withdrawal extensor’ movement is suppressed by the influence of the pyramidal tract over the spinal reflex arc. The toe then goes down instead of up, as a result of a segmental reflex involving small foot muscles and the overlying skin.This is considered to be normal in adults and is termed - flexor plantar response. With lesions of the pyramidal system, structural or functional, this segmental downward response of the toes disappears, the flexion synergy may become disinhibited and the EHL muscle is again recruited into the flexion reflex of the leg producing the sign of 'Babinski'. The pyramidal tract thus maintains a suppressor action on the ‘flexion reflex’synergy. Pyramidal tract dysfunction however, allows the response to revert to the withdrawal movement by releasing or facilitating the ‘flexion reflex synergy’ of which contraction of the extensor hallucis longus muscle forms an integral part. A Babinski sign can appear only if the intraspinal pathways of the ‘flexion reflex synergy’are operative, however severe the motor deficit in the foot. The motor neurons of the
leg muscles are laminated into separate columns within the anterior horns of the cord, each of which supply proximal or distal flexor or extensor muscles. Both structural as well as functional lesions of the pyramidal tract fibres projecting onto the lumbosacral anterior horn cells and interneurons supplying the leg muscles subserving the ‘flexion reflex synergy’ can release the
Babinski sign. Reversible pathophysiologic conditions result in, or produce, a transient extensor plantar response.Structural lesions produce more lasting effects
The muscles taking part in a fully developed response include extensor hallucis longus, tibialis anterior, extensor digitorum longus, hamstring group of muscles and tensor faciae latae. The characteristic response is dorsiflexion (extension) of the [big toe], which precedes all other movements. It is followed by fanning out and extension of the other toes, dorsiflexion of the ankle and flexion of the hip and knee joint. This response represents 'positive' Babinski sign. There is no such thing as a 'negative' Babinski sign.
The dorsiflexion of the toes may be the only visible effect, but the contraction of the thigh and leg muscles is always present and can be detected by palpation. Contraction of the tensor fasciae
latae has been referred to as Brissaud’s reflex.
So the fully developed extensor plantar response forms part of the primitive ‘flexion reflex synergy’ of the lower limbs designed to withdraw the limb from a painful stimulus.
This spinal defence reflex mechanism described by Sherrington, activates all the muscles involved in
shortening the stimulated limb. It involves flexion of the hip and knee, dorsiflexion of the ankle and extension of the great toe. The ‘toe and foot extensors’ although named extensors by anatomists, are in fact flexor in a physiological sense, because their action is to shorten the limb and
contract reflexly along with other flexor muscles. The physiologist looks on the Babinski sign as simply a part of the ‘primitive flexion reflex’. 
The function of the pyramidal tract may not only be disturbed by structural lesions of myelin sheaths, axons, or both, but also by non-neurological conditions [Table I].ni_2000_48_4_314_1509_3 

Types of Babinski sign

a) Minimal Babinski sign : Contraction of hamstring muscles and tensor faciae latae.
b) True Babinski sign : Includes all the components of the fully developed extensor plantar reflex.
c) Pseudo Babinski sign : One may encounter this type of response in sensitive individuals, plantar hyperaesthesia, and choreo-athetosis due to hyperkinesis. True Babinski can be clinically distinguished from the false Babinski by the contraction of hamstring muscles in the former, and failure to inhibit the extensor response by pressure over the base of the great toe. The true Babinski sign is reproducible, unlike voluntary withdrawal of the toes.
d) Exaggerated Babinski sign : It can either be in the form of 'flexor spasm' or 'extensor spasm', depending upon the muscles i.e. whether flexors or extensors, have excess of tone. Flexor spasms occur in spinal cord disease, bilateral upper motor neuron lesion at a supraspinal level, multiple sclerosis and subacute combined degeneration of the cord, while 'extensor spasm' occurs in patients with corticospinal tract lesion when the posterior column function is normal.
e) Inversion of plantar reflex : If the short flexors of the toe are paralysed or flexor tendons are severed accidentally, an extensor response may be obtained.
f) Tonic Babinski reflex : Characterised by slow prolonged contraction of extensors of toe, seen in frontal lobe lesions and extrapyramidal involvement.
g) Crossed extensor response/bilateral Babinski sign : Unilateral stimulation produces bilateral
Babinski in patients with bilateral cerebral disease and spinal cord disease.
h) Spontaneous Babinski : In infants and children following manipulation of the foot, and in patients with extensive pyramidal tract diseases, passive extension of the knee or passive flexion of the hip and the knee, may produce a positive Babinski sign.

