Physioworld's blog

Stress test uses and procedure

2022-06-09T21:20:00.002-07:00

Stress test uses and procedure

The stress test is also called a Treadmill test, stress ECG, nuclear stress test, stress echocardiogram, or treadmill test. There are 3 main types of stress tests: nuclear stress tests, stress echocardiograms, & exercise stress tests.

The stress test is used to find heart disorders. During physical activity, the heart pumps more complex and faster. The stress test assesses heart function using the treadmill or stationary bike.

Stress Test

Uses of stress tests?

Most often used for diagnosis of:

Coronary artery disease
Heart attack or other serious heart conditions
Arrhythmia

It also finds out what level of exercise is safe for an individual and how well treatment is working.

Why stress test is needed?

Angina
Rapid heartbeat
Arrhythmia
Shortness of breath
Recent heart surgery
Family history of heart problems.

Procedure

During an exercise stress test:

Electrodes are placed on the arms, legs, and chest.
Electrodes are attached by wires to an EKG machine. This EKG machine records the electrical activity of the heart.
The health care provider then tells you to initially start walking slowly on a treadmill or ride a stationary bike. Then after a few minutes, you will be asked to walk or pedal faster with the incline and resistance.
The target heart rate is set by the provider, you will be asked to continue walking or riding until you reach a target heart rate.
If you feel dizziness or fatigue the test will stop.
After the test, you will be monitored for 10-15 minutes.

Treadmill Test

During a nuclear stress test:

The health care provider will ask you to lie down on an examination table.
The Healthcare provider will insert radioactive dye through an intravenous (IV) into your arm. This dye helps to view images of the heart clearly.
Heart absorb dye between 15-20 minutes. A special camera will inspect or scan the heart.
As the nuclear stress test is an imaging test, the camera will create images of the heart when the heart is at rest.
You will be hooked up to an EKG machine, then you will be asked to walk on the treadmill or ride a stationary bike.
The health care provider will compare two Images of the heart: when the heart is at rest and another white exercising.
After the test, you will be monitored for 15-20 minutes or until you feel normal.

During a stress echocardiogram

The health care provider will ask you to lie down on an examination table.
The health care provider will rub a special gel on a transducer and create moving pictures of the heart.
The transducer is held against your chest. This device makes sound waves.
After these images, the healthcare provider will ask you to walk on the treadmill or ride a stationary bicycle.
Then images of the heart are taken when it is working at its hardest.
The Healthcare provider will compare 2 sets of images: A heart at rest & another one when the heart is working.
After the test, you will be monitored for 15-20 minutes or until you feel normal.

Hope you all find this helpful for you, if you have any queries related to this topic or any other topic then you all are free to contact me via contact us or you can also ask your doubts in the comment box. Thank you!

Disclaimer for https://physioworldblog.blogspot.com/ If you require any more information or have any questions about our site's disclaimer, please feel free to contact us by email at deepikajoshi12347@gmail.com. Disclaimers for Physioworld's blog All the information on this website - https://physioworldblog.blogspot.com/ - is published in good faith and for general information purposes only. Update Should we update, amend or make any changes to this document, those changes will be prominently posted here.

Thoracic cage abnormalities and their management

2022-01-31T09:04:00.008-08:00

Thoracic Cage abnormalities and their management

Hello students and friends, today we are going to discuss what are the abnormalities seen in a thoracic cage or rib cage. These abnormalities can develop due to any disease or trauma to the rib cage.

What is thoracic cage abnormality?

Thoracic cage abnormalities include:

PECTUS EXCAVATUM

It is a congenital or genetic condition in children where several ribs and sternum (breastbone) grow abnormally inward. This gives a hollow appearance in the center of the chest. The posture of the patient also gets disturbed.

Also called “sunken chest” or “funnel chest.”
It can be mild, if it becomes severe then it can affect the heart and lungs. When it becomes severe, it may lead to breathlessness, chest pain, and irritation.

Treatment

Surgical repair is done under local anesthesia. Repair is typically done in the teenage years, once the pubertal growth spurt is completed.
Ravitch procedure and minimally invasive repair (Nuss procedure) are done to correct the deformity.

PECTUS CARINATUM

Anterior protrusion of the chest due to abnormal growth of the cartilages of the rib bones and the sternum. The costal cartilage overgrows forward or outward. There can be asymmetry of the chest (one side more prominent than the other).

Also known as pigeon chest.
Boys>Girls
The heart and lungs don’t get affected. It is not always present at birth rather it can get worsen as the child grows older.
Associated with disorders including heart disease, scoliosis, kyphosis, Down syndrome, and Marfan syndrome.

Treatment

Bracing of the chest wall;
Surgery is usually not needed and it is done under local anesthesia.
Ravitch procedure is done through a horizontal chest incision (mid-chest). Abnormal costal cartilages are drawn, preserving the lining that covers the outside of the cartilage, allowing the sternum to be driven downward in a more normal position.

Impingement Syndrome and its types

2021-08-21T01:24:00.006-07:00

Impingement Syndrome and its types

Hello students and friends, today we are going to discuss what is impingement syndrome and its type.

Impingement syndrome is also called shoulder impingement syndrome.

Shoulder impingement syndrome occurs when acromion rubs against the rotator cuff, causing pain and irritation. It's a clinical syndrome within which soft tissue becomes painfully entrapped within the enarthrodial joint space (shoulder joint area).

What is the role of the rotator cuff muscle?

The rotator cuff consists of muscles and tendons. These muscles and tendons keep the ball of the humerus in the socket and help in arm rotation. Rotator cuff muscles include:

Supraspinatus
Infraspinatus
Teres minor
Subscapularis.

These 4 muscles originate on the shoulder blade and attach as a "cuff" of the tendon on the humerus.

These rotator cuff muscles sit on a small space between the acromion and the humerus, because of this arrangement of rotator cuff it becomes more susceptible to impinge which leads to impingement syndrome.

Clinical manifestations

The affected patients are generally over 40 years of age. These patients generally suffer from persistent pain without any known preceding trauma.

Shoulder impingement may be caused due to excessive stress on the shoulder joint or it can be caused due to any injury.

Types of impingement syndromes

Shoulder impingement syndrome is classified into 4 types:

Subacromial impingement syndrome(external impingement)
Subcoracoid impingement
Posterosuperior inner impingement
Anterosuperior inner impingement.

Subacromial impingement syndrome

Commonest type.
In subacromial impingement syndrome, the elevation of the arm ends up in abnormal contact between the rotator cuff muscle and therefore roof of the shoulder.

Subcoracoid impingement syndrome

Less common.
Subscapularis tendon impinges between the coracoid and the humerus (lesser tuberosity). This causes pain & tendinosis in the soft tissue structure.

Posterosuperior inner impingement

Also known as internal impingement syndrome.
An uncommon form of shoulder impingement.
Primarily it involves the infraspinatus tendon and the posterosuperior glenoid labrum.
It occurs in the ABER position ( the shoulder is abducted and externally rotated).

Anterosuperior inner impingement syndrome

Impingement of the subscapularis tendon between the anterior humeral head and the anterosuperior glenoid and labrum during flexion (forward) of the arm.

Hope you all find this helpful for you, if you have any query related to this topic or any other topic then you all are free to contact me via contact us or you can also ask your doubts on the comment box. Thank you!

Disclaimer for https://physioworldblog.blogspot.com/ If you require any more information or have any questions about our site's disclaimer, please feel free to contact us by email at deepikajoshi12347@gmail.com. Disclaimers for Physioworld's blog All the information on this website - https://physioworldblog.blogspot.com/ - is published in good faith and for general information purpose only. Update Should we update, amend or make any changes to this document, those changes will be prominently posted here.

Mechanism of respiration

2021-08-12T04:10:00.010-07:00

Mechanism of respiration

Hello students and friends, today we are going to discuss the mechanism of respiration or how our lung helps in breathing. Here we will learn the steps involved in the mechanism of respiration and how respiration takes place.

What is breathing?

Breathing is a process that involves in and out of the air from the lungs. This process is carried out by various respiratory organs of our body. Inhalation of air is the process in which oxygen-rich air goes into the lungs and exhalation is the process in which carbon dioxide-rich air goes out from the body.

The breathing rate of a normal adult= 15-18 times per minute.

During heavy exercise= exceeds 25 times per minute.

Mechanism Of Breathing

Mechanism of breathing involves two processes:

Inspiration
Expiration

Inspiration

In the process of inspiration, there is the contraction of muscles that are attached to the outer side of the ribs. These muscles pull out the ribs and result in an expansion of the chest cavity.

Diaphram contracts and moves downwards resulting in expansion of the chest cavity and contraction of abdominal muscle takes place.

A partial vacuum is made within the thoracic cavity which sucks air into the lungs and fills the expanded alveoli.

Mechanism Of Inspiration

It is an active process in which the intake of atmospheric air takes place.
When the volume of the thoracic cavity (rib cage) increases and the air pressure decreases, inspiration takes place.
The volume of the thoracic cavity(rib cage) increases due to the contraction of external intercostal muscles.
Contraction of the diaphragm further increases the dimension of the chest cavity. Simultaneously expansion of lungs takes place.
As the lungs expand pressure of the air inside the lungs gets decreased.
The pressure equalizes and therefore the atmospheric air which is inhaled rushes inside the lungs.

Expiration

In the process of gaseous exchange, when the air is expelled out, expiration takes place.

During the process of expiration, the muscles which are attached to the ribs contract, and the muscles of the diaphragm and abdomen relax.

The volume of the chest cavity decreases so the pressure inside the lungs increases. When the pressure increases the air in the lungs is pushed out and expiration takes place.

Mechanism Of Expiration

It is a passive process.
Carbon dioxide is exhaled out in the process of expiration.
Expiration occurs when the size of the thoracic cavity decreases and the pressure of the air outside increases.
As the pressure gets increased, the external intercostal muscles relax and internal intercostal muscles contract.
When muscles contract and relax, the ribs are pulled inwards and therefore the size of the chest cavity is reduced.
Diaphragm gets to relax and the lung compressed.
Consequently, the pressure of air increases, and therefore the air is forced out.

Mechanism of Respiration

It involves an exchange of gases and breathing mechanisms.

Exchange of Gases

Transport of Oxygen

Oxygen within the blood is carried to the tissue by two forms-

Oxyhaemoglobin- chemical composition of oxygen with haemoglobin(Hb), and solution of oxygen in plasma.

The O2 in the blood combines with haemoglobin(Hb) when the concentration of oxygen is high in the blood.
Oxyhaemoglobin, being unstable, dissociates to release oxygen. Low O2, low pH and high temperatures stimulate the dissociation process.

Internal Respiration

When the gaseous exchange takes place in the tissues, it is known as internal respiration.

Here, the oxygen carried in the form of oxyhaemoglobin gets dissociated to release oxygen.

This oxygen breaks down the glucose to release CO2, H2O, and energy. The energy is utilized by the body, while carbon dioxide is diffused from the tissues.

2. Transport of CO2 from Tissues to the Lungs

CO2 is transported by 3 mechanisms:

Some CO2 dissolves in the water of plasma to form carbonic acid.
Carbonic acid ionizes to form bicarbonate ions.
The H+ ions are catalyzed by the enzyme carbonic anhydrase.
Bicarbonates ions combine with sodium(Na+) and potassium(K+) to form sodium bicarbonate and potassium bicarbonate.
Some carbon dioxide(CO2) combines with haemoglobin for the formation of carbaminohemoglobin.
At last, it is carried to the lungs and released out by the body through the method of expiration.

Respiratory Gas Transport

After the blood becomes oxygenated, and carbon dioxide is removed, the next phase is the transportation of oxygen-rich blood to the tissues. The cardiovascular system contributes to the transportation of gases. It consists of blood vessels and the heart.

The oxygenated blood leaves the lungs and enters the heart through the pulmonary veins(the only vein which carries oxygenated blood).

Then the blood is pumped to the rest of the body from the left ventricle through the aorta and its corresponding branches.

Disclaimer for https://physioworldblog.blogspot.com/ If you require any more information or have any questions about our site's disclaimer, please feel free to contact us by email at deepikajoshi12347@gmail.com. Disclaimers for Physioworld's blog All the information on this website - https://physioworldblog.blogspot.com/ - is published in good faith and for general information purpose only. Update Should we update, amend or make any changes to this document, those changes will be prominently posted here.

Lung abscess

2021-08-09T20:38:00.001-07:00

Lung abscess

Hello students and friends, today we are going to discuss what is lung abscess is and how it affects our body. Here we will learn how we can treat this condition by using medical and physiotherapy approaches.

A lung abscess is a pus-filled cavity within the lung surrounded by inflamed tissue that sometimes results from bacteria(i.e breathing bacteria) that normally live in the mouth or throat into the lungs, leading to an infection.

Is Lung abscess is serious?

A collection of pus in the lung tissue dies due to infection, which makes lung abscess life-threatening. If it lasts for under 4-6 weeks, then it is considered acute. If it lasts for longer then it is considered chronic.

What happens if a lung abscess ruptures?

Formation of bronchopleural fistula takes place which causes secondary empyema. This condition arises when there is no proper management of lung abscess in acute form by giving postural drainage and appropriate antibiotics.

Do we drain lung abscesses?

Yes, lung abscesses drain spontaneously during the course of therapy by using bronchoscopy and chest physiotherapy. Thoracocentesis and thoracotomy can be done.

Symptoms of lung abscess

Mainly symptoms are seen slowly in the patients. They may include:

Breathing difficulty or chest pain during breathing
Cough
Sweating in the nighttime
Cough is seen with sputum
Formation of pus with sputum(streaked with blood)
Weight loss
Fever
Fatigue
Loss of appetite
Bad breath
Clubbing

Cause of Lung Abscess

Primary lung abscess

In primary lung abscess, there is an infection caused within the lungs.

It mainly occurs due to the consumption of alcohol. As a person drinks alcohol he experiences an altered level of consciousness, nausea, and even vomiting, this results in inhalation of stomach content and bacteria into the lungs through which infection is caused.

