Set the Language

We weren't able to detect the audio language on your flashcards. Please select the correct language below.

Front

Back

Hint

Flashcards
»
Pathology I - Red Blood Cell Disorders

Pathology I - Red Blood Cell Disorders

by RabiaNaseem, Feb. 2015

Subjects: 2010 class pathology

Favorite

Add to folder

Flag

Shuffle
Toggle On

Toggle Off
Alphabetize
Toggle On

Toggle Off
Front First
Toggle On

Toggle Off
Both Sides
Toggle On

Toggle Off
Read
Toggle On

Toggle Off

Reading...

Front

Card Range To Study

through

Play button

Progress

1/621

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

621 Cards in this Set

Front
Back
3rd side (hint)

Anemia	inability of blood cells to carry sufficient oxygen to body cells	inadequate no. of blood cells deficiency of oxygen carrying hemoglobin can occur if hemoglobin is inadequate
Anemia Causes	Blood loss by hemorrhage blood forming tissue can not maintain normal numbers of blood cells -cancer, chemotherapy -radiation	certain types of infections
Polycythemia	too many RBC - blood to thick to flow properly
Pernicious Anemia	Low RBC - dietary deficiency of B12
Folate Deficiency Anemia	Decrease in RBC Folic Acid deficiency
Blood Loss Anemia	Hemorrhaging associated w/trauma -extensive surgeries
Anemia of Chronic Disease	Serious complications -chronic inflammatory disease -cancer causes unknown
Hyperchromic	abnormally high hemoglobin count
Hypochromic	abnormally low hemoglobin count
Leukopenia	abnormally low WBC
Leukocytosis	abnormally high WBC
Multiple Myeloma	Cancer of antibody secreting B lymphocytes
Leukemia	blood cancer affecting WBC
CML	Chronic Myeloid Leukemia
AML	Acute Myeloid Leukemia
CLL	Chronic Lymphatic Leukemia
ALL	Acute Lymphatic Leukemia
Thrombus	clot which stays in the place it is formed.
Thrombosis	condition of having blood clot
Embolus	dislodged clot which circulates through blood stream
Embolism	condition of having dislodged blood clot
Hemophilia	X- linked inherited disorder failure to produce 1 or more plasma proteins for clotting
Hempohilia A	caused by absence of Factor VIII protein
Thrombocytopenia	Most common type of clotting disorder platelet count decrease
Lymphedema	edema = swelling lymph = water swelling of extremities because of obstruction of lymphatics and accumulation of lymph
Congenitial Lymphedema	Most common in women 15-25 obstruction in both lymph vessels and nodes
Lymphangitis	Acute inflammation of lymphatic vessels lymph = water angi= vessels itis= inflammation
Tonsilitis	acute or chronic infection of tonsils
Lymphoma	tumor of lymphoid tissue -often malignant Two major categories: HL - Hodgkins Lymphoma NHL - Non - Hodgkins Lymphoma
Hodgkins Lymphoma	malignancy cause unknown enlarged nodes in neck and axilla curable if detected early, and confined to lymphatic system
Non Hodgkins Lymphoma	Maglinant lymphoid tissue other than Hodgkins Lymphoma - thought to be caused by virus -more generalized involvement of nodes - Central Nervous System involved
Hypersensitivity	inappropriate or excessive reponse of immune system
Allergy	hypersensivity of immune system to relatively harmless environmental antigens
Contact Dermatitis	local skin inflammation hours after initial contact ex: exposure to poison ivy soaps certain cosmetics
Autoimmunity	inappropriate, excessive response to self antigens ex: MS, Lupus, Diabetes Mellitus, Rhemuatoid Arthritis
Isoimmunity	Undesirable reaction of immune system to antigens from different individuals of same species ex: pregnancy tissue transplant
Reaction Syndrome	When body rejects against foreign grafted tissue
Host vs. Graft	Recipient system recognizes foreign matter attacks and destroys donated tissue
Graft vs. Host	Donated tissue attacks recipient tissue destroying all tissue. Leads to death
Immunodeficiency	failure of immune system mechanisms to defend against pathogens
Congenital Immune Defiency	-Rare -Improper Lymphocyte development at birth -causes SCID - b and t immunity defective
Pathology	Study of disease
history	imbalance of the 4 humors or basic substances of the body
Disease	abnormal state in which part or all of body is incapable of maintaining homeostasis
Injury	Damage to tissue from excessive external physical or chemical force
Definition	description of the disease
Etiology	the cause of the disease
Idiopathic	unknown cause
iatrogenic	disease due to medical treatment
pathogenesis	how disease develops
incidence	frequency of occurrence where disease occurs geographically who is likely to be affected
pathophysiology	changes in structure and function characteristics of disease
Signs and Symptons	manifestation of the disease
Sign	objective findings that can be seen by observer
Symptons	subjective experience that can only be felt by patient
Syndrome	cluster of signs and symptoms that tend to occur together
Diagnosis	indentification of disease - must be done by physician
Prognosis	prediction of the course the disease is like to take
Treatment	whatever is done to cure or manage disease and to rehabilitate during recovery
Contraindication	some element of the disease which precludes/prevents certain kinds of treatment
Complications	additional syndromes or disease can occur as a result of an initial disease
Infection	colonization of body to hostile organisms
Congential causes	injury occuring during development of fetus
Genetic causes	disease due to undesirable mutations to choromosomes
Immune System dysfunction	Immune system over-reaction to harmless minor antigen (allergies) or it may attack the body its supposed to protect (auto-immune disorders)
External causes of injury	physical trauma radiation (electric shock, solar radiation, radioactive contamination)
High Risk Behaviors	cigarette smoking lack of adequate exercise poor nutrition (poor food choices, starvation) inadequate sleep abuse of drugs and alcohol
Symbiotic/mutualistic relationship	organism and host both benefit
Commensal relationship	organism neither hurts or helps the host
Parasitic relationship	organism benefits but hurts host
Host	organism that supports the growth of another organism
Infection Types: local systemic	presence of pathogenic organism on or in the host
localized infection	confined to one area of the host
systemic infection	involves a large area of the whole body
Virulence	disease causing potential of an organism
Susceptibility	how vunerable the host is to infection
Opportunistic infection	infection that occurs when immunity has been comprimised and host defenses are weak
Epidemiology	study of how disease spreads and are distributed geographically
Epidemic	disease affects large number of people in a paticular area
Pandemic	an epidemic that is very widespread or even worldwide in distribution
Sporadic	ocassional outbreaks that do not become epidemic or pandemic
endemic	When a disease is most often found in a paticular population
Bacteria	usually very small single cell organisms- lack mitochondria often form colonies tough, rapidly adaptible/survive hostile environments can survive for thousands of years
Bacteria characteristics	no nucleus - DNA is floating cytoplasm -have rigid cell walls instead of membranes made of protein and sugars-cause illness by competing for resources (nutrients) destroying tissue
prokaryotes (bacteria)- name for all bacteria	Non-nucleated microbes
eukaryotes	nucleated microbes
Bacteria endotoxin	part of cell wall
Bacteria exotoxin	secreted into the surrounding fluid
Common bacteria disease	tuberculosis pneumonia, syphllis lyme disease bacterial tetanus gangrene
Virus	much smaller than bacteria consist of no more than outer envelope or capsule and core of genetic material (DNA or RNA)
Virus characteristics	no organells no nucleus no cytoplasm incapable of independent movement or reproduction, must infect a living cell
Virus types	DNA viruses - host cell's organelles "read" viral DNA and produce more virus RNA virsuses - RNA gets turned into DNA in host cell; DNA is then read to produce more viruses
Viral life cycle	sticks to host cell=injects DNA/RNA=RNA read=proteins and the new DNA/RNA synthesize by host cell=new virus assembles inside host=virus ruptures through cell membrane=killing host cell and spilling into environment
Common viral infections	common cold the flu AIDS cold sores herpes infections
Protozoa	general term for single celled eukaryotic organisms, have distinct nucleus, organelles and mitochondria. Includes ameoba Toxoplasma gondii is included
Protozoan disease	Toxmoplasma, malaria, amebic infection of GI tract or liver
Fungi	separate kingdom of life -colonies of cells that can take of a variety of shapes from a single layer of mold to a mushroom to a huge colony covering acres of ground
Fungi characteristics	not plants have rigid cell walls made of chitin includes yeast, mushroooms, molds the reproduce by forming spore
Fungal infection often infect	human skin respiratory tract
Fungal infections include:	athlete's foot ringworm (tinea) jock itch vaginal and oral yeast
Anthropods	animals, including insects, crustceans (crabs) and spider
Anthropod characteristics	exoskeleton made of chitin ventral nervous system open circulatory system
Anthropods make cause injury	bites injections of venom carrier or vectors of disease
Anthropod parasites and disease carriers include.....	fleas and ticks which carry Typhus, Lyme disease, bubonic plague biting insects which carry marlaria
Helminths:	worms, specficially parastic worms. They are multicellular, sometimes very large organisms-complex life cycles involving 2 or more hosts