Alternate methods The late 19th and early 20th century was abound with disclaimers associated with founders of new reflex movements of the great toe. These movements are known by the term 'Babinski like responses'. These responses can be elicited by the following techniques, each with its own eponym.
  1. Chaddock's sign:The extension of the big toe may be obtained by stimulating the dorsal lateral aspect of the foot from the posterior portion of the skin beneath the external malleolis anteriorly along the external edge of the foot.
  2. Gordon's sign: squeezing the calf muscle
  3. Oppenheim sign: applying pressure along the shin of tibia
  4. Gonda's sign: pressing the 4th toe downwards and then releasing it with a snap
  5. Stransky sign: vigorous adduction of the little toe followed by its sudden release
  6. Schaefer's sign: squeezing the Achilles tendon
  7. Rossolimo's sign: flexion of the toes, on quick percussion of the tips of the patients toes with the finger tip
  8. Mendal Bechtrew sign: flexion of the four outer toes induced by tapping the dorsum of the foot in the region of cuboid bone
  9. Bing's sign:  giving multiple pinpricks on dorsolateral surface of the foot
  10. Moniz sign: forceful passive plantar flexion of the ankle
  11. Throckmortan sign: pressing over the dorsal aspect of the metatarsophalangeal joint of the great toe
  12. Strumpell sign: application of forceful pressure over anterior tibial region
  13. Cornell sign: scratching the dorsum of the foot along the inner side of the extensor tendon of the great toe
  14. plantar flexion and fanning of the toes on tapping the mid plantar region of the foot or base of the heel.
Most of these signs imply an increase in the reflexogenous zone and denote responses from different parts of the receptive field. When sufficiently facilitated, the reflex may be elicited by other stimuli as well. Infact, in extreme cases of UMN deficit, the complete ‘flexion reflex’ may be exhibited spontaneously and continuously; the patient lies in bed, the hip and knee flexed, and the ankle and great toe dorsiflexed. In other cases of severe UMN deficit, almost any unpleasant stimulus, such as scratching, pinching, or pricking, will evoke the ‘flexion reflex’, even when applied as high as the thigh, far from the usual reflexogenous zone.

Fallacies 
An extensor response may be present when there is no damage to the pyramidal tract. A possible explanation being the excitation of the distal motor neurons and inhibition of the impulses via flexor reflex afferent
nerve fibres can be dissociated because they are mediated by different neurons, however closely linked. On the contrary, cases with proven damage to the pyramidal system have had normal plantar response. We should understand that corticospinal fibres not only originate in different parts of the cortex, but also have different terminations. Babinski sign can be expected only when 'leg fibres' of the pyramidal tract are involved. Plantar areflexia can be noted in cases with loss of sensation of sole due to lesion of the first sacral cutaneous distribution. The same can be observed in paralysis of extensors or long flexors of great toe. In spinal shock, cessation of tonic discharge of spinal neurons by excitatory impulses in descending pathways may explain its non existence. Drugs like parenteral physostigmine in physiological doses may also abolish a plantar response.
    »   Conclusion        
Despite the continuing controversy and observer bias, clinical utility of Babinski sign remains unchallenged. The role of pyramidal system in the pathophysiology of this sign is quite clear. Pyramidal tract dysfunction releases the flexion reflex synergy, of which contraction of the extensor hallucis longus muscle forms an integral part. The most important and vital question in interpreting the plantar response is not, whether the great toe goes up or not, but is whether an upgoing toe is pathological or not. For an appropriate answer the method of observation is much more important than the method of elicitation.