Alcohol also weakens the immune system. When immune systems get weak, there are more chances of getting an infection.

Another cause of primary lung abscesses is pneumonia(Aspiration Pneumonia).

Secondary lung abscess

Occurs due to:

Obstruction of the large airways of the lungs
The infection spread from any other part of the body to the lung
Coexisting diseases in the lungs.

The ratio of secondary lung abscess is less than primary lung abscess.

Complications

Empyema
Bronchopleural fistula
Secondary amyloidosis
Gangrene of the lungs
Bleeding into the lungs(hemorrhage).

Diagnosis

History of the Patient
X-ray or CT scan
A bronchoscope (take a sample of fluid from the area of the abscess to diagnose)
If pus or sputum is detected, then they will analyze the sputum or pus.

Treatment

Primary treatment of lung abscess includes antibiotics( typically this treatment lasts 3 weeks - 8 weeks).
Avoid smoking.
Some cases are treated with invasive procedures- A tube can be inserted to drain pus from the abscess.
Surgery can be used to remove infected or damaged lung tissue.
If in case of antibiotics don't work then lung drainage is done. Drainage of the lung is done via inserting a needle through the chest wall or through bronchoscopy and endobronchial ultrasound(US).

Disclaimer for https://physioworldblog.blogspot.com/ If you require any more information or have any questions about our site's disclaimer, please feel free to contact us by email at deepikajoshi12347@gmail.com. Disclaimers for Physioworld's blog All the information on this website - https://physioworldblog.blogspot.com/ - is published in good faith and for general information purpose only. Update Should we update, amend or make any changes to this document, those changes will be prominently posted here.

Septic arthritis and its aetiopathogenesis

2021-01-12T00:03:00.002-08:00

Septic arthritis and its aetiopathogenesis

Hello students and friends, today we are going to learn what is septic arthritis, its aetiopathogenesis, symptoms, diagnosis, treatment, and complications.

Firstly we have to know the meaning of septic and arthritis.

Septic: sepsis is a term that generally refers to a severe infection that transmits via the bloodstream.

Arthritis: swelling and pain in the joints.

Now let's discuss what is septic arthritis?

Septic arthritis is caused by pyogenic organisms that is why it is also termed as pyogenic arthritis, infective arthritis(as there is an infection in a joint through the bloodstream), or supportive arthritis.

There is a painful infection in the joint which is typically acute at present, but it may present as sub-acute or chronic arthritis.

Commonest joint affected- Knee joint is more prone.

Other joints- Hip joint, shoulder joint, Elbow joint.

Aetipathogenesis

Males>Females.
Commonly children are affected.
Staphylococcus aureus is the commonest causative organism.

Other organisms are:

Streptococcus pneumococcus
Gonococcus.

Other predisposing factors are:

Poor hygiene
Diabetes
Poor resistance

Infants and elderly ones are at higher risk of developing septic arthritis.
Septic arthritis can also occur due to any injury through which germs enter into the joint.
The organisms will follow any of the following routes to reach the joint and cause septic arthritis-

Hematogenous route

It is the commonest route.
Infection is caused in the form of pyoderma, septicemia, throat infection, etc.

Penetrating wound

By penetrating any cut wound organism may enter and cause septic arthritis.
Commonly knee joint is affected.

Iatrogenic

Infection may cause during femoral artery puncture or by intra-articular steroid injection used in different arthritis.

Umbilical cord sepsis

Sepsis in infants.
When sepsis occurs in the umbilical cord it can travel to the joints.

~When organisms reach the joint by following any of the above routes, there is an inflammatory response generated in the synovium which results in the exudation of fluid within the joint.
~In joint exudate, inflammatory granulation tissue, and lysosomal enzymes are present which destroys the joint cartilage.
~As joint cartilage is destroyed and exudation of joint fluid is caused, at the latter stage there is a complete loss of movement in the joints(ankylosis).

Symptoms

Swelling in the joint
The joint area becomes red and warm
Fever
Discomfort
Difficulty in using affected limb.

Diagnosis

Diagnosis in an early stage is important for improvement in joints.

1. Physical examination

A child with acute septic arthritis shows the following symptoms-

Swelling
Redness
Acute septic arthritis is associated with high-grade fever and malaise.
Difficulty in using affected limb.
Throbbing pain.

A child with subacute septic arthritis shows the following symptoms-

A child does not allow anybody to touch the joint.
The movement of the joint is improper.
Painful limps in the lower limb can be noticed.
Some amount of joint movement is possible.

By palpating the joint we can diagnose high temperature around the joint, tenderness, and effusion.

When any active or passive movement is initiated, there is severe pain and muscle spasm is seen.

2. Radiological examination

X-ray- It helps in the diagnosis of joint spaces and soft tissue shadow corresponding to the distended capsule due to swelling of the joint.
Ultrasound- It helps in detecting deep joints like the shoulder and hip joint.

3. Blood test

The blood test shows neutrophilic leucocytes.
Erythrocyte sedimentation rate is markedly elevated in the case of septic arthritis.

4. Joint aspiration

It is the fastest and best method for the diagnosis of septic arthritis.
The fluid which is aspirated through the joint shows features of acute septic inflammation.
Till one gets the culture reports, gram staining is done to provide clues to the type of organism.

Treatment

In early-stage

By parenteral route, a broad spectrum of antibiotics is administered.
A combination of Cefratriaxone and cloxacillin is given in an appropriate dose.
As per sensitivity reports and aspirate culture, medications are subsequently changed.
The joint must be at rest by using a splint or traction.
Whenever pus is aspirated through the joint(arthrotomy) or fluid is aspirated arthroscopically for culture or investigation, the joint must be washed and closed with a suction drain.
As the inflammation is controlled in an early stage, the patients improve and the joint is then gradually mobilized.

In late-stage

The joint doesn't move.
In such cases, after an arthrotomy and extensive debridement of the joint, the joint is immobilized in the position of optimum function.
By immobilizing, the disease heals and ankylosis occurs in that position.

Complications

Pathological dislocation of the joint.
Osteoarthritis
Deformity and stiffness in the joint.

Disclaimer for https://physioworldblog.blogspot.com/ If you require any more information or have any questions about our site's disclaimer, please feel free to contact us by email at deepikajoshi12347@gmail.com. Disclaimers for Physioworld's blog All the information on this website - https://physioworldblog.blogspot.com/ - is published in good faith and for general information purpose only. Update Should we update, amend or make any changes to this document, those changes will be prominently posted here.

Osteochondritis and its cause

2021-01-07T20:39:00.000-08:00

Osteochondritis and its cause

Hello students and friends, today we are going to learn what is osteochondritis, its cause, symptoms, diagnosis, and treatment.

It is also termed osteochondritis dissecans.

It is a painful type of osteochondrosis.

Occurs in the joints when blood supply to the joint is reduced and the bone gets soften.

In osteochondritis dissecans the cartilage or bone in the joint is inflamed.

Symptoms may appear late because it takes months or even years.

It usually affects the knee, ankle, and elbow.

It can occur in other joints also(shoulder and hip).

Sporadic osteochondritis dissecans- When only one lesion occurs in a single joint.

Symptoms

Pain
Weakness
Swelling
Stiffness in the joints
Clicking sound when joint moves
Joint locking in one position

It occurs most often in children and adolescents (10-20years age).

It especially affects young athletes or those individuals who are most active in physical activities.

Causes

The cause of sporadic osteochondritis is unknown.
If it is familial osteochondritis then it is inherited by mutation of a gene(ACAN).
Repeated trauma and stress to the joint can lead to osteochondritis.

Diagnosis

Physical examination- people who have familial osteochondritis have short stature.
Joint stability assessment
X-ray- shows bone and its location with lesion and its size.
CT-scan- it displays more internal details(blood vessels, soft tissue)
Genetic testing is done to find out changes in genes, chromosomes, and protein.
MRI(Magnetic Resonance Imaging)- it is done along with ultrasound(US) to produce clear images of the affected cartilage.

Treatment

In children's and youngsters- sporadic osteochondritis dissecans will usually heal on their own as age increases.
Pain-relieving medications are administered- ibuprofen(Advil, Motrin).
Children and younger teens can relieve their pain and swelling on their own with rest and decreasing their physical activities(running, jumping, etc.)
After 6-12 weeks, the injured joint will start its normal functioning.
Activities must resume gradually to avoid joint damage again.
Crutches, braces, splints, and casts are used if healing is slow.
Physiotherapy management should be done for improvement in healing and normal joint functioning.

Surgical treatment

Surgery is performed arthroscopically.
Surgery is done through three techniques:

A hole is drilled into the affected bone and cartilage.
Screwing the detached bone and cartilage.
Replacing the detached bone and cartilage by grafting.

When surgery is done successfully, crutches are suggested for about 6 weeks.

Physiotherapy for at least 2-4 months.

After 4-5 months, patients can gradually resume their activity.

Disclaimer for https://physioworldblog.blogspot.com/ If you require any more information or have any questions about our site's disclaimer, please feel free to contact us by email at deepikajoshi12347@gmail.com. Disclaimers for Physioworld's blog All the information on this website - https://physioworldblog.blogspot.com/ - is published in good faith and for general information purpose only. Update Should we update, amend or make any changes to this document, those changes will be prominently posted here.

Menstrual cycle and its phase

2021-01-06T20:07:00.000-08:00

Menstrual cycle and its phase

Hello students and friends, today we are going to learn what is the menstrual cycle, its phase, symptoms, complications, and how the uterine changes occur.

So, let's start with what is puberty?

Puberty is the stage of life when childhood converts into adulthood.
At this stage of life, the body will grow faster than at any other time.
Development of secondary sexual characteristics.
Male: 12-16 years
Female: 10-16 years.

There are five signs of puberty, given by Thanners and Marshal(scientists)-

Thelarchae- Development of breast
Adrenarche- Development of axillary hair(underarm hair)
Pubarchae- Pubic hair
Increase in height
Menarche- In girls starting of the menstrual cycle(1st menses).

There are 2 types of puberty-

Precocious- there is the development of secondary sexual characteristics before the age of 10 years.
Delayed- puberty comes after the age of 16 years.

What is the menstrual cycle?

In the female reproductive system, natural changes occur in a cyclic manner due to the shedding of endometrium through the vagina that makes pregnancy possible.
The menstrual cycle occurs due to the rise and fall of estrogen levels in females.
Menses are necessary for the production of oocytes.
There is a thickening of the lining of the uterus due to the menstrual cycle.
When there is a thickening of the lining occurs there is the growth of the egg and it is released around the 14th day of the cycle.
If pregnancy does not occur due to any reason then the lining is released and this is known as menstruation(period).

Criteria for normal menstrual cycle

The normal menstrual cycle is termed as eumenorrhoea.
Menarche- 13 years of age.
Every cycle must repeat in 28-30 days.
As per year- 13 menses.
From menarche to menopause(15-45 years), approximately 30 years- 400 menses.
Blood loss- 20-80 ml.

Average blood loss- 35ml/menses.

Bleeding phase- 1-5 days.
Bleeding duration- 2-7 days.
Range- 21-35 days.
The outflow tract must be normal.

Phases of the menstrual cycle(ovarian changes)

Ovarian cycle
Uterine cycle

Ovarian cycle-

Follicular phase
Ovulation
Luteal phase.

Uterine cycle-

Menstruation
Proliferative phase
Secretory phase.

Ovarian cycle

Follicular phase

Duration- 14 days.
The first part of the ovarian cycle.
When this phase occurs, the ovarian follicles mature and prepare to release an egg.
Level of FSH(follicle-stimulating hormone)- 3-10mIU/ml.
A few ovarian follicles are stimulated during the first days of the cycle due to the rise in the follicle-stimulating hormone.
One dominant follicle in the ovary will mature known as the Graafian follicle and it contains the ovum.
The development of follicles is known as folliculogenesis.
At a late stage, it overlaps with the proliferative phase(uterine cycle).

Ovulation

A second phase of the ovarian cycle.
In the ovulation phase, the ovarian follicle releases the mature egg into the oviduct.
FSH acts on follicles which results in the growth of the follicles, and the dominant follicle grows fast and the growing follicle then releases the estrogen which gives negative feedback to the follicle-stimulating hormone and suppresses the FSH, and simultaneously stimulates the luteinizing hormone(LH).
This process is known as LH surge(starts around the 12th day of the average cycle and it may last up to 48 hours).
LH works on the Graafian follicle(mature follicle) and the Graafian follicle rupture into pieces(these rupture pieces of Graafian follicle is known as corpus luteum) and results in ovulation(ovum is released).

Luteal phase

The final phase of the ovarian cycle.
FSH and LH transform the dominant follicle into the corpus luteum.
Then progesterone is produced.
Production of estrogen is induced by the increased progesterone in the adrenal gland.
FSH and LH production is suppressed by the hormones produced by the corpus luteum.
It is a phase of 14 days.
Mainly progesterone is produced by the corpus luteum to maintain pregnancy.
Up to 15-28 days.
Falling in the level of progesterone triggers menses and the next cycle begins.

Uterine changes

Bleeding phase/menstruation/catamania

The first phase of the uterine cycle.
Usually 1-5 days.
Heavy periods- menorrhagia.
Plasmin is an enzyme that inhibits clotting in the menstrual fluid and this condition will lead to iron deficiency.
Corpus luteum disappears and estrogen and progesterone level are decreased.
Dysmenorrhea(severe uterine pain) is felt in felt during menstruation.
Estrogen works as a vasodilator and helps in vasodilation, when it gets reduced, the uterine artery goes into vasoconstriction.
Some condition arises such as hypoxia, ischemia, and irreversible necrosis in the uterine endometrium.
Endometrial cells died and bleeding of the uterine artery starts.
As blood fillup in the uterus(hematometra), this sensation then goes into the hypothalamus.
From the hypothalamus, this information goes into the posterior pituitary, and oxytocin hormone is released which contracts the uterus, and outflow of blood occurs.
This results in menstruation.
The normal thickness of the endometrium is 5-6mm.
At the end of the bleeding phase, the thickness remains 1mm.

