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The moment the tips of my fingers detected a lump in my breast, a white, cold fear flooded through me.

It was a nondescript day during the usual end-of-year chaos, so the mental turbulence of receiving the eventual breast cancer diagnosis mingled with prize-givings and school concerts.

To steady my mind, I reassured myself that early-stage breast cancer was curable, my doctors were confident and the course was clear.

So, when my surgeon told me after she had removed the tumour that there was also a second type of cancer in my breast, I fell apart.

By this point, I had undergone a mammogram and an ultrasound and there was no hint of a second cancer.

The original tumour was obvious to the touch, but neither I nor the doctors who examined me had detected any other change.

A few weeks earlier, I didn't know there were different forms of breast cancer. Now, the disease was landing a one-two punch.

The second blow had me reeling because my doctors had no idea how big the cancer was, or where it was located.

I now know all of that is typical of this type of breast cancer - including the lack of awareness.

The second cancer I had is called lobular breast cancer.

No-one I've spoken to outside of medical circles or cancer support groups has heard of it.

Most women I've told about my diagnosis are visibly shocked to discover there's a detection-evading form of the disease.

So, over the past few months, I've gone back to the clinicians who treated me and other experts in the field to find out what we know about lobular breast cancer, and how women can look out for it.

How common is lobular breast cancer?

Lobular breast cancer accounts for 10-15 per cent of all breast cancers.

Around the world and in Australia it is on the rise.

In the four years to 1990, lobular cancer accounted for about 8 per cent of Australian breast cancer cases.

By 2019, that had risen to around 13 per cent, which is between 2,000 and 3,000 women per year.

If the number of lobular breast cancer cases were recorded separately from other breast cancers, lobular would be more common in Australian women than ovarian and cervical cancer.

And yet there is only one government-funded Australian project researching lobular cancer.

The National Health and Medical Research Council said that in the past 12 years, it had only received one application that contained the term "lobular".

Cancer researcher Dr Amy McCart Reed from the University of Queensland is working on the project.

She said there was a strong push in the US to raise awareness about lobular breast cancer and drive more research funding towards it.

"In Australia, not a huge amount of lobular breast cancer research is undertaken," she said.

Her team is looking at the special features of lobular cancer cells to see if they can find a drug that could target them.

"We should have targeted therapies for lobular breast cancer patients because these tumours are inherently different," she said.

How is lobular cancer different to other types of breast cancer?

The most distinct feature of lobular cancer is that it often grows in single-file strands of cells that spread out through the tissue.

This was clear to me when Professor Andrew Field - the pathologist who discovered lobular cancer in my breast - showed me images of the two cancers I was diagnosed with.

At his laboratory at St Vincent's Hospital in Sydney, he pulled up a photo of the lump I had removed.

The cancerous mass is obvious to a naked eye, but what was hiding alongside it took a microscope to find.

In an astonishing stroke of good luck (which he called "doing his job"), when Professor Field examined the tumour, he spotted cells of lobular cancer in the thin margin around it.

Even on the images he showed me under a microscope, it's hard to discern the strings of cells that spread out like lines of little ants.

Because of what Professor Field discovered, I went back for more extensive surgery, which revealed multiple sites (or foci) of lobular cancer throughout my breast.

"We found 13 of these little foci and they are very separate from each other," Professor Field said.

It is this diffuse growth pattern that helps lobular cancer stay hidden and means it is often diagnosed at a more advanced stage.

Why is lobular breast cancer harder to detect on medical images?

Before we go any further, it's important to note that mammograms are effective tools for picking up breast cancer.

In fact, Australia's breast screen program, which uses mammograms, detects about half of all invasive breast cancer cases in women aged 50-74 and nearly 60 per cent of those are caught early.

That said, none of the 13 places lobular cancer set up shop in my breast showed up on my mammogram.

So, I took my images to radiologist Professor Mary Rickard, who specialises in breast imaging at the Sydney Breast Clinic, to find out if she could see anything other radiologists missed.

She couldn't.

Because lobular cancer forms as strings of cells, it doesn't always show up as a discernible shape on a mammogram.

What made it extra difficult was breast density.

My breasts happen to be extremely dense. In fact, my surgeon once described my mammogram as "like looking at a snowstorm".

When you look at a mammogram, the white bits are the glands, ducts and fibrous tissue; the black is fatty tissue.

Women who have dense breasts, or more fibro-glandular tissue, will have more white show up on a mammogram.

Because radiologists look for changes in the shape or pattern of the tissue, cancers can be hard to spot in mammograms for women with dense breasts.

"The denser the breast, the more difficult to find a cancer generally, and lobular is more difficult than other cancers," Professor Rickard said.

What should women do to check for lobular cancer?

Professor Rickard wants all women who have a mammogram to know their breast density, which is rated from A to D, with D being the most dense.

"We would normally recommend that anybody who has a C or D density went on to ultrasound examination," she said.

Ultrasound imaging uses high-frequency soundwaves to examine internal structures, so it can be useful for finding tumours in dense breasts.

But Professor Rickard said this technique could also struggle to identify a lobular cancer that has grown in between the breast tissue, rather than as a mass.

"Mammograms are not sensitive for it, ultrasound is not sensitive for it," she said.

That's not to say they will never pick it up, but rather that women who are still worried should consider a form of imaging that uses an injected contrast dye.

Professor Rickard said MRIs and contrast-enhanced mammography detect 90 to 95 per cent of cancers.

"All tumours are more likely to be picked up by a contrast image," she said.

Why you should 'advocate strongly for yourself'

Unfortunately, the government does not subsidise contrast mammograms and only offers a subsidy for MRI to very high-risk patients.

But knowing your own breasts is free.

That's why women are now recommended to not just check for lumps, but to be "breast aware".

Read more about this story:

Professor Rickard said that meant knowing the size and shape of your breasts and looking for any change such as a thickening or hardening, the skin or nipple pulling in, discharge from the nipple, or distortion in the shape of the breast.

"People need to be aware that their breast looks different, feels different, not just that they have a lump," she said.

Vicki Durston from the Breast Cancer Network Australia said her organisation now promoted "breast awareness", encouraging women to be familiar with their breasts so they could pick up changes early.

"If you notice a change that is unusual for you, it is important you see your doctor as soon as possible," she said.

Dr McCart Reed said many lobular patients reported a sense of thinking something was not right.

She wants women to know they should see a doctor about any changes they notice and to follow up if they still think something is wrong.

"Advocate strongly for yourself," she said.

It's now been four years since the day I sat across from my breast surgeon trying to wrap my head around having the misfortune of being diagnosed with two types of breast cancer at once.

Now, I'm thankful I did, because the one that was possibly the biggest threat would have gone unnoticed, had it not been for the luck of finding the other one.

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This tricky breast cancer is sneaking up on women, and there's very little research into it

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Four years after being diagnosed with a form of breast cancer that's hard to detect, ABC journalist Mary Lloyd goes back to her doctors to find out how women can look out for it.

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Inflammatory Breast Cancer: Rare, Not Impossible | Tatiana Cordts | TEDxACU

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Learning Objectives

Define the different types of body movements

Identify the joints that allow for these motions

Synovial joints allow the body a tremendous range of movements. Each movement at a synovial joint results from the contraction or relaxation of the muscles that are attached to the bones on either side of the articulation. The type of movement that can be produced at a synovial joint is determined by its structural type. While the ball-and-socket joint gives the greatest range of movement at an individual joint, in other regions of the body, several joints may work together to produce a particular movement. Overall, each type of synovial joint is necessary to provide the body with its great flexibility and mobility. There are many types of movement that can occur at synovial joints (Table 1). Movement types are generally paired, with one being the opposite of the other. Body movements are always described in relation to the anatomical position of the body: upright stance, with upper limbs to the side of body and palms facing forward.

Watch this video to learn about anatomical motions. What motions involve increasing or decreasing the angle of the foot at the ankle?

Flexion and Extension

Flexion and extension are movements that take place within the sagittal plane and involve anterior or posterior movements of the body or limbs. For the vertebral column, flexion (anterior flexion) is an anterior (forward) bending of the neck or body, while extension involves a posterior-directed motion, such as straightening from a flexed position or bending backward. Lateral flexion is the bending of the neck or body toward the right or left side. These movements of the vertebral column involve both the symphysis joint formed by each intervertebral disc, as well as the plane type of synovial joint formed between the inferior articular processes of one vertebra and the superior articular processes of the next lower vertebra.

In the limbs, flexion decreases the angle between the bones (bending of the joint), while extension increases the angle and straightens the joint. For the upper limb, all anterior-going motions are flexion and all posterior-going motions are extension. These include anterior-posterior movements of the arm at the shoulder, the forearm at the elbow, the hand at the wrist, and the fingers at the metacarpophalangeal and interphalangeal joints. For the thumb, extension moves the thumb away from the palm of the hand, within the same plane as the palm, while flexion brings the thumb back against the index finger or into the palm. These motions take place at the first carpometacarpal joint. In the lower limb, bringing the thigh forward and upward is flexion at the hip joint, while any posterior-going motion of the thigh is extension. Note that extension of the thigh beyond the anatomical (standing) position is greatly limited by the ligaments that support the hip joint. Knee flexion is the bending of the knee to bring the foot toward the posterior thigh, and extension is the straightening of the knee. Flexion and extension movements are seen at the hinge, condyloid, saddle, and ball-and-socket joints of the limbs (see Figure 1).

Hyperextension is the abnormal or excessive extension of a joint beyond its normal range of motion, thus resulting in injury. Similarly, hyperflexion is excessive flexion at a joint. Hyperextension injuries are common at hinge joints such as the knee or elbow. In cases of "whiplash" in which the head is suddenly moved backward and then forward, a patient may experience both hyperextension and hyperflexion of the cervical region.

Abduction, Adduction, and Circumduction

Abduction and adduction are motions of the limbs, hand, fingers, or toes in the coronal (medial-lateral) plane of movement. Moving the limb or hand laterally away from the body, or spreading the fingers or toes, is abduction. Adduction brings the limb or hand toward or across the midline of the body, or brings the fingers or toes together. Circumduction is the movement of the limb, hand, or fingers in a circular pattern, using the sequential combination of flexion, adduction, extension, and abduction motions.

Adduction, abduction, and circumduction take place at the shoulder, hip, wrist, metacarpophalangeal, and metatarsophalangeal joints.

Abduction and Adduction

Abduction and adduction motions occur within the coronal plane and involve medial-lateral motions of the limbs, fingers, toes, or thumb. Abduction moves the limb laterally away from the midline of the body, while adduction is the opposing movement that brings the limb toward the body or across the midline. For example, abduction is raising the arm at the shoulder joint, moving it laterally away from the body, while adduction brings the arm down to the side of the body. Similarly, abduction and adduction at the wrist moves the hand away from or toward the midline of the body. Spreading the fingers or toes apart is also abduction, while bringing the fingers or toes together is adduction. For the thumb, abduction is the anterior movement that brings the thumb to a 90° perpendicular position, pointing straight out from the palm. Adduction moves the thumb back to the anatomical position, next to the index finger. Abduction and adduction movements are seen at condyloid, saddle, and ball-and-socket joints (see Figure 2).

Circumduction

Circumduction is the movement of a body region in a circular manner, in which one end of the body region being moved stays relatively stationary while the other end describes a circle. It involves the sequential combination of flexion, adduction, extension, and abduction at a joint. This type of motion is found at biaxial condyloid and saddle joints, and at multiaxial ball-and-sockets joints (see Figure 2).

Rotation

Rotation can occur within the vertebral column, at a pivot joint, or at a ball-and-socket joint. Rotation of the neck or body is the twisting movement produced by the summation of the small rotational movements available between adjacent vertebrae. At a pivot joint, one bone rotates in relation to another bone. This is a uniaxial joint, and thus rotation is the only motion allowed at a pivot joint. For example, at the atlantoaxial joint, the first cervical (C1) vertebra (atlas) rotates around the dens, the upward projection from the second cervical (C2) vertebra (axis). This allows the head to rotate from side to side as when shaking the head "no." The proximal radioulnar joint is a pivot joint formed by the head of the radius and its articulation with the ulna. This joint allows for the radius to rotate along its length during pronation and supination movements of the forearm.

Rotation can also occur at the ball-and-socket joints of the shoulder and hip. Here, the humerus and femur rotate around their long axis, which moves the anterior surface of the arm or thigh either toward or away from the midline of the body. Movement that brings the anterior surface of the limb toward the midline of the body is called medial (internal) rotation. Conversely, rotation of the limb so that the anterior surface moves away from the midline is lateral (external) rotation (see Figure 3). Be sure to distinguish medial and lateral rotation, which can only occur at the multiaxial shoulder and hip joints, from circumduction, which can occur at either biaxial or multiaxial joints.

Turning of the head side to side or twisting of the body is rotation. Medial and lateral rotation of the upper limb at the shoulder or lower limb at the hip involves turning the anterior surface of the limb toward the midline of the body (medial or internal rotation) or away from the midline (lateral or external rotation).

Supination and Pronation

Supination and pronation are movements of the forearm. In the anatomical position, the upper limb is held next to the body with the palm facing forward. This is the supinated position of the forearm. In this position, the radius and ulna are parallel to each other. When the palm of the hand faces backward, the forearm is in the pronated position, and the radius and ulna form an X-shape.

Supination and pronation are the movements of the forearm that go between these two positions. Pronation is the motion that moves the forearm from the supinated (anatomical) position to the pronated (palm backward) position. This motion is produced by rotation of the radius at the proximal radioulnar joint, accompanied by movement of the radius at the distal radioulnar joint. The proximal radioulnar joint is a pivot joint that allows for rotation of the head of the radius. Because of the slight curvature of the shaft of the radius, this rotation causes the distal end of the radius to cross over the distal ulna at the distal radioulnar joint. This crossing over brings the radius and ulna into an X-shape position. Supination is the opposite motion, in which rotation of the radius returns the bones to their parallel positions and moves the palm to the anterior facing (supinated) position. It helps to remember that supination is the motion you use when scooping up soup with a spoon (see Figure 4).

Dorsiflexion and Plantar Flexion

Dorsiflexion and plantar flexion are movements at the ankle joint, which is a hinge joint. Lifting the front of the foot, so that the top of the foot moves toward the anterior leg is dorsiflexion, while lifting the heel of the foot from the ground or pointing the toes downward is plantar flexion. These are the only movements available at the ankle joint (see Figure 4).