IMPORTANT TRIADS IN MEDICINE

IMPORTANT TRIADS IN MEDICINE

►TRIAD OF ALPORT'S SYNDROME --
• SENSORINEURAL DEAFNESS,
• PROGRESSIVE RENAL FAILURE,
• OCULAR ANOMALIES
►TRIAD OF BEHCET'S SYNDROME --
• RECURRENT ORAL ULCERS,

• GENITAL ULCERS,
• IRIDOCYCLITIS.
►BECK'S TRIAD --
• MUFFLED HEART SOUND,
• DISTENDED NECK VEINS,
• HYPOTENSION.
►CHARCOT'S TRIAD --
• PAIN+FEVER+JAUNDICE
►GRADENIGO'S TRIAD -
• SIXTH CRANIAL N. PALSY,
• PERSISTANT EAR DISCHARGE,
• DEEP SEATED RETRO-ORBITAL PAIN
►Triad Of Hypernephroma --
• pain+
• hematuria+
• renal Mass
. ►Triad of Wilm's tumor:
• Fever +
• Mass +
• Hematuria
►Hutchinson's Triad ---
• Hutchison's Teeth,
• Interstitial Keratitis,
• Nerve Deafness.
►Triad Of Kwashiorkar-
• Growth Retardation,
• Mental Changes,
• Edema.
►Saint's Triad ---
• Gall Stones,
• Diverticulosis,
• Hiatus Hernia.
►Trotter's Triad --
• Conductive Deafness,
• Immobility Of Homolateral Soft Palate,
• Trigeminal Neuralgia.
Mnemonic: NPC- neuralgia, palatal paralysis, conductive 

deafness
►VIRCHOW'S TRIAD --
• STASIS+
• HYPERCOAGULABILTY+
• VESSEL INJURY.
►SAMTER'S TRIAD --
• ASPIRIN SENSITIVITY,
• BRONCHIAL ASTHMA,
• NASAL POLYP.
►Grancher's triad--
• lessened vesicular quality of breathing,
• skodaic resonance, and
• increased vocal fremitus; seen in early pulmonary tuberculosis.
►Osler's triad--
• telangiectasis,
• capillary fragility, and
• hereditary hemorrhagic diathesis seen in hereditary

hemorrhagic telangiectasia.
►BARTTER'S SYNDROME -
• METABOLIC ALKALOSIS,
• HYPOKALEMIA,
• NORMAL OR DECREASED BP.
►Weil's Disease--
• Hepatorenal Damage,
• Bleeding Diathesis,
• Pyrexia.
►Meniere's Disease --
• Vertigo,
• Tinnitus,
• Sensorineural Hearing Loss.
►Melkersson Rosenthal Syndrome--
•recurrent Facial Palsy,
•Plication Of Tongue,
•Facial Edema.
►Parkinsonism--
•Rigidity,
•Tremor

•Hypokinasia
►Cushing's traid --
•Bradycardia,
•hypertension &
•irregular respirations in increased intracranial
pressure.
►Kartagener’s Syndrome--
•bronchiectasis,
•Recurrent sinusitis, and
•Situs inversus.
►Hemobilia(Triad of Sandblom)--
•Malena,
•Obstructive jaundice,
•Biliary colic.
►Murphy's triad(in order)-
•Pain,
•Vomitting,
•Fever.
►WHIPPLE'S TRIAD Of INSULINOMA--
•HYPOGLYCAEMIA DURING ATTACKS,
•S.GLUCOSE <40 mg%,
•PROMPT RELIEF ON GLUCOSE ADMINISTRATION.
►Triad of HUS
•hemolytic anemia +
•acute renal failure +
•thrombocytopenia
►Triad of alkaptonuria
•Homogentistic aciduria
• Black pigmentation of cartilage and collagenous tissue

•Ochronotic arthritis
►Classic triad of Chronic mercury poisoning
•Excessive salivation and gingivitis

•Tremors
•Neuropsychiatric changes
►Adams triad or Hakim's triad for Normal Pressure 