Proliferative phase

The second phase of the uterine cycle.
6-14 days.
During the follicular phase, estrogen level increases in the ovary and initiates the formation of a new layer of endometrium in the uterus.
Uterine endometrium thickness increases up to 2-3 mm.

Secretory phase

The final phase of the uterine cycle.
Corpus luteum forms and releases two hormones, one is estrogen(which helps to increase the number of cells-hyperplasia), and progesterone(which helps in increase in the size of the cells-hypertrophy).
Endometrium thickness in this phase becomes 5-6mm.

Symptoms of menstruation

Acne
Tenderness in the breasts
Tiredness
Irritation
Mood swings
Bloating
Pain in the abdomen

Complications

Iron deficiency anemia
Dysmenorrhea

Disclaimer for https://physioworldblog.blogspot.com/ If you require any more information or have any questions about our site's disclaimer, please feel free to contact us by email at deepikajoshi12347@gmail.com. Disclaimers for Physioworld's blog All the information on this website - https://physioworldblog.blogspot.com/ - is published in good faith and for general information purpose only. Update Should we update, amend or make any changes to this document, those changes will be prominently posted here.

Head injury

2020-11-06T19:58:00.000-08:00

Head injury

Hello students and friends, today we are going to learn what is head injury, how it is caused, its mechanism of injury, classification, and management.

Let's discuss first what is a head injury?

Head injury is also termed as traumatic brain injury.
Head injury is caused by any external physical force.
In traumatic brain injury, there is an impairment of the functioning of the body or cognitive abilities.
Behavioral or emotional functioning also gets disturbed.
The impairments are either temporary or permanent depending upon the type of head injury.

Mechanism of brain injury

The mechanism of head injury includes:

Acceleration: In this head is fixed and the object is moving.

If the head is hit by a stick, in this stage the head is fixed and the stick is considered as a moving object.

Deceleration: In this, the head is moving but the object is fixed.

In this case, we can consider the case of a car accident or hit by a wall.
Here, the wall is the object and the head is moving.

Causes

Road traffic accident(50%)
By fall of injury(21%)
Violence and assaults(12%)
Sports(10%).

Traumatic brain injury

Contusion- Brushing type injury, blood from small blood vessels are leaked due to injury; the arterial supply to the brain starts leaking due to the indirect effect of trauma.
Concussion- It is a mild traumatic injury; in this type of injury brain is hit in the cranial cavity or skull, the term used for this type of injury is the jarring type of injury.
Countre coup injury- It is also a jarring type of traumatic injury but in this case, injury occurs to the opposite side means when there is any condition in which the brain gets hit by the skull, then the opposite side of the brain gets injured.

Signs and symptoms

Symptoms gradually develop over 1-6 weeks.

CSF leakage from ears and nose.
Minor blunt head injury.
Penetrating trauma.
Increase in ICP(intracranial pressure).
Positive Babinski's sign(indicate upper motor neuron lesion).
Raccoon eyes.
Ecchymosis below the ear(battle sign).
Loss of consciousness.
Vomiting and nausea.
Persistent headache which gets worsens with time.
Seizures and convulsions.
Confusions
Personality changes
Mild paralysis.
Memory loss.
Loss of hearing or eyesight.
Dizziness or vertigo.
Peripheral nerves are often injured which leads to numbness and tingling.
Coordination problems.
Aphasia.

Fracture of the skull in head injury

There are 4 types of fractures seen in head injury patients-

Linear fracture
Depressed fracture
Diastatic fracture
Basilar fracture.

Linear Fracture: Most common type of skull fracture during a head injury.

In this type of fracture, depression is not seen.
There is a simple break in the skull that follows a simple straight line in the skull.
Not a serious injury.

Depressed Fracture: Type of comminuted fracture.

There is a breakage in the bone into many parts.
Depression is also seen at the site of fracture.

Diastatic Fracture: It is seen commonly in young children.

Fracture of sutural line.
Cause pits in the bone of the skull.
The fracture occurs on one or more sutures.

Basilar Fracture: It is the most severe type of fracture.

Usually caused by severe blunt head trauma.
In the basilar type of fracture, fracture of the base forming bone.
Mostly temporal bones are involved.
It also involves occipital, sphenoid, ethmoid, and frontal bone(orbital plate).

Management

If there is an increase in ICP(intracranial pressure) then we have to alter the patient's position for maintaining ICP.
The flat supine or prone position of the patient must be avoided.
To decrease intracranial pressure, osmotic diuretics(mannitol 20%) is administered.
If CSF(cerebrospinal fluid) production increase, then acetazolamide and glycerol is administered which decreases the production of CSF and increases its absorption.
Nose blowing and coughing must be avoided because they increase intracranial pressure.
Surgeries[craniotomy, craniectomy, and burr holes].

Indications

Large hematomas
The patient is in a coma.
CT-scan shows midline shifts.
Rapid deterioration.
Complications of brain surgeries
Infections(meningitis).
Chances of damage to the surroundings parts or structures.
Hope you all find this helpful for you, if you have any query related to this topic or any other topic then you all are free to contact me via contact us or you can also ask your doubts on the comment box. Thank you!
Disclaimer for https://physioworldblog.blogspot.com/ If you require any more information or have any questions about our site's disclaimer, please feel free to contact us by email at deepikajoshi12347@gmail.com. Disclaimers for Physioworld's blog All the information on this website - https://physioworldblog.blogspot.com/ - is published in good faith and for general information purpose only. Update Should we update, amend or make any changes to this document, those changes will be prominently posted here.

Parkinson's Disease

2020-11-04T22:14:00.000-08:00

Parkinson's Disease

Hello students and friends, today we are going to learn what is Parkinson's disease, how it is caused along with their pathophysiology, signs and symptoms, diagnosis, and treatment.

Let us discuss first what is Parkinsonism?

It is a neurological disorder.
Also known as paralytic agitans.
It is slowly, progressive, and degenerative disorder of the brain in which dopamine level gets decreased.

~Destruction of a dopaminergic neuron(neuron which synthesizes dopamine).

~Dopaminergic neurons are present in the midbrain(basal ganglia), in basal ganglia substantia nigera is present which releases dopamine.

~The important point related to Parkinson's is that it is not a muscle disease, because there is no muscle weakness in the case of parkinsonism as basal ganglia are not involved with muscle strengthening.

As there is a deficiency of dopamine in the case of Parkinson's, then we have to understand first its function.

Function of Dopamine

Dopamine is a neurotransmitter or messenger which helps in sending signals or impulses between the brain and the distal part of the neuron.
It gives inhibitory responses, the impulses which the brain sends to the distal parts get filtered and extra impulses get eliminated by its inhibitory response.
Mood changes are also associated with the level of dopamine. If there is euphoria, then the level of dopamine is increased.
Memory(if the level of dopamine is less then the memory also gets decreased).
It also regulates behavior and cognition.

As there is a decreased level of dopamine, then its functions also get altered.

Etiology

The cause is idiopathic.
It might be genetic, present from birth(juvenile).
Trauma

Damage in the mid-brain after head injury which leads to damage in the brain stem and subsequently decreases in dopamine production cells and the level of dopamine gets decreased.

Stroke

As the artery of the brain gets damaged and oxygen supply gets disturbed means condition of hypoxia is seen.
Hypoxia leads to a decrease in the level of substansia nigera(dopamine production cells), subsequently a decrease in the level of dopamine.

Hydrocephalus.
Excessive use of drugs, especially anti-psychotic drugs(which is mainly used in depression).
Inflammation in the brain parenchyma(encephalitis).

Signs and symptoms

In parkinsonism, there are 4 major cardinal signs.

Tremors(first sign)- mostly resting tremors.
Rigidity(second sign)- cogwheel rigidity.
Bradykinesia(movements get slow down).
Postural changes- shuffling gait, slurred speech, torticollis movement, propulsive gait.

Other signs and symptoms are:

Speech changes.
Writing changes
Loss of autonomic movements.

Pathophysiology

Due to any etiological cause, the level of dopamine gets decreased(decrease of sensory inhibitor) and the level of acetylcholine gets increased(excitatory activity increased).
When an excitatory activity is increased at the neuromuscular junction, sodium channels get open and it enters through the channel and then the development of positivity increases the muscle tone and stimulation contraction.
This will rise to tremors and extra contraction of muscles leads to stiffness and spasm of the muscle and there is overstimulation of neuron which leads to an increase in muscle tone.
As muscle tone increases, it gives rise to tremors and tremors are the first sign of Parkinson's disease.

Management

Levodopa+Carbidopa.
Bromocriptine.
Amantadine
Monoamine Oxidase inhibitor(MOAI)- Rasagiline.
Anticholinergic drugs(Benzotropine).
Physiotherapy management(exercises, using gait-aids, movement strategy training).

Effects of drugs

Levodopa is given to stimulate basal ganglia to covert it in dopamine.
Carbidopa helps in the crossing of the blood-brain-barrier and prevents levodopa from a breakdown in the blood due to enzyme dopadihydroxinase.
Bromocriptine increases the production of dopamine.
Amantadine increases the level of dopamine if there is a decrease in dopamine levels.
Anticholinergic drugs increase dopamine levels and decrease the Ach level.

Side-effects of drugs

Levodopa+Carbidopa may lead to nausea and dysrhythmia.
Bromocriptine decreases the level of prolactin hormone synthesis, which leads to decrease in milk production in the female which hinder in breastfeeding of baby, that is why it is recommended that pregnant female will not use this medicine during pregnancy.
Amantadine will cause nausea, constipation, drowsiness, headache, and blurred vision.
Anticholinergics drugs should be avoided in glaucoma patients and in alcoholic patients.
MOAI is avoided with levodopa as well as with tyramine food(vine, beer).

Disclaimer for https://physioworldblog.blogspot.com/ If you require any more information or have any questions about our site's disclaimer, please feel free to contact us by email at deepikajoshi12347@gmail.com. Disclaimers for Physioworld's blog All the information on this website - https://physioworldblog.blogspot.com/ - is published in good faith and for general information purpose only. Update Should we update, amend or make any changes to this document, those changes will be prominently posted here.

Syphilis and its cause

2020-11-03T21:53:00.007-08:00

Syphilis and its cause

Hello students and friends, today we are going to discuss syphilis, its cause, mode of spread, pathogenesis, stages, diagnosis, and treatment.

Let us discuss first what is syphilis and its cause?

Syphilis is a sexually communicated disease caused by the bacteria Treponema pallidum.
Due to unsafe sex practices, syphilis is occurring in developing countries like Canada, Russia, the USA, and England.
If we talk about the size of the organism, it is very small. Its length is 6-20micrometer and diameter range of 18-20micrometer.
Spirochete bacterium Treponema pallidum is the bacteria that is responsible for bacterial infection and causes syphilis.

Spirochetes

Long, slender, helical tightly coiled bacteria.
Gram-negative bacteria.

Treponema Pallidum

It is a microaerophilic spirochete means it require less oxygen for their growth.
It is gram-negative bacteria and doesn't see in gram stain.
It is transmitted only amongst humans.
6-15 micrometer long and 0.1-0.2 micrometer wide.

Mode of the spread of syphilis

It is transmitted through unsafe sexual contact:

When one partner is infected with syphilis he/she may cause syphilis to their partner also.
Usually, the bacteria enter into the body through the damaged or broken skin/mucous membrane during sexual contact.
It may be transmitted through the mouth, genitalia, or rectum through sexual contact or it can be transmitted by kissing also.
If an infected partner kissed or made intimate contact with his non-infected partner then there are chances of transmission of syphilis to the non-infected partner also.

If we talk about non-sexual contact:

Syphilis through non-sexual contact is rare.
It involves transmission by infected blood transfusion through needle(horizontal transmission) and through the mother to the fetus during pregnancy(vertical transmission).

Pathogenesis

During sexual contact, bacteria penetrate via skin and mucus membranes.
It can also transmit through the placenta.
Incubation period: 10-90 days(usually 21 days) before the manifestation of the initial stage.

How syphilis transmit?

The only way of transmission is through direct contact, it doesn't transmit through sharing clothes, and food.

If we talk about its type we describe its type on the basis of its stages.

Stages of syphilis

Congenital syphilis:

It is transmitted from the mother to child in the uterus.

2 stages are:

Early means in the first 2 years of the life of the child.
Late

Acquired syphilis:

It is transmitted through sex or blood transfusion.

2 stages are:

Early syphilis
Late syphilis

In early syphilis, there are 3 stages-

Primary
Secondary
Early latent.

In late or tertiary syphilis, there are 4 stages-

Neurological
Cardiovascular
Gummatous
Late latent

If we consider stages of syphilis depending upon the period after which the lesion occurs, there are manly 4 stages-

Primary stage
Secondary stage
Tertiary stage
Latent stage.

Primary syphilis-

The appearance of the chancre usually associated with regional lymph node enlargement.

Chancre: chancre is single, firm non-tender, raised red lesions.

It progresses from macule to papule to ulcer.
The ulcer can be seen on an anogenital site or at extra-genital sites like the mouth and lips.
It lasts usually from 3-6 weeks.
It usually heals without treatment.
They are painless.
The person is highly contagious.

If sufficient medication is not administered it progresses to the secondary stage.

Secondary syphilis

Ordinarily occurs after 2-3 months following primary syphilis.
It is characterized by rashes that arise from 2-8 weeks after the chancre develops and sometimes before it heals.
If primary syphilis is left untreated, then it will lead to secondary syphilis.
In the case of secondary syphilis, lymph nodes get enlarged, and with enlargement of the lymph nodes, cutaneous lesions in the skin on the palms and soles, which are painless are seen in the whole body.
Lesions are symmetrical, pale, red, or pink.
They are round and are distributed on the trunk and proximal extremities.
Diameter= 5-10mm.
Infection is spread throughout the body.

Tertiary syphilis

If secondary syphilis is not treated then it will lead to tertiary syphilis.
Usually develops after 2-3 years if secondary syphilis is not treated.
Lesions are less infective.
Bacterial organisms are difficult to detect.

Some complications of tertiary syphilis are:

Cardiovascular syphilis
Neurosyphilis
Benign tertiary syphilis.