Helminthic infections	very common roundworm(ascarias lumbricoides) may infest up to 1.5 billion people. trichinois, hookworms, pinworms are example
Prions	abnormal mutant version on normal CNS proteins may be produced by genetic mutation or by eating prion contaminated animal flesh best know is "Mad Cow Disease"
Incubation	pathogen is present and reproducing but not enough yet to produce symptons
Prodromal stage	first appearance of mild, vague, non-specific symptons
Acute stage	Symptoms become more severe and also typical of a specific disease
convalescene	infection is contained and being eliminated, tissue repair start
Resolution	pathogen eliminated. tissue repair complete. no remaining symptons
Chronic infection	when host can not resolve the infection. Pathogen may stay in body for months or years. producing periods or persistent symptoms.
Subclinical/subacute	infection is resolved without producing symptons
Insidious	disease has very gradual onset
Fulminant	disease with very abrupt severe onset
Sepis	Widespread infection with critical levels of toxins in blood and body fluids
Septic shock	sudden severe drop in blood pressue due to sepsis: occurs because toxins cause body wide vasodilation. Possibly fatal
Disease prevention Public Health measures	sewage treatment waste disposal purification of drinking water food inspection and preservation
Asepsis	killing or removing of microbes as well as prevention of reproduction
Sterilization	killing all microbes on a surface
disinfection	preventing infection by applying disinfectants to kill bacteria, usually to treat environmental surfaces, not tissue
Antisepsis:	preventing sepsis by preventing multiplication of bacteria; applies to living tissue (people)
Drug therapy/Chemotherapy	includes antibotics, antivirals, antiparastic. Can refer to any drug therapy including cancer chemotherapy.
Immunotherapy	boosting or supporting the immune system with chemical that stimulate the immune response
Immunizations	using antigenic substances to produce immunity to the pathogen in which the antigens occur
Cellular adaption	How cells change in response to environmental stresses
Atrophy	shrinkage in cell size. Causes: reduced nutrition reduced stimulation, disuse. also refer to decrease in size of organ
Hypertrophy	Increase in cell size Cause: increased workload may cause disease if too extreme/prolonged ex: kidney
hyperplasia	increase in cell number, actual cell division occurs. Also occurs with hypertrophy
Metaplasia	conversion of one adult cell type to another. Usually caused by chronic imitation/inflammation. Ex: replacement of cilliated tissue in bronchi of smokers replacement of epithelial tissue with grandular in esophagus of patients with acid reflux
Dysplasia	abnormal cell proliferation. pre-cancerous cells. Usually result of chronic inflammation/irritation, stress. May revert if irritant is removed
Anaplasia = synomous with malignancy	lack of cellular differentation. Usually occur as a progression of dysplasia.
apoptosis	controlled cell destruction = as in destruction of worn out RBC
Necrosis	cell death in organ/tissue that is still part of living organism. Triggers inflammation in surrounding tissue.
Necrosis types:	Coagulative necrosis liquefactive necrosis Caseous necrosis
Coagulative necrosis	cells die and their proteins denature and coagulative (cooked egg) but tissue outline is preserved - heart attack
Liquefactive necrosis	usually occurs due to the presence of bacteria= Pus
Caseous necrosis	casein is a milk protein. Caseous means "cheesy". An area of necrosis that appears cottage cheese like white matter- associated w/ TB
Gangrene	necrosis of large mass of tissue
Dry gangrene	gangrene due to coagulative necrosis
Wet gangrene	gangrene due to liqufactive necrosis
Gas gangrene	due to infection by certain types of bacteria - large amount of gas waste- painful and fatal
calcification	accumulates in inflamed or necrotic tissue altherosclerosis (arteries) heart valve damage kidney stones
hypercalcemia	calcium is not necessarily present causing kidney stones
inflammation	the response of vascularized tissue to injury or irritation
Possible irritants include	biological physical, chemical, mechanical damage ischemic damage (blood)
Healing Process	injured tissue progresses through 3 stages of healing: acute stage subacute (prolferation) maturation (remodeling)
Acute Stage	characterized by acute inflammation which limits infection, removes necrotic tissue and sets stage for healing
subacute state	aka proliferation stage characterized by presence of granulation tissue, which generates scar tissue
maturation	aka remodeling stage characterized by formation and consolidation of scar tissue
Acute Inflammation - Stage 1	Four classic signs of acute inflammation calor (heat) Rubor (redness) Tumor (swelling) Dolor (pain) - sometimes loss of function
Inflammatory mediators:	prostaglandins (cause pain) histamines chemotatic factors chem= chemical, tatic= movement draw white blood cells into area causes vasodilation
With inflammation two types of basic changes occur	vascular cellular
Vascular changes: substances such as prostaglandins and histamines cause:	vasodilation: increase in vascular permeability both changes allow for fluid with plasma proteins to enter tissue space and for WBC to enter tissue space as well
Cellular changes: chemotatic factors attract WBC to injury site	chemotaxis pavementing/margination emigration by diapedesis wound resolution
Chemotaxis	WBC are attracted to area of inflammation by chemotatic factors released by injured/irritated tissue
Pavementing/Margination	endothelial cells in capillaries retract exposing basement membrane. WBC stick to exposed basement membrance "pavmenting it"
Emigration by diapedesis	WBC squeeze through gaps between endothelial cells and enter tissue space; begin tissue destruction of pathogens and phagocytosis of debris
wound resolution	WBC remove debris, dead cells, toxins etc. to set stage for the proliferative phase
Acute phase Response	systems sign and symptoms which may appear if inflammation/infection is widespread. This includes increased WBC count, fever, aches and pains, loss of apetite fatigue etc.
Swelling	build up of inflammatory exudate
Pressure from the build up of fluid at the site of injury can....	increase pressure on nerves, increasing injury -increased pressure on vessels restricts the amount of blood that can get into the site
Subacute/Profilerative Stage	clot begins to dissolve cells are mostly fibroblasts new capillaries are laid down by angioblasts fluid in GT has lots of growth factors
Subacute /Profilerative stage II	as collagen fibers accumulate, cells begin to withdraw as scar starts to fully form, capillaries and nerve fibers withdraw as well, but fresh scar tissue may still be vascularized
Chronic/Maturation = Remodeling Stage Scar takes on final shape, takes on strength and stretch necessary to permit normal function	As cells of GT retract, collagen fibers start to cross link collagen fibers shrink pulling on surrounding tissue tensile strength of scar increase blood vessels gradually withdraw
Outcomes of Acute Stages	Healing by Primary intention Healing by Secondary intention Regeneration Chronic Inflammation
Healing by Primary Intention	wound edges have been approximated properly. Scar tissue formation minimal, fibrosis/contracture usually minimized or non-existent
Healing by Secondary Intention Secondary Healing	Contracture: excessive pulling together of wound and/or scar produces dysfunction Fibrosis formation of abnormal or excessive amount of scar tissue Adhesions - sticking together of structures that should not adhere to each other
Regeneration/parenchymal	liver, the epidermis, kidneys (some degree)
Chronic Inflammation causes	weak initial inflammatory response: incomplete wound resolution due to debris or persistent infection repetitive re-injury continuous abnormal stress, inadequate nutrition or presence of disease
Chronic Inflammation (contributing factors)	poor bio-mechanics, change in training intensity environmental factors ex. poorly designed work station
Chronic Inflammation (Possible outcomes)	formation of fibrous capsule around area of inflammation forming abcess which must be drained to promote healing formation of abnormal scar tissue in chronically inflamed tissue
factors in wound healing	nutrition adequate blood flow impaired inflammatory and immune response wound separation foreign objects
when to refer an acute injury for medical care	you feel or hear a popping sound swelling or discoloration is present there is deformity 25% or more loss of function nausea or vomiting, dizziness or fainting severe pain conditions fail to improve
Massage therapy modalities - External	heat - vasodilator, causes hypermia cold - vaoconstrictor, reduces metabolic activity contrast bathing - alternating heat and cold
Massage therapy modalities - external	Liniments and essential oils liniments - essential oils aromatherapy
Sarcomere	contractile unit of muscle cells
Dysfunctional Alpha Motor neurons	release excessive Ach causing increased activity in post synaptic membrance at nueromuscular junction causing increased activity of sarcomeres in the vicinity
myofascial trigger point	hyper-irritable locus (area) within a taut band of skeletal muscle. Spot is painful upon compression can evoke characteristic of referred pain and autonomic phenomena