Inversion and Eversion

Inversion and eversion are complex movements that involve the multiple plane joints among the tarsal bones of the posterior foot (intertarsal joints) and thus are not motions that take place at the ankle joint. Inversion is the turning of the foot to angle the bottom of the foot toward the midline, while eversion turns the bottom of the foot away from the midline. The foot has a greater range of inversion than eversion motion. These are important motions that help to stabilize the foot when walking or running on an uneven surface and aid in the quick side-to-side changes in direction used during active sports such as basketball, racquetball, or soccer (see Figure 5).

Protraction and Retraction

Protraction and retraction are anterior-posterior movements of the scapula or mandible. Protraction of the scapula occurs when the shoulder is moved forward, as when pushing against something or throwing a ball. Retraction is the opposite motion, with the scapula being pulled posteriorly and medially, toward the vertebral column. For the mandible, protraction occurs when the lower jaw is pushed forward, to stick out the chin, while retraction pulls the lower jaw backward. (See Figure 5.)

Depression and Elevation

Depression and elevation are downward and upward movements of the scapula or mandible. The upward movement of the scapula and shoulder is elevation, while a downward movement is depression. These movements are used to shrug your shoulders. Similarly, elevation of the mandible is the upward movement of the lower jaw used to close the mouth or bite on something, and depression is the downward movement that produces opening of the mouth (see Figure 6).

Excursion

Excursion is the side to side movement of the mandible. Lateral excursion moves the mandible away from the midline, toward either the right or left side. Medial excursion returns the mandible to its resting position at the midline.

Superior Rotation and Inferior Rotation

Superior and inferior rotation are movements of the scapula and are defined by the direction of movement of the glenoid cavity. These motions involve rotation of the scapula around a point inferior to the scapular spine and are produced by combinations of muscles acting on the scapula. During superior rotation, the glenoid cavity moves upward as the medial end of the scapular spine moves downward. This is a very important motion that contributes to upper limb abduction. Without superior rotation of the scapula, the greater tubercle of the humerus would hit the acromion of the scapula, thus preventing any abduction of the arm above shoulder height. Superior rotation of the scapula is thus required for full abduction of the upper limb. Superior rotation is also used without arm abduction when carrying a heavy load with your hand or on your shoulder. You can feel this rotation when you pick up a load, such as a heavy book bag and carry it on only one shoulder. To increase its weight-bearing support for the bag, the shoulder lifts as the scapula superiorly rotates. Inferior rotation occurs during limb adduction and involves the downward motion of the glenoid cavity with upward movement of the medial end of the scapular spine.

Opposition and Reposition

Opposition is the thumb movement that brings the tip of the thumb in contact with the tip of a finger. This movement is produced at the first carpometacarpal joint, which is a saddle joint formed between the trapezium carpal bone and the first metacarpal bone. Thumb opposition is produced by a combination of flexion and abduction of the thumb at this joint. Returning the thumb to its anatomical position next to the index finger is called reposition (see Figure 6).

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Define the different types of body movements Identify the joints that allow for these motions Synovial joints allow the body a tremendous range of movements. Each movement at a synovial joint results from the contraction or relaxation of the muscles that are attached to the bones on either side of the articulation.

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Carpal Tunnel Syndrome Provocative Tests & Physical Exam

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What is the temporomandibular joint (TMJ)?

The temporomandibular joint (TMJ) is the joint that connects the jaw to the skull. There is a TMJ on each side of the face, in front of each ear. These joints allow the movements needed for speaking, eating and facial expression.

TMJ dysfunction can cause pain, abnormal jaw movements and joint noises. They are quite common.

What are the symptoms of TMJ dysfunction?

If you have TMJ dysfunction, you may have:

discomfort or pain in the jaw, especially when eating

an aching pain in front of your ear, which may spread to your face

'locking' of the jaw, making it difficult to open or close your mouth

a clicking or grating noise when you open your mouth or chew

an uncomfortable or uneven bite

headache (especially in the temples, under the eyes and at the sides of the lower jaw)

earache

neck or shoulder pain

What causes TMJ dysfunction?

TMJ dysfunction can be caused by a number of different things, including:

Sometimes, people have TMJ dysfunction without any obvious cause.

When should I see my doctor?

If you think you might have TMJ dysfunction and it is bothering you, see your doctor or dentist. They will do a physical examination. You might be asked to have an x-ray, CT or MRI scan.

How is TMJ dysfunction treated?

TMJ pain may go away without any treatment. In the meantime, there is plenty you can do to relieve the symptoms of TMJ pain:

eat soft food

avoid chewing gum

cut all food into small pieces

avoid clenching your jaw

avoid opening your mouth wide

wear a mouthguard while you sleep to prevent jaw clenching or teeth grinding

You can also try relaxation techniques to relieve stress. Gentle jaw-strengthening exercises might also help.

It is not known which medications are effective for TMJ dysfunction. However, medications that may be tried include pain relief medication, medications that treat inflammation, and muscle relaxants.

In most cases, TMJ dysfunction improves over time. Very few people need surgery.

Last reviewed: August 2021

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The temporomandibular joint (TMJ) is the joint that connects the jaw to the skull. There is a TMJ on each side of the face, in front of each ear. These joints allow the movements needed for speaking, eating and facial expression. TMJ dysfunction can cause pain, abnormal jaw movements and joint noises.

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Examination of the Lymph Nodes - Clinical Examination

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This is a unique online course which teaches students the basics of blood film analysis. This course is specifically tailored to those with a background in Medical Science, Medicine or Pathology who are studying or starting work in a haematology laboratory but also serves as a valuable continuing education resource. To be successful in this course, access to a haematology laboratory is desirable but not essential.

This is not a textbook or a laborious examination of every blood film abnormality but rather focusses on the approach - both an overall method for analysing a blood film, and a framework for analysing quantitative and qualitative changes in blood cells. At each step students are taught a method, provided with the theoretical framework for interpreting abnormalities, and shown examples of abnormalities highlighting their clinical significance. This is reinforced with frequent in-lecture interactive quizzes, end of lecture mcqs, and suggested lab exercises which engage the student with the laboratory and their colleagues. At the end of each module and at the end of the whole series are summative assessments which must be successfully completed to attain the course certificate.

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Blood Film Morphology - A Practical Guide

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This is a unique online course which teaches students the basics of blood film analysis. This course is specifically tailored to those with a background in Medical Science, Medicine or Pathology who are studying or starting work in a haematology laboratory but also serves as a valuable continuing education resource.

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Coursera - Fundamentals of innate immunity and B cell function

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Coursera - Fundamentals of innate immunity and B cell function

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About this Course

Course 1 of a three course specialization called Fundamentals of Immunology. Each course in the specialization presents material that builds on the previous course's material.

This is the first leg of a three-part journey through the defenses your body uses to keep you healthy. In this part we hope to give you the vocabulary and concepts you need to interact with the medical community and to provide them in a context that makes them memorable. Fundamentals of Immunology introduces students to the basic functions of the adaptive and innate immune systems. The early lectures survey cells, tissues and organs using metaphors, cartoons and models to improve understanding and retention. After describing the form, function, origin and varieties of antibodies, subsequent lectures provide details on the mechanism of the generation of variation. The course provides animations of gene rearrangement and class switching and descriptions of affinity maturation correlated with detailed physical models of antibody structure. The final lecture reviews these concepts in anatomical context. Testing employs multiple choice questions testing facts, concepts, and application of principles. Questions may refer to diagrams, drawing and photographs used in lecture and reproduced in the outline. What You'll Learn: The difference between adaptive and innate immune systems, the characteristics of various pathogens that they protect you from and the overall strategies employed in this protection. The detailed structure of antibodies and related immunoglobulin receptors, the characteristics and function of the different antibody classes and the mechanism for producing both the recognition regions and stem regions. Finally, how these structures are coded for in the DNA and expressed in the B cells.

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Subtitles: Arabic, French, Portuguese (European), Chinese (Simplified), Italian, Vietnamese, Korean, German, Russian, Turkish, English, Spanish

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Approx. 16 hours to complete

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Rice University

Rice University is consistently ranked among the top 20 universities in the U.S. and the top 100 in the world. Rice has highly respected schools of Architecture, Business, Continuing Studies, Engineering, Humanities, Music, Natural Sciences and Social Sciences and is home to the Baker Institute for Public Policy.

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About the Fundamentals of Immunology Specialization

This specialization is designed to equip students with the basic concepts and vocabulary of immunology. The goal is to provide students from different backgrounds with a fundamental understanding of immunology and the ability to appreciate and analyze new developments in immunological therapies designed for the treatment of disease.

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Fundamentals of Immunology: Innate Immunity and B-Cell Function

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Offered by Rice University. Course 1 of a three course specialization called Fundamentals of Immunology. Each course in the specialization presents material that builds on the previous course's material. This is the first leg of a three-part journey through the defenses your body uses to keep you healthy.

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About this Course

Over 500,000 people in the United States and over 8 million people worldwide are dying every year from cancer. As people live longer, the incidence of cancer is rising worldwide and the disease is expected to strike over 20 million people annually by 2030. This open course is designed for people who would like to develop an understanding of cancer and how it is prevented, diagnosed, and treated.

The course introduces the molecular biology of cancer (oncogenes and tumor suppressor genes) as well as the biologic hallmarks of cancer. The course also describes the risk factors for the major cancers worldwide, including lung cancer, breast cancer, colon cancer, prostate cancer, liver cancer, and stomach cancer. We explain how cancer is staged, the major ways cancer is found by imaging, and how the major cancers are treated. In addition to the core materials, this course includes two Honors lessons devoted to cancers of the liver and prostate. Upon successful completion of this course, you will be able to: - Identify the major types of cancer worldwide. (Lecture 1) - Describe how genes contribute to the risk and growth of cancer. (Lecture 2) - List and describe the ten cellular hallmarks of cancer. (Lecture 3) - Define metastasis, and identify the major steps in the metastatic process. (Lecture 4) - Describe the role of imaging in the screening, diagnosis, staging, and treatments of cancer. (Lecture 5) - Explain how cancer is treated. (Lecture 6) We hope that this course gives you a basic understanding of cancer biology and treatment. The course is not designed for patients seeking treatment guidance - but it can help you understand how cancer develops and provides a framework for understanding cancer diagnosis and treatment.

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Approx. 8 hours to complete

Subtitles: Arabic, French, Portuguese (European), Italian, Catalan, Portuguese (Brazilian), Vietnamese, Dutch, German, Russian, Turkish, English, Hebrew, Spanish

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The mission of The Johns Hopkins University is to educate its students and cultivate their capacity for life-long learning, to foster independent and original research, and to bring the benefits of discovery to the world.

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About the Cancer Biology Specialization

The healthcare system is a rapidly evolving field with new research leading to advancements in medicine. Developed at Johns Hopkins University and led by top-ranked Hopkins faculty and cancer experts, this specialization on Cancer Biology focuses on the basics of cancer biology, how cancer metastasis occurs, and specifically, screening guidelines for prostate cancer, the most common cancer in American men.

This specialization starts with an Introduction to the Biology of Cancer, introduces the molecular biology of cancer and the biologic hallmarks of cancer. The course also describes the risk factors for the major cancers worldwide, including lung cancer, breast cancer, colon cancer, prostate cancer, liver cancer, and stomach cancer. Experts at Johns Hopkins University explain how cancer is staged, the major ways cancer is found by imaging, and how the major cancers are treated. The specialization takes a deeper dive in Understanding Cancer Metastasis, explaining how cancer spreads or metastasizes. This course will describe the major theories of metastasis and then describe the biology behind the steps in metastasis. The course also describes the major organs targeted by metastasis and describes how metastases harm the patient. Lastly, it focuses on Understanding Prostate Cancer, providing you with the tools to examine the incidence of prostate cancer, including risk factors, stages, and treatments at each stage.

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Is financial aid available?

More questions? Visit the Learner Help Center.

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Over 500,000 people in the United States and over 8 million people worldwide are dying every year from cancer. As people live longer, the incidence of cancer is rising worldwide and the disease is expected to strike over 20 million people annually by 2030.

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About this course: This course covers chemicals in our environment and in our bodies and how they impact our health. It addresses policies and practices related to chemicals, particularly related to how they get into our bodies (exposures), what they do when they get there (toxicology), how we measure them (biomonitoring) and their impact on our health. Most examples are drawn from the US.

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About this course: This course covers chemicals in our environment and in our bodies and how they impact our health. It addresses policies and practices related to chemicals, particularly related to how they get into our bodies (exposures), what they do when they get there (toxicology), how we measure them (biomonitoring) and their impact on our health.

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The Gut Movie - A story about poo & the future of medicine. In The Gut Movie, we follow the journey of researcher Kale Brock in the quest to discover whether the 'optimal microbiome' does in... Read all The Gut Movie - A story about poo & the future of medicine. In The Gut Movie, we follow the journey of researcher Kale Brock in the quest to discover whether the 'optimal microbiome' does indeed exist. The Gut Movie - A story about poo & the future of medicine. In The Gut Movie, we follow the journey of researcher Kale Brock in the quest to discover whether the 'optimal microbiome' does indeed exist.

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The Gut Movie: Directed by Kale Brock. With Thomas Borody, Kale Brock. The Gut Movie - A story about poo & the future of medicine. In The Gut Movie, we follow the journey of researcher Kale Brock in the quest to discover whether the 'optimal microbiome' does indeed exist.

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Assessment 1 Part A - Case Study

End of Module 2.2 (Week 4)

Assessment 1 Part B - Case Study
End of Module 5.2 (Week 10)

Assessment 2 - Mid-term
Practical Exam

End of Module 3.2 (Week 6)

Assessment 3 - End of Term Practical Exam

End of Module 6.2  (Week 12)

Attendance

Students enrolled on campus are required to attend 80% of classes

Students enrolled online are required to attend 2 weekend workshops in full (ie 4 days in total)
Hurdle assessment:
This assessment item must be successfully completed in order for the overall subject to be satisfactorily completed.
| Hurdle  | Pass/Fail

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452K likes, 998 comments - world_of_biology_wob on July 3, 2023: "3.5 million views and counting.
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7,834 likes, 108 comments - nurse_human on August 28, 2023: "🌟🌟Let’s talk about Right vs Left side Heart Failure 🫀🫀. I hope this explanation helps you understand the symptoms better!!! 🥰

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Abnormal Breath Sounds | Respiratory System

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What Is It, How Is It Assessed, Uses, and More

What is tactile fremitus?