Cardiovascular syphilis: Syphilitic aortitis is seen.

This occurs from 10-40 years after infection.
Affects the heart and blood vessels.
Usually seen in 10% of patients with the tertiary disease.

Neurosyphilis syphilis: mainly symptomatic.

Appears within few months of primary infection.
It can appear after 20-30 years later also.
Affects the nervous system.

Benign tertiary syphilis- includes Small bumps of tissue and fiber in the bone, skin, and mucous membrane(gummas).

Gummas are nodular lesions and result from delayed hypersensitivity reaction.
Usually, disappear after treatment with antibiotics.

The latent stage of syphilis

If syphilis left untreated then it will lead to latent syphilis.
The rash will go away in this stage.
This period is brief as 1-year or it may vary from 5-20 years.
During the latent stage, there is relapsing of the secondary stage of syphilis.
If there is relapsing at the time of pregnancy then the infection will transfer to the newborn and he/she will birth with congenital syphilis.

It may occur between secondary relapses, and after the secondary stage.

Lesions are not clinically visible.
The host suppresses the infections here.

Diagnosis

Asses a history of syphilis.
The most recent serological test should be done for syphilis.
The serological test for syphilis may not be positive during early primary syphilis.
The antibody tests are always positive at the secondary stage.
If we take laboratory diagnosis-
Firstly we have to identify lesions of Treponema pallidum.

Darkfield microscopy.
Direct fluorescent antibody- Treponema pallidum(DFA-TP)[This is the most specific test].

Serological tests-

Non-treponemal tests.
Treponemal tests(FTA-ABS, EIA).

Treatment

It is curable.
Signs and symptoms of secondary syphilis may go away on their own without any kind of treatment in 2-6 weeks.
If the right antibiotics are administered on time then it is curable.
We can give penicillin and other antibiotics[doxycycline, azithromycin, and ceftriaxone] to primary and secondary syphilis patients.
Penicillin is injected intravenously if the patient is suffering from neurosyphilis.
Damage through late syphilis can not be reversed.

Disclaimer for https://physioworldblog.blogspot.com/ If you require any more information or have any questions about our site's disclaimer, please feel free to contact us by email at deepikajoshi12347@gmail.com. Disclaimers for Physioworld's blog All the information on this website - https://physioworldblog.blogspot.com/ - is published in good faith and for general information purpose only. Update Should we update, amend or make any changes to this document, those changes will be prominently posted here.

Cirrhosis of liver

2020-11-02T21:10:00.003-08:00

Cirrhosis of liver

Hello students and friends, today we are going to discuss cirrhosis of the liver means how the liver gets damaged, its cause, etiology, pathophysiology, risk factors, complications, and medications.

If you are suffering from this condition or your family/friends are suffering from this disease then it might be helpful to you all.

Let us discuss some basics of the liver and its functions.

~The liver is anatomically located in the right upper quadrant of the abdomen below the diaphragm.

Basic functions are-

Regulated chemical level in the blood.
Secretion of bile.
Excretion of bilirubin, cholesterol, and waste products.
Metabolize fats, proteins, and carbohydrates.
Helps in the synthesis of plasma proteins(albumin and clotting factors).
Helps in the activation of enzymes.

When there is cirrhosis of the liver all the functions of the liver get disturbed.

Let us start with cirrhosis of the liver-

~Cirrhosis of the liver is a chronic progressive disease that is characterized by nodule formation and scarring of the liver.

It is irreversible means if the liver gets damaged then we cant restore its normal shape and size and their functions.
There are fibrotic regeneration and diffuse destruction of the hepatic cells of the liver.
In this condition, necrotic tissue is replaced by fibrotic tissue.
The normal structure of the liver and vasculature of the liver is altered, as there is damage to blood vessels there is impairing of the blood and lymph flow.
Because of the impairment of blood, hepatic insufficiency, and portal hypertension occur.
Liver tissue is damaged as this is a chronic disease, there is a replacement of liver tissue by fibrosis, there is scar tissue formation, and regenerative nodules are formed which leads to loss of function of the liver.

Cirrhosis of liver

Causes of cirrhosis of the liver

Viral hepatitis B & C
Autoimmune hepatitis
Gall bladder obstruction
Genetic
Certain medications(methotrexate, and acetaminophen)
High blood pressure
Diabetes
High body fat
Alcohol
Liver diseases

Rate of the population affected by cirrhosis of the liver

About 2.8 million people are affected in which 1.3 million died in 2015.
The most common cause of cirrhosis is HVB(hepatitis virus B), HBC(hepatitis virus C), and alcohol.

Symptoms

~Initially, it is asymptomatic.

If we see early symptoms of the onset of disease-

Nausea
Vomiting
Abdominal discomfort(mostly upper)
Weakness
Tiredness or fatigue
Diarrhea
Mild fever
Swelling of ankle

As the disease progresses-

Jaundice.
Ascites.
In male: Loss of hairs from the body, gynecomastia, and testicular atrophy.
In females: Reduce in breast size, and loss of sexual drive.
Spider naevi.
Anemia.
Purpura.
Fetor hepaticus(musty smell from breath).

Due to portal hypertension

Caput medusae(the network of dilated veins that surrounds the umbilicus).
Splenomegaly(WBC count decreases and platelet count decreases).
oesophageal varices(mouth bleeding).

Other symptoms-

Clubbing of nails.
Dupuytren's contracture.

When the disease gets advance-

Hepatic encephalopathy.
Kidney damage.
Bruising.
Muscle wasting or cachexia.

Pathophysiology

Liver cells get damaged due to the formation of fibrous tissue.
The destructed cells are replaced gradually by scar tissue.
There is obstruction of the blood and lymph flow.
There are hepatic insufficiency and damage to liver tissue by cirrhosis of the liver.
Due to etiological factors, there is diffuse destruction and regeneration of the cells and the formation of fibrous tissue.

Classification

Alcoholic
Post necrotic
Biliary
Cardiac

Alcoholic- also called portal cirrhosis.

Men>women.
Because of some offending agents, there is the formation of small nodules.
Fibrosis occurs- mainly around the central and portal vein areas.

Post necrotic- most common

Scar tissue formation.
Mainly caused by HBV and HBC.
It is caused by industrial chemicals also.
Women>men.

Biliary cirrhosis- scarring around the lobes of the liver and bile ducts.

It results from obstruction of the intrahepatic or extrahepatic biliary system and chronic biliary injury.

Cardiogenic cirrhosis- it is rare.

It is a chronic liver disease.
Associated with long-term severe right-sided heart failure.
Caused by atrioventricular valve disease or constrictive pericarditis.

Etiology and risk factors

Cystic fibrosis.
Autoimmune hepatitis.
Biliary atresia(GI disorder).
Hemochromatosis(too much iron in the body).
Wilsons disease.
Alcohol abuse.
Chronic viral infections of the liver.

Diagnosis

Blood test(WBC count and platelet count is low).
Enzyme test- SGPT, alkaline phosphate, and SGOT.
The serum bilirubin level is raised.
PTC(percutaneous transhepatic cholangiography)
Low protein level.
Prothrombin time increases.
USG.
CT-scan.
MRI.
Biopsy(later stage).

Management

Ask the patient to minimize the deterioration of the liver the use of alcohol, toxic substances, and drugs must be stopped.
Treat ascites and electrolytic imbalance.
Diuretic therapy is given frequently with spironolactone(Aldactone).
Abdominal paracentasis.
If ascites are not treated by other means then the TIPS(Transjugular intrahepatic portosystemic shunt) procedure is used to treat it. It is an interventional radiological procedure.
Antiemetics.
Pain-relieving medications.
For hepatic encephalopathy- lactulose(cephulac) or neomycin(myciguent).
The original liver of the patient is removed and replaced by the donor liver(organ) in the same anatomical position of the liver. This procedure is called Orthotropic liver transplantation, it may be required.

Complications

Bleeding esophageal varices.
Coagulopathies(bleeding disorder).
Hepatic encephalopathy.
Bleeding esophageal varices(when blood flow to the liver is blocked).
Hyponatremia(level of sodium gets too low in the body).
Water retention.

Disclaimer for https://physioworldblog.blogspot.com/ If you require any more information or have any questions about our site's disclaimer, please feel free to contact us by email at deepikajoshi12347@gmail.com. Disclaimers for Physioworld's blog All the information on this website - https://physioworldblog.blogspot.com/ - is published in good faith and for general information purpose only. Update Should we update, amend or make any changes to this document, those changes will be prominently posted here.

Ankylosing spondylitis

2020-11-01T21:32:00.003-08:00

Ankylosing spondylitis

Hello students and friends, today we are going to discuss what is ankylosing spondylitis, its cause, signs and symptoms, risk factors, and its treatment.

Let us discuss first what is ankylosing spondylitis,

Ankylosing spondylitis is an inflammatory disease/arthritis in which the spine and large joints are affected.

~It primarily affects the spine and it also affects other joints.

~It is an autoimmune illness in which immune cells get activated when certain bacteria enter or pass into the bloodstream and cytokines(chemical) produced by the immune cells.

~When cytokines get activated, they active other cells, and these cells migrate to the joints through the blood which leads to swelling in the joints. When joints swell it results in pain and swelling of the joints.

~Especially sacroiliac joint is affected more.

~Pain in the ribs, chest, buttocks, and in the entire back or neck also occur.

~Pain is felt generally at night and in the early morning.

~The blood supply to the joints reduces during sleep, cytokines get pent up and induces stiffness and pain in the joints.

~When a person sleeps, he/she may felt pain(nocturnal) during turning into the bed.

~When a person wakes up in the morning, blood flow increases or back to normal, cytokines washed away and the pain reduces.

~Sometimes it also affects other joints of the body- knee, shoulder, and ankle.

Normal spine view

Causes

Its exact cause is still unknown, but genetic and environmental factors can cause ankylosing spondylitis.
Almost 80-90% of patients with ankylosing spondylitis have the HLA-B27 gene.
HLA-B27 increases the risk of having ankylosing spondylitis, however other genes with respect to environmental factors also cause ankylosing spondylitis.
According to researchers, more than 60 genes are associated with ankylosing spondylitis.
Genes are identified as- ERAP 1, IL-12, IL-17, and IL-23.

Early signs and symptoms

Symptoms ordinarily begin to appear in late adolescence or early adulthood.

Some symptoms are:

Neck pain
Mild fever
Loss of appetite
Sweating at night
Stiffness and pain in the lower back, hips, and buttocks.
Pain in tendon and ligaments.

Late symptoms include-

Pain, stiffness, and tenderness are seen on both sides of the body
Postural changes occur
Tiredness.

Ankylosing spondylitis

Risk factors

Mostly affect a person with age 15-40years.
Men(3times)>women.
Genetic or any family history.

Which areas are most affected?

Areas which are mainly affected are-

Spine
Shoulder joint
Joints of the hands and feet
Thigh area
Hip joint
Neck
Ribs.

Diagnosis

Physical examination is done to examine the range of motion(ROM) in the spine.
When a physical examination is done, it shows a change in posture with pain in a different position with difficulty in breathing(expansion of chest).
X-ray is done to check changes in bone and joints.
MRI used for scanning more detailed images of bone and soft tissue. It is expensive.
The blood test can be done but it doesn't reveal that much information about ankylosing spondylitis as it gives information about inflammation and inflammation can be caused by many diseases not only ankylosing spondylitis.
HLA-B27 gene is tested in the blood test, but most of the people who have that gene don't have ankylosing spondylitis.

Treatment

NSAIDs(non-steroidal anti-inflammatory drugs)- indomethacin, and naproxen.
TNF blockers(tumor necrosis factor)- adalimunab, certolizumab, etanercept, golimumab and infliximab.
Interleukin-17 inhibitor(IL-17)- secukinumab and ixekizumab for body defense against infection and inflammation.
Physiotherapy is an important part of the treatment- includes deep breathing exercises, jogging(moderate to high impact exercises are recommended but with some restrictions), group exercises, PNF(proprioceptive neuromuscular facilitation), and an exercise program.
Electrotherapy
TENS(transcutaneous electrical nerve stimulation)
Hot compression
Locally injected corticosteroids
DMARDs(disease-modifying anti-rheumatic drugs)- sulfasalazine and methotrexate.
Surgery- however, surgery is not required as such but artificial joint replacement surgery may be the last option for some people with an advanced joint disease which affects hips or knees.

Disclaimer for https://physioworldblog.blogspot.com/ If you require any more information or have any questions about our site's disclaimer, please feel free to contact us by email at deepikajoshi12347@gmail.com. Disclaimers for Physioworld's blog All the information on this website - https://physioworldblog.blogspot.com/ - is published in good faith and for general information purpose only. Update Should we update, amend or make any changes to this document, those changes will be prominently posted here.

Varicose vein

2020-10-31T01:52:00.006-07:00

Varicose vein

Hello students and friends, today we are going to discuss what is the varicose vein, its main cause, types, etiology, risk factors, symptoms, and treatment.

So let us first discuss varicose vein.

Varicose veins= term commonly refers to the veins of the legs.

Varicose veins are veins that have enlarged and become twisted.
Varicose veins can occur anywhere in the body but it commonly refers to the veins of the legs.
When there is a condition of varicose veins, the leaflets of the valves are no longer properly meet and doesn't work properly.
Veins have a pair of leaflet valves, which prevent blood from flowing backward means it prevent retrograde flow of the blood.
There is valvular incompetence when these leaflets are unable to meet properly.
When a person remains in a standing position for a long period of time, pressure in the veins is high, varicose veins may occur.
This mainly affects the superficial veins of the legs.
A varicose vein is painful(especially in a standing position) and it is also considered a cosmetic problem because of its appearance.
Leg swelling, venous edema, lipodermatosclerosis, and ulceration are seen.

Is varicose vein is life-threatening?

Mostly uncommon, but it may be confused with deep vein thrombosis(DVT), which may be considered a life-threatening condition.