Capillary constriction	sustained contraction of sarcomeres causes an increase in metabolic demand and local ischema due to capillary constriction
Sustained Muscle contraction	with inadequate ATP, disturbance of calcium re-uptake channels within the membrane resulting in calcium ions concentrating in sarcoplasm. actin-myosin bonds do not break and muscle contraction is sustained
Sensitized nociceptors (pain receptors)	release of vasoreactive substance in area that could sensitize local nociceptors, producing the hyer-irritability and "exquisite pain"
central trigger points	located middle/center of muscle belly
attachment trigger points	located near muscle attachment sites. sarcomeres on either side of attachment site are taut. These are called taut bands.
enthesopathy	process of developing the attachment trigger point
Enthesitis	fibrous and inflammatory calcification that may develop in the area of the attachment trigger points
Active Trigger points	spontaneously produces pain. Does not require pressure to be activated
Latent Trigger Points	Produces pain only upon compression
Key trigger point	Can activate trigger points in other muscles
Satellite trigger points	Develop in reference zone of trigger point, in an overloaded synergist, in an antagonist, or muscle linked only neurologically
Direct causes of trigger point	acute overload overwork fatigue direct trauma radiculopathy - nerve inpingement chilling - sitting in front of air condition
Trigger Point - Indirect causes	other trigger points visceral disease (organs) arthritic joints other joint dysfunctions - misalingment emotional distress - sensitized people
Trigger Point - Signs	-Referred Pain -Dysesthesia - unpleasant abnormal sensation -Hyperesthesia - increased sensitivity to sensation
Trigger Point Signs (continued)	Pain - dull and aching, often deep with varying intensity -present only in motion -spontaneous -with stretching (active and passive) -increases when affected muscle is strongly contracted
Trigger Point Signs (autonomic symptons)	vasoconstriction sweating increased goosebumps persistent tearing(neck & face) persistent runny nose excessive salivation (head and face)
Trigger Point Signs	stretch range is restricted muscle weakened muscle spasm referred spasm reflex inhibition sleep is often disturbed
trigger Point signs to look for during palpation	Palpable bands contracted spots- Contraction nodules reproduction of patients pain (by pressure of needling of tender spot) Jump sign twitch response Dermographia (skin writing) Panniculosia- (thickenning of subcutaneous tissue)
Trigger Point - Perpetuating factors - anything that chronically overloads a muscle or acutely irritates a chronically irritated muscle or reduces energy metabolism in a diseased individual	Mechanical stress nutritional inadequacies Anemia or boderline anemia Hypothyroid Hypoglycemia hyperuricemia
Trigger Point - perpetuating Factors (continued)	Pyschological Allergy Chronic infection Impaired Sleep Radiculopathy - nerve Joint distrubances Visceral disease
Trigger point - Treatment	Initial application of local heat slow skin rolling slow repetitive muscle stripping Alternating ischemic compression Prolong ischemic compression Repetitive petrissage and gentle stretch
Trigger point - Treatment Other techniques	Stretch Avoid over treatment Combination cold and stretch technique
Creating Functional Scar Wolf's Law: organized arrangement according to the mechanical forces acting on the tissue.	long term goal of treatment formation of strong, mobile scar at site of the lesion that is complete and painless and function has been restored
Acute stage heat (calor) Redness (rubor) Swelling (tumor) Pain (dolor) loss of function	Last 0-48 hours five signs all present at same time loss of normal ROM empty end feel protective muscle spasms antalgic position - part will be held in a position that will not cause pain
Acute stage therapeutic goals	Reduce the inflammatory response Rest Ice- cold applications; full immersion, local application Compression - elastic ace bandage Elevation NSAIDS: Non Steroid Anti inflammatory Drugs; Ibuprofen
Acute stage therapeutic goals (cont)	Collateral massage: maintain lymph flow - avoid site of injury Maintain normal ROM - in related areas Gentle pain free ROM Do not try to reduce protective spasm increased pain/increased inflammation - signs too much movement
Subacute Phase Proliferative Phase	begins 2 to 4 days after injury- continues to 14 -21 days collagen fibers are being laid down tissues appear red or pink pain is lessening pain is now felt near the normal point of tissue resistance
Therapeutic Goals in Subacute Phase	Increase circulation - effleurage, skin rolling, petrissage Reduce swelling reduce the formation of adhesions mobilize the forming scar begin strengthening the tissues
Chronic Stage Maturation (ReModeling Phase)	Last 14-21 days post injury to up to 1 year Continuous strengthening of the scar substantial decreased swelling Full (or near) pain free ROM normal end feel Pain on over-pressure Increased tensile strength of tissue little further remodeling
Chronic Stage (Maturation/eModeling Phase) in some cases..............	Limited ROM due to extensive contractures and adhesions to avoid recurrence of pain, tissue must be stretched or adhesions broken up
treatment guidelines for Chronic/ReModeling Stage	mobilize any adhesions restore full pain free ROM reduce any remaining swelling increase strength and endurance of muscle
Subacute Phase Proliferative Phase	begins 2 to 4 days after injury- continues to 14 -21 days collagen fibers are being laid down tissues appear red or pink pain is lessening pain is now felt near the normal point of tissue resistance
Therapeutic Goals in Subacute Phase	Increase circulation - effleurage, skin rolling, petrissage Reduce swelling reduce the formation of adhesions mobilize the forming scar begin strengthening the tissues
Chronic Stage Maturation (ReModeling Phase)	Last 14-21 days post injury to up to 1 year Continuous strengthening of the scar substantial decreased swelling Full (or near) pain free ROM normal end feel Pain on over-pressure Increased tensile strength of tissue little further remodeling
Chronic Stage (Maturation/eModeling Phase) in some cases..............	Limited ROM due to extensive contractures and adhesions to avoid recurrence of pain, tissue must be stretched or adhesions broken up
treatment guidelines for Chronic/ReModeling Stage	mobilize any adhesions restore full pain free ROM reduce any remaining swelling increase strength and endurance of muscle correct ay postural imbalances
Subacute Phase Proliferative Phase	begins 2 to 4 days after injury- continues to 14 -21 days collagen fibers are being laid down tissues appear red or pink pain is lessening pain is now felt near the normal point of tissue resistance
Therapeutic Goals in Subacute Phase	Increase circulation - effleurage, skin rolling, petrissage Reduce swelling reduce the formation of adhesions mobilize the forming scar begin strengthening the tissues
Chronic Stage Maturation (ReModeling Phase)	Last 14-21 days post injury to up to 1 year Continuous strengthening of the scar substantial decreased swelling Full (or near) pain free ROM normal end feel Pain on over-pressure Increased tensile strength of tissue little further remodeling
Chronic Stage (Maturation/ReModeling Phase) in some cases..............	Limited ROM due to extensive contractures and adhesions to avoid recurrence of pain, tissue must be stretched or adhesions broken up
treatment guidelines for Chronic/ReModeling Stage	mobilize any adhesions restore full pain free ROM reduce any remaining swelling increase strength and endurance of muscle correct any postural imbalances
Correct posture	position that minimizes the stress on each joint and requires minimal muscle activity to maintain
Faulty posture	any position that increases stress to the joints
Center of gravity higher center - less stability	in children - at level of 12 thoracic vertebrae as one ages the center drops to the level of the second sacral vetebra in adult women, slightly higher in men
Level	flat or horizontal line that water will settle to
Plumb line/gravity line	string w/weight (plumb bob) attached to that hangs from a fixed point on wall or ceiling. Used as reference for assessing client's posture
spinal curves in normal posture	spinal curves are named for the direction of the convexity of the curve
Anterior Curves (lordosis) aka Secondary curves	cervical and lumbar curves
Posterior curves (kyphosis) aka primary curves	Thoracic and sacral curves
primary curves	at birth, all sections of spine are curved posteriorly. Sacral and thoracic sections maintain this original posterior curve so they are considered primary
Deformity	malformation or malpositioning of any part of the body
Degrees of deformity etiologies: congenital or acquired	1st degree (functional) 2nd degree (transitional) 3rd degree (structural)
1st degree deformity (functional)	changes in muscle tone and structure no bony changes no soft tissue contracture patient can usually self correct usually disappear with movement
2nd degree deformity(transitional)	definite contracture of soft tissue w/slight bony changes. Can not self-correct May be able to change length of self-tissue over time (months to years)
3rd degree deformity (structural)	structual deformities will not disappear with time will not correct soft tissue work, there can be improvement in soft tissue patterns, decrease spasm, decrease pain, improved circulation and available Rom