Tactile fremitus, also known as tactile vocal fremitus, refers to the vibration of the chest wall that results from sound vibrations created by speech or other vocal sounds. When a person speaks, airflow from the lungs causes the vocal cords in the larynx to vibrate. These vibrations, which are also known as vocal fremitus, are transmitted down the tracheobronchial tree and through the lung tissue to the chest wall, where they can be felt by the hand as a palpable vibration.

Tactile fremitus is a clinical sign commonly assessed as part of a routine physical examination of the lungs. Respiratory physical examination generally consists of a visual assessment of the chest wall, palpation of chest expansion symmetry, tactile fremitus, percussion of the chest (which refers to the tapping of the thorax with the fingers), and lung auscultation (which uses a stethoscope to listen to an individual's breathing sounds).

In individuals with healthy lung tissue, tactile fremitus can be felt symmetrically along both sides of the chest. Normally, tactile fremitus is more pronounced near the clavicles and in between the shoulder blades, with a decreasing intensity towards the base of the lungs. Abrupt or asymmetrical changes in the intensity of tactile fremitus are considered to be an unusual finding, and may reflect the presence of an underlying lung condition.

How do you assess tactile fremitus?

Tactile fremitus is assessed by asking an individual to repeat a certain phrase while the examiner places the palms or the bony edge of their hands on the individual's chest wall to feel for sound vibrations. Low-frequency vibrations, such as those created by two adjacent vowel sounds (e.g. "coin", "sound", or "boat"), are transmitted more effectively down the tracheobronchial tree, and thus evoke a more noticeable fremitus.

Examination of tactile fremitus is typically performed in all the major regions of the chest wall, covering the posterior, lateral and anterior chest. The examiner usually feels both sides of the chest wall at the same time to detect subtle changes between either side of the chest. Alternatively, one hand can be used to palpate one side of the chest and then moved back and forth to compare both sides.

What is tactile fremitus used for?

Changes in the intensity of tactile fremitus can be used to detect areas of unusual lung tissue density. The assessment of tactile fremitus is based on the principle that sound vibrations are conducted better through solid or fluid mediums, as opposed to air, which causes a decay in sound transmission. As a result, areas of increased lung tissue density are better conductors of sound, and generally present a more noticeable fremitus than normal air-filled lung tissue. Conversely, an excessive amount of air within the lungs may cause impaired sound transmission, leading to a decreased or absent tactile fremitus.

In combination with other clinical findings, tactile fremitus may be useful in suggesting an initial diagnosis that can then be confirmed by specific diagnostic tests. These tests may include blood tests, imaging techniques ( chest x-ray, CT scan), or pulmonary function tests, depending on the potential clinical concern.

What causes decreased tactile fremitus?

Decreased intensity of tactile fremitus may occur as a result of excessive amounts of air in the lungs (also known as hyperinflation). Hyperinflation can be seen in individuals with pulmonary emphysema, chronic obstructive pulmonary disease (COPD), asthma, or severe airway obstruction.

Additionally, decreased or absent tactile fremitus may also occur when there is an increased distance between the lungs and the chest wall. For instance, excess fluid or air can collect in the pleural space; the thin fluid-filled cavity that forms between the two layers of serous membrane between the lungs and the chest wall. The buildup of excess fluid in the pleural space is known as a pleural effusion, whereas accumulation of air in the pleural space is known as a pneumothorax.

Finally, tactile fremitus may also have decreased intensity in individuals with obesity or increased muscular mass, due to increased thickness of the chest wall.

What causes increased tactile fremitus?

Increased intensity of tactile fremitus generally occurs as a result of increased density within the lung tissue. This commonly occurs as a result of lung consolidation, which refers to the replacement of the air within healthy lung tissue with another substance; either inflammatory exudate, blood, pus, or cells. The most common cause of a consolidated lung is a lung infection, such as pneumonia. Other causes of increased tactile fremitus include partial or total collapse of a lung (known as atelectasis) or the presence of a solid mass in the lungs, such as a tumor.

What are the most important facts to know about tactile fremitus?

Tactile fremitus refers to the palpable vibration of the chest wall that results from the transmission of sound vibrations through the lung tissue to the chest wall. It is a clinical sign commonly assessed as part of routine physical examination of the lungs. Tactile fremitus can be assessed by asking an individual to repeat a certain phrase while the examiner palpates the individual's chest wall to feel for vocal vibrations. Changes in the intensity of tactile fremitus can be used to detect areas of increased or decreased lung density. Tactile fremitus typically has a greater intensity in areas of increased lung density, such as a consolidated lung. Conversely, excess air within the lungs, or increased thickness of the chest wall, may lead to a decreased intensity of tactile fremitus.

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Tactile Fremitus: What Is It, How Is It Assessed, Uses, and More | Osmosis

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Tactile fremitus, also known as tactile vocal fremitus, refers to the vibration of the chest wall that results from sound vibrations created by speech or other vocal sounds

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Overview

What is postural orthostatic tachycardia syndrome (POTS)?

Postural orthostatic tachycardia syndrome (POTS) is a condition that affects circulation (blood flow). It involves the autonomic nervous system (which automatically controls and regulates vital bodily functions) and sympathetic nervous system (which activates the fight or flight response).

POTS is a form of orthostatic intolerance, the development of symptoms that come on when standing up from a reclining position, and that may be relieved by sitting or lying back down. The primary symptom of an orthostatic intolerance is lightheadedness, fainting and an uncomfortable, rapid increase in heartbeat.

Heart rate and blood pressure work together to keep the blood flowing at a healthy pace, no matter what position the body is in. People with POTS can't coordinate the balancing act of blood vessel squeeze and heart rate response. This means the blood pressure can't be kept steady and stable.

Each case of POTS is different. POTS patients may see symptoms come and go over a period of years. In most cases, with adjustments in diet, medications and physical activity, a person with POTS will see an improvement in quality of life. And POTS symptoms may subside if an underlying cause is found and treated.

There are various forms of POTS. The most common are:

Neuropathic POTS: Peripheral denervation (loss of nerve supply) leads to poor blood vessel muscles, especially in the legs and core body.

Hyperadrenergic POTS: Overactivity of the sympathetic nervous system.

Low blood volume POTS: Reduced blood volume can lead to POTS. Low blood volume can cause similar symptoms that may overlap in neuropathic and hyperadrenergic POTS.

Who is at risk for POTS?

The majority of POTS patients are women ages 13-50 years old. About 1 to 3 million people suffer from POTS in the United States.

Patients may develop POTS after a viral illness, serious infections, medical illness, pregnancy and trauma such as head injury. The condition may develop as aftermath of a significant illness (especially associated with hospitalization and prolonged immobilization).

POTS may develop in those who have had a recent history of mononucleosis.

People with certain autoimmune conditions such as Sjogren's syndrome and celiac disease can be at higher risk. Sjogren's can be evaluated by blood testing, dry eye test, lip biopsy and rheumatology consult. Celiac disease can be tested through blood work, gastroenterology consult and if needed biopsies of the small intestines.

Symptoms and Causes

What are the symptoms of postural orthostatic tachycardia syndrome (POTS)?

POTS symptoms can be uncomfortable and frightening experiences. Patients with POTS usually suffer from two or more of the many symptoms listed below. Not all patients with POTS have all these symptoms.

Diagnosis and Tests

How ispostural orthostatic tachycardia syndrome (POTS) diagnosed?

POTS can be difficult to diagnose due to so many symptoms occurring in the body over time. Before diagnosis of POTS, various symptoms may lead patients to try many doctors. Patients with POTS may have symptoms for months to years before finally being diagnosed with the condition.

A tilt table test is the gold standard of POTS diagnosis. The tilt table measures your heart rate and blood pressure as you change posture and position.

Besides the tilt table, other testing may be done for POTS:

Management and Treatment

How is postural orthostatic tachycardia syndrome (POTS) treated?

Medications like salt tablets, fludrocortisone, pyridostigmine, midodrine, and/or a beta blocker may be prescribed to help control POTS.

You may be prescribed thigh-high medical compression stockings. These stockings help push the blood up from the legs to reduce POTS symptoms.

You should obtain a blood pressure monitor to check blood pressure and pulse. Blood pressure monitors may be purchased at most drug stores, online or at a medical supply store. Have your blood pressure monitor checked at your doctor's office to make sure your machine's readings correlate with your doctor's blood pressure readings.

Although the heart is healthy in most POTS patients, you may be evaluated to enter a cardiac rehab program. This exercise template uses the cardiac rehab model to recondition and help improve health and control POTS. Some of the best data for treating POTS comes from cardiac rehab.

What are everyday ways to help manage POTS?

Diet and nutrition

Increase sodium in your diet to 3,000 mg to 10,000 mg per day.

Drink 2-2.5 liters per day of fluids. Water is a good choice. Sports drinks are OK, but watch calories and if you have food sensitivities to these drinks' ingredients.

Small and frequent meals are better tolerated and reduce POTS symptoms.

Diet with high fiber and complex carbohydrates may help reduce blood glucose (sugar) spikes and lessen POTS symptoms.

Keep your nutrition balanced with protein, vegetables, dairy and fruits.

Plan meals as POTS patients may occasionally not have stamina for grocery shopping and preparing meals. Plan meals when your energy is at its peak. If possible, make it a family plan to prepare food and share grocery shopping responsibilities.

Don't over-rely on processed foods. Processed foods are easy to prepare and are appealing when you have reduced energy, but usually have less nutritional value.

Beneficial salty snacks may include chicken or beef broth, vegetable broth, pickles, olives, salted fish like sardines/anchovies and nuts. Don't over-rely on snack chips and crackers for salt.

Plan grocery store shopping using a list to make sure you pick up healthy food choices and POTS care (hydration and salty supplements). If your stamina is reduced have someone help you shop, carry and put away your groceries.

Health conditions can be costly. Do your best not to compromise nutrition and food choices to save money.

You may need a dietary and nutrition consult ordered by your doctor to help you with your diet. This consult can be especially helpful for those with celiac and other dietary sensitivities.

Often in early phase of POTS patients don't like how their bodies feel and look. Be careful of fad diets or diet supplements for weight loss.

Monitoring POTS

Taking and writing down your vital information (blood pressure and pulse) can give you insight and better control over your POTS, and helps your doctor fine tune your treatment.

Check blood pressure and pulse at the same time daily (in the morning and after dinner). It's very helpful to do this for the first few months of your diagnosis. Also check blood pressure and pulse when you aren't feeling well.

Heart rate/pulse

Measuring heart rate can give you insight as you deal with POTS. Other facts about heart rate and POTS:

A normal heart rate is between 60 to 100 beats per minute.

A fast heart rate over 100 beats per minute can be a condition called tachycardia.

A slow heart rate under 60 beats per minute is called bradycardia.

High or low rates can cause symptoms of POTS.

Blood pressure

Blood pressure is the pressure of the blood in the blood vessels in the circulatory system. Blood pressure is related to the heart beating and the diameter and elasticity of the artery walls.

Blood pressure has two components, systolic and diastolic. Blood pressure is recorded as systolic/diastolic. For example, a blood pressure reading of 120/80 represents the systolic number as 120 and the diastolic number as 80.

The systolic refers to the amount of pressure in the arteries during the contraction of your heart muscles (heart beats). The diastolic refers to the blood pressure between heart beats.

Normal blood pressure is between is 90-120 for systolic and 60-80 for diastolic.

Many patients will have stable blood pressure readings since the adrenergic response to keep heart rate increased will reduce blood pressure drops.

POTS patients can have moments of hypertension with the systolic over 140 or diastolic over 85. If hypertension occurs in many readings, inform your POTS specialist of these consistent readings of hypertension.

Low blood pressure is below 90/60. Blood pressure logging that reveal low blood pressure readings can be helpful for POTS treatment.

Exercise and physical activity

Exercise and physical activity are key to managing POTS. Here are important things to know as you undergo an exercise program such as cardiac rehab, as well as other physical activities. Talk with your healthcare provider for specific instructions on these exercises.

Isometric exercises involve contracting your muscles without actually moving your body. Isometrics squeeze the muscle and push the blood back toward the heart. They are simple to do and can be done lying in bed or seated in a comfortable chair. It's a good idea to do these in bed before getting up to prepare your body for sitting and standing.

Transition slowly with your body. Go from lying to sitting on the edge of the bed. Stay there for several minutes, allowing the body to naturally adjust to the change in position. Once you are standing, pause and wait before walking to allow blood pressure to adjust again. If you feel lightheaded at any point, wait for a few minutes in that position to see if it resolves. If not, then return to the prior position as your body isn't adjusting properly. SLOWLY is the key.

Begin a modest walking program. Count how many steps you can do without inducing symptoms. These steps are your initial baseline. Start with walking once a day and go a little further in time, distance or by adding steps. If you feel good, add a second walk in the day. A simple strategy for counting steps is to do 100- 300 steps per awakening hour during the day. Fitness trackers can monitor steps and distance easily. Every week or every few weeks add more steps to your daily total.

Simple yoga with focusing on breathing may help reduce POTS symptoms.

As you do better with your POTS, more fitness and exercise regimens may be started.

Sleep

Try to maintain a typical sleep schedule. Go to bed consistently at a certain time and set a consistent time to wake up. The best sleep hygiene and good rest comes from staying consistent with your sleep schedule every day. Even if you had a poor night of sleep, try to get up at your regular time. A consistent sleep schedule, even with a bad night's sleep, helps you feel better in the long term.

Excessive daytime napping may make nighttime sleep less restful.

Most people need 7 to 10 hours sleep at night.

Be aware of POTS symptoms of chest pain, sweating, restlessness and racing heart rate during bedtime. These symptoms interfere with sleep quality and may have to be addressed by your POTS specialist

Avoid excessive television viewing or use of tablet/smartphone/computer in bed. These technologies can interfere with sleep quality.

Raise the head of your bed 6-10 inches to help alleviate POTS symptoms. The entire bed must be at an angle. Raising the head of the bed will reduce urine formation overnight and increase fluid volume in your circulation in the morning. This may help you wake up more easily.

Make sure the temperature is ideal in your bedroom to help you get proper rest.

Living With

How do I coordinate and organize my care with postural orthostatic tachycardia syndrome (POTS)?

Start a binder or folder containing your basic notes and testing results. Periodically review this binder to remove out-of-date data. As a rule, about 20-30 pages of pertinent medical data will help guide your POTS medical team most effectively.

You'll need a healthcare provider or primary care physician to go to for routine care and health wellness management. Your POTS specialist may ask you to see your healthcare provider periodically. Get copies of your medical visit notes from your healthcare provider - especially any additional testing results - to have in your record binder (see above).