•Hydrocephalus
•urinary incontinence,
•gait disturbance, and dementia
►Bezold's triad: Three symptomatic indications of 

otosclerosis:
•diminished aural perception of low frequency tones,
• retarded bone conduction,
• negative Rinne test
►Hand-Schüller-Christian disease triad of
•exophthalmos,
•lytic bone lesions (often in the skull), and
•diabetes insipidus
►UNHAPPY TRIAD
An unhappy triad (or terrible triad, "horrible triangle",

O'Donoghue's triad or a "blown knee") is an injury to the

anterior cruciate ligament, medial collateral ligament, and

the meniscus. The triad refers to a complete or partial tear of

the anterior cruciate ligament, medial collateral ligament,

and the meniscus.

►Dieulafoy's triad:
•hyperesthesia of the skin,
•exquisite tenderness and
•guarding over McBurney's point, considered a classic sign

of acute appendicitis
►Vogt Triad of tuberus sclerosis: Mental Retardation

Adenoma Sebaceum Seizures
►Miller fisher syndrome:Variant of GBS. It usually affects the

eye muscles first and presents with the triad of 

•ophthalmoplegia, •ataxia, and •areflexia.
►Classic triad of Wernicke encephalopathy are 

•encephalopathy, •ataxic gait, •ophthalmoplegia!
►Carney Triad :::
•gastric epithelioid leiomyosarcoma (these are now known to 

actually be malignant gastrointestinal stromal tumors),
• pulmonary chondroma, and
•extra-adrenal paraganglioma. .
►Atta's triad of bilharzial dysentery:-.
•Bleeding per rectum.
•Polyposis.
•Clubbing of fingers
►Loeys-Dietz syndrome is phenotypically distinct from 

Marfan syndrome... Loeys-Dietz syndrome is an aggressive, 

autosomal dominant condition that is distinguished by the 

triad of
•arterial tortuosity and aneurysms,
•hypertelorism (widely spaced eyes), and
•bifid uvula or cleft palate.
►Classic triad in Gardner's Syndrome:
colonic polyps
bone tumors
soft tissue tumors
►Borchardt's triad
epigastric pain, nausea, inability to pass nasogastric tube..

seen in gastric volvulus
►Triad of shaken baby syndrome:
•subdural

•hematoma , retinal hemorrhage , and
•cerebral oedema.
►Beck's cognitive triad is a triad of types of negative thought present in depression:
•The self (i.e., self is worthless)
•The world/environment (i.e., world is unfair), and
•The future (i.e., future is hopeless).
►Felty triad
•Neutropenia
•RA
•SPlenomegaly
►Behcet's syndrome
The clinical triad of uveitis with recurrent oral and genital ulcers--
►Macdonald triad
The Macdonald triad is a set of three behavioral 

characteristics which are associated with sociopathic

behavior. These behavioral characteristics are found in the

childhood histories of individuals with sociopathic behavior:
•Enuresis (bedwetting)
•Firesetting
•Torturing small animals
►MARSHALL'S TRIAD, when considering the pathology of
trauma of bomb explosions. The triad includes
•punctate-bruises,
•abrasions and

•small punctate lacerations all of which are typically found in 

an explosive bomb blast. Although many similarities exist 

between injury patterns seen in lightning and concussive 

injuries, Marshall's Triad findings are not typically found in 

lightning strike injuries.


►Van der Hoeve syndrome presents with the triad of 

•osteogenesis imperfecta,
•otosclerosis and
•blue sclera.
►Classical triad of Aortic stenosis(valvular dx)-
• dyspnea,
• angina and
• syncope.
►the classic Rigler's triad of gallstone ileus:
• pneumobilia;
• small bowel obstruction; and
• an ectopic gallstone
►VIRchow’s triad for venous thrombosis:
Vascular trauma
Increased coagulability
Reduced blood flow
►Mackler's triad which includes
• chest pain,
• vomiting and
• subcutaneous emphysema,
while classical, is only present in 14% of

people with Boerhaave syndrome .