Pelvic Tilt (normal posture)	sacral angle 30 degrees sacral angle = superior margin of sarum for the horizontal plane ASIS and pubic crest in same vertical plane (plumb to each other) PSIS and ASIS should be in the same horizontal plane or ASIS should be no more than 5-10 degrees below PSIS
Deformities/Deviations of Pelvis	Anterior Tilt Posterior Tilt Lateral Tilt Small Hemipelvis Anterior/Posterior Rotation
Anterior Tilt	ASIS lies in front of the pubic crest. ASIS is significantly lower than PSIS 5-10 degrees. Anterior posterior cures will be exagerated (increase lumbar lordosis
Posterior Tilt	ASIS lies behind the pubic crest. PSIS is lower than the ASIS (lumbar curve will be diminished)
Lateral Tilt	Illiac crest on one side is higher than the other Both ASIS and PSIS are higher on the high side sid to be abducted on lower side, adducted on higher side
Small Hemipelvis	one os coxa is small than the other
Anterior/Posterior Rotation	one os coxa rotates/tilts anteriorly or posteriorly on the sacrum
Deviations/Deformities of the Spine	Lordotic Postures Lower Crossed Syndrome Kyphotic Postures Kyphosis Arcuata Upper crossed syndrome kyphosis angularis
Swayback	pelvis is tilted forward. Entire pelvis shift anteriorly. sharp lumbosacral angle. thoracolumbar. hips in extension lower lumbar extensor - tight upper lumbar extensors - overstretched
Lower crossed syndrome- Lordotic postures	Type 1 postural deformity QL, lumbar erectors, illopsoas, rectus femoris shortened abdominals, gluteals, hamstrings, stretched by anterior tilt
Lordotic Postures	any exaggerated anterior curvature. Typically occurs in lumbar and cervical spine. spine in hyperextension
Kyphotic Postures	any exaggerated posterior curvatures. Sometime reduced or reversed anterior curve. Possible to have cervical kyphosis
Kyphosis Arcuata	Type 1 Postural deformmity, Posterior curve is a continuous arc, usually due to muscle imbalance
Upper crossed syndrome	Pec Maj. and Minor, Cervical Erectors, SCM, Levator Scapula, and Upper Trapezius and sub-occipitals are shorten thoracic erectors and anterior cervicals are lengthened increasing thoracic curve of spine
Flatback - Kyphosis	posterior tilt of pelvis (sacral angle of 20 degrees = diminised flattend lumbar curve. lumbar spine become hypermobile. The other curves are reduced also.
Kyhosis angularis	Type 3 Struture deformity. Posterior curve is sharply angled. Usually due to changes in bony structure. Wedge shaped (compressed anteriorly) . Occurs most frequently in osteoporosis.
Scoliosis	deformity characterized by lateral curvature of the trunk combines with rotation of the vertebrae
Scoliosis (continued)	vertebral bodies - rotated toward the side of the convexity (more room) spinous processes rotate toward the concavtity Ribs position will be altered flare and bulge posteriorly on the convex side compress and shift anteriorly on the concave side
Scoliosis	deformity characterized by lateral curvature of the truck combined with rotation of the vertebrae
Vertebral bodies (scoliosis)	rotated toward the side of convexity (where there is more room)
Spinous Processes (scoliosis)	rotate toward the concavity
Ribs (scoliosis)	will be altered - flare and bulge posteriorly on the convex side compress and shift anteriorly on concave side
Varieties of Scoliosis	-Simple Curves -Compound Curves -Transitional Curves
"C" curves (scoliosis)	single curve in one direction in any portion of the column or a long "C" curve involving the whole or large part of the spine. Right thoracic most common
Compound curve	Consists of 2 or more curves. Can be double curves ("S"), triple curves, rarely quadruple curve. Most common right thoracic, left lumbar curve
Transitional vertebrae	Vertebrae where the direction of the curve changes
Classifications of Scoliosis	-Primary -Secondary -Functional -Structural
Primary Scoliosis	-first or primary problem -muscular imbalance Idiopathic (genetic) Most common adult females Usually begins to appear between 8 to 10 years progressive form leads to mild to severe 3rd degree scoliosis severe may compromise cardiorespiratory function
Secondary scoliosis	Result of some previous deformity or disease
Secondary scoliosis deformity list	-legs or feet, structural leg length discrepancy -Unilateral paralysis of abdominals, illiopsoas, or back muscles -injuries to spine -Nerve root irritation -unilateral lung disease -malformed vertebrae -hemipelvis
Functional Scoliosis	Curve disappears with movement -indicates its a type 1 or postural deformity (ex. leg length discrepancy)
Structural scoliosis	caused by abnormally shaped vertebrae. Will not disappear with movement
Signs and Symptoms of Scoliosis	-Head tilted laterally -shoulder height uneven -Ribs bulge on one side, flatten on other -uneven waist indentations -one hip higher than other -lateral pelvic tilt or rotation
Signs and Symptons (scoliosis) continued	One arm hangs farther from the side than the other -palpate spinous processes for deviations from a straight line
Torticollis (stiff neck)	malposition of the head due to unilateral shortening of the SCM and other cervical muscles (upper traps, scalenes, levator scapula)
Congenital Torticollis	due to birth trauma -unilateral SCM tear as baby comes through birth canal -head laterally flexed toward affected side -and face is rotated away (2nd degree deformity)
Acquired Torticollis	unilateral sprain or strain of neck -whiplash injury -trigger point activation of neck muscles (sleeping posture, work posture, infection) may be due to hemiplegia (paralysis from stroke)
Acquired Torticollis (contd)	Usually limited to 3-5 days treaments include massage, gentle Tense and Relax, Reciprocal inhibition gentle stretching, Trigger point work - best to wait until acute symptons abate
Valgus/Valga	distal end of bone distal to to the affected joint is positioned further laterally than in a normal joint
Varum/Vara	distal end of the bone distal to the affected joint is positioned further medially than in a normal joint
Lower Extremity - Hip (coxa) Coxa Valga Coxa Vara Femoral Anteversion Femoral Retroversion	neck shaft angle of the femur - angle between femur neck and shaft when viewed from the front. Normally between 120 - 135 in an adult
Coxa Valga	neck shaft greater than 135 affect joint: hip distal bone: femur distal end of femur more lateral
Coxa Valga results in:	subtalar supination lateral tibial torsion long ipsilateral (same side) leg posterior pelvic rotatoin
Coxa Vara	neck shaft angle less than 120 afftected joint: hip distal bone: femur distal femur is positioned more medial
Coxa Vara results in:	subtalar pronation medial tibial torsion short ipsilateral (same side) leg anterior rotation at pelvis
Femoral Anteversion	degree of forward projection of the neck of the femur compared to the coronal plane.
Excessive femoral anteversion may cause;	Toeing in (pigeon toes) Medial femoral torsion lateral tibial torision subtalar pronation medial rotation of hip beyond normal range > 60
Femoral Retroversion	projects backward in relation to the coronal plane of the femoral shaft
Excessive femoral retroversion may cause	Toeing out lateral femoral torsion lateral tibial torsion subtalar supination
Genu Valgum	knock knee - knees touch, space between feet -affected joint - knee -distal bone - tibia -distal end of tibia is position laterally
Genu Vargum	two or more finger widths can fit between the knees with the ankles together - "bow legged" affected joint: knee distal bone: tibia distal end of tibia positioned medially
Genu	knee
Q-Angle	Quadriceps angle. Angle between rectus femoris and patellar tendon line drawn from ASIS to midpoint of patella -from tibial tuberosity to midpoint of patella men 13, women 18
Increased Q-Angle	Associated with patella alta, superior resting position of patella
Increased Q-Angle	associated with chondromalacia as well as genu valgum, subluxing patella femoral and tibial rotation (femoral anteversion)
Squinting Patella	medial resting position of patella (inward)
Frog/Grasshopper Eye Patella	lateral resting position of patella (outward)
tibial torsion	Angle formed by the intersection of a line through axis of the knee and through medial and lateral malleoli (ankle axis). Normal amount of rotation at tibia 12-18
Medial tibial torsion	tibia rotated medially (less than 12) associated with decreased Q-angle normal patella tracking -pronation of foot
Lateral tibial torsion	tibia rotated laterally (more than 18) associated with increased Q-angle lateral tracking of patella medial rotation of femur supination of foot
Tibial Vara	Bowed tibia -increased Q-angle -lateral tracking of patella -chondromalacia -"bayonet" knee/leg
Foot Talipes - Club foot Pes Planus (Flat Feet) Pes Cavus (Hollow or Rigid Foot)	Pes
Talipes (club foot) Equinovarus - inward Calcaneovalgus- outward	-developed in utero -orthopedic care including repeated cast application required soon after birth -severe cases surgery required
Equinovarus (club foot - inward)	most common, -plantar flexed -inverted -markedly adducted
Calcaneovalgus (club foot - outward)	-less common -flat of convex arch -dorsiflexed, can be easily approximated against lower tibia -early treatment, with cast or corrective shoes
Pes Planus (flat feet)	refers to fallen medial longitudinal arch Head of talus displaces medially and plantarwise