If you're feeling very ill or something doesn't feel right, you may need to go to the ER or Urgent Care immediately. If you call your POTS specialist you may be told to go to the ER or Urgent Care

Be sure to follow up with your POTS specialist.

How do I cope emotionally with POTS?

Be open and honest with loved ones and support groups about your diagnosis of POTS. Talk about your fears, hopes, struggles and challenges with the condition. Encourage the people who support you to learn more about POTS.

Get enough sleep and eat well to help manage stress.

Shared medical appointments and POTS support groups (either online or in person) will help reduce the feeling of being alone and different.

Be careful with social media. Be mindful of the accuracy of any particular website's data. Some POTS patients find comfort in social media. For others, social media can cause unnecessary and excessive stress and worry.

Be very cautious of quick solutions from non-medical sources and people. Quick solutions usually don't help POTS and can even cause more emotional distress.

We recommend counseling to help you learn to cope with a chronic health condition. Counseling may help to control other co-existing mental health issues that may negatively influence POTS.

Meditate or take even just a few minutes of a time-out to help reduce some of your POTS symptoms.

Emotions can have a significant influence on your daily life and health. Identifying them can be useful if you are talking with a counselor or POTS support group.

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POTS: Causes, Symptoms, Diagnosis & Treatment

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Postural orthostatic tachycardia syndrome (POTS) is a condition that affects circulation (blood flow). It involves the autonomic nervous system (which automatically controls and regulates vital bodily functions) and sympathetic nervous system (which activates the fight or flight response).

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S1 Heart Sound | S2 Heart Sound | S3 Heart Sound | S4 Heart Sound | Extra Heart Sounds

Introduction

Heart sounds are produced from a specific cardiac event such as closure of a valve or tensing of a chordae tendineae.

Many pathologic cardiac conditions can be diagnosed by auscultation of the heart sounds. Note that heart sounds are discrete, short audible events from a specific cause - different from a heart murmur. A murmur is due to turbulence of blood flow and can, at times, encompass all of systole or diastole.

The main normal heart sounds are the S1 and the S2 heart sound. The S3 can be normal, at times, but may be pathologic. A S4 heart sound is almost always pathologic. Heart sounds can be described by their intensity, pitch, location, quality and timing in the cardiac cycle.

Intensity: Heart sounds can be described as increased in intensity (loud), decreased in intensity (soft) or absent.

Pitch: Heart sounds can be described as high pitched (heard best with the diaphragm of the stethoscope).

Location: The location of the heart sound can help determine the etiology. The standard listening posts (aortic, pulmonic, tricuspid and mitral) apply to both heart sounds and murmurs. For example, the S1 heart sound - consisting of mitral and tricuspid valve closure - is best heard at the tricuspid (left lower sternal border) and mitral (cardiac apex) listening posts.

Timing: The timing can be described as during early, mid or late systole or early, mid or late diastole.

Although terms such as "click," "snap" or "knock" are sometimes used, they have no specific quality or meaning. They will be referenced in the following sections.

First Heart Sound (S1)

The first heart sound results from the closing of the mitral and tricuspid valves. The sound produced by the closure of the mitral valve is termed M1, and the sound produced by closure of the tricuspid valve is termed T1. The M1 sound is much louder than the T1 sound due to higher pressures in the left side of the heart; thus, M1 radiates to all cardiac listening posts (loudest at the apex), and T1 is usually only heard at the left lower sternal border. This makes the M1 sound the main component of S1.

CLINICAL PEARL: A split S1 heart sound is best heard at the tricuspid listening post, as T1 is much softer than M1.

The M1 sound occurs slightly before T1. Because the mitral and tricuspid valves normally close almost simultaneously, only a single heart sound is usually heard. However, in about 40% to 70% of normal individuals - as well as in certain cardiac conditions - a "split S1" sound can be appreciated. This occurs when the mitral valve closes significantly before the tricuspid valve, allowing each valve to make a separate audible sound. Inspiration delays the closure of the tricuspid valve in a normal person, due to increased venous return, thereby enhancing the splitting of the S1 sound.

A split S1 sound is common in the setting of a right bundle branch block or ventricular tachycardia/premature ventricular contractions, or PVCs, with a right bundle branch block morphology. A RBBB causes the electrical impulse to reach the left ventricle before the right ventricle. Dyssynchrony then occurs, resulting in the left ventricle contracting before the right ventricle, thus the pressures in the LV rise before that of the right ventricle.

This delays the closure of the tricuspid valve, resulting in a split S1 sound. A left bundle branch block has the opposite effect on S1. In this setting, the electrical impulse reaches the RV before the LV, thus the pressure in the RV rises before that of the LV. This forces the tricuspid valve closed earlier, resulting in complete overlap of M1 and T1, and thus no audible split S1 sound.

CLINICAL PEARL: A RBBB results in a widened split S1, whereas a LBBB results in the absence of a split S1.

Four factors affect the intensity of the first heart sound. Because the M1 portion of S1 is much louder than T1, it is only important to discuss what affects the intensity of M1.

1. Chest wall thickness: The first factor is the thickness of the chest wall. Individuals with obesity will have a soft S1, whereas thinner people will have a more intense S1. The greater the distance separating the leaflets of the mitral valve at the beginning of systole, the louder the S1; this is affected by the duration of the PR interval on the ECG.

2. Length of PR interval: Remember that the PR interval represents part of diastole, meaning a longer PR interval would result in a longer diastolic filling time. As the LV fills, the pressure gradually increases. This gradual increase in pressure causes the mitral valve leaflets to slowly drift together. Therefore, when ventricular systole occurs in the setting of a long PR interval, the leaflets will be separated by a smaller distance, and the S1 sound will be softer. The converse is also true. A short PR interval results in an accentuated S1, as the mitral valve leaflets will be further apart at the onset of ventricular systole.

CLINICAL PEARL: A short PR interval results in an accentuated S1, whereas a long PR interval results in a soft S1.

3. Valve leaflet mobility: The mobility of the valve leaflets is another factor influencing the intensity of M1. In mild to moderate mitral stenosis, the increased left atrial pressure causes the mobile portions of the mitral valve leaflets to be more widely separated, resulting in an accentuated M1 sound. In severe to critical mitral stenosis, the valve leaflets are so calcified and immobile that the M1 sound is diminished or absent.

CLINICAL PEARL: Mild to moderate mitral stenosis results in a loud S1, whereas severe to critical mitral stenosis results in a soft S1.

4. Ventricular contraction rate: The rate of ventricular contraction also affects the intensity of S1. The faster the heart rate and the faster the rise in ventricular pressure, the louder the S1. Thus, high flow states such as anemia, thyrotoxicosis or sepsis would result in an accentuated S1. Also, during exercise or any other setting of tachycardia, the S1 will be accentuated.

Second Heart Sound (S2)

The second heart sound is produced by the closure of the aortic and pulmonic valves. The sound produced by the closure of the aortic valve is termed A2, and the sound produced by the closure of the pulmonic valve is termed P2.

The A2 sound is normally much louder than the P2 due to higher pressures in the left side of the heart; thus, A2 radiates to all cardiac listening posts (loudest at the right upper sternal border), and P2 is usually only heard at the left upper sternal border. Therefore, the A2 sound is the main component of S2.

CLINICAL PEARL: A split S2 is best heard at the pulmonic valve listening post, as P2 is much softer than A2.

Like the S1 heart sound, the S2 sound is described regarding splitting and intensity. S2 is physiologically split in about 90% of people. The S2 heart sound can exhibit persistent (widened) splitting, fixed splitting, paradoxical (reversed) splitting or the absence of splitting. The S2 heart sound intensity decreases with worsening aortic stenosis due to immobile leaflets. In severe aortic stenosis, the A2 component may not be audible at all.

CLINICAL PEARL: In severe hypertension, a loud S2 may be prolonged and slurred - falsely mimicking a split S2.

Physiologic Split S2

Normally, A2 occurs just before P2, and the combination of these sounds make up S2. A physiologic split S2 occurs when the A2 sound precedes P2 by a great enough distance to allow both sounds to be heard separately. This happens during inspiration when increased venous return to the right side of the heart delays the closure of the pulmonic valve (major effect), and decreased return to the left side of the heart hastens the closure of the aortic valve (minor effect), thereby further separating A2 and P2. During expiration, the distance narrows, and the split S2 is no longer audible.

Paradoxical Split S2

A paradoxical split S2 heart sound occurs when the splitting is heard during expiration and disappears during inspiration - opposite of the physiologic split S2. A paradoxical split S2 occurs in any setting that delays the closure of the aortic valve including severe aortic stenosis and hypertrophic obstructive cardiomyopathy, or in the presence of a left bundle branch block.

CLINICAL PEARL: A paradoxical split S2 is heard in AS, HOCM or in the presence of a LBBB.

Persistent (Widened) Split S2

Persistent (widened) splitting occurs when both A2 and P2 are audible during the entire respiratory cycle, and the splitting becomes greater with inspiration (due to increased venous return) and less prominent with expiration. This differs from a fixed split S2, which exhibits the same amount of splitting throughout the entire respiratory cycle and is explained below.

Any condition that causes a nonfixed delay in the closure of the pulmonic valve, or early closure of the aortic valve, will result in a wide split S2. Therefore, a persistent split S2 would occur in the setting of a RBBB, pulmonary hypertension or pulmonic stenosis (delayed P2) or severe mitral regurgitation/ventricular septal defect (early A2 closure).

A RBBB causes a delay in the closure of the pulmonic valve, and thus a delay in P2, without any effect on A2. In severe MR or in the setting of a VSD, the A2 occurs early. In mitral regurgitation, this is due to a large proportion of the left ventricular stroke volume entering the left atrium, causing the left ventricular pressure to decrease faster. In a VSD, a large proportion of the stroke volume goes into the RV, similarly decreasing LV pressure quickly. The P2 is not affected in severe MR or VSD unless pulmonary hypertension is present.

CLINICAL PEARL: A persistent (widened) split S2 occurs in the setting of a RBBB or severe MR.

Fixed Split S2

A fixed split S2 is a rare finding on cardiac exam; however, when found, it almost always indicates the presence of an atrial septal defect. A fixed split S2 occurs when there is always a delay in the closure of the pulmonic valve, and there is no further delay with inspiration; compare this to a widened split S2, as described above.

To explore why an ASD results in a fixed split S2, we must consider the altered cardiac hemodynamics present, which result in a fixed delay in PV closure. During inspiration, as usual, there is an increase in venous return to the right side of the heart and thus increased flow through the PV - delaying its closure. The alteration in a person with an ASD occurs during expiration. As the person expires, the pressure in the right atrium decreases because there is less venous return. The decreased pressure allows more blood to flow abnormally through the ASD from the high pressured left atrium to the right atrium, ultimately resulting again in increased flow through the pulmonic valve - again, delaying its closure.

CLINICAL PEARL: A fixed split S2 is pathognomonic for the presence of an ASD.

Third Heart Sound (S3)

The third heart sound, also known as the "ventricular gallop," occurs just after S2 when the mitral valve opens, allowing passive filling of the left ventricle. The S3 sound is actually produced by the large amount of blood striking a very compliant LV.

CLINICAL PEARL: A S3 heart sound is produced during passive left ventricular filling when blood strikes a compliant LV.

If the LV is not overly compliant, as is in most adults, a S3 will not be loud enough to be auscultated. A S3 can be a normal finding in children, pregnant females and well-trained athletes; however, a S4 heart sound is almost always abnormal.

CLINICAL PEARL: A S3 heart sound is often a sign of systolic heart failure, however it may sometimes be a normal finding.

A S3 can be an important sign of systolic heart failure because, in this setting, the myocardium is usually overly compliant, resulting in a dilated LV; this can be seen in the image below.
Normal LV vs. Dilated LV (S3 Present)
S3 is a low-pitched sound; this is helpful in distinguishing a S3 from a split S2, which is high pitched. A S3 heart sound should disappear when the diaphragm of the stethoscope is used and should be present while using the bell; the opposite is true for a split S2. Also, the S3 sound is heard best at the cardiac apex, whereas a split S2 is best heard at the pulmonic listening post (left upper sternal border). To best hear a S3, the patient should be in the left lateral decubitus position.

Fourth Heart Sound (S4)

The fourth heart sound, also known as the "atrial gallop," occurs just before S1 when the atria contract to force blood into the LV. If the LV is noncompliant, and atrial contraction forces blood through the atrioventricular valves, a S4 is produced by the blood striking the LV.

CLINICAL PEARL: A S4 heart sound occurs during active LV filling when atrial contraction forces blood into a noncompliant LV.

Therefore, any condition that creates a noncompliant LV will produce a S4, while any condition that creates an overly compliant LV will produce a S3, as described above.

A S4 heart sound can be an important sign of diastolic HF or active ischemia and is rarely a normal finding. Diastolic HF frequently results from severe left ventricular hypertrophy, or LVH, resulting in impaired relaxation (compliance) of the LV. In this setting, a S4 is often heard. Also, if an individual is actively having myocardial ischemia, adequate adenosine triphosphate cannot be synthesized to allow for the release of myosin from actin; therefore, the myocardium is not able to relax, and a S4 will be present.

It is important to note that if a patient is experiencing atrial fibrillation, the atria are not contracting, and it is impossible to have a S4 heart sound.

CLINICAL PEARL: A S4 heart sound is often a sign of diastolic HF, and it is rarely a normal finding (unlike a S3).

Like S3, the S4 sound is low pitched and best heard at the apex with the patient in the left lateral decubitus position. Below is comparative information for S3 and S4.
S3 - "ventricular gallop"

Occurs in early diastole

Occurs during passive LV filling

May be normal at times

Requires a very compliant LV

Can be a sign of systolic congestive HF

S4 - "atrial gallop"

Occurs in late diastole

Occurs during active LV filling

Almost always abnormal

Requires a noncompliant LV

Can be a sign of diastolic congestive HF

Extra Heart Sounds

There are a few common extra heart sounds that the clinician may encounter. These include ejection sounds that occur with pulmonic or AS heard in early systole, "clicks" that are heard in mitral or tricuspid valve prolapse occurring later in systole, as well as "snaps," "knocks" and "plops."

Systolic ejection click: A systolic ejection click frequently indicates a bicuspid aortic valve. This sound is heard just after the S1 heart sound. Usually, the opening of the aortic valve is not audible; however, with a bicuspid aortic valve, the leaflets dome suddenly prior to opening and create a systolic ejection click. The click may be difficult to hear in the presence of significant AS.