Signs and symptoms

Heavy legs
Aching
The appearance of spider veins(telangiectasis)
Swelling of ankle(especially in the evening)
Venous eczema
Brownish-yellow shiny skin discoloration near the affected veinous area
When a person stands up or moves suddenly then there are chances of developing cramps.
Atrophile Blanche(whitened and irregular sac-like patches can appear at the ankles).
Lipodermatosclerosis(shrinking of skin above the ankle)
Clotting time increases.

Types of varicose veins

Trunk varicose veins
Reticular varicose veins
Telangiectasis varicose veins(spider or thread veins).

Trunk varicose veins- Thick and long; near to the skin surface.

Reticular varicose vein- They from network and red in color.

Telangiectasis varicose veins(spider veins)- Usually harmless, the appearance of red/blue clusters of veins on the legs or anywhere in the body where varicose vein occurs.

Etiology

There is the failure of venous veins in the saphenous veins, this results in retrograde flow of venous blood in the branches of saphenous veins.
Ambulatory venous pressure elevates and symptoms of varicose veins occur.

Ambulatory venous pressure(AVP) is the ankle venous pressure when a person is walking.
It is the gold standard test for testing the efficiency of the calf musculovenous pump.

Epidemiology

Early stage- women-25% & men-15%.
Venous ulceration- 5% of the population.
More common in women than in men.

Complications

Poor circulation of blood through the affected limb may lead to complications but most of the varicose veins are reasonably benign.

Some complications are-

Skin ulcers or venous ulcer(especially near the ankles)
Pain, tenderness, heaviness in the affected limb
Long-standing for many hours may lead to pain and may hinder work
Dermatitis
In long-standing venous ulcers, there may be a development of carcinoma or sarcoma
In overweight patients, acute fat necrosis can occur at the ankle
Venous eczema
Superficial thrombophlebitis
Minor trauma may lead to heavy blood loss.

Causes

Menopause
Elevation of venous pressure
Defective venous valves
Infection or trauma
Incompetent venous valves.

Risk factors

As age increases, risk factor increases
Genetics
Pregnancy
Obesity
Men<women

Diagnosis

When you visit your doctor, firstly he will examine your legs and if there is a condition of varicose veins and the veins are visible on the calf itself and he may ask you about pain or symptoms you are having.
Doppler test is done to diagnose it and it is painless(non-invasive).
Ultrasound can also be done to check the blood flow through the veins.
A venogram may be done for the assessment of veins. This is done to ensure that any blood clot or blockage is not present in the veins which causes pain and swelling in the legs.
An X-ray may be done by injecting a special dye into the legs, this will give a better view of the flow of blood.

Clinical tests

Trendelenburg test
Multiple tourniquet tests
Lower limb venous ultrasonography
Fegans test

Treatment

Non-surgical treatment includes sclerotherapy, exercise, physiotherapy, elevating the legs, and elastic stockings.
The traditional surgical treatment includes vein stripping to remove the affected veins.
Alternative techniques- radiofrequency ablation, endovenous laser treatment, and US-guided foam sclerotherapy.
Microsclerotherapy(block off smaller veins using a liquid chemical injection)
Endovenous ablation therapy.

What is the physiotherapy management for a varicose vein?

Varicose vein mainly caused due to inactivity of the legs or body for a long period of time(as in standing posture).

Exercises increase the blood flow in the body and increase the flow of blood to the heart.

We can also relieve its symptoms by-

Walking and running
Bicycling
Lunges
Leg lifts.

Disclaimer for https://physioworldblog.blogspot.com/ If you require any more information or have any questions about our site's disclaimer, please feel free to contact us by email at deepikajoshi12347@gmail.com. Disclaimers for Physioworld's blog All the information on this website - https://physioworldblog.blogspot.com/ - is published in good faith and for general information purpose only. Update Should we update, amend or make any changes to this document, those changes will be prominently posted here.

Bronchiectasis and its cause

2020-10-17T23:59:00.001-07:00

Bronchiectasis and its cause

Hello students and friends, today we are going to discuss bronchiectasis and its cause along with their symptoms, treatment, diagnosis, and pathogenesis.

So, let's discuss what is bronchiectasis?

Bronchiectasis is described as chronic permanent dilation and destruction of bronchi due to destructive changes in the elastic and muscular layers of bronchial walls.

In bronchiectasis, lung airways become damage. There is impairment of the drainage of bronchial secretions.

Pathogenesis

In bronchiectasis, there is difficulty in clearing the secretions & recurrent infections with infection & inflammation which results in airway injury and remodeling.
It is the long-term condition in which cilia get damage and thus lungs become vulnerable to infections.
In this, one or more of the conducting bronchi/airways gets damage{muscular and elastic component of bronchi damaged}.
Abnormal dilation of bronchial tract leading to accumulation of the thick pool of purulent material and occlusion due to fibrosis thickening.
Enlargement of the bronchial artery and increased anastomosis between them leads to an increase in vascularity.
As infection increases, mucus gets increased along with microorganisms. Then this infection leads to damage to the airways.
This is called a vicious cycle.

We can classify bronchiectasis according to the amount of sputum production-

If sputum is produced less than 10ml= mild

If sputum is produced 10-15ml= moderate

If sputum is produced more than 150ml= severe.

If we discuss how serious is bronchiectasis is, then we conclude that the complications are rare, but they can be serious(coughing with a large amount of blood).

Types of bronchiectasis

Cystic fibrosis- genetic condition; thick sticky mucus buildup in the lungs which results in recurrent pulmonary/lung infections.
Non-cystic fibrosis- if the person has asthma, COPD, cilia gets damage, and there is a problem in clearing mucus from the lungs then bronchiectasis occurs in that person.

Clinical features and symptoms

Chest pain
Dyspnea
Fatigue
Cough with mucopurulent sputum(mucus discharge+pus)
Weight loss
Blood in sputum
Weakness
Chronic cough
Fever
Wheezing
Decreased appetite
Cyanosis.

Causes of bronchiectasis

Some common causes are:

Immunodeficiency
Aspiration
Cystic fibrosis(a most common cause which gets worsen over time)
The disease of connective tissue
Abnormalities of cilia
ABPA(allergic bronchopulmonary aspergillosis)
Severe lung infections in childhood.

Signs/findings on physical examination

Crackle sound
Wheezing sound
Abnormal sounds
Bluish discoloration(cyanosis)
Loss of weight
Deoxyhaemoglobin>5gm.
Rhonchi(low pitched sound)
Digital clubbing.

Diagnosis

Pulmonary function test
X-Ray chest
Bronchoscopy
HRCT-scan
Respiratory function test
ABG
Sweat test(for cyanosis of cystic fibrosis).

Treatment

Physiotherapy
Antibiotics
Oxygen therapy
Bronchodilators
Penicillin
Steroids
Mucus reducing drugs.

If we discuss the best treatment for bronchiectasis, then we can prefer inhaled tobramycin(nebulized treatment) which is widely used nowadays. Gentamicin and colistin are also used.

Can bronchiectasis cure permanently or it can go away?

No this is not curable as well as there is no treatment of bronchiectasis which helps to cure it permanently.

It is a lifelong condition in which each cycle of infection lungs becomes more damaged.

Its symptoms can be prevented by removing mucus from the lungs.

Foods which are useful and foods which we have to avoid

We have to eat a healthy balanced diet and avoid food that has excessive salts, sugar, and saturated fats.

Disclaimer for https://physioworldblog.blogspot.com/ If you require any more information or have any questions about our site's disclaimer, please feel free to contact us by email at deepikajoshi12347@gmail.com. Disclaimers for Physioworld's blog All the information on this website - https://physioworldblog.blogspot.com/ - is published in good faith and for general information purpose only. Update Should we update, amend or make any changes to this document, those changes will be prominently posted here.

Poliomyelitis, its types and prevention

2020-10-13T02:56:00.005-07:00

Poliomyelitis, its types, and prevention

Hello students and friends, today we going to discuss what is poliomyelitis?

Here you will get to know-

What is poliomyelitis?

Poliomyelitis is caused by which virus?

Poliomyelitis vaccine

How poliomyelitis is spread?

Prevention, complications, symptoms, treatment, and many more.

So, let us start with the meaning of poliomyelitis-

Polio= grey(grey matter of spinal cord)

Mye= Spinal cord

Litis= Inflamation

First-person who discovered polio- Karl Landsteiner & Erwin proper(1908).

Is poliomyelitis is a viral or bacterial disease?

Poliomyelitis is caused by poliovirus(RNA virus).
Hence it is an RNA virus, it is non enveloped; outermost covering- capsid(protein coat).
Poliovirus is an enterovirus(of high infectivity), which invades the intestine.
It is the viral disease in which the destruction of nerves occurs in the spinal cord.
The main reservoir of infection lies in the human GI tract(gastrointestinal tract).
The virus enters through:

the mouth(oral route) and then multiply in the throat/pharynx[multiply in mucosal cells of throat, then virus goes into the stomach and then to the intestine] and intestine[here virus again multiply in the mucosal cell] during 1-3 week incubation period before going into the blood, then it goes to the spinal cord and infects motor neurons.

The virus continues to be excreted in saliva for 2-3 days, and in the feces for a further 2-3 weeks.
Because the inflammation occurs and the signals from the brain and spinal cord are no longer received from that infected nerve area, this leads to atrophy of muscles(muscle wasting), and the muscle shrinks.

In which age polio attacks?

Mostly in children's, but no age is considered as such.

Male:Female= 3:1

How polio is transmitted/spread?

Polio is transmitted through sneezing, coughing, contaminated food & water.

It is highly contagious.

Symptoms

90-95%- asymptomatic
4-8%- symptomatic(non-paralytic)
0.5%- get polio(paralytic polio)
The most severe form can cause paralysis and even death of an individual.

Non-paralytic polio symptoms: if an individual has non-paralytic polio then there may be flue like symptoms that are present like coughing, sneezing, etc.

Paralytic polio symptoms: if an individual has paralytic polio then his initial symptoms are flu-like, the later on loss of muscle reflexes is seen, pain in muscles and spasm is seen.

Types of poliomyelitis

Non-Paralytic/Pre-Paralytic Poliomyelitis
Paralytic Poliomyelitis
Spinal poliomyelitis
Bulbar poliomyelitis
Bulbospinal poliomyelitis

Non-paralytic poliomyelitis:

If we see early signs and symptoms of patients, the patient develops a high fever with pharyngitis, myalgia, anorexia, nausea and vomiting, and headache with neck stiffness due to meningitis.
Symptoms subside within 1-2 weeks.

Paralytic poliomyelitis:

It is not clearly understood which factors are in favor of the development of this type of poliomyelitis but there is some evidence that physical activity and intramuscular injection during the prodrome may be important exacerbating influences.

Spinal polio:

Severe muscle pain begins frequently with spasm in muscles, then weakness and fasciculation develop.
The lower limbs being affected more as compared to the upper limbs, it tends to become maximal within 48 hours.
It causes paralysis in arms and muscles.
Weakness tends to be asymmetrical.
Muscle tone is flaccid, the reflexes are initially brisk, then become absent.

Bulbar polio

Particularly occurs in children.
It may occur without any limb weakness.
It is more common in those individuals whose tonsils and adenoids have been removed.
Adult individuals have spinal as well as bulbar involvement.
The virus mainly infects neurons of the diaphragm, because of this difficulty in breathing occurs.

Bulbospinal polio:

Contain symptoms of both spinal and bulbar polio.
Very lethal and rare.

Treatment

Medicines(NSAIDs, Analgesics)
Warm towel
Heating pad
Physical therapy
Self-care

Poliomyelitis vaccine-

We can prevent polio through vaccination.

The vaccine can prevent polio in 2 types-

Inactivated poliovirus vaccine~ injection given to an individual; a killed form of the virus is used.
Oral polio vaccine~ weak strain of poliovirus is used.

How long poliovirus can survive?

Poliovirus can survive for a long period of time in an external environment.
It survives 4 months in water and 6 months in feces.
Polio is more likely to occur in the rainy season, overcrowding area, and area with poor sanitization.
Polio is present only in Pakistan, Afghanistan & Nigeria.

Incubation period

It incubates in 7-14 days.

Complications

As severity increases,

Stiffness in the neck occurs.
Joints flexed; muscles become painful and tender.
When we do passive stretching it provokes painful spasm.

Prevention of poliomyelitis

If a patient has had an attack of poliomyelitis, then he should be immunized with a vaccine.
There is no cure, it can only be prevented through vaccination at an early stage.
If the polio vaccine is given multiple times to a child then it can protect the child for the whole life.

Disclaimer for https://physioworldblog.blogspot.com/ If you require any more information or have any questions about our site's disclaimer, please feel free to contact us by email at deepikajoshi12347@gmail.com. Disclaimers for Physioworld's blog All the information on this website - https://physioworldblog.blogspot.com/ - is published in good faith and for general information purpose only. Update Should we update, amend or make any changes to this document, those changes will be prominently posted here.

Pericarditis and its treatment

2020-10-09T20:19:00.004-07:00

Pericarditis and its treatment

Hello students and friends, today we are going to learn what is pericarditis.

For understanding better about pericarditis, firstly let's discuss pericardium.

The pericardium is the heart covering which has 2 layers:
Parietal layer: also called as parietal pericardium; outer layer.
Visceral layer: also called as epicardium; inner layer.
These layers are separated by a pericardial cavity. It contains 15-50 ml of an ultrafiltrate of plasma.

So, this is a brief explanation of pericardium, now let us discuss pericarditis.

Pericarditis is the condition in which inflammation of the pericardium occurs.
It is classified into 3 types:

Acute- less than 3 weeks.
Sub-acute- 6 weeks to 6 months.
Chronic- more than 6 months.

CAUSES

Most commonly caused by echovirus or coxsackievirus.
It is most commonly caused by viruses like echovirus or coxsackievirus & less frequently by influenza or HIV infections.
Bacteria can also lead to bacterial pericarditis(also c/d as purulent pericarditis).
Pericarditis can also be caused due to fungal infections.
Some causes of pericarditis are unknown and this condition is termed as idiopathic pericarditis.
Men>Women.
Mostly affect men of age- 20-50 years.
Other causes also include:
Heart attack.
Myocarditis.
Radiation therapy to the chest.
Immunosuppressants.
Trauma or surgery to the chest, esophagus, or heart.