Pes Planus (functional)	-1st degree -fallen arch only when standing -arch will reappear with they stand on toes, or when non-weight bearing
Pes Planus (structural)	fallen arches when weight bearing or non-weight bearing
Pes Cavus (hollow foot/Rigid Foot)	accentuated longitudinal arch. both medial and lateral longitudinal arches are accentuated
Pes Cavus (results)	claw toes ((ext. of Metatarsal phlangeal joints, with flex of DIPS and PIPS) metatarsal heads are sore, often deformed -toes do not touch ground in active or passive movement
Toes = great Hallux Hallux Valgus	lateral deviation of great toe -deviation can cause great toe to overlap 2nd toe -cause formation of hammer toes -can cause inflammation of soft tissue caught between head of first metatarsal and wall of shoe "bunion"
Hammer Toes	extension of MP (metatarsalphlangeal) joint, flexion of PIP, and Extension of DIPS (2nd joint)
Claw toes	Extension of MPJ, flexion of PIP and DIP joints
Morton's Toe/Foot (Greek foot)	second toe is longer than the great toe due to short 1st metatarsal.
Morton's Neuroma	Entrapment of digital nerve of the foot between 3rd and 4th metatarsal heads -intial stages causes metatarsalgia -progression forms localized enlargement of the nerve
Metatarsalgia	syndrome describing pain over the metatarsal heads or in the metatarsalphalangeal (MP) joints
Winging of scapula	medial border of scapula lifts off the ribs and resembles a wing
Static winging	structural deformity of ribs, scapula, clavicle or spine
Rotary wining	one inferior angle of scapula has rotated further from the spine than the other
Dynamic winging	wings during movement. Usually caused by palsy for the long thoracic nerve
Sprengel's deformity	congenitally high or undescended scapula, (usually fibrosis) -can be unilateral or bilateral -result in decreased abduction, ROM daily living not affected
Carrying Angle (Elbow) elbow = cubitus	angle formed by long axis of humerus and long axis of ulna. most easily seen when elbow extended, forearm supinated men - 5-10 women 10-15
Cubitus Valgus	carrying angle more than 15
Cubitus Varum	carrying angle less than 5
Hand Dupuytren's Contracture	flexion contracture of palmar fascia and tendons of flexor digitorium superficialis
dupuytren incidence	-condition more common in men than women -familial tendency -incidence increases in people who sustain repetitive trauma in the wrist
Dupuytren' pathophysiology	-low grade chronic inflammatory response with proliferation of fibroblasts --fascia contracts, nodules form in tendons, skin begins to pucker -fourth finger is most commonly involved -extreme conditions entire hand closes can not flex or extend fingers
Dupuytren's Sign and Symptoms	-thickening palmar fascia -nodules in the flexor tendons puckered, adherent skin -reduced extension range of motion -
Dupuytren Treatment	-Trigger Point and deep tissue massage for the entire forearm and wrist complex -myofascial strokes to forearm, wrist, hand -deep friction to palmar fascia -Passive stretching for the fingers, into extension and abduction -moist heat treatments
Inflammatory Conditions	due to results of overuse w/resulting microtrauma, or due to single traumatic episode. -sometimes caused by pathogens -sometimes idiopathic
Myositis fibrositis myofascitis tendinitis tenosynovitis	-inflammation of actual muscle tissue -inflammation of connective tissue wrapping of muscles -inflammation of muscles and its fascia -inflammation of a tendon -inflammation of synovial sheath of tendons
muscle pull	refers to tears in the tendon
Muscle tear	rupture in the belly
Basic types/Etiologies	-distraction ruptures -compression ruptures
Distraction ruptures	occur to an inadequately warmed-up muscle an exhausted muscle or has suffered previous injury -overstretching -contraction overload -eccentric (sudden decleration) -concentric (sudden acceleration)
Compression rupture	due to direct trauma (blow disrupts the fibers) -sometimes refered to as charley horse
Degree of muscle Injury	first degree - 0 to 10 percent second degree = 10-99 percent third degree = full 100 of fibers
Signs and Symptoms (Rupture	pain and itching swelling all movements painful and limited 1st degree - mild, 2nd degree mild - severe 3rd degree - little or no pain, severe weakness tenderness altered consistency tremor or spasm
Sequelae	Condition following and resulting from a disease
Compartment Syndrome	May develop because of severe bleeding: -intracompartmental pressure rises to point where blood flow is significantly reduced or even stopped -risk of ischmic necrosis -medical emergency and may require surgery
Mulscle tear/Rupture Treatment Acute	-Acute no massage is given RICE - first aid Compression bandages and splints MD must determine the extent of damages immobilization in a cast for 2 weeks
Muscle tear/rupture Treatment Subacute	(after 72 hours) general massage, light direct work never pull on granulation tissue mild isometric contractions "muscle setting" no stretching until tear is healed
Muscle tear/rupture Treatment (continued)	heat and contrast bathing applications direct transverse and longitudinal friction muscle stripping chronic conditions direct fiber cross friction fascial strokes AROM and PROM
Whiplash (aka acceleraton injury)	Most commonly occurs when car is still and struck from behind sending head and neck into rapid extension
Whiplash Signs and Symptons	swelling and tenderness injury in neck flexors -SCM, Scalenes, - Supra and infrahyoid - deep anterior cervicals injury to extensors, anterior longitudinal ligaments, intervertebral discs
Myositis Ossificans	ossification of muscles
Myositis Ossificans etiology	Complication of a fracture or an injury to the periosteum May develop in any torn muscle with hematoma formation - develop after initial trauma - callus tissue develops within the belly or tendon of a muscle - contraction of the muscles lead to irritation and inflammation
Myositis Ossificans Signs and Symptoms	Increase of pain in the area of an injury several weeks into the healing process - Pain increase wih movement of an involved muscle -Decrease in the mobility of the joint acted on by the muscle -local tenderness -local swelling -X-ray reveals the fragment
Mositis Ossificans Treatment	No massage over the area, but general massage and collateral massage to reduce swelling and increase circulation -Rest and ice to reduce the inflammation -Anti-inflammatory medications -Sometimes immobilized
Repetitive Use Syndromes	"overuse syndromes" caused by - overload or repeated microscopic injuries to the musculoskeletal system
Repetitive Use Syndromes Factors which contribute to these injuries	muscle imbalance training errors faulty mechanics incorrect equipment hard surfaces skeletal malalignment
Repetitive Use Syndromes Results of overuse	-muscle and soft connective tissues = inflammation, microruptures and macroruptures In bone= stress fractures
Repetitive Use Syndrome Causes	Single load which exceeds the tissue limits - (trauma w/o tear) Repeated smaller loads examples: Shin splints Tendinitis and tenosynovitis ITB Syndrome Tennis Elbow/Golfer's Elbow
Overuse Tendinitis Definition & Causes	inflammation of tendon Causes: Repetitive one-sided movement, especially under load. Persistent mechanical irritation -Excessive single trauma or strain short of rupture (microtrauma) -Unaccustomed exercise that exceeds the load limits of the tendon (weekend warrior)
Overuse Tendinitis Signs & Symptons	Pain -when resting, increases when resisted isometric contraction, stretching Tenderness-site of lesion or inflammation Inflammation - entire muscle Reduced or painful ROM Swelling Crepitus
Overuse Tendinitis Treatment - Acute	Rest and ice Ice massage to tendon General collateral massage Pain free passive ROM NSAIDS in severe cases, cortisone injections
Overuse Tendinitis Treatment - subacute	-Direct cross fiber friction over tendon-followed by ice massage -Gentle stretches -Fascial Work -Increase the duration of treatment as the healing continues -Long term cases may require up to 10-12 minutes of direct massage per treatment -Exercise and stretches to gradually increase strength and ROM
ITB Friction Syndrome	inflammation of the periosteum occuring as a result of tight ITB rubbing over the lateral femoral condyle
ITB Friction Syndrome (Biomechanics)	-full extension lies anterior to femoral condyle -30 degree knee flexion lies over femoral condyle -greater than 30 degree flexion lies posterior to femoral condyle
ITB Friction Syndrome	-congenital -due to injury -repetitive use
ITB Friction Syndrome Predisposing factors	postural factors: leg-length disrepancy medial tibial torision pronation of feet contracture of hip gluteus medius, minimus, maximus and/or TFL
ITB Friction Syndrome Predisposing biomechanical factors	cross over gait when running loss of flexibility in hamstrings, quadriceps, Achilles and/or tibial posterior
ITB Friction Sequence and Associated Conditions	-general fibrosis of ITB and lateral retinaculum of knee -trochanteric bursitis -SI joint dysfunction, lordosis and lumbar dysfunction
ITB Friction Incidence	Common with -runners -speed skaters -roller bladers -soldiers in basic training
ITB Friction Sign and Symptons	-Pain over lateral femoral condyle -Positive Ober's Test -Pain with adduction of hip w/knee flexed to 30 degrees -Pain with standing on affected leg w/knee flexed to 30 -40 of flexion -Positive Noble's Test
ITB Friction Treatment	Rest Anti-inflammatory and analgesic medications