Mitral valve prolapse click: Mitral valve prolapse produces a mid systolic click, usually followed by a uniform, high-pitched murmur. The murmur is actually due to MR that accompanies the MVP; thus, it is heard best at the cardiac apex. MVP responds to dynamic auscultation. After sudden standing, preload is decreased, and the click moves earlier in systole. With sudden squatting, preload increases, and the click moves later in systole.

Opening snap: In the setting of MS, the increased left atrial opening pressures cause an opening snap to occur when the mitral valve leaflets suddenly tense and dome into the LV in early diastole. This high-frequency sound is best heard at the apex.

Tumor plop: A tumor plop is an early diastolic low-pitched sound just after the S2 heart sound. This is in contrast to the opening snap of rheumatic mitral valve stenosis, which is high pitched. A tumor plop may be followed by a low-pitched diastolic murmur. If the mitral valve inflow obstruction is significant enough, physical exam findings of congestive HF will be present.

Pericardial knock: A pericardial knock can be present in patients with constrictive pericarditis, as the early filling of the LV is limited from the constrictive process. The knock occurs earlier than a S3 heart sound. which is the distinguishing factor; this is because the S3 heart sound occurs from a stretch of a very compliant LV, which takes a short time longer.

# data[].attributes.attachment_link.description
S1 Heart Sound | S2 Heart Sound | S3 Heart Sound | S4 Heart Sound | Extra Heart Sounds Heart sounds are produced from a specific cardiac event such as closure of a valve or tensing of a chordae tendineae. Many pathologic cardiac conditions can be diagnosed by auscultation of the heart sounds.

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108. Wavreille G, Baroncini M, Rtaimate M. A rare cause of pseudoclubbing (pseudohippocratic finger): The acrometastasis.A case report. Chir Main. 2009;28:381–3. [PubMed] [Google Scholar]

109. Farzaneh-Far A. Images in clinical medicine. Pseudoclubbing. N Engl J Med. 2006;354:e14. [PubMed] [Google Scholar]

110. Santiago MB, Lima I, Feitosa AC, Braz Ade S, Miranda LG. Pseudoclubbing: Is It different from clubbing? Semin Arthritis Rheum. 2009;38:452–7. [PubMed] [Google Scholar]

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Digital clubbing is an ancient and important clinical signs in medicine. Although clubbed fingers are mostly asymptomatic, it often predicts the presence of some dreaded underlying diseases. Its exact pathogenesis is not known, but platelet-derived growth ...

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Introduction

Welcome to our vesicular breath sounds page. On this page we provide a definition of vesicular breath sounds, and then we compare vesicular breath sounds to bronchial sounds using audio recordings and text. Finally, there is a link to the training lessons available on this site.

What Are Vesicular Breath Sounds

Vesicular breath sounds are heard across the lung surface. They are lower-pitched, rustling sounds with higher intensity during inspiration. During expiration, sound intensity can quickly fade. Inspiration is normally 2-3 times the length of expiration.

Listen

Audio Playback

Waveform

Compare To Bronchial Breath Sounds

Bronchial breath sounds are heard when auscultating over the large airways.

Respiratory Sounds Reference Guide

Our auscultation reference guide provides quick access to this sound as well as many other adventitious sounds. Each sound is described also with an audio recording and waveform.

Quick Links to Other Breath Sounds

While we have many breath sound lessons and quick references on this website. Please use the links below.

Basics of Lung Sounds
The goal of this basic course in lung sounds is to improve auscultation observational skills. We focus on describing important breath sounds and in providing recordings of each. Many students find that waveform tracings aid in learning lung sounds; we have included dynamic (moving cursor) waveforms with each lesson. The anatomy pages use illustrations to reveal an example of each lung sound (anatomy not yet available on smartphones).

Intermediate Lung Sounds
The goal of this intermediate course is to expand your observational skills when auscultating breath sounds. The course lessons include voiced sounds: bronchophony, egophony and whispered pectoriloquy. We also provide auscultation lessons on several types of wheezes, crackles and stridor. Each of these lung sound lessons includes audio, text and dynamic waveform. The anatomy pages use illustrations to reveal an example of each lung sound (anatomy not yet available on smartphones).

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Welcome to our vesicular breath sounds page. On this page we provide a definition of vesicular breath sounds, and then we compare vesicular breath sounds to bronchial sounds using audio recordings and text. Finally, there is a link to the training lessons available on this site.

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Identifying Nutritional Deficiencies Through Nails, Skin & Hair – Dr.Berg's Webinar

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Thanks Holly Barrow for creating these

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I found these on Quizlet - https://quizlet.com/472640720/print

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Things to commit to memory for Week 6 prac exam

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Things to commit to memory for Week 6 prac exam

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Skin cancer occurs when skin cells are damaged, for example, by overexposure to ultraviolet (UV) radiation from the sun.

There are three main types of skin cancer:

Both basal cell carcinoma and squamous cell carcinoma are known as non-melanoma skin cancer or keratinocyte cancers. Keratinocyte cancer is more common in men, with almost double the incidence compared to women.

Melanoma is the third most common cancer in Australians excluding keratinocyte cancers as data on incidence is not routinely collected).

Every year, in Australia:

skin cancers account for around 80% of all newly diagnosed cancers

the majority of skin cancers are caused by exposure to the sun

the incidence of skin cancer is one of the highest in the world, two to three times the rates in Canada, the US and the UK.

Learn more about how Cancer Council funded researchers are working on curing Australia's national cancer.

Skin cancer symptoms

The sooner a skin cancer is identified and treated, the better your chance of avoiding surgery or, in the case of a serious melanoma or other skin cancer, potential disfigurement or even death.

It is also a good idea to talk to your doctor about your level of risk and for advice on early detection.

Become familiar with the look of your skin, particularly spots and moles, so you pick up any changes that might suggest a skin cancer.
Look for:

any crusty, non-healing sores

small lumps that are red, pale or pearly in colour

new spots, freckles or any moles changing in colour, thickness or shape over a period of weeks to months.

Causes of skin cancer

Australia has one of the highest rates of skin cancer in the world. Anyone can be at risk of developing skin cancer, though the risk increases as you get older.

The majority of skin cancers in Australia are caused by exposure to UV radiation in sunlight.

Some factors that increase your risk of skin cancer include:

Diagnosis of skin cancer

It is important to check your skin regularly and check with your doctor if you notice any changes.

In the majority of cases, your GP will examine you, paying attention to any spots that may look suspicious. Your GP may perform a biopsy (remove a small sample of tissue for examination under a microscope). In some cases your GP may refer you to a specialist, such as a dermatologist, if necessary.

Skin cancer clinics

Usually operated by GPs, skin cancer clinics can offer a variety of services. Some clinics are run by dermatologists.

Skin cancer clinics may not offer higher levels of expertise than your GP, so it is important to look into what services are offered and the training of the staff.

When choosing a skin cancer clinic consider:

staff - qualifications and experience

costs

diagnosis and services offered

follow-up provided.

Cancer Council does not operate or recommend any particular skin cancer clinics or doctors.

Treatment for skin cancer

Skin cancers are almost always removed. In more advanced skin cancers, some of the surrounding tissue may also be removed to make sure that all of the cancerous cells have been taken out.

The most common treatment for skin cancer is surgery to remove the cancer (usually under a local anaesthetic). Common skin cancers can be treated with ointments or radiation therapy (radiotherapy). Skin cancer can also be removed with cryotherapy (using liquid nitrogen to rapidly freeze the cancer off), curettage (scraping) or cautery (burning).

For more detailed information about skin cancer please phone Cancer Council 13 11 20 or talk to your GP.

Palliative care

In some cases of skin cancer, your medical team may talk to you about palliative care. Palliative care aims to improve your quality of life by alleviating symptoms of cancer.

As well as slowing the spread of skin cancer, palliative treatment can relieve pain and help manage other symptoms. Treatment may include radiotherapy, chemotherapy or other drug therapies.

Treatment Team

Depending on your treatment, your treatment team may consist of a number of different health professionals, such as:

GP (General Practitioner)- looks after your general health and works with your specialists to coordinate treatment.

Dermatologist- specialises in preventing, diagnosing and treating skin diseases.

Surgeon- Surgeon which can be a general surgeon, a surgical oncologist to manage complex skin cancers or a plastic surgeon trained in complex constructive techniques, including surgery if the cancer has spread..

Screening for skin cancer

There is currently no formal screening program for skin cancers in Australia. It is recommended that people become familiar with their skin. If you notice any changes consult your doctor.

More information about early detection is available in Cancer Council's position statement on screening and early detection of skin cancer.

You can also explore our section on how to check your skin for signs of skin cancer.

Download Cancer Council's skin cancer identification poster to help identify potential skin cancers:

Preventing skin cancer

Protect your skin

For best protection, when the UV level is 3 or above, we recommend a combination of sun protection measures:

Slip on some sun-protective clothing - that covers as much skin as possible.

Slop on broad spectrum, water resistant SPF30 sunscreen. Put it on 20 minutes before you go outdoors and every two hours afterwards. Sunscreen should never be used to extend the time you spend in the sun.

Slap on a hat - that protects your face, head, neck and ears.

Seek shade.

Slide on some sunglasses - make sure they meet Australian standards.

Be extra cautious in the middle of the day when UV levels are most intense.

For further information please visit our page on preventing skin cancer.

Prognosis for skin cancer

It is not possible for a doctor to predict the exact course of a disease. However, your doctor may give you the likely outcome of the disease. If detected early, most skin cancers are successfully treated.

Most non-melanoma skin cancers do not pose a serious risk to your health but a cancer diagnosis can be a shock. If you want to talk to someone see your doctor. You can also call Cancer Council 13 11 20.

Sources

Understanding Skin Cancer, Cancer Council Australia, © 2020. Last medical review of source booklet: January 2020.

Australian Institute of Health and Welfare (AIHW). Australian Cancer Incidence and Mortality (ACIM) books. Canberra: AIHW.

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Skin cancer | Causes, Symptoms & Treatments

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Skin cancer occurs when skin cells are damaged, for example, by overexposure to ultraviolet (UV) radiation from the sun. There are three main types of skin cancer: Both basal cell carcinoma and squamous cell carcinoma are known as non-melanoma skin cancer or keratinocyte cancers.

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Intended for healthcare professionals

1. How to use an...

2. How to use an ophthalmoscope

Career Focus BMJ 2004; 329 doi: https://doi.org/10.1136/bmj.329.7461.s56 (Published 07 August 2004) Cite this as: BMJ 2004;329:s56

1. David Spokes, ophthalmology senior house officer

1. Kidderminster General Hospital, Kidderminster

Abstract

When we asked for tips on practical medical skills, many readers sent us guidance on using an ophthalmoscope. Here is a selection and amalgamation of five readers' collected wisdom—from senior house officer to consultant ophthalmologist

The ophthalmoscope seems a simple tool. But in reality, “fundi NAD” written in the notes often means “not actually discerned.” The ophthalmoscope is not difficult to use but it requires some practice. Try to get in the habit of using it in every neurological examination—you'll soon get the hang of it.

Prepare your equipment

Does it work?

Check that the ophthalmoscope actually works—the batteries may be flat or it may not have been charged. Some ophthalmoscopes have a small cover over their aperture which, if closed, may lead you to think that it is not working.

How does it work?

There are different types of ophthalmoscope, and it always pays (with the lights still on) to familiarise yourself with the various dials and levers. When switched on, the emitted light should be:

Bright—turn it to maximum

White—ignore all other colours

Circular—again, ignore all the slits and crosses; turn the dial until you get a round circle.

Many people find it confusing to have to think about their own glasses and the patient's glasses. Don't worry about this—set all the numbers on the ophthalmoscope to “0.” Ask the patient to remove his or her glasses—you can keep your own on or remove them as you prefer. Contact lenses do not need to be removed.

Room lighting

Switch the room lights off or dim them, but don't make the room too dark.

Prepare your patient

Dazzling examination

Explain what you are going to do to the patient. Warn the patient that the bright light can temporarily dazzle them.⇑

Position

Position the patient so that he or she is comfortable but sitting up (if possible).

To dilate or not to dilate?

Pupil dilatation (with one drop tropicamide 1% in each eye and wait for 15 minutes) is useful to acquaint yourself with the normal fundus but may not always be possible, especially in neurology patients or those with a head injury.⇓

Even with dilatation, only about a third of the fundus is visible with a direct ophthalmoscope. Fortunately, the area most visible is the posterior pole (including the disc and the macula), where you should be able to see the ocular findings of many systemic diseases such as hypertension and diabetes

Where the patient should look

It is important to get your patient to fixate on a precise area (for example, the corner of the room or curtain rail). If you are too vague about this they will move their eyes. Instruct the patient to look at this spot no matter what—even if you get in the way. This spot should be located so that they are looking slightly away from you when they are examined—that is, to the left when you examine the right eye and vice versa.

Get your own position right

Eye to eye

It is best to examine the patient's left eye with your own left eye and right eye with your own right eye—this takes practice. Try to keep your other eye open. Certainly, in an examination, such as for membership of the Royal College of Physicians (MRCP) part 2, you shouldn't close your other eye while examining the retina.⇑

Place your hand on the patient's forehead so that your fingers are splayed but your thumb is on the upper lid. This is important as you will use your thumb to hold the patient's lid open and also the joint of your flexed thumb is exactly where your forehead needs to end up.

What am I looking for?

Red reflex

Media opacities obscure the red reflex (corneal scars, cataract and vitreous haemorrhage, and asteroid hyalosis).

Optic disc

Look for optic disc size, colour (pallor, congestion), cup disc ratio, margins, haemorrhages, new vessels, collaterals. Pale and clearly demarcated disc: optic atrophy. Pathological cupping: glaucoma. New vessels on the disc: proliferative diabetic retinopathy is the most common cause. Yellow-grey disc with blurred margins ± haemorrhages: papilloedema—bilateral.

Vessels

Start at the disc and follow the vessels out to look for hypertensive and arteriosclerotic changes. Look as far as the mid-periphery for scars (inflammatory, laser), haemorrhages, exudates, pigment (white, black), and pigmented lesions. Examine arteries, veins (slightly thicker), and perivascular fundus. A-V nipping is seen in hypertension.

Look also for: microaneurysms, blot haemorrhages, hard exudates—background diabetic retinopathy; cotton wool spots (fluffy white patches), vessel changes such as venous beading, and venous loops are preproliferative changes; leashes of new vessels.