►Ohashi triad:
• Neoplasms with mucin hyper— production,
• dilatation of the duct of Wirsung, and
• protruding papilla (the Ohashi triad)
►Abnormalities in Congenital Rubella: Triad of Gregg :
• cataract,
• deafness, and
• heart defect
►Currarino syndrome (or triad) is defined as a partial sacral 

agenesis associated with a presacral mass and ano-rectal 

malformation.

►Triad of alkaptonuria
• Homogentistic aciduria
• Black pigmentation of cartilage and collagenous tissue
• Ochronotic arthritis

►Dieulafoy's triad::
• Hypersensitivity of the skin,
• tenderness and
• muscular contraction at McBurney's point in acute 

appendicitis.
►Triad of somatostatinoma:-
• Diabetes mellitus
• Steatorrhoea 
• CholecystolithiasisChat Conversation End

Tuesday, June 16, 2015

Why we don’t get Heart Cancer?

Why we don’t get Heart Cancer?



We all heard of cancers of the brain, blood, lymph nodes, lungs, bone, and every other bodily organ, part, or system imaginable. Have you heard about heart cancer?

Heart long symbolized as the root of loving emotion are somehow immune to the dreaded disease. Tumors occur in the heart also, but are not as common as other parts, so don't hear about them.

Malignant heart tumors, known as rhabdomyosarcomas, are extremely rare. Sarcoma is a type of tumor that originates in the soft tissues of the body, a rhabdomyosarcoma occurs in the muscle tissue of the heart. Their incidence is estimated at less than 0.1 percent, based on a study of more than 12,000 autopsies, which identified only seven cases of any kind of primary cardiac tumor. Most cancers found in the heart are secondaries, have come from elsewhere in the body.

Cancer begins when cells start to grow out of control. This is due to damaged DNA, the genetic material carried in the nucleus of each and every cell. Normally, a cell repairs any damaged DNA, or simply dies, but cancer cells do not repair or die. Instead, they divide and make many more abnormal cells with damaged DNA. Another unusual property possessed by cancer cells is they are able to grow and invade other tissues. Normal cells cannot do the same.

Cancers in the heart have come from “elsewhere in the body,” means an invasion. The cancer began somewhere else in the body and it has infiltrated the heart. This is called secondary tumor. The most common secondary tumors spreading to the heart “come from the lung, from the esophagus, and from the liver, and the stomach. Even nests of leukemia cells form tumors in the heart. More importantly, all of these different types of tumors “usually go to the right side of the heart. That’s where the blood enters the heart, on the right side.

A tumor is a tumor. How do doctors know where a tumor originates especially when a new tumor appearing years later in a part of the body far from the original cancer site? When a new tumor appears, its cells are identical to those of the original tumor. So if a person had pancreatic cancer, and it spread to the brain, the tumor appearing in their brain, when viewed through a microscope, would look nothing like the tumor of a person with brain cancer, the cells of this brain tumor would look identical to pancreatic tumor cells.

If secondary tumors invade the heart, why is it so rare for primary tumors to develop there? 

Genetic fate is sealed. One receives half the genes from mothers and half from father. The gene expression can be modified throughout the life and that can create cancer. Environment affects which genes become expressed (activated) as well as how frequently they become activated.

Carcinogens coming from the food and environment are one of the many factors that influence which genes are activated or not. Human body has some defenses against these contaminants, in the form of detoxifying enzymes, and the body is supported by micronutrients which turn on tumor suppressor genes, dangerous toxins found in the fat tissue still modify the genes, which can result in cancers forming in the organs of the body, especially those containing fatty tissue. A lot of toxins are found in breast tissue, because there are a lot of fat cells there. And toxins are found wherever there is the most fat. This is why the heart is so exceptional. There’s not much of fatty tissue in the heart. The heart is enclosed in a membrane, the pericardium. This fluid-filled sac itself become engulfed by cancer, with tumors metastasizing to the outside of it, but still it does its job of protecting our precious hearts.

So, even though cancer can happen anywhere there are cells, your heart remains virtually immune due to its muscular nature and the assistance of the pericardium. Smart heart.