SYMPTOMS

Anxiety.
When a person goes into a lying down position then the difficulty in breathing occurs.
Chest pain(may radiate to the neck, shoulder, back, or abdomen) due to rubbing of pericardium against the heart.
Dry cough.
Fatigue.
Fever.
In the case of pleuritis, when a person starts breathing, he/she need to bend over or hold the chest.

Pericarditis can be associated with some diseases like:

Autoimmune disorders.
HIV infection/ AIDS.
Kidney failure.
Tuberculosis.
Cancer.
Hypothyroidism.
Rheumatic fever.

SIGNS

When we place the stethoscope on the chest, then the sound of pericardial rub can be heard.
The heart sound may be muffled.
Pericardial effusion is seen in the heart when fluid is filled in the pericardium. So, muffled or distant sound can be heard.

If the disease is severe,

Crackle sound produced.
Breath sound gets decreased.

TESTS

If the fluid is build-up in the pericardial sac, it may be seen in-

Chest X-Ray
ECG
Heart MRI & CT-scan
Echocardiogram
Radionuclide scanning.

These test shows-

Heart enlargement
Inflammation signs
Constrictive pericarditis(scarring & contracture of pericardium).

Laboratory test-

Blood culture
CBC
C-reactive protein
ESR
Tuberculin skin test
HIV serology.

TREATMENT

Analgesics- for pain relief
Antibiotics- for treatment of bacterial pericarditis
NSAIDs or aspirin- for the reduction in inflammation of the pericardium
Antifungal drugs- for treatment of fungal pericarditis
Corticosteroids(prednisolone)- in some patients
If the fluid is build-up in the pericardium, then it affects the heart, and heart function gets affected and produces cardiac tamponade, it is necessary to drain fluid from the sac. This procedure of removal of fluid from the sac is called pericardiocentesis.

May be done using echocardiography- guided needle or minor surgery

If pericarditis is chronic, recurrent, or causes constrictive pericarditis, then the part of the pericardium must be removed.

Disclaimer for https://physioworldblog.blogspot.com/ If you require any more information or have any questions about our site's disclaimer, please feel free to contact us by email at deepikajoshi12347@gmail.com. Disclaimers for Physioworld's blog All the information on this website - https://physioworldblog.blogspot.com/ - is published in good faith and for general information purpose only. Update Should we update, amend or make any changes to this document, those changes will be prominently posted here.

Bronchial Asthma and its treatment

2020-10-08T23:44:00.010-07:00

Bronchial Asthma and its treatment

Hello students and friends, today we are going to learn about what is chronic asthma, its triggers, cause, symptoms, medications as well as first-aid for an asthmatic attack.

Lets clear one thing that there is no difference between asthma and bronchial asthma, bronchial asthma is another name for asthma.

Inflammatory disease of small airways of the lungs characterized by episodic reversible bronchial obstruction due to hyperresponsiveness of the tracheobronchial tree.

Asthma is associated with mast cells, eosinophils & T-lymphocytes.

MAST CELLS- they release histamine which is released when there is an allergic reaction in the body.

EOSINOPHILS- a type of WBC(white blood cell).

T-LYMPHOCYTES- a type of lymphocyte, plays a central role in immune responses and associated with allergy & inflammation.

Asthma can increase the risk of developing bronchitis.

Bronchial Asthma Triggers/Main cause of asthma

Smoking/second-hand smoking
Excercise
Air pollution or inhalation of toxins
Anxiety
Emotional stress
Perfumes & fragrance
Wheather(cold weather mainly)
Acid reflux
Allergens(dust mites, pollen)
Certain drugs(NSAIDs, aspirin, &beta-blockers)

Foods that should be avoided-

Cow milk
Peanut
Wheat
Fish
Eggs

Signs and symptoms

Shortness of breath
Excessive coughing or a cough that stays, which leads to sleep disturbances
Chest tightness
Wheezing sound during breathing.

Factors affecting asthma

Respiratory infections
Tobacco smoking
Dust pollutants
Cold weather
Emotional stress.

Types of asthma

2 types:

Extrinsic asthma
Intrinsic asthma

Extrinsic Asthma

Begins usually in childhood.
Family history of preceding allergies is involved
Hypersensitivity to allergens.
IgE level in the serum increases.
Increase in eosinophils.
Atopic.
Most episodic.
Positive skin sensitivity test.

Intrinsic Asthma

Develops later in adulthood.
Family history is not involved.
Normal IgE level.
Symptoms develop after any trigger factors(respiratory infections, exercise, emotional stress, etc.)
Non-atopic.
Negative skin sensitivity test.

Pathophysiology

Chronic inflammation of respiratory tubes, tightening of respiratory smooth muscles, and episodes of bronchoconstriction.
When an asthmatic episode occurs, an inflamed airway responds to environmental triggers(smoke, dust, etc.).
Narrowing of airways in asthma occurs due to inflammation and bronchoconstriction of the airways.
When airways get narrow, a wheezing sound is produced.
There are various ways of inflammation- macrophages, mast cells, lymphocytes, eosinophils, neutrophils.
Breathing gets difficult due to the narrowing of airways, thus airways get narrow, excess production of mucus occurs.
The immune system of the body gives a response in the bronchial airways, results in asthma.
The airways exhibit hypersensitivity to particular triggers(stimuli). It is usually categorized as a Type I hypersensitivity reaction.
When the bronchi expose to these triggers, they contract and go into a spasm(asthmatic attack).
Inflammation occurs which leads to further narrowing of airways, thus mucus production increases which leads to coughing and other breathing difficulties.
Then vascular leakage increases which leads to edema and an increase in mucus secretion.
When mucus secretion increases, airways obstruct and remodeling of airways occurs leads to smooth muscle hypertrophy/hyperplasia.

Hyperplasia- increase in the number of cells.
Hypertrophy- increase in the size of cells.

Diagnosis

Pulmonary function test
Spirometry
Peak expiratory flow
Chest X-Ray
The wheezing sound produced; difficulty in breathing.

Treatment

Bronchodilator- beta-adrenergic blockers; helps to open the lung airways.
Self-care- it is an important factor, if we want to cure this condition then we have to care for ourselves.
Anti-inflammatory drugs- corticosteroids; prevent joint swelling and inflammation of the tissues.
Inhalers(dry powder inhalers)
Breathing exercises

In the case of mild asthma-

Asthalin inhalers are given; sorbitol.

If severity increases-

Corticosteroids: we can give corticosteroids in 2 ways- either by inhalers or by nebulizer
Inhalers: salbutamol, declasone
Nebulizer: they are rest fumes; in this mixing of salbutamol & declasone is done.
We can give some drugs through IV- Aminophylline and theophylline.
Aminophylene(250mg) is given over 20 minutes.
Theophylline is given in a slow manner, as it has a narrow therapeutic range; if it goes beyond the 20 micrograms per liter serum level then the patient will collapse.
The normal level of theophylline- 10-20 micrograms per milliliter.

Acute severe asthma- systemic steroid

If uncontrolled- apetroprium bromide

70-80% Helium

Decrease airway resistance; improve the effect of aerosolized bronchodilators.

First Aid

First Aid is given in the case when there is no medication available at that moment:
Loose clothing of the patient
Airway assist
Maintain the position of the patient.

During an asthma attack:

Respiratory rate>25 breaths per minute
Heart rate>110 beats per minute
Oxygen saturation<92%
Cyanosis occurs
The partial pressure of oxygen< 8 KPa
Peak Expiratory flow<50%; If PEF<33%, then this will lead to a life-threatening condition.
Silent chest
Effect on the central nervous system- drowsiness, confusion.

If life-threatening symptoms are seen in asthma-like cyanosis of lips or nails of fingers,then immediate medical care is required.

If someone questions that his asthma can go away, then the answer is `yes' it can go away. It mainly goes away in that condition when it occurs in childhood as compared to adults.

Disclaimer for https://physioworldblog.blogspot.com/ If you require any more information or have any questions about our site's disclaimer, please feel free to contact us by email at deepikajoshi12347@gmail.com. Disclaimers for Physioworld's blog All the information on this website - https://physioworldblog.blogspot.com/ - is published in good faith and for general information purpose only. Update Should we update, amend or make any changes to this document, those changes will be prominently posted here.

Epilepsy and its types

2020-10-06T22:10:00.010-07:00

Epilepsy and its types

(EPI= upon; LEPTOS= seizures)

Epilepsy is a medical condition that mainly affects the nervous system.
Also known as a seizure disorder.
Disorders in brain cells occur because of genetic influence, head trauma, or any infectious disease.
Unusual electrical activity occurs which leads to repetitive seizures.

Abnormal behavior is seen in the case of epilepsy.
Involuntary muscle movement occurs with unusual perception.
The consciousness level also gets disturbed.

TYPES OF EPILEPSY

GENERALISED SEIZURES:

The whole brain is involved.
Immediate loss of consciousness.
2 subtypes:
Tonic-clonic epilepsy-
Also known as Grand mal seizures.
Consciousness is lost and muscle convulsions.
Carbamazepine, phenytoin, oxcarbazepine, valproic acid, lamotrigine is the first-line drugs used in this condition.
Absence seizures-
Also known as Petit mal seizures.
Children>adults
Starring at some site for a few seconds.
Include brief, sudden lapses of consciousness.
Valproic acid & ethosuximide are the first-line of drugs used in this type of seizure.
PARTIAL SEIZURES:

Cortical discharge occurs locally & remains localized in one region.
Symptoms vary according to the region affected:
Abnormal sensory experience and behavior.
Involuntary muscle contraction.
Carbamazepine, phenytoin, lamotrigine, valproic acid, oxcarbazepine are the first line of drugs used in this type of seizure.
STATUS EPILEPTICUS:

In this, seizures occur repeatedly and there is no recovery in between the repeated seizures.
MYOCLONIC SEIZURES:

Sudden brief muscular contraction occurs in one part of the body or in the whole body in a repeated manner.
Falling tendency increases & stiffness of the body is seen.
This seizure can occur alone or with other seizures.
Valproic acid and clonazepam are the first-line of drugs used in this type of seizure.

FEBRILE SEIZURES:

Seen in children's due to an increase in the temperature of the body.

ETIOLOGY

Some conditions can help us to understand the cause of epilepsy, otherwise, the cause of epilepsy is idiopathic.

Head trauma
Meningitis
AIDS
Prenatal injury
Genetically influenced individual
Brain tumors
Stroke

SIGNS AND SYMPTOMS

Loss of consciousness
Uncontrolled jery movements of arms & forearms
Problem in speaking
Temporary confusion
Mental problem symptoms

RISK FACTORS

Metabolic disturbances.
Sleep deprivation
Intercurrent infections
Alcohol withdrawals.
Physical fatigue.
Mental fatigue.

PATHOGENESIS OF EPILEPSY

Brain functions get altered, this results in generating abnormal electrical activity which results in seizures/epilepsy.
Epilepsy is caused due to some genetic influence, trauma/brain injury, and infectious diseases.
Neurons get stimulated and pass signals/waves of excitation to other neurons.
It results in the development of a paroxysmal depolarization shift which shows the characteristics of giant excitatory postsynaptic potential, thus the neuronal network begins bursting.
GABA inhibition & Dopamine level gets decreased.
GABA & Dopamine are neurotransmitters.

DIAGNOSIS

Medical history- an important aspect that has to be considered while examining the patient. It helps in understanding the main root cause of the patient(genetic).
Neurological examination- Electroencephalogram(EEG)
CT-scan
MRI-scan
Genetic testing- CMA(chromosomal microarray) to check whether the patient is having any gene of epilepsy from his/her family or a mutation occurs.

COMPLICATIONS

Injury to the skull- when an individual falls down because of a seizure, the skull can get damaged as it hits directly the surface which is close to an individual(ground, table, etc.).
A shoulder dislocation-(seizures can lead to dislocation of the shoulder because of jerky movements of arm and forearm).
Fracture of the vertebra- vertebra get fractures when jery movements of the body occur or fall down from some height.
During an epileptic attack, the patient can injure his tongue, lip, or chick.
When an individual vomits, the contents of the vomited stomach may go into the lungs.
Limbic structures(hypothalamus, hippocampus, and amygdala) can also get damage that is involved in regulating emotions.

Disclaimer for https://physioworldblog.blogspot.com/ If you require any more information or have any questions about our site's disclaimer, please feel free to contact us by email at deepikajoshi12347@gmail.com. Disclaimers for Physioworld's blog All the information on this website - https://physioworldblog.blogspot.com/ - is published in good faith and for general information purpose only. Update Should we update, amend or make any changes to this document, those changes will be prominently posted here.

Osteoporosis and its management

2020-10-05T02:25:00.008-07:00

Osteoporosis and its management

Hello students and friends, today we are going to learn about osteoporosis, which is the most common bone disease which can occur with an increase in age.

Here we will discuss their risk factors, clinical features, investigations, and management.

Osteoporosis is a condition in which new bone formation doesn't occur with the removal of old bone.
The bone becomes weak and brittle in this condition.
This is the most common bone disease characterized by reduced bone mineral density.
Risk of fracture increase with an increase in age.
Women affect(30%) more than men(12%).
The bone turnover throughout life depends on the balance between bone formation(by osteoblasts) and bone reabsorption(by osteoclasts). When the rate of bone reabsorption exceeds the rate of formation of bone, then osteoporosis occurs.
After menopause, bone reabsorption in women increases as there is an increase in loss of bone, and estrogen deficiency occurs.
After menopause, the risk of osteoporosis and fracture increases as some women attained a low peak bone mass after menopause.
Fracture risk increases.
The individual shows a stooped posture or curved back.