Macula

You will find the macula temporal to the disc. The foveal reflex is seen better with a green (red-free) filter and is at two disc diameters away from the disc and 1.5 degrees below the horizontal (your whole field of view is 8 degrees). A circinate ring of hard exudates, haemorrhage (dot, blot, or flame), or pigment deposition are the most common things you will see.

Begin at arm's length

Begin at arm's length by shining the ophthalmoscope light into the patient's pupil (you will then see the red reflex). Follow this reflex until your forehead rests on your thumb—you should immediately see the optic disc. It will probably be out of focus so, without moving your head, turn the lens dial either way—if the disc becomes clearer keep turning. If it becomes more blurred, turn the dial the other way.

To look at the macula, ask the patient to look directly into the ophthalmoscope light. The ophthalmoscope can also be used for examining the anterior part of the eye by turning the lens dial to ∼ +10.

What am I looking for?

Follow a routine: red reflex, anterior segment, disc, vessels, and lastly macula (see box). In an exam, once you have found an abnormality, keep looking for a second one.

When examining the vascular arcades, ask the patient to look in the appropriate direction to extend your field of view. The red-free (don't call it “green”) filter is useful for enhancing the appearance of blood vessels and haemorrhages by making blood show up black.

Record your findings

Record any abnormalities in a diagram, using the disc diameter as a reference measure. Remember, the image is not inverted, so you can draw it as you see it. Seek expert advice if needed.⇑

Common mistake

The biggest mistake doctors make when using the ophthalmoscope is not getting near enough to the patient. Don't be shy. Make sure you are very close to the patient, almost cheek to cheek, and that you maintain this throughout the examination. The closer you get, the wider your field of view.⇑

If you dilate the patient's pupils remember that he or she should not drive for at least one or two hours after dilatation, and longer if they feel their vision has not returned to normal.

View Abstract

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It is best to examine the patient's left eye with your own left eye and right eye with your own right eye-this takes practice. Try to keep your other eye open. Certainly, in an examination, such as for membership of the Royal College of Physicians (MRCP) part 2, you shouldn't close your other eye while examining the retina.

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Acute Otitis Media (Causes, Pathophysiology, signs and symptoms, treatment and complications)

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Quick Explainer: Grommets (A procedure for recurrent ear infections).

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Mayo Clinic Minute: The A, B, C, D, Es of skin cancer

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Indian Dermatol Online J. 2015 Mar-Apr; 6(2): 67-74.

Abstract

Certain nail changes are specific for various dermatological disorders. In addition, examination of nails may also provide an insight into more sinister systemic manifestations in the form of both subtle as well as specific changes. These findings may present as a defect of various anatomical components of the nail unit; nail matrix, nail plate and/or nail bed or vasculature. This article is an attempt to equip the dermatologists with a foresight to suspect and diagnose the unapparent systemic connotations that may be possible by a simple but detailed nail examination.

Keywords: Matrix, nail, nail bed, nail plate, nail unit, systemic diseases

INTRODUCTION

Subtle nail abnormalities can harbinger appalling systemic diseases. Hippocrates in the fifth century described clubbing as an important clue to myriad of systemic manifestations.[ 1] Since then many more nail findings have been found to be associated with systemic diseases. Therefore, examination of the nails should be an integral part of a complete dermatological examination. Clinicians must acquaint themselves with these nail findings as they can provide a clue in diagnosing certain systemic diseases. Moreover, at times, some nail changes can be a presenting feature before other signs of a systemic disease become clinically evident. With the convenience with which all 20 nails can be examined; certainly, they serve as an important diagnostic tool. Fingernails usually provide more accurate information than toenails, because clinical signs on toenails are often modified by trauma.

CLASSIFICATION

It is important to classify the nail involvement in systemic diseases according to its specificity of association [ Box 1 ].[ 2]

Box 1

However, for a dermatologist, it is also important to classify them according to the clinical presentation, that is, morphological changes in the nail unit [ Box 2 ]. We will discuss briefly the importance of these changes and their possible association with various systemic diseases.

Box 2

Abnormalities of nail shape

Koilonychia

It is the presence of reverse curvature in the transverse and longitudinal axis, giving a concave dorsal aspect to the nail. These changes result in spooning of the nails capable of retaining a drop of water. It is appreciable more on fingernails then toenails [ Figure 1 ]. Koilonychia can be idiopathic or associated with a variety of conditions such as iron deficiency anemia (Plummer Vinson syndrome), malnutrition, hemochromatosis, coronary disease, thyroid disorders, Upper gastrointestinal malignancy, traumatic injury, or occupational.[ 2, 3] Koilonychia is of common occurrence in young infants but tend to disappear in early years of life in majority. Subungual hyperkeratosis accompanying koilonychias is suggestive of psoriasis. A number of factors, such as old age, digital ischemia, and so on, leading to thinning of nails may cause koilonychia. Occupational softening and iron deficiency are probably the most common causes.[ 4, 5] Mild nail-plate thickening and discoloration are also indicative of an occupational cause. The petaloid nail is an early stage of koilonychia and is characterized by flattening of the nail.[ 6]

Hereditary and congenital forms are rare and are sometimes associated with other nail signs such as leukonychia. Transmission is dominant with high penetrance.

The exact cause of koilonychia is at best elusive. An angulation of the nail matrix secondary to connective tissue changes or spooning of the nail resulting from a relatively low distal matrix as compared with the proximal matrix, are some of the proposed hypotheses.[ 7]

Clubbing

It is characterized by increased nail plate curvature longitudinally and transversely with soft tissue hypertrophy of the digital pulp usually involving all 20 digits. Clubbing has been studied extensively and rationally and forms an integral component of any general physical examination in clinical practice. Because of an exhaustive list of systemic associations, it is classified into three major categories: Idiopathic, hereditary-congenital, and acquired.[ 6, 7] It may have connotations with systemic diseases, such as cyanotic congenital heart diseases, infective endocarditis, primary and metastatic lung cancer, bronchiectasis, lung abscess, cystic fibrosis, mesothelioma, inflammatory bowel disease, and hepatic cirrhosis.[ 8, 9]

Clubbing may be an early sign of AIDS in pediatric HIV-positive patients. It may be associated with hypertrophic osteoarthropathy, in which subperiosteal new bone formation in the distal diaphysis of the long bones of the extremities causes pain and symmetric arthritis-like changes in the shoulders, knees, ankles, wrists, and elbows.

Three forms of geometric assessment can be performed in clubbing. (1) Lovibond's angle at the junction between nail plate and proximal nail fold and it is normally less than 160°. In clubbing, this is increased to over 180°. (2) Curth's angle at distal interphalangeal (DIP) joint is normally approximately 180° and this diminishes to less than 160° in clubbing [ Figure 2 ]. (3) Schamroth sign refers to the obliteration of normally diamond-shaped space formed when dorsal sides of the distal phalanges of corresponding right and left digits are opposed [ Figure 3 ].[ 10]

Dolichonychia

It is defined as the length of nails greatly exceeding the width of nail and has been associated with Marfan's syndrome and hypopituitarism.[ 12]

Macronychia and micronychia

These constitute nails that are too large or too small compared with other nails on nearby digits. Macronychia may be due to local gigantism, whereas micronychia may occur in association with plexiform neuromas.[ 10]

Abnormalities of nail attachment

Onycholysis

Onycholysis refers to the distal separation of the nail plate from the nail bed [ Figure 4 ]. Areas of separation appear white or yellow due to air beneath the nail and sequestered debris. It is more frequently associated with diverse local conditions such as trauma, psoriasis, fungus, and contact irritant reactions (nail cosmetics) than systemic disease. The correlation of onycholysis with the systemic diseases appears to be over-rated. Systemic associations include anemia, brochiectasis, lung cancer, cutaneous T-cell leukemia, diabetes mellitus, thyroid disorders, porphyria, lupus erythematosus, psoriatic arthritis, Sezary syndrome, drugs (psoralens and tetracyclines), and Vitamin C deficiency.[ 15, 16] When it happens in thyrotoxicosis, the earliest stage is conversion of the curved adhesion line to a straight line. This adhesion line later dips proximally into the nail bed as a jagged projection. This description is that of Plummer's nails, which usually involves fourth and fifth fingers.[ 2]

Abnormalities of nail surface

Longitudinal ridging (Onychorrhexis)

Longitudinal lines, or striations, may appear as indented grooves or projecting ridges and may represent long-lasting abnormalities [ Figure 6 ]. Although a single nail fissure is most likely due to a minor trauma, systemic connotations have been found with systemic amyloidosis, nail-patella syndrome, collagen vascular diseases, graft versus host disease, and rheumatoid arthritis.[ 4, 10]

Central ridges can also be caused by iron, folic acid, or protein deficiency.

Beau's lines

Described first in 1846, Beau's lines are band-like depressions extending from one lateral edge of the nail to the other. It is the most common and least specific nail change in a systemic disease. Its exact cause is not known but there is temporary cessation of nail growth in the matrix by various factors, for example, trauma involving proximal nail fold, severe acute illness such as fever, heart attack, exposure to extreme cold, psychological stress, and poor nutritional status. Idiopathic and inherited forms also occur. If there is complete inhibition of nail growth for around 2 weeks, Beau's line will reach maximum depth resulting in onychomadesis [ Figure 7 ]. Recurrent bouts of illness may lead to the formation of series of transverse furrows/grooves [ Figure 7 ]. The width of the transverse groove relates to the duration of the disease that has affected the matrix. The distal limit of the furrow, if abrupt, indicates a sudden attack of disease; if sloping, a more protracted onset.[ 18] The presence of Beau's lines on all 20 nails is usually the result of systemic disease such as mumps, pneumonia, coronary thrombosis, Kawasaki disease, syphilis, and hypoparathyroidism.[ 4, 10]

Nail pitting/trachyonychia

Pits result from a defective keratinization of the proximal matrix with persistence of parakeratotic cells in the nail plate surface.[ 19] Its role and diagnostic utility is doubtful as a large number of local factors affect the matrix function. It may occasionally be useful in diseases such as psoriasis, psoriatic arthritis [ Figure 8 ], SLE, dermatomyositis, syphilis, sarcoidosis, and pemphigus vulgaris.[ 2, 19, 20]

Abnormalities of nail color

Leukonychia

Leukonychia refers to the white discoloration of nail. It is traditionally classified into three subtypes.[ 22]

True, when pathology originates in matrix and emerges in the nail plate.

Apparent, when pathology is in the nail bed.

Pseudo, when nail plate pathology is exogenous, for example, onychomycosis [ Figure 9 ].

Leukonychia associated with systemic disease is usually true or apparent

Mees lines: True leukonychia due to arsenic intoxication is characterized by a single or multiple, transverse, narrow whitish line running along the width of the nail and parallel to lunula, and may involve multiple nails. These lines do not disappear on blanching and move distally with time.[ 23, 24] Histology shows fragmented nail plated with foci of parakeratotic cells. They have been reported with other conditions as well such as Hodgkin's disease, leprosy, tuberculosis, malaria, herpes zoster, chemotherapeutic drugs, carbon monoxide (CO) and antimony poisoning, renal and cardiac failure, pneumonia, and childbirth.

Muehrcke's lines: These are apparent leukonychia characterized by double white transverse line [ Figure 10 ], resulting possibly from a localized edematous state in the nail bed exerting pressure on the vascular bed. They are specific for hypoalbuminic state (occur in patients albumin <2 g/dL) and disappear when the protein level normalizes. Muehrcke's lines are seen in nephrotic syndrome, glomerulonephritis, liver disease, chemotherapeutic drugs, and malnutrition.[ 22, 25, 26]

Half and half nail or Lindsay nail: Apparent leukonychia with a normal proximal half and abnormal brownish discolored distal half [ Figure 11 ]. It is seen in patients of chronic kidney disease with uremic renal failure.[ 26, 27]

Terry nails: Apparent leukonychia with nail that is white proximally and normal distally [ Figure 12 ]. It is associated with congestive cardiac failure, adult-onset diabetes mellitus, peripheral vascular disease, hemodialysis, and HIV.[ 27, 28]

Cyanosis

Cyanosis may manifest as blue or purple discoloration of the nail bed and digits as a result of lower oxygen saturation causing accumulation of deoxyhemoglobin in the small blood vessels of the extremities. Central cyanosis is caused by congenital heart diseases and may manifest on mucosa and extremities, whereas peripheral cyanosis is usually diagnosed by examination of the nail and digits and is caused by vasoconstriction and diminished peripheral blood flow as occurs in cold exposure, shock, congestive cardiac failure, and peripheral vascular disease.[ 10]

Icterus

Yellowish discoloration of the mucosae as a result of deposition of bilirubin may extend to involve the nails in severe cases and may represent severe form of liver disease or hemolysis.[ 10]

Splinter hemorrhages

Splinter hemorrhages in nails are formed by the extravasation of blood from the longitudinally oriented vessels of the nail bed. They occur commonly in psoriasis but may be seen in the setting of infective endocarditis [ Figure 14 ], rheumatic heart disease, valvular replacement, SLE, antiphospholipid syndrome, IV drug abusers, and congenital heart diseases. A simultaneous occurrence in multiple nails is indicative of a systemic cause.[ 2, 22, 31]

Nail abnormalities in specific organ system

Table 1 depicts nail involvement associated with certain specific organ systems. Although overlap in findings is common, subtle changes may predict sinister internal involvement.[ 22]

Table 1

Nail involvement in genodermatosis

Genodermatosis may present with a constellation of signs and symptoms thereby clinching the diagnosis. However, many times subtle but characteristic findings in nails bring us very close to the diagnosis itself. Table 2 depicts genodermatosis associated with nail involvement.[ 22, 35]

Table 2

Hence, nail findings may not only be window to a plethora of possible systemic associations, but also a window of opportunity as a profound knowledge of the associations may be useful in a complete and targeted workup of the patient to pre-empt the clinching of a more sinister systemic disease.

Footnotes

Source of Support: Nil

Conflict of Interest: None declared.