Dr. Jacqueline Barrientos,
Assistant professor, Hofstra North Shore-LIJ School of Medicine 
Dr. Mitchell Gaynor,
Assistant professor at Weill Cornell Medical College

Thursday, June 11, 2015

BREATH SOUNDS : NORMAL AND ABNORMAL MNEMONICS

Breath sounds mnemonic



Breath sounds!

Vesicular sounds:
Inspiration is longer than expiration. No pause in between.
They are normal. 

Mnemonic:-
VE is short. (Expiration is short)
VesI is long. (Inspiration is long)

Bronchial breath sounds:
Inspiration and expiration occupy the same duration of time and are separated by a pause.
Heard in:- Consolidation or a large cavity. 

Mnemonic:-
B for Bronchial, B for Both are equal.
Broncho-vesicular sounds:
Both are equal with a pause.
Heard in: Bronchial asthma, Emphysema. 

Mnemonic:-
The B for Both are equal. The hyphen reminds me of the pause.

Abnormal breath sounds: Crackles, Wheeze, Rhonchi and Stridor


Crackles (Also Known as Rales)

What do crackles sound like? 

Roll your hair between your fingers next to your ear.. That's what fine crackles sound like! (Or the sound of salt heated on a frying pan, if you've ever tried cooking :P)
Coarse crackles sound like ripping open Velcro.

When are crackles heard?
Crackles are much more common during the inspiratory than the expiratory phase of breathing, but they may be heard during the expiratory phase.

Mechanism of crackles:
Crackles are the sounds you will hear in a lung field that has fluid in the small airways or if atelectasis is present.

Causes of crackles:
Crackles is often a sign of adult respiratory distress syndrome, early congestive heart failure, asthma, and pulmonary edema.

Rhonchi
What do Rhonchi sound like?
Try making a snoring sound or try to make a sound as if you're gargling your mouth. That's what Rhonchi sounds like!

When are Rhonchi heard? 
Rhonchi are more prominent on exhalation.

Mechanism of Rhonchi:
Secretions in large airways, as occurs with bronchitis, may produce these sounds; they may clear somewhat with coughing.

Causes of Rhonchi:
Pneumonia, chronic bronchitis, and cystic fibrosis are patient populations that commonly present with rhonchi.

Wheezes
What do wheezes sound like? 
Try whistling slowly while exhaling.. That's what wheezes sounds like! Wheezes are continuous musical tones. 

When do wheezes occur? 
Wheezes are most commonly heard at end inspiration or early expiration.

Mechanism of wheeze:
As the airway lumen becomes smaller, the air flow velocity increases resulting in harmonic vibration of the airway wall and thus the musical tonal quality. They result as a collapsed airway lumen gradually opens during inspiration or gradually closes during expiration. 

Causes of wheezes:
Heard when listening to an asthmatic patient. Sibilant wheezes are caused by asthma, congestive heart failure, chronic bronchitis, and COPD too.
PS: Wheeze is also known as sibilant rhonchi. 
Rhonchi is also known as sonorous wheeze.

Stridor
What does stridor sound like? 
Stridor are intense, high-pitched, continuous monophonic wheezes (musical sound) heard loudest over extrathoracic airways.  Similar to a creaking or a grating sound.

When is stridor heard? 
They tend to be accentuated during inspiration when extrathoracic airways collapse due to lower internal lumen pressure.

Mechanism of stridor:
It usually caused by a foreign body obstruction of the larger airways, such as the trachea or a main bronchus.

Causes of stridor:
It is also the most common type of breath sound heard in children with croup (Laryngotracheobronchitis caused by parainfluenza) and a foreign body airway obstruction.
Also heard in Bacterial tracheitis, Diphtheria, Epiglottitis (H. Influenza) and Broncholitis (RSV).

Stertor
What is Stertor?
It is like stridor but it's more harsh, less musical and low pitched.

Mechanism of stertor: Respiratory sound that originates from pharynx, basically, anywhere  above larynx.

Causes of stertor: Seen in partial obstruction  of airway above larynx characterised by heavy snoring  and gasping like in obstructive sleep apnea.