CAUSES

Menopause in females.
Protein deficiency
Malnutrition
Long term steroid therapy
Cushing syndrome
Phenobarbitone therapy

RISK FACTORS FOR OSTEOPOROSIS

Drugs- Corticosteroids(reduce bone formation by inhibiting osteoblast function & promoting apoptosis in osteoblasts & osteocytes), anticonvulsants.
Endocrine diseases- Early menopause, hyperthyroidism, Cushing syndrome.
Inflammatory diseases- Rheumatoid arthritis, ankylosing spondylitis, Inflammatory bowel disease.
Respiratory diseases- Cystic fibrosis, COPD.
Gastrointestinal diseases- Chronic liver disease, malabsorption,
Miscellaneous- Poor diet, smoking, HIV, myeloma.

Most important cause - corticosteroid therapy.
Risk increases when the dose of prednisolone exceeds 7.5mg daily for more than 3 months.
Corticosteroids inhibit intestinal calcium absorption

Corticosteroids also lead to secondary hyperparathyroidism because of the renal calcium leakage and thus reduce in serum calcium level.
Osteoclastic bone reabsorption also gets increased.
If the steroids dose becomes high then hypogonadism occurs.

Risk factors can be split between-

Nonmodifiable
Modifiable

Nonmodifiable:

Age of an individual.
Sex(as females are more prone to osteoporosis because of estrogen deficiency, males also have decreased testosterone levels but they are less suffered as compared to women).
Family history.
If the height of an individual is short then the individual is more prone to osteoporosis.
If an individual suffers from a fracture earlier are likely to have another fracture.

Modifiable:

Alcohol intake
Deficiency of VITAMIN D
Malnutrition
Antacids
Lack of exercises
Tobacco smoking.

Medical disorders:

Kidney diseases
Immobility in the body of an individual
Parkinson's disease
Rheumatological disorders
Disorders which are inherited through genes
Disorders in blood

CLINICAL FEATURES

Asymptomatic until a fracture occurs.
Loss of strength.
Most frequent site: forearm(colles' fracture), dorso-lumbar spine, hip fracture.
Pain
Slight height loss & increased kyphosis.

INVESTIGATIONS

DEXA(dual-energy X-Ray absorptiometry)- For the Bone mineral density of the lumbar spine and hip.
For measuring bone density-

T- score.
Z- score.
Osteoporosis is diagnosed when the T-score value falls to -2.5 or below.
T- score above -1.0 is regarded as normal.

3. Neutron activation analysis.

4. bone biopsy.

Other tests include- Blood test

TFTs(thyroid function test).
Immunoglobulins.
ESR(erythrocyte sedimentation rate).
25(OH) vitamin D.
Sex hormone & Gonadotrophin level.
Calcium phosphate.

MANAGEMENT

MEDICAL MANAGEMENT:

Calcium supplementation.
Vitamin D.
Androgens.
Estrogens.
High protein in the diet.
Alandronate.
Calcitonin.
Teriparatide.
Strontium ranelate.
Biphosphonates.
Hormone replacement therapy.
Pharmacological treatment is indicated in patients: T-score- below -2.5.

ORTHOPEDIC TREATMENT

Exercise.
Bracing.

Limitation of alcohol intake.
Cessation of smoking.

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Stages of fracture healing

2020-09-30T21:35:00.004-07:00

Stages of fracture healing

Hello students and my dear friends, today I'm going to discuss the healing of fractures of cortical bone & cancellous bone along with the factors affecting fracture healing.

Let's first discuss the stages of healing fracture of cortical and cancellous bone.

The healing of bone differs from soft tissue healing from the stage of granulation tissue formation.

STAGES IN FRACTURE HEALING( CORTICAL BONE )

Stage of hematoma
Stage of granulation tissue
Stage of callus
Stage of remodeling (consolidation)
Stage of modeling (remodeling)

1) STAGE OF HAEMATOMA

It lasts up to 7 days
Formation of hematoma after the fracture of the bone, between and around the fracture, as blood leaks out through torn vessels in the bone.
From the fracture ends, the periosteum and local soft tissues are displaced. Because of this, ischemic necrosis of the fracture ends occur over a variable length(usually only a few mm).
The blood supply in the area is thin, some oocytes die whereas others are stimulated to react afterward by modifying into daughter cells.
Later, these cells contribute to the healing process.

STAGE OF GRANULATION TISSUE

It lasts for about 2-3 weeks.
Daughter cells produce cells in this stage which alters and designs to provide blood vessels, fibroblasts, osteoblasts, etc.
Collectively they form soft granulation tissue in the spaces between the fractured segments.
This cellular tissue eventually gives a soft tissue facility to the fracture; without any fundamental rigidity.
The blood clot gives rise to loose fibrous tissue mesh.
The loose fibrous mesh helps as a core for the ingrowth of fibroblasts and new capillaries.
This clot is sequentially eliminated by macrophages, giant cells, and other cells arising in the granulation tissue.
Granulation tissue further differentiates to create osteoblast then finally form bone.

STAGE OF CALLUS

Last for about 4-12 weeks.
The granulation tissue differentiates further and creates osteoblasts. An intercellular matrix becomes impregnated with calcium salts. This results in the formation of woven bone(callus).
Usually, after 3 weeks of fracture, the callus is the first sign of union visible on X-Ray.
It gives good strength to the fracture.
Callus formation- Adults < Children ; Cortical bone < cancellous bone.

STAGE OF REMODELING

Stage of consolidation.
Woven bone is substituted by mature bone with a typical lamellar structure.
It is a slow process and takes 1-4 years.

STAGE OF MODELING

Stage of remodeling.
The bone is gradually strengthened in this stage.
At the endosteal and periosteal surfaces, the sharpening of cortices occurs.
Weight-bearing stresses and muscle forces of a person when it resumes its activity are the major stimulus to this process which comes from local bone strains.

HEALING OF CANCELLOUS BONE

Cancellous bones have a large area of contact between trabeculae as the bone is of uniform spongy texture and has no medullary cavity.
The union can occur right between the bony trabeculae.
Mature osteoblasts lay down the woven bone in the intracellular matrix and join the two fragments together.

PRIMARY AND SECONDARY BONE HEALING

In primary fracture healing, bone healing occurs directly without the formation of callus.
As there is no callus formation, it is difficult to evaluate union on X-Ray.
Primary fracture healing occurs when edges are touching each other exactly.
It occurs where the hematoma has been disturbed.

SECONDARY BONE HEALING

This occurs where the hematoma is not disturbed.
Healing occurs with callus formation.
It can be evaluated on X-Ray.
Eg. Comminuted fracture.
It occurs in those fractures which operated without disturbing the fracture hematoma.

FACTORS AFFECTING FRACTURE HEALING

Age of the patient- Children > Adults > Old
Type of bone- Flat and cancellous bones > Tubular and cortical bones
The pattern of fracture- Spiral fracture > Oblique fractures
Immobilization- not necessary to immobilize all fractures( fractures of ribs, scapula) they heal itself anyway; some fractures need immobilization and still not heal( fracture of the neck of femur).
Compression at fracture sites- it enhances the rate of the union of cancellous bone.
Open fracture- they often go into delayed union and non-union.

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Anatomy of bone

2020-09-27T04:55:00.008-07:00

Anatomy of bone

Bone is the hardest part of the body which is covered by muscle.

Classification of bone

Long bone
Short bone
Flat bone
Irregular bone

Let's discuss the structure of the typical long bone

In children, a typical long bone lets take an example of the femur has 2 ends which are also known as epiphyses, and an intermediary portion called the shaft, which is also known as diaphysis.

The part of the shaft which joins the epiphyses is called metaphysis.

Epiphyses and metaphyses are separated by a thin plate of growth cartilage, one at each end.

This plate is known as the epiphyseal plate.

At maturity, the epiphyses are fuses with the metaphysis.

The epiphyseal plate gets replaced by bone.

Articular cartilage covers the articular ends of the epiphyses.

Periosteum covers the rest of the bone and it provides attachment to the tendons, muscles, ligaments, etc.

Sharpey's fibres are present which connects the bone to the periosteum & they are the strands of fibrous tissue.

Now, If we classify bone microscopically then the bone can be classified as woven and lamellar.

Woven bone(fibrous bone): Immature bone; and is characterized by random organisations of osteocytes (bone cells) and collagen fibres.

At the initial stages of fracture healing, woven bone is formed at periods of rapid bone formation.
Woven bone is mechanically more immature(weaker) bone.
It can be found in the foetal skeleton.

Lamellar bone( mature bone): It has orderly arrangments of osteocytes (bone cells) and collagen fibres.

Lamellar bone constitutes of both cortical and cancellous bone.
But there is a difference between lamellae in these bones, i.e. the cortical bone lamellae are densely packed, and the cancellous bone lamellae are loosely packed.
Osteon– a basic structural unit of lamellar bone. Central canal or Haversian the canal is surrounded by a series of concentric laminations or lamellae.
These canals move longitudinally and join freely to each other and with volkmann's canal.
The following runs horizontally from an endosteal to periosteal surfaces.
The shaft of the bone is made up of cortical bone and the ends are mainly made up of cancellous bone. The junction between the cortical bone and the cancellous bone is termed as corticocancellous junction which is the most common site of fractures.

Haversian canal- series of minute tubes in the outermost zone of the compact bone or cancellous bone, that allows blood vessels and nerves to travel through them.

Each Haversian canal usually contain one or two capillaries and nerve fibres.
The channels are grown by concentric layers called lamellae.
Envelops the blood vessels and nerve cells throughout the bones and communicates with bone cells through connections termed as canaliculi. This unique pattern is carried to mineral salt deposits & storage which gives bone tissue its strength.
Most of the individual lamella form concentric rings around the larger longitudinal canal in the mature compact bone, within the bone tissue, these canals are called as Haversian canal.
Osteons are present in the Haversian canal.

Volkmann's canals: tiny channels in the bone that transmit blood vessels from the periosteum into the bone and that interact with the Haversian canals.

It provides energy and nourishing element for osteons.

Let discuss the composition of bone :

Bone is made up of:

Bone cells
Extracellular matrix (organic and inorganic)

Bone cells:

a) osteoblast

b) osteocytes

c) osteoclasts

Blood supply of bones

Nutrient artery
Metaphyseal vessels
Epiphyseal vessels
Periosteal vessels

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Fracture and its classification

2020-09-25T23:57:00.014-07:00

Fracture and its classification

Hello students and friends, today we are going to discuss what is a fracture and its classification. So let's discuss first what is a fracture.
There are 206 bones in the body.
A fracture is a breach within the continuity of a bone.
Here we discuss different types of fractures according to their classification.

Types of fractures

The fracture can be classified as:

Based on Aetiology

Traumatic fracture

 A traumatic fracture is defined as a continuous fracture of bone due to trauma.
Due to excessive force, the normal bone can break as in the case of an accident or when a person is hit by a heavy object.
Traumatic fracture includes day to day practice fall.
Fracture caused by a fall, road traffic accident, etc. is included in a traumatic fracture.

Pathological fracture-

A pathological fracture is defined as a fracture of a bone which has been made weak by some underlying disease.

This fracture is caused due to pathological factors, there is no force required to cause such type of fracture.

For example fracture through a bone that gets weakened by metastasis.

The most familiar cause of pathological fracture is osteoporosis.

Some other factors are-

Tumors

Bone cyst

Osteomyelitis

Osteoporosis

Rickets

Stress fracture-

a stress fracture is defined as the fracture occurring at a site in the bone which is subjected to repeated minor stresses/injury causing a break in bony trabeculae over a while.

If there is a condition of osteoporosis but the person uses the bone repeatedly then the condition of stress fracture may occur.

Repetitive force and overuse of bone may lead to a stress fracture and tiny cracks in the bone may occur.

Pain is there but stress fracture may not be visible on X-Ray.

Based on displacements

Undisplaced fracture: there is a breakage of bone in which the bone remains aligned and these fractures are easy to identify by the absence of vital displacement.
Displaced fracture: there is a breakage in the bone in which the fragments are not aligned.
In displaced fracture fragments are separated and fracture may be displaced.
Factors which are responsible for displacement are:
Fracturing force
Muscle pull on the fracture fragment
Gravity
Displacement of the distal fragment to the proximal fragment occurs.
The displacement can exist in the form of-
Angulation
Shift
Rotation
Based on the association with the external environment

Open fracture: open fracture is defined as a fracture with a break in the overlying skin and soft tissue which then leads to the fracture communicating with the external environment.

The open or compound fracture includes wounds that communicate with the fracture or where the fracture hematoma is exposed.

Contamination occurs at the site where fracture hematoma is exposed.

Open lesions carry a higher risk of infection.

a) Internally open fracture- internally open fractures are sharp fracture end pierces the skin from within.

b) Externally open fracture- fracture by an object which tears the skin and soft tissue over the bone, as the object breaks then this fracture resulting in an open fracture.

Closed fracture: in closed fracture, the overlying skin and soft tissue structures are intact with each other and the fracture is not communicating with the external environment.

Based on the complexity of treatment

Simple fracture: simple fracture is easy to treat and it can be defined as a fracture in two pieces.

Eg. Transverse fracture of the humerus.

Complex fracture: complex fracture is usually difficult to treat and it can be defined as a fracture in multiple pieces.

Eg. Comminuted fracture of the tibia.

Based on the amount of force causing a fracture

High-velocity injury: These are fractures sustained as a result of severe trauma force, as in road traffic accidents.

In these fractures, there is severe soft tissue damage (periosteal and muscle injury).

Such fractures are often unstable, and slow to heal because there is extensive devascularisation of fracture ends.

Low-velocity injury: These fractures are sustained as a result of mild fracture force.
For example when a person falls.
These fractures often heal as expected because there is little soft tissue injury.
Later, there is a change in the pattern of fracture due to shifting from low velocity to high-velocity injuries.
More complex fractures are arises which are difficult to treat.

Based on pattern

Transverse fracture: In the transverse fracture, the line is perpendicular to the long axis of the bone.

Tapping or bending force results in such type of fracture.

Oblique fracture: The fracture in which the fracture line is at an oblique angle to the long axis of the bone.

Bending force results in such type of fracture.

Spiral fracture: An important form of oblique fracture in which the fracture line rotates along the long axis of the bone.

In this fracture, the fracture line goes spirally in more than one plane.
The primary twisting force results in such type of fracture.
This fracture occurs secondary to the rotational force.