REFERENCES

2. Lawry M, Daniel CR., 3rd . Nails in systemic disease. In: Scher RK, Daniel CR, editors. Nails: Diagnosis, Therapy, Surgery. 3rd ed. Philadelphia: Elsevier Science Limited; 2005. pp. 147-69. [ Google Scholar]

4. Baran R, Dawber RP, Haneke E, Tosti A, Bristow I. Martin Dunitz. 3rd ed. 2005. Nail configuration abnormalities. A Text Atlas of Nail Disorders: Techniques in Investigation and Diagnosis; pp. 18-24. [ Google Scholar]

8. Braunwald E. Hypoxia and cyanosis. In: Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo DL, Jameson JL, editors. Harrison Principles of Internal Medicine. 16th ed. New York: McGraw-Hill; 2009. pp. 209-12. [ Google Scholar]

27. Tosti A, Daniel CR, 3rd, Piraccini BM, Iorizzo M. Heidelberg: Springer Verlag; 2010. Color Atlas of Nails; p. 3. [ Google Scholar]

Articles from Indian Dermatology Online Journal are provided here courtesy of Wolters Kluwer -- Medknow Publications

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Certain nail changes are specific for various dermatological disorders. In addition, examination of nails may also provide an insight into more sinister systemic manifestations in the form of both subtle as well as specific changes. These findings may ...

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Medical Terminology - The Basics - Lesson 1

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A Trauma-informed Facilitation Course Offered for the Healers - The Urban Alchemist

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Do you know how trauma shows up in the body for your clients? What to do when you see it? And how to manage the impacts on you of holding space alongside trauma? Calling all therapists, bodyworkers, natural therapy practitioners, teachers, support workers, coaches, yoga teachers and anyone who wor…

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Clinician's Corner: Taking a good patient history

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Body fatness has been an important psychosocial issue among humans for millennia. It is clearly manifested by paleolithic statuettes of exceedingly plump women. This suggests being "full figured" was highly desirable at least for women. In contrast, images of obese people, males or females, are never exhibited in ancient Egyptian funerary wall paintings, stellae, or statues suggesting that fatness was not considered to be a desirable trait there. This also is the case in artifacts from other cultures in the Middle East in that era. Why the degree of fatness has varied in different cultures is not clear. However, it may have depended on the availability of a reliable food supply and the effort required in obtaining it.

More recently, the degree of rotundity considered ideal also has varied considerably in the general population, but particularly for young women. Before the 1920s, "full figured" women were considered to be desirable as long as the distribution was hourglass in type. However, the 1920s Flapper era introduced abbreviated and revealing dresses. The result was that thinness was not only desirable but also required. This concept has moderated but still influences women's views of beauty and eating habits at present.

Fatness as a Personal or Society Issue

Traditionally, a person's fatness has been defined at a personal level as well as at a societal level. However, this is difficult to quantify. That is, each individual has his/her own perception of how fat he/she should be. As indicated above, this often depends on a general concept of societal norms or is due to peer pressure. For example, currently in Western societies, young women are often concerned about their body image, and most consider themselves to be too fat, even though they are well within population-based references. This is not only due to societal concepts of an ideal degree of fatness, but also due to thinness being a goal promulgated by the fashion industry and reinforced by commercial advertising.

At a societal level, although poorly described or quantified, there also is a degree of fatness beyond which a person generally is considered to be unacceptably fat; that is, there is an ill-defined threshold at which a person is labeled as being "fat" or "obese." However, it is based on the "I can't define it but I know it when I see it" concept. In addition, implicit in this context is that the location of the excess fat plays a role, as does a person's age. It is much more acceptable to be "overweight" when one is old than when one is young. Also particularly in women, the accumulation of fat in certain areas of the body is considered to be much more acceptable than in other areas. For example, truncal (belly fat) accumulation would be considered to be less acceptable than the accumulation of fat in the peripelvic and thigh areas as well as in the breast area 1; that is, one may be statistically "fat" but with an appropriate figure be merely referred to "as amply endowed" or "pleasingly plump."

The social consequences of being "too fat" are severe. Discrimination begins in childhood and results in serious emotional scars. Societal discrimination limits career choices, and indeed many career paths are closed to those considered to be too fat. Also, societal stigmatization often impairs a person's ability to express his/her intellectual and other talents; that is, they become underachievers. In addition, the potential pool of mates is limited because of their perceived unattractiveness. Thus, obese people tend to marry other obese people and, parenthetically, to produce obese children. 2- 4

Fatness as a Medical Issue

Not only the societal but also the functional and indirectly the medical consequences of an excessive accumulation of fat also have been recognized for millennia. Nevertheless, the concept that "body build" (fatness) is a major population-based medical issue gained popularity in this country only shortly before 1900. Life insurance data accumulated at that time 5 and subsequently 6 indicated that body weight, adjusted for height (Wt/Ht), was an independent determinant of life expectancy, and in 1910, the effects of being overweight were noted to be greater for younger people than for the elderly. 6

Subsequently, the Metropolitan Life Insurance Company in 1959 published tables of average body weights for heights (Wt/Ht) by gender and at different ages. 7 This was based on data from 1935 to 1953 from more than 4 million adults, mostly men, insured by 26 different insurance companies. The risk for development of certain diseases as well as mortality data related to Wt/Ht differences also were analyzed and reported in the 1960 Statistical Bulletin of the Metropolitan Life Insurance Co. 8, 9

The Wt/Ht tables were used for many years as a reference for population-based studies. If a person's Wt/Ht was 20% above or below the mean for that height category, he/she was considered to be overweight or underweight, respectively. The insurance data also indicated the ratios of weights for heights (the term used was "body build") at which mortality was lowest in adults. The latter was referred to as the "ideal" or later the "desirable" weight. All of these data were periodically updated. 10 Interestingly, from 1959 to 1983, the desirable weight, that is, the weight/height representing the lowest mortality had increased. 10- 12 However, a "desirable body" weight for height was invariably lower than the average weight for height in the insured population. 7, 10, 13

Problems With the Wt/Ht (Body Build) Index

Early on it was recognized that tall people had a lower death rate than did short people 7, 8, 13 with the same Wt/Ht ratio. It also was recognized that a person's height in general and leg length in particular could affect the calculated body mass adjusted for height. A person's bony frame, that is, bone mass, also could affect the interpretation of this ratio. In general, it reflected whether one was narrowly or broadly built. Thus, efforts were made to eliminate lower limb length and frame size as variables. 7, 10 The strategy was to develop representations of body build, that is, charts of weight/height that were independent of these variables. The overall goal was to have the same distribution of Wt/Ht at each level of height.

Mathematical Adjustment of Body Build

Mathematically, the issue of adjusting body build for differences in height was approached with the concept that the body, particularly the trunk, could be considered as being a 3-dimensional volume or mass. Thus if a tall person were simply a scaled-up version of a short person, weight would increase approximately with the cube of height. 16 Indeed, several equations were developed and tested based on this concept; that is, the cube root of weight divided by height ( ³√Wt/Ht) or weight/height, 3 and so on, but none were ideal. 17 This is because tall people are not just scaled-up versions of short people. As indicated previously, they tend to be more narrowly built resulting in a greater lean/fat proportion of body mass.

Later, it was shown that the body mass for height actually scaled best with weight for height when the height was raised to the 1.6 to 1.7 exponent (Wt/Ht, 1.6 etc). 18 Thus, with an increase in Ht, the effect of Ht on the ratio is exponential, whereas the change in Wt is linear. This has the effect of Ht on the ratio to be magnified as Ht increases. Overall, it results in a lower ratio in tall people than will be obtained with just a Wt/Ht ratio. Thus, it potentially compensates for a narrower build in tall compared with short people.

This exponent is not convenient for use in population-based studies, and it was determined that Wt/Ht ² generally was satisfactory. 16, 18 The latter represents the Quetelet Index. It was developed by Dr Quetelet in the 1800s.

Lambert Adolph Jacque QueteletAdoption of the BMI as an Index of Obesity

In 1972, Keys et al 16 severely criticized the validity of Metropolitan Life Insurance published data per se, and the then-published tables of desirable weight for height, as well as the tables used to define people who were underweight or overweight. 7 (The pejorative term "obese" was rarely used in that era.) Instead, Keys et al, using better documented weight for height data, popularized the Quetelet Index in population-based studies. They referred to it as the body mass index (BMI). Thus, Quetelet Index = body weight (kilograms) divided by height squared (meters) = BMI.

As indicated above, by squaring the height, it reduces the contribution of leg length in the equation and tends to normalize the body mass distribution at each level of height; that is, it reduces the effect of a variance in height in the relationship of weight to height. This was considered to be important because most of body fat is in the trunk. Nevertheless, as also pointed out by Keys et al, 16 even the BMI rather poorly represents a person's percent of body fat.

BMI Distribution in a Normal Population

Although a BMI determination reduces the effect of lower-extremity length on the Wt/Ht ratio, whether one uses the BMI or merely the ratio of weight to height, the population distribution is still not Gaussian. That is, it is not symmetrical but is always skewed to the right, that is, toward a higher ratio of weight (body mass) to height. For example, the distribution of BMIs in adult American men and women was determined in 1923 in 1026 individuals (Figure). 27 The median BMI was 24, but the mean BMI was 25. The distribution curve clearly indicated a skewing toward an increase in BMI, and this trend has continued. 26

WHO and the Categorization of BMIs Into Quartiles

In 1993, the WHO assembled an Expert Consultation Group with a charge of developing uniform categories of the BMI. The results were published as a technical report in 1995. 25 Four categories were established: underweight, normal, overweight, and obese. An individual would be considered to be underweight if his/her BMI was in the range of 15 to 19.9, normal weight if the BMI was 20 to 24.9, overweight if the BMI was 25 to 29.9, and obese if it was 30 to 35 or greater. Using linear regression, a BMI of 16.9 in men and 13.7 in women represents a complete absence of body fat stores. 31

The above 4 categories are similar to those suggested by John S. Garrow in 1981, 31, 32 but the terminology was changed. The terminology he used was "desirable" for a BMI up to 25, "grade I obesity" between 25 and 29.9, "grade II obesity," between 30 and 40, and "grade III obesity" for BMI greater than 40.

The latter classification was based on Rosenbaum and colleagues' 33 own data obtained in a survey of an adult population, aged 16 to 64 years, in Great Britain and published in 1985.

The population-based data indicated the majority of people were in the "desirable" range of the BMI distribution as indicated in Table . Unfortunately, this distribution is not and has not been similar to those found in other surveys. The BMIs have been higher.

TABLE 1

At the time that the WHO classification was published, the National Institutes of Health (NIH) in the United States classified people with a BMI of 27.8 (men) and 27.3 (women) or greater as being overweight. If they were below this BMI, they were considered to be "normal." This was based on an 85% cutoff point of people examined in the National Health and Nutrition Examination Study (NHANES) II. 12, 22, 34 Subsequently, in 1998, the cutoff point between normal and overweight was reduced to a BMI of 25 to bring it into line with the 4 categories in the WHO guidelines. 25, 35 Parenthetically, this instantaneously converted millions of Americans from being "normal weight" to being "overweight."

The new terminology appears to be a bit presumptuous and careless because the BMI is not a direct measure of percent of fat mass, and the dynamic concept that those in the former "overweight" category are now in the "preobesity" category invariably going on to "obesity" is not the case. Also those with a lower BMI initially, but with a dynamic weight gain over time, would have to transition through this category in order to become classified as "obese" regardless of the terminology. By analogy, should those classified as "underweight" now be referred to as being "prenormal"?

Distribution of BMI in the General Population

Regardless of the terminology and population reference issues, at present the BMI is the currency by which we define the obesity issue throughout the Western world. It was developed for the convenience of the epidemiologists, and indeed it did provide a uniform codification of body weight for height reporting. The BMI categories are shown in (Table ).

Table 2

BMI as a Determinant of Body Fat Mass

From an anatomical and metabolic perspective, the term obesity should refer to an excessive accumulation of body fat (triacylglycerols), and upon these grounds, the accuracy of the BMI as a determinant of body fat mass has been repeatedly questioned, 16, 39- 41, 46- 48 because it clearly has limitations in this regard. Gender, age, ethnic group, and leg length are important variables. 45, 49- 55 It should be noted that in population-based studies women generally have a BMI that is lower than that in men, even though their fat mass relative to their body build or BMI is considerably greater (~20% to 45%+).

The relatively poor correlation between percent of body fat mass and BMI also clearly has been shown more recently in the NHANES III database in which bioelectrical impedance was used to estimate the fat component of body composition. 51 In subjects with a BMI of 25 kg/m ², the percent of body fat in men varied between 14% and 35%, and in women it varied between 26% and 43%. Thus, using the NIH-suggested criterion based on percent of body fat to define obesity, subjects with a BMI of 25, a group that would be considered to be essentially normal, were associated with a body fat mass that varied again between low normal to obese. Also it is of interest that in the entire NHANES cohort, the BMI correlated better with lean body mass than with fat mass in men. 51 More recent NHANES data also indicate a poor correlation of BMI with percent of body fat, particularly in men. 58

In addition, in a recent study in individuals with or without diabetes in which the loss of lean body mass with aging was reported, the mean BMI in those without diabetes was 26.8. In those with diabetes, the BMI was 29.1; that is, it was higher as generally expected. However, the percent of lean body mass was the same; that is, the increased BMI in those with diabetes was not due only to an excessive accumulation of fat. 59

Trends in Body Weight and Height

Over the past several decades, there has been an increase in BMI in the general population. This has resulted in predictions of a public health disaster. It should be recognized that in the United States during the period from 1960 to 2002 not only has the mean weight increased by 24 lb among men aged 20 to 74 years, but also the height has increased by about 1 in. We can then calculate that the weight increase per year has only been 0.57 lb, and as indicated above, this could be due to an increase in lean mass rather than fat mass, or it may be a combination of the two. In women, there was a similar increase in weight and height. 40

Overall, the history of changes in height and weight in Western European men and probably women has been that of an increase in both weight and height. In the 17th century, the average height of men in Northern Europe was ~5 ft 3 in. It now approaches 6 ft. 61 These data suggest that the BMI categories should be adjusted upward periodically to accommodate population-based changes. Improvements in mortality rates also suggest an adjustment would be useful.

Body Fat Location

More specifically, both visceral fat accumulation 68, 69 and an expanded girth have been associated with development of insulin resistance, diabetes, and risk for coronary heart disease and hypertension. 63, 64, 70- 74 Accumulation of fat in the abdominal area appears to correlate best with triacylglycerols accumulating in the liver and skeletal muscle. These may actually represent the pathogeneticially important metabolic consequences that result in insulin resistance and more directly correlate with development of the above adverse medical conditions. 68, 75, 76 Incidentally, the relatively small accumulation of fat in these organs would not be detectible by BMI determinations, and they do not correlate simply with total body fat mass. 75

The Life Cycle and Location of Accumulated Fat

It is of some interest that accumulation of fat in the lower body at puberty in females is unique to humans, is not present in any of the great apes, and most likely is estrogen mediated. 1

In a teleological sense, why this occurs, if due to estrogen, is uncertain. It could represent a means of maintaining body fat during pregnancy without an undue expansion in abdominal girth. It also may act as a counterbalance when women carry a child either during pregnancy or afterward. It also may be a space-filling fat site due to the relatively larger pelvis in postpubertal females. 81 Overall, it may represent an adaptation to the human upright bipedal posture. In any event, it results in a lower center of gravity among women compared with men. Indeed, the lower body segment in females becomes ~40% greater than in males (quoted in Singh, 1993), 1 and it has strong sex-related overtones.