ITB Friction Massage Treatment	-Ice Massage -Friction massage -Myofascial release to low back, hip, thigh, leg and foot -Soft tissue mobilization around greater trochanter Exercise to strengthen and balance muscle of lower extremity, esp. tibialis group
Upper Patellar Tendinitis (Runner's Knee)	Tendonitis of quadriceps tendon at it's attachment to patella
Lower Patellar Tendinitis (Jumper's Knee)	Tendinitis to the patellar ligament
Signs and Symptons	-Swelling and tenderness on palpation in the area directly above or below patella -Onset is gradual over a period of several weeks -Pain exacerbated by squatting, jumping or resisted isometric contraction of the quadriceps
Achilles Tendinitis	Tendinitis of Tenosynovitis of Calcaneal/Achilles tendon
Achille Tendinitis Signs and Symptoms	-Swelling over the tendon -Redness to skin over tendon -Intense, diffuse tenderness -Crepitus w/pressure on tendon during movement Pain on using the Achilles tendon, contracting or stretching
Patellofemoral Syndrome & Chondromalacia Patella	Chrondromalacia means softening of artucular cartilage of patella Patellofemoral Tracking Dysfunction - means the patella is pulled too far laterally each time the knee is extended under load
Patellofemoral Syndrome Etiology - Predisposing factors	-Increased Q-Angle- caused by increased femoral anteversion -Patella Alta - high riding patella is outside of the groove -Tibia vara - hyperextension
Patellofemoral Syndrome Predisposing biomechanical factors	Insufficiency of the vastus medialis - may occur from lack of conditioning before activities involving loaded knee extension -Soft tissue restrictions - lateral reticulum tightness, may be congenital or due to increased tightness of ITB, hamstrings tightnees, tight quadriceps
Patellofemoral Syndrome Pathological Changes	Excess lateral movement during knee extension causes rotation of patella which pulls the posterior surface of the patella into the femoral condyle (instead of in between them) increases wearing away of cartilage
Patellofemoral Syndrome Signs and Symptons	Client will describe recent increase in activity involving extensor loading -Gradual onset of pain felt in a generalized area over the medial aspect of the patella -Pain is increased by increasing patellofemoral compression, such as sitting with knee bent for long periods of time descending stairs -Patella malalignment
Patellofemoral Syndrome Treatment	-Rest -Anti-inflammatory, analgesic medication -Knee braces or tapings -Shoe orthotics (pronated feet) -Corrective exercise, postural reeducation
Patellofemoral Syndrome Massage Treatment	-Deep tissue to quads, hamstrings, TFL and ITB, medial and lateral patellar retinacula, gastrocnemius -Stretching all tight musculatture using tense/relax, passive stretch -Strengthen/reeducate the client how to properly recruit the vastus medialis, hip adduction exercise
Shin Splints : most commonly involve Tibialis Anterior Tibialis Posterior	General terms for a number of conditions which produce an aching pain the the front lower leg. Most involve inflammation of the periosteum and muscles due to the the constant tugging of the contracted muscles during excess activity
Periostitis Tenoperiostitis Osteoperiositis Stress factures	-inflammation of the periosteum -inflammation of the tendon and the periosteum -inflammation of the bone and periosteum -the tibia may fracture due to fatigue failure within the bone
Anterolateral Shin Splints	Pain over lateral aspect of tibialis anterior, extensor digitorium longus and extensor hallicus longus
Posteromedial shin splints	pain over medial aspect - tibialis posterior aka Medial Tibial Stress Syndrome - refers specifically to periostitis of the tibia and the interosseous membrane at the attachment of the tibialis posterior
Shin splint Etiology	Overuse- usually runners or joggers -too rapid increase in mileage training -training on hard surfaces, inadequate footwear, insufficient warm-up
Shin splint etiology (predisposng)	Postural factor excessive pronation of foot Biomechanical factors -muscle imbalance between anterior compartment and posterior compartment
Sequellae/Related conditions Shin splint	anterior compartment syndrome - fascia of anterior compartment is too tights for overdeveloped muscles -intercompartmental pressure increases and pain results
Shin Splint Anterolateral/Postmedial Signs	Pain in shins --gradually and increases over time --may not appear until 2 or 3 hours after activity has ceased --occur during activity only --may be constant --occur during activity and persist for several hours after Weakness in the involved muscles Pain on resisted isometric contraction Pain with stretching
Shin Splints Signs - Anterior Compartment Syndrome	deep aching pain throughout the anterior compartment lateral to shin area
Shin Splints - signs Stress Fractures	Gradual onset of pain Initial stages, pain during activity, relieved by rest As conditions progress, pain persist after activity, perhaps worsening during the night swelling persisting after activity localized tenderness percussion of bone at another site causes pain at fracture site
Shin Splint - treatment Anteriolateral/posteromedial Acute	rest w/cold applciation twice a day for (up to) twenty minutes for 2 to 3 days Anti-inflammatory medications
Shin Splint Treatment Anterolateral/posteromedial Subacute and Chronic	after 3 days general massage is indicated rest may be indicated to 2 to 4 weeks or up to several months in the case of stress fracture after 3 weeks gradual return to activity is begun, including progress exercise and stretching and massage fascial work is indicated as well as friction to any adhesions and fibrosis
Plantar Fascitis	inflammation of plantar fascia. Microruptures in the fascia in the area just anterior to the calcaneal attachment. Repeated trauma my result in growth of bone spurs in the calcaneus
Plantar Fascitis (Etiology)	Predisposing Postural factors -excessive pronation of foot Pes cavus biomechanical factors shortness in triceps surae (gastroc soleus complex) lifting the heel during take-off while running, jumping, or walking Vigorous take-off or repeated fast take-off is most likely inadequate support from shoes
Plantar fascia Signs & Symptons	-Pain at the origin of the fascia when the foot is weight-bearing -morning stiffness and pain which decreases with activity -marked tenderness on pressure, especially medial bands
Planatar Fascia Signs and Symptoms (cont'd)	-palpable bands of scar tissue -swelling over the calcaneus (occassionally) -Pain when standing on tiptoe and walking on the heels Numbness along the outside of the foot -Xray may reveal bony outgrowth at point of tear
Plantar Fascia Treatment	-rest, usually to the point of cessation of the activity -arch supports realignment of subluxated bone -myofascial strokes and stretches to release the plantar fascia and the posterior compartment of the leg
Shoulder Tendinitis	Inflammation of the tendons of the SITS muscles and the longhead of the biceps brachii
Shoulder Tendinitis Etiology	Overuse in contract sports Common in throwers, weight lifters, racket sport players and wrestlers -overuse in occupations that require repeated upper extremity movements
Shoulder Tendinities Sequellae and Related Conditions	calcification sub-acromial bursitis Impingement Syndrome/Swimmer Shoulder weakness in infraspinatus and teres minor allow the head of the humerus to elevate in the glendoid fossa
Shoulder Tendinitis Signs and Symptoms	-Local and referred pain -swelling -point tenderness -Painful Arc - felt between 60-120 deg. of abduction when tendon passes under the coracoacromial arch -pain at end of ROM
Shoulder Tendinitis Signs and Symptoms (contd)	Painful resisted contraction - medial rotation for subscapularis - abduction for supraspinatus - lateral rotation for infraspinatus and teres minor -flexion of shoulder
Shoulder Tendinitis Massage Treatment	-Friction after acute stage -Release scapula to improve shoulder joint complex mechanics -strengthen lateral rotators of shoulder to keep head of humerus depressed during overhead movements
Lateral Epicondylitis/Tennis Elbow	Inflammation of muscles tendons and periosteum of lateral epicondyle -extensor carpi radialis brevis - most frequently involved muscles other muscles: extensor carpi longus extensor digitorum, brachioradialis, supinator, triceps and anconeous
Tennis Elbow/ Etiology	overstrain of muscles at lateral epicondyle -mechanical faults and poor equipment found in tennis players, musicians, potters, painters, carpenters, chefs, massage therapists
Lateral Epicondyle/Tennis Elbow Sequellae and Related Conditions	Radial nerve entrapment of the supinator muscle
Lateral epicondyle/Tennis Elbow Signs and Symptoms	-Onset is gradual, often related to poor mechanics or equipment -pain and aching at the elbow radiating down the wrist -weak grip -painful resisted extension of wrist, fingers and/or supination of the forearm
Lateral Epicondyle/Tennis Elbow Sign & Symptoms (cont'd)	-Area tender on palpation -swelling is not uncommon -Police stop, (pain in fingers, wrist and elbow in extension outstretched)
Tennis Elbow (treatment)	Rest up to 2 weeks of complete cessation of activity is often recommended -compression brace just distal to elbow when any work is performed -NSAIDS exercise, stretch