Comminuted fracture: In comminuted fracture, the bone is broken into many fragments.

A comminuted fracture is caused by crushing or compression force along the long axis of the bone.

Segmental fracture: When there are two fractures in one bone, but these fractures are at a different level then the fracture is termed as a segmental fracture.

OTHER FRACTURES:

GREENSTICK FRACTURES: Fracture in the young bone of children.

MONTEGGIA FRACTURE- DISLOCATION: It is the fracture of the proximal third of the ulna with dislocation of the head of the radius.

SMITHS FRACTURE: This fracture happens in adults, at the cortico-cancellous junction of the distal end of the radius with ventral tilt and other displacements.

COLLE'S FRACTURE: This fracture occurs in adults, at cotico- cancellous junction of the ventral end of the radius with dorsal tilt and other displacements.

RONALDO FRACTURE: It is the fracture of the base of the 1st metacarpal.

MARCH FRACTURE: Fracture of the distal 1/3rd of the metatarsals head.

HANGMAN'S FRACTURE: It is a fracture through the pedicle and lamina of the C2 vertebra, with partial dislocation of C2 over C3, and sustain hanging.

POTT'S FRACTURE: In this fracture, one or both malleoli are affected.

MASSONIASE FRACTURE: Fracture of the ankle occurs, there is a fracture of the neck of the fibula.

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Chronic Bronchitis

2020-09-23T21:36:00.006-07:00

Chronic Bronchitis

Hello students and friends, today we are going to discuss chronic bronchitis.

Here you will get what is chronic bronchitis, its signs, and symptoms, causes, pathophysiology, risk factors, complications, diagnosis, and treatment.

If your family member or friends are suffering from chronic bronchitis then preventive measures which have to be taken are discussed here.

Now, let us start with its basic definition,

Chronic bronchitis is defined as a productive cough that leads for 3 months or at least two years.
Most people with chronic bronchitis have COPD.
This is a serious condition which is caused by inflammation and irritation of the bronchial tubes due to the overproduction of mucus.When mucus builds up there is this disallowing of sufficient air into the lungs.
The major cause of CB. is tobacco smoking.

Signs and symptoms

Chronic bronchitis is often characterized by persistent cough with sputum or mucus.
Shortness of breath
Chest pain
Fatigue
Ankle, feet, and leg swelling
Frequent cold or flu
Low-grade fever and chills
Wheezing
Lung infections
Sputum (yellow or green color or sometimes bloody)
Chest discomfort

Causes of chronic bronchitis

Chronic bronchitis is caused by smoking.
Inhaling irritating fumes or dust.
Viruses such as the flu virus or influenza virus.
Inflammation of bronchi is normally caused by paralysis of cilia which stops the normal movement of mucus from the Airways and this is the primary cause of mucus buildup due to pathogenic microbes.
Chronic inhalation of air pollution or irritating fuels or dust from industries of coal mines, textile manufacturing, livestock farming, and grain handling may also, be risk factors for the development of chronic bronchitis.
Air pollution allergy and infection can make it worse.
Chronic bronchitis occurs most often during the cold and flu season.

Pathophysiology

In chronic bronchitis, there is a narrowing of the airway starting with bronchi and there is an increase in airflow resistance and breathing rate also gets increases.
Hypoxemia and hypercapnia occur
Hypoxemia is a decrease in oxygen level in the blood and hypercapnia is increase in carbon dioxide.

Risk factors

People who are at high risk are:

Smokers
The elderly, infants, and young children
Patient with heart or lung disease
Weekend immune system with an increase in age
COPD
Repetitive exposure to lung irritants.

Major complications

Breathing difficulty
Pneumonia
Pneumothorax
Enlargement and weakening of right heart ventricle muscle
Respiratory failure
Emphysema
Lung transplantation
Cor pulmonale
Pulmonary hypertension
Polycythemia

Diagnosis

Physical examination
Chest X-Ray
Medical history and examination of the lung
Pulse oximetry (Oxygen saturation may be measured by placing a sensor on the finger)
Pulmonary function test
Spirometry (spirometry measures the inhalation and exhalation of the lungs as well as the efficiency rate of transfer of oxygen to the blood. This is performed in the patient who is having a persistent cough)
Peak flow meter (it assesses the change in breathing)
A microscopic examination or culture of a sample of phlegm may be obtained to look for a bacterial infection(Phlegm is a type of mucus produced in the lungs and lower respiratory tract).
Arterial blood gas (ABG)- it is a type of blood test which evaluates the carbon dioxide and oxygen levels in the blood.
CT scan

Treatment

Chronic bronchitis is a long-term disease of the lung which never goes away completely.
Symptoms may be treated by the means of :

Lung volume reduction surgery
Inflammation and edema of the respiratory tract epithelium may be reduced with inhaled corticosteroids.
Lung transplantation
Pulmonary rehabilitation
Supplemental Oxygen
Bronchodilators - wheezing and shortness of breath can be treated by reducing bronchospasm with bronchodilators
Oral medications
Cough suppressants or expectorants
Nebulizer treatment
Antibiotics
Drinking a lot of water breathing techniques and nutritional counting and stop smoking may help in treating the symptoms.

Prevention and control

Chronic bronchitis can be prevented by:

No smoking
Stay away from environmental pollution
Washing hands often to avoid the spreading of microbes.

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EMPHYSEMA

2020-09-23T00:25:00.006-07:00

EMPHYSEMA

Emphysema ( Greek : emphysan: inflate Itself composed of en meaning in and physan meaning breath, blast)

Emphysema means swelling.
Emphysema is included in a group of the disease called chronic obstructive pulmonary disease (COPD).
It is often caused by long term exposure to air pollution or smoking.
Emphysema causes dilation of air spaces by the destruction of the alveolar wall, leading to the collapse of alveoli during expiration.
Emphysema is a long-term progressive disease of the lungs that primarily causes shortness of breath.
There is the destruction of lung tissue around smaller sacs, called alveoli, which makes their air sacs unable to hold their functional shape upon exhalation. That is why it is called obstructive lung disease.

ETIOLOGY

1)Tobacco smoking

2) Atmospheric pollution
3) Infections
4) Genetic factor
5) Alpha-1 antitrypsin deficiency
6) Inherited diseases (rare) [ Marfan syndrome, Menke's syndrome]

7) Severe cases of Alpha I antitrypsin deficiency may also develop cirrhosis of the liver, where Alpha I antitrypsin gets accumulated and then leads to fibrotic reaction.

8) When persons enter at the age of 20 years, the new alveoli tissue development stops and simultaneously the lung tissue starts to deteriorate. Pulmonary elasticity will also be lost as alveoli die, the number of lung capillaries starts declining and after the breakdown of the lung, elastin begins.

As the age increases, they will also lose strength along with the mass in their chest muscles and the muscles get weaken.
With the increasing age, our bone density also gets reduced, and bones start to deteriorate and this will affect the posture of the body.
Together, if we see all age-related aspects then we conclude that they can cause the development of emphysema. Though it is not necessary, there is a risk of having decreased respiratory function.

9) Second-hand smoke

10) Chemicals and toxins

CLINICAL FEATURES

"Pink puffer"

1) Barrel chest deformity
2) lung volume increases
3) Vital capacity decreases
4) Loss of weight
5) Peptic ulceration
6) Speaks in short, jerky sentences
7) Purse lip breathing
8) Minimal cyanosis
9) Cough with or without expectorant
10) Hyperventilates and less hypoxemia (pink)
11) Prolonged expiratory time
12) Anxious
13) Use of accessory muscles
14) Thin appearance

CLASSIFICATION

1) Centriacinar emphysema :

• Also called as centrilobular emphysema.
• Occurs most commonly in the upper lobes.
• The respiratory bronchiole is expanded.
• There is dilation of the respiratory bronchiole.
• The distal acinus or alveoli are unchanged.
• It can co-exist with chronic bronchitis.
• Invariably occurs in smokers.
• Mostly coal mine workers which exposed more to carbon and dust are affected.

2) Panacinar emphysema:

• Also called as pan lobular emphysema.
• Whole of acinus is uniformly affected.
• The entire respiratory acinus, from respiratory bronchioles to alveoli, is expanded.
• Occurs more commonly in lower lobes(especially basal segments, and anterior margins of the lungs).
• Associated with:
1) Alpha antitrypsin deficiency
2) Cigarette smokers

3) Paraseptal emphysema

• Distal acinar.
• Involves alveolar ducts and sacs at the lung periphery.
• Associated with spontaneous pneumothorax.
• It may also be seen in older patients with centrilobular emphysema.
"Both centrilobular and paraseptal emphysema may progress to bullous emphysema"

~Bulla - Bulla is defined as being atleast1 cm in diameter, and with a wall less than 1 mm thick.

When the air gets trapped inside the emphysematous spaces, there is a local expansion of the structure.

• Least common.
• Localized along pleura- peripheral part of the acinus.

4) Irregular emphysema:

• Most common.
• Least significant.
• Common around scar tissue

• There is congenital extrinsic compression by an abnormally large pulmonary artery. This causes malformation of bronchial cartilage, making them soft and collapsible.

There is a special type of emphysema. congenital lobar emphysema.

CONGENITAL LOBAR EMPHYSEMA

• CLE is potentially reversible.
• CLE cause respiratory distress in the neonates.
• Life-threatening.
• CLE is a severe case of bullous emphysema.
• CLE results in over expansion of a pulmonary lobe and resultant compression of the remaining lobes of the ipsilateral lung, and possibly also the contralateral lung.

SIGNS AND SYMPTOMS

Alpha-1 antitrypsin destruction
Smoking
Shortness of breath(Dyspnea)
Tachypnea(rapid breathing)
Anteroposterior diameter of the chest increase(Barrel chest)
Hypoxia
Cyanosis

PATHOPHYSIOLOGY

Smoking is the main cause of emphysema.
In the case of emphysema, the elasticity of the lung is lost.
Bronchioles gets enlarged and the walls of the alveoli get destructed.
Alveoli and small distal airways are affected and then the larger airways also get affected by emphysema.
The stabilizing function of the bronchioles loses and there is collapsing of airways so gases will remain in it and the bronchioles get enlarged.
Blisters are formed and the walls of the lungs tissue get diminished.
As smoking is the main cause of emphysema, so the inhaled irritants cause inflammatory cells to release from polymorphonuclear leukocyte(basophils, eosinophils, and neutrophils) and alveolar macrophages to move into the lungs.
The irritants which released from smoking will affect on Alpha I antitrypsin and reduce its activity. Therefore, emphysema develops.
As there is a reduction of the alveolar tissue then there is a reduction in the surface area for the exchange of gases.
It can also lead to Cor pulmonale.

Cor pulmonale is also called as right-side heart failure. The right ventricle of the heart gets enlarged due to high blood pressure in the lungs and it is usually caused by chronic lung disease.

SOME IMPORTANT POINTS TO BE REMEMBERED:

Here I'm including some important points about Alpha I antitrypsin and some medical terminologies which are important for understanding emphysema.

If there is a genetic deficiency of Alpha I antitrypsin -

Non-smokers- its deficiency will not affect that much in non-smokers.
Smokers- low level of Alpha I antitrypsin increases the risk of emphysema in smokers because it may progress more rapidly in smokers as smoking reduce its activity. If there is a low level of Alpha I antitrypsin then the chances of lung diseases also get increases and the person is more likely develops chances of COPD( chronic obstructive pulmonary disease)

As we find out the deficiency of Alpha I antitrypsin affects our lung as well as leads to COPD, so let's discuss COPD & Alpha I antitrypsin.

COPD( Chronic Obstructive Pulmonary Disease)

In COPD, there is a blockage in the airflow which leads to breathing problems.
As airflow blocks so there is difficulty in breathing.
It gets block by a group of lung diseases.
Most common conditions involve in COPD-

Emphysema
Chronic bronchitis

Damage to both acinar level- emphysema
Damage at bronchial level- bronchitis.
Common extrinsic trigger- cigarette smoking.

ALPHA I ANTITRYPSIN :

Alpha I antitrypsin is a protein made by the liver.
Its function is to protect the lungs.
If there is a deficiency of Alpha I antitrypsin then the risk of developing emphysema and other disorders related to AAT deficiency will increase.
It is a rare hereditary condition.
Both parents must have at least 1 copy of the abnormal alpha I antitrypsin deficiency gene. If they have a copy of an abnormal gene then the disease will inherit to their child.
Basically, it is caused by changes in the SERPINA1 gene. This gene gives the instruction to make the alpha 1 antitrypsin protein.
AAT's main function is to protect the body from another protein called neutrophil elastase.
Neutrophil elastase is an enzyme that helps the body to fight with infections, but it can also attack the lungs and also to the other healthy tissues of the body if it is not controlled by AAT.
As there is a deficiency of AAT, then this allows the neutrophil elastase to destroy the lung tissue, and thus lung disease occurs.
Testing is done by taking blood samples and it is simple, quick, and highly accurate.
Normal Range- 100-300 mg/dL ; Less than 80 mg/dL- significant risk for lung diseases.

DIAGNOSIS OF EMPHYSEMA

X-Ray of chest[ lungs are hyper- expanded; coarse bronchovascular markings; increase in anteroposterior diameter; diaphragm has normal contour].
Atrial Blood Gas analysis[measures how well your lungs transfer oxygen to your bloodstream and how well carbon dioxide removes from the body].

TREATMENT OF EMPHYSEMA

Oxygen therapy
Bronchodilators
Steroids
Corticosteroids in an inhaler form
Surgery or lung transplant
Pulmonary rehabilitation
Antibiotics
Vaccines ( to prevent the disease, the patient should receive a flu shot annually and pneumonia shot every 5-7 years)
Protein therapy.

Disclaimer for https://physioworldblog.blogspot.com/ If you require any more information or have any questions about our site's disclaimer, please feel free to contact us by email at deepikajoshi12347@gmail.com. Disclaimers for Physioworld's blog All the information on this website - https://physioworldblog.blogspot.com/ - is published in good faith and for general information purpose only. Update Should we update, amend or make any changes to this document, those changes will be prominently posted here.