Not only is thigh fat greater in women than in men, but also women generally have a preponderance of slow-twitch fibers, whereas men have a preponderance of fast-twitch fibers in their quadriceps muscles, as do upper-body-obese women, 82 suggesting either genetic or earlier developmental differentiation events. Could this be an adaptation for load-bearing versus speed as a group survival adaptation?

As indicated above, the accumulation of fat with aging in both sexes tends to occur in the truncal area and is associated with an increase in visceral fat. In women, this could be explained by a decrease in circulating estradiol, that is, a decreased estrogen/testosterone ratio associated with the menopause. (Again of some interest, it is only humans who have a defined menopause).

In men, with aging, there is a decrease in testosterone and a relative increase in estrogen, resulting in a decrease in the testosterone/estrogen ratio. 83 Thus, in men, a change in sex hormone concentrations could possibly explain the increased accumulation of fat in general. However, why there is a preferential accumulation in the truncal location, that is, why they too develop an increase in visceral fat, is unclear. Clearly, location of fat in this area would help to maintain mobility. The latter could be of great importance in hunter-gatherer societies and in defense of the tribe. Perhaps the distribution is programmed by gender earlier in life.

Methods of Estimating Body Fat Mass and Location of the Fat

At present, simple, accurate methods for measuring percent of body fat and, in particular, body fat in different fat depots are not available. The indirect methods currently in use for estimating total percent of body fat include underwater weighing, an air displacement and density determination using a Bod Pod, a bioelectrical impedance analyzer, and a determination of the isotopically labeled water mass. In the past, determination of the total body radioactive potassium and thus metabolizing tissue mass have been used to estimate lean body mass, and by difference, the fat mass. 86

Anthropometric determination of fat mass directly has been done using skin-fold thickness measured at various sites. 87 A dual-energy x-ray absorptiometry (DEXA) scan, which provides a 3-dimensional picture of body organ densities, can be used for estimating total body fat. Its location also can be determined. Single computed tomography (CT) slices of the abdomen and thigh can be used to obtain 2 dimensions of those fat depots from which a 3-dimensional fat area can be reconstructed. This also can be done using magnetic resonance imaging, but magnetic resonance imaging is very expensive. One cannot do serial sections of the body using CT to determine fat mass because of the excess radiation associated with this procedure.

All of the previously mentioned methods use certain assumptions in the calculation of body fat mass, and all are subject to potential error. Nevertheless, there are more specific methods of determining body fat mass than is the BMI. Important information regarding the location of the stored fat also can be determined with some methods.

BMI and Morbidity and Mortality

The BMI classification system currently is being widely used in population-based studies to assess the risk for mortality in the different categories of BMI. It also is being used in regard to specific etiologies for mortality risk. However, as with its use to estimate percent of body fat, it is a rather crude approach. Even when some comorbidities are considered, the correlation of mortality rates with BMI often does not take into consideration such factors as family history of diabetes, hypertension, coronary heart disease, metabolic syndrome, dyslipidemias, familial longevity or the family prevalence of carcinomas, and so on. Recently it has been reported that more than 50% of susceptibility to coronary artery disease is accounted for by genetic variants. 92

Frequently, when correlations are made they also do not take into consideration a past as well as a current history of smoking, alcohol abuse, serious mental disorders or the duration of obesity, when in the life cycle it appeared, and whether the body weight is relatively stable or rapidly progressive, that is, type 1 or type 2 obesity. 93, 94 In most population-based studies, only the initial weight and/or BMI are given, even though weight as well as fat stores are known to increase and height to decrease with aging. In addition, the rate of weight gain varies among individuals, 7, 94, 95 as does the loss of muscle mass. 95 Muscle mass has been correlated negatively with insulin resistance and prediabetes. 96 Lastly, population-based studies do not take into consideration the present and past history of a person's occupation, medication-induced obesity, and how comorbidities are being treated. All of the above are significant issues.

More Explicit Problems in Relating the BMI to Medical IssuesThe "Obesity Epidemic"

Recently, there has been concern that an epidemic of obesity is occurring, not only in the United States, but also worldwide based on BMI data. In the NHANES data, there has been a change in the mean but to a greater extent in the distribution of BMI for adults aged 20 to 74 years in the United States. 26 That is, the mean BMI has increased, but there has been a greater increase in skewing toward the right and very large BMI. This results in more individuals being categorized as "obese." The reason for the recent increase in mean BMI, but particularly in those in the obese category, is unknown, although there are many speculations. The dramatic decrease in smoking is likely to have been a contributor. 91, 103- 106 Smoking contributes to population-based BMI by at least 2 mechanisms. Smoking impairs appetite per se. It also is pathogenetically important in the development of chronic obstructive pulmonary disease, which itself results in a lower body mass. Of some interest, NHANES data also indicate that the trend of an increase in BMI has not continued since 1999 in women and only modestly in men. 58 Smoking rates also have stabilized at a low level.

Is Being "Overweight" by BMI Criteria a Medical Issue?

Regardless of an observed increased skewing in the BMI distribution, it is important to note that several recent studies indicate that for most of us being a bit overweight (preobese?) as determined by BMI may not be so bad. 107- 111

The EPIC observational study is a population-based study that includes 359 387 individuals aged 25 to 70 years living in Europe. 109 The mean age of this group at the initiation of the study was 51.5 years, and the mean follow-up has been 9.7 ± 2 years. In this study, both the crude and adjusted relative risk of death among men was actually the lowest in those with a BMI of 26.5 to 28, that is, those in the overweight (preobese) category. Also, a significant increase in risk of death was present only among those with a BMI of less than 21 or greater than 30. That is, there is a wide range of BMIs in the central part of this population in which there was relatively little impact of BMI on risk of death over a 9.7-year period.

Similar data were obtained in the NIH-American Association of Retired Persons study of 527 265 men and women between the ages of 50 and 71 years in the United States and followed for up to 10 years. 110 The lowest death rate in the entire cohort was among those in the "overweight" category, and this was particularly true among the men. There also was a broad range of BMIs over which there was little difference in mortality (BMI of 23.5 to 30).

The NHANES data going back to 1971 and up to 1994 also indicate that the relative mortality risk is lowest in men with a BMI of 25 to 30 in all age groups, that is, from the age of 25 years up to the age of 70 years. 107 In addition, the risk of mortality was little affected by a BMI from 18.5 up to a BMI of 30 in all age categories. Indeed, in those older than 70 years, there was little impact on the death rate even if they were in the obese category. Similar results have been reported for women in the NHANES reports. 112 The lowest mortality occurred with a BMI of 27.

In a Canadian study, the age-adjusted mortality rate over 13 years in men was essentially unchanged in those with a BMI of 18.5 up to 35, that is, from the Normal Weight category through the obesity class I category. In women, there was only a modest increase over the same range. 113

In summary, there is a large range of BMIs over which there is little association with the death rate. Generally, the range is from a BMI of 21 up to and often including 30. It is centered in the 24-to-28 BMI range. This information is not entirely new. Andres 114 in 1980 summarized 16 different population-based studies in which anthropometrically determined obesity was not associated with increased mortality rate. A detailed analysis in 1960 of the Metropolitan Life Insurance data also suggested little increase in mortality rates in people with a degree of overweight less than 20% or more above the average for a given height and age (quoted in Keys et al 97).

Interestingly, in the EPIC observational Study, 109 when the waist circumference-to-BMI ratio was calculated, that is, adjusting the waist circumference for BMI, it tended to linearize the association of BMI with risk for death, and the ratio was greatest for those with a low BMI. Thus, even if an individual had a low BMI but a relatively increased waist circumference, the risk was increased. Indeed, for any given BMI, a 5-cm increase in circumference increased the risk of death by a factor of 1.17 among men and 1.13 for women. Also in this study, the overall greatest mortality risk was in those individuals with the lowest BMI and not those with the highest BMI. Nevertheless, even in the category with the lowest BMI, adjusting for waist circumference affected the mortality rate negatively. This again indicates the importance of the location of body fat in addition to the total amount of fat accumulated.

A recent analysis of 50 prospective observational studies indicated the lowest mortality at a BMI of 23 to 25. However, these data were obtained in the 1970s and 1980s in an aggregate population with a mean BMI of 24.8, that is, lower than at present. The increased mortality at higher BMI's was modest up to a BMI of 27.5, and the authors could account for the excess mortality largely on the risk factors known to be associated with obesity. The latter are currently being much better treated than in that era. 115

Issues to be Resolved When Relating BMI With Health Determinants

Overall, a major unresolved issue is which factor of the following is more important in the prediction of comorbidities such as cardiovascular disease, diabetes, hypertension, malignancies, or overall death rates. Is it BMI, total body fat mass, or the distribution of body fat, that is, visceral versus subcutaneous, or upper body fat accumulation (as determined by abdominal circumference, or a waist/hip ratio, or some combination of these, and so on)? The EPIC 109 data suggest that where fat is accumulated is much more important than merely the BMI, with the exception of those with an exceeding large total fat mass.

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Body Mass Index: Obesity, BMI, and Health: A Critical Review

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Body fatness has been an important psychosocial issue among humans for millennia. It is clearly manifested by paleolithic statuettes of exceedingly plump women. This suggests being "full figured" was highly desirable at least for women.

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Clinical Examination

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A comprehensive collection of medical revision notes that cover a broad range of clinical topics.

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A collection of interactive medical and surgical clinical case scenarios to put your diagnostic and management skills to the test. Each clinical case scenario allows you to work through history taking, investigations, diagnosis and management. We also have a collection of 500+ OSCE cases with mark schemes and answers to relevant questions.

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History taking | OSCE | OSCE Practice | Geeky Medics

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A collection of history taking guides with included checklists, covering common OSCE stations, to help practice your history taking skills.

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Taking a history from a patient is a skill necessary for examinations and afterwards as a practicing doctor, no matter which area you specialise in. It tests both your communication skills as well as your knowledge about what to ask. Specific questions vary depending on what type of history you are taking but if you follow the general framework below you should gain good marks in these stations. This is also a good way to present your history.

In practice you may sometimes need to gather a collateral history from a relative, friend or carer. This may be with a child or an adult with impaired mental state.

Procedure Steps

Step 01

Introduce yourself, identify your patient and gain consent to speak with them. Should you wish to take notes as you proceed, ask the patients permission to do so.

Step 02 - Presenting Complaint (PC)

This is what the patient tells you is wrong, for example: chest pain.

Step 03 - History of Presenting Complaint (HPC)

Gain as much information you can about the specific complaint.

Sticking with chest pain as an example you should ask:

Site: Where exactly is the pain?

Onset: When did it start, was it constant/intermittent, gradual/ sudden?

Character: What is the pain like e.g. sharp, burning, tight?

Radiation: Does it radiate/move anywhere?

Associations: Is there anything else associated with the pain, e.g. sweating, vomiting.

Time course: Does it follow any time pattern, how long did it last?

Exacerbating / relieving factors: Does anything make it better or worse?

Severity: How severe is the pain, consider using the 1-10 scale?

The SOCRATES acronym can be used for any type of pain history.

Step 04 - Past Medical History (PMH)

Gather information about a patients other medical problems (if any).

Step 05 - Drug History (DH)

Find out what medications the patient is taking, including dosage and how often they are taking them, for example: once-a-day, twice-a-day, etc.

At this point it is a good idea to find out if the patient has any allergies.

Step 06 - Family History (FH)

Gather some information about the patients family history, e.g diabetes or cardiac history. Find out if there are any genetic conditions within the family, for example: polycystic kidney disease.

Step 07 - Social History (SH)

This is the opportunity to find out a bit more about the patient's background. Remember to ask about smoking and alcohol. Depending on the PC it may also be pertinent to find out whether the patient drives, e.g. following an MI patient cannot drive for one month. You should also ask the patient if they use any illegal substances, for example: cannabis, cocaine, etc.

Also find out who lives with the patient. You may find that they are the carer for an elderly parent or a child and your duty would be to ensure that they are not neglected should your patient be admitted/remain in hospital.

Step 08 - Review of Systems (ROS)

Gather a short amount of information regarding the other systems in the body that are not covered in your HPC.

The above example involves the CVS so you would focus on the others.

These are the main systems you should cover:

Please note these are the main areas, however some courses will also teach the addition of other systems such as ENT/ophthalmology.

Step 09 - Summary of History

Complete your history by reviewing what the patient has told you. Repeat back the important points so that the patient can correct you if there are any misunderstandings or errors.

You should also address what the patient thinks is wrong with them and what they are expecting/hoping for from the consultation. A useful acronym for this is ICE [I]deas, [C]oncerns and [E]xpectations.

Step 10 - Patient Questions / Feedback

During or after taking their history, the patient may have questions that they want to ask you. It is very important that you don't give them any false information. As such, unless you are absolutely sure of the answer it is best to say that you will ask your seniors about this or that you will go away and get them more information (e.g. leaflets) about what they are asking. These questions aren't necessarily there to test your knowledge, just that you won't try and 'blag it'.

Step 11

When you are happy that you have all of the information you require, and the patient has asked any questions that they may have, you must thank them for their time and say that one of the doctors looking after them will be coming to see them soon.

This guide is designed for students and doctors. If you are applying for medical school and would like more information on the UCAT please check out our complete guide and our guide on how to practice for your exam. We've also prepared a UCAT Practice Test to help you prepare for the exam.

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Taking a history from a patient is a skill necessary for examinations and afterwards as a practicing doctor, no matter which area you specialise in. It tests both your communication skills as well as your knowledge about what to ask.

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Click when you are logged in to BB and it should take you to the page

Galvin, K., &amp; Bishop, M. (2011). Case studies for complementary therapists : a collaborative approach. Churchill Livingstone/Elsevier. https://ebookcentral-proquest-com.torrens.idm.oclc.org/lib/think/reader.action?docID=1722061&ppg=642

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Torrens University Australia Limited ABN 99 154 937 005, CRICOS Provider Code: 03389E. RTO No. 41343