Tennis Elbow/Lateral Epicondyle Massage Treatment	-Ice massage to area of inflammation -General collateral massage -As inflammation subsides heat application or contrast bathing may be used -Friction massage to lesion, followed by ice massage -passive and pain free active movements are advised -exercise and stretches to condition the entire forearm and upper extremity
Tennis Elbow/Lateral Epicondyle Massage (Follow-up)	-Patient should always properly warm up and maintain the strength of the muscles -new equipment and retraining may be needed -wearing a heat retaining supportive bandage over the tendons to relieve the stress load on the muscle
Medial Epicondyle (Golfer's Elbow)	Inflammation of common flexor tendon at medial epicondyle of the humerus. Symptoms same as tennis elbow except present on anteromedial aspect of the forearm.
Medial Epicondyle (Golfer's Elbow)	treatment is same as lateral epicondyle and flexor musculature
Insertional Wrist tendinitis/tenosynovitis	inflammation of the insertions of the wrist tendons. Sign and symptons include: pain and tenderness at point of insertion of tendons of: Extensor Carpi Ulnaris, Extensor carpi radialis longus and brevis. Treatment same: friction ice, strengthening
De Quervain Disease/Tenosnovitis	tenosynovitis at base of thumb involving abductor policis longus and extensor policis brevis. (border of anatomical snuffbox). inflammation of the lining of a tendon sheath
DeQuervain Disease Eitology	-overuse microtrauma- especially repeated wrist motion w/forearm rotation and excessive use of thumb -direct trauma - volleyball players -fairly common in massage therapists
DeQuervain Disease Predisposing factors	more common in persons who have lateral epicondyle, cervical spinal and postural problems -systemic disease such as diabetes rheumatoid arthritis, gout and other
DeQuervain Disease Signs and Symptoms	Same as tendinitis but in tendons that have synovial sheaths -putting these tendons on the stretch often increases the pain as pull on the sheath increases - Positive Finklestein's test -resisted testing of thumb abduction and extension of the PIP of thumb
DeQuervain's Disease Treatment	rest splinting NSAIDS and steriodal anti-inflammation
DeQuervain's Disease Massage Treatment	same as tendinitis but the tendon must be on the stretch when the friction is applied to the be most effective -short term work is indicated in subacute phase -ice massage -gentle AROM (within pain free range) -exercises to strengthen
Myofascial dysfunction syndrome	soft tissue mechanical dysfunction myofascial pain syndrome fibromyalgia syndrome
soft tissue dysfunction	overuse conditon that lead to the development of detectable soft tissue changes characteristic of micro trauma
Myofascial pain syndromes	soft tissue pain dysfunctions characterized by the development of trigger point
Fibromyalgia Syndrome	soft tissue dysfunctions which are characterized by central pain mechanisms w/ global pain patterns and little characteristics tissue change
MPS - Myofascial Pain Syndrome	soft tissue pain syndrome presence of trigger points in soft tissue. Arises primarily from trigger points acute, reccuring, chronic
Myofascial Pain Syndrome Etiology	-idiopathic -possibly result of repeated microtrauma from a build up of overuse syndromes
Myofascial Pain Syndrome Sign and Symptons	-usually regional in character -several to many trigger points but in non-specific locations
Fibromyalgia	non-articular rheumatic disorders characterized by -diffuse, widespread pain -tenderness at specific locations -stiffness of muscles, tendon insertions, non-specific locations -
Fibromyalgia etiology	-idiopathic -central mechanism in (CNS) Hypothesis: deficiency in serotonin Hypothesis; deficiency in endorphins and enkephalins, excess substance P -genetic predisposition
fibromyalgia etiology (cont'd)	possible build up of overuse conditions leading to mps which then leads to fibromyalgia. Can be diagnosed with fibromyalgia w/o being diagnosed with MPS
Fibromyalgia Contributing factors	-physical or mental stress -poor sleep -trauma -exposure to cold or dampness -occupational or recreational stress -lack of exercise - becomes more significant as the condition persists -over-exercise in a few cases
Fibromyalgia Incidence	70 - 90 percent patients are women age range from 20-50 years
Fibromyalgia Signs and Symptoms	-no inflammation -generalized muscloskeletal pain pain aggravated by stretching and overuse -stiffnes -fatigue -disturbed sleep tender points -11 to 18 tender points active @ specific locations in the body at one time.
Fibromyalgia Sequella and Related Conditions	-sleep disturbance -anxiety and depression -hypersensitivity - cold, heat, pressure which can increase after stimulus is removed -parasthesias - numbing and tingling -edema as condition progress: irritable bowel syndrome, chronic headache and memory loss
Fibromyalgia Pathogenesis/Pathological Changes	-onset is typically gradual -often experience symptons between 4-6 years or more
Fibromyalgia Treatment	-medication for depression (tri-cyclic anti-depressant) -stress reduction techniques: biofeedback, mediation -education about nature of condition -exercise/stretching: aerobic, low grade strength training -swimming and aquatics
Fibromyalgia Massage Treatment	-general massage and ROM work -heat applications -myofascial manipulation -trigger point work
Muscle Disease 2 diseases muscular weakness contractures and deformities Death (pulmonary conditions)	Duchenne's Muscular Dystrophy Myasthenia Gravis
Muscular Dystrophy (muscle growing wrong)	disease the affects the muscle tissue directly w/o affecting the nervous system - degenerative muscle tissue
Muscular Dystrophy/ Pseudohypertrophic	characterized -extensive degeneration of proximal mucle tissue followed by fibro-fatty replacement (muscles appear enlarged although they are weak)
Muscular Dystrophy Etiology	-inherited X-link recessive trait -absence of dystrophin (protein w/i muscle cell membranes)
Muscular Dystrophy Incidence	affects 1 in 3000 live male births incidence and age of onset boys age 3 to 7
Muscular Dystrophy Signs and Symptoms	In early stages: wadding gait, toe walking, lordosis, frequent falls -By 10 to 12 years of age - most patients are confined to wheelchairs flexion and contraction and scoliosis -early 20's death occurs, usually due to respiratory complications
Muscular Dystrophy treatment	-no specific medical treatment -daily prednisone (glucocorticoid) -Exercise is encouraged as long as is possible
Muscular Dystrophy Massage Treatment	- Passive exercise -increase circulation to the muscles -moderate full body massage w/active and passive movements
Myasthenia Gravis	characterized by episodic muscule weakness and easy fatigue -disorder of nueromuscular transmission -autoimmune disease
Myasthenia Gravis Etiology	autoimmune disorder - acetylcholine receptors @ nueromuscular joints are destroyed by white blood cells (antibodies) -considered idiopathic -initiating event is unknown
Myasthenia Gravis Incidence and onset	Most common in women Onset usually between 20-24 years of age, but may occur anytime
Myasthenia Gravis Signs and Symptoms	-may fluctuate in intensity over the course of hours and days - as with other autoimmune disease often alternate periods of flare up and remission -no sensory symptoms -fatigability of muscles
Myasthenia Gravis Signs and Symptoms (cont'd)	Plosis (dropping eyelid) Diplopia (double vision) weakness in chewing muscles (dysarthia) -unclear speech (dysphagia)- difficulty swallowing Proximal muscle weakness Enlarged thymus Life threatening respiratory involvement
Myasthenia Gravis Treatment	Use of drugs: Anicholineserase drugs Corticosteriods and other immunosuppressive druges Plasmapheresis (blood treatment that removes circulating antibodies) active periods - exercise is contraindicated active exercise program s/b included respiratory support when needed
Sprains ligament injuries	injuries of the joint capsule or ligaments classfied by degree of overstretching or rupture that has occurred
Sprain degrees	1st degree- overstretched w/o tearing ligamentous laxity (sometimes congenital) 2nd degree-between 5 and 100% of the fibers are torn 3rd degree - total disruption of ligaments
Sprain Types	Simple - no fibers torn - 1st degree Severe - some fibers are torn. 2nd and 3rd degree sprains
Common sprains	ankle (most common), wrist finger toes knee sacroilliac joint
Sprains Signs and Symptoms	-Immediate pain -Trearing or popping -Swelling -ecchymosis (significant w injury to blood vessels -pain w/ specific ligament stress -pain w/distraction of the joint surface -point tenderness on palpation
Sprains Treatment First Aid	-local cold application -compression bandage -elevation -rest
Sprain Treatment - simple sprain	first aid treatment - intermittent cold application w/elevation and compression should continue 24 to 48 hours -gentle, pain free ROM -muscles that stabilizes that joint s/b strengthened -cross fiber friction massage to involved ligament to reduce ahesions -
Sprain Treatment - severe	-sometimes surgery is indicated -no direct massage during acute stage -pain free ROM (subcute stage) -direct massage to healing ligament may be performed only to mobilize -during subacute stage, massage will address the tissue in the area of injury. attempt to improve drainage an circulation
Sprain Treatment - Severe (cont'd)	Passive pain free ROM - reduce adhesions an align new collagen fibers -Active ROM w/i tolerable limits. resistance is increased gradually Chronic stage - Normal pain free ROM is restored - (pain on over pressure) perform direct massage to maturing ligament
Sprain Treatment - Severe (cont'd)	-Passive and active ROM exercise performed -Resistance exercises -Proprioceptive and postural re-education -Serious injury causes compensating distortions to posture and proprioception that must be addressed
Ankle sprain- inversion	anterior tibular ligament - most commonly sprained ligament in body. other ligaments: calcaneocuboid and calcaneofibular
Ankle sprain causes:	most common mechanism of injury -plantar flexion inversion stress -dorsiflexion street (less common)
Ankle sprain Signs and Symptoms	-pain over ligaments involved -positive anterior draw test -localized swelling over the ligament -articular effusion of the ankle joint in some cases -muscle spasm end feel is typical -ecchymosis -warmth -capsular limitation
Ankle sprain treatment	-taping -crutches -ice massage -friction massage -mobilization -myofascial work -strengthening and stretching -balance training
Meniscus Injuries	common with trauma to knee. Medial meniscus is injured more frequently than lateral meniscus
Meniscus injuries	made from fibrocartilge -non vascular -outer edges do receive some blood from arteries of knee capsule -slow to heal - sometimes do not heal
Meniscus Imjury Mechanisms of Injury	-compression and twisting forces applied to knee -twisting on a semi-flexed knee -Valgus or varus blows -degenerative changes to the joint
Meniscus Injuries Sequella and related conditions	Knee sprains Terrible Triad - (medial menicus, medial collateral ligament, anterior cruciate ligament)
Meniscus Injuries Signs and Symptoms	-something "gives" in the joint. -pain along intra-articular line -Onset is usually sudden -Pain along the intra-articular line -tissue is tender to palpation -pain deep in the knee joint, pain is nauseating -restricted ROM
Meniscus Injuries Signs and Symptoms (con't)	-extension is more limited than flexion -knee may "lock" - full extension or flexion does not occur -joint effusion (swelling- fluid accumulation) -Hemarthrosis (bleeding into joint) -clicking -chronic or intermitten effusion -take months or years to heal w/conservative treatment
Meniscus Injuries (Evaluation)	-functional test not conclusive -refer to physician if you suspect meniscus problems -refer to physician if recovery from ligament is not progressing as expected -Evaluation of knee joint by arthroscopy or MRI
Meniscus Injuries (treatment)	-knee brace -Surgery: 1. Arthroscopic -shave away fragments 2. removal of meniscus with no replacement 3. Replacement with artificial meniscus
Meniscus Injuries Massage treatment - Acute	Rest Ice Compession Elevation
Meniscus Injuries Massage (subacute)	Contrast bathing - massage to lower extremity, ROM for the knee -begin w/muscle setting and isometric exercise for the quadriceps -myofascial work to balance the muscles that affect knee from the hip: address- adductors, rectus femoris, TFL/ITB and hamstrings
Meniscus Injuries Massage (chronic stage)	-progressively strengthen quadriceps -avoid positions or activities that cause compression of the knee joint -if ROM is restricted PROM may help. No excessive stretching force to joint
Dislocation	articulating bones in a joint become partially or completely displaced from each other and remain displaced. when this occurs other joints structures (ligaments, capsules, labrums, cartliage) are disrupted to some degree
Types of dislocation	Luxation =complete dislocation. Oppossing articular surfaces are separated and are no longer congruent with each other. Complications are typical Subluxation = a partial dislocation w/each other but no longer correctly aligned. Complication can occur, but less common
Where dislocations occur	luxation = complete patella, fingers, toes, elbow sublocations = partical dislocation spine, knee, ankle, acromiocavicular joint (shoulder separation)
Dislocation - Mechanisms of Injury	-trauma -congenital (cause unknown) -previous disease that produces destabilization of joint (ex., RA can cause joint disruption)
Dislocation Signs and Symptoms	-intense, nauseating pain at the time of injury -joint is fixed by muscle spasm -deformity: bones/joints appear out of place Ex. humeral head is below coracoid, below glenoid fossa or below clavicle -depression below the acromion posteriorly (sulcus sign)
Dislocation Signs and Symptoms (cont'd)	-Swelling and ecchymosis -function of limb is lost -Nerve and blood vessel damage -In weeks after injury there is often severe apprehension about any movement of joint
Shoulder Dislocation/Luxation Anterior dislocation	-most common dislocation -humeral head displaced anteriorly and is inferior to coracoid process -usually occurs due to a fall on an outstretched abducted arm -possible injury to blood vessels and nerves in the area high incidence of recurrence especially in younger persons
Shoulder Dislocation /Luxation Posterior dislocation	- also possible -less common
Shoulder dislocation Treatements First Aid	-immobilization and protection -cold application -elevation if possible
Dislocation Medical Treatment	-physician must reduce the dislocation -radiologic exam is indicated before reduction s/b attempted -Reduction may be open (surgical) or closed (by manipulation) -Fixation - (tapping, ating, strapping, bracing, splinting) - up to 3 weeks in patients younger than 30 - up to 1 weeks for patients over 30 - protection (soft cast)
Dislocation Massage therapy	-Once devices are removed massage can begin to improve circulation, relive spasm, reduce fibrosis and adhesions -PROM - only be with movement range that won't stress joints -Avoid any abduction and lateral rotation for first 1 to 2 months (anterior dislocations) -avoid medial rotation w/posterior dislocations)
Spinal subluxations	-most common subluxation is vertebral column due to laxity of spinal ligaments -vertebra may shift anteriorly, posteriorly or rotate from correct position
Spinal subluxations Causes	-induced by muscle spasm or traumatic injury -may cause compression of the nerves where they emerge causing radiculopathy -may irritate joint capsules on the posterior vertebrae joint and referred pain my result usually to paraspinal muscles
Radiculopathies characterized by	-radiating pain -spasm an/or weakness -decreased deep tendon reflexes -reflex autonomic distrubances
Radiculopathies Radiating pain	radiating pain/parasthesias (numbness, tingling and pins and needles) - dermatomal and sclermatomal patterns
Radiculopathies (con'td)	Spasm and/or weakness - mytomal distribution decreased deep tendon reflexes (stretch reflex) associated w/that segments
Radiculopathies (cont'd ) Reflex autonomic distrubances	-in skin innervated by posterior ramus of spinal nerve root associated with that segment 1. simple test - drag fingers along spine from head to tail and notice the sequence of color changes that occur 2. skin should first blanch due to ischemia then beome hperemic then normal -w/i a few seconds 3. if transition is not smmoth and rapid a pathology is indicated
Radiculopathies (cont'd) Treatment	-physicians will prescribe muscle relaxers -manipulation and mobilization by chiropractor, osteopath or PT -manipulation is beyond scope of MT license
Radiculopathies Massage treatments	-heat and cold used to alleviate pain, spasm and other symptoms -massage to release spams my be sufficient to release sublaxation -myofascial work may also achieve the same result -massage before and after manipulation -erector spinae and transversospinals should be specifically addressed -once subluxation has been reduced the client should attempt to strengthen and stretch erectors and abdominals and correct postural distortions
spondylosis	condition of the vertebrae Usually vertebrae ankylosis (degenerative joint condition)
Spondylitis	inflammation of the vertebrae
Spondylolysis lolysis = break down of vertebrae	defect in pars interarticularis (region between superior and inferior facets of vertebrae
Spondylolisthesis= spondy = joint lolisthesis = displacement	forward displacement of one vertebrae over another
Etiology:	trauma degenerative processes
Spondylolisthesis	L5 - most commonly involved vertebrae it slips over S1 -overstretched anterior longitudinal ligament may be cause -fracture of pars interarticularis -common in people who exhibit hypermobility -may be no clinical problem -2-4% of the population
Spondylolisthesis Signs and Symptoms	-back pain with insidious onset -pain increases with standing or bending -pain decreases with sitting
Spondylolisthesis Assessment	-restrictions in active flexion of lumbar spine -step deformity (L5 obviously anteriorly displaced relative to L4 and sacrum) -visible or palpatable depression -Lordosis -straight leg raise test is usually negative -standing on one leg, balancing and extending the spine will generate pain
Spondylolisthesis Diagnosis	-X-ray will reveal the fault -scottie dog fracture (spondylosis) or napolean hat (spondylolisthesis) -degenerative changes in the intervertebral discs (spondylosis)
Spondylolisthesis Treatment	-fixation and stabilization until fracture heals -manipulation to reduce the fracture -possible surgery
Spondylolthesis Massage Treatment	-may be indicated to treat spasms and increase ROM -myofascial release
Disc Injuries what they are	Intervertebral disc injuries are injures to the substance of the fibrocartilaginous discs which lie between vertebral bodies
Disc injuries where they occur	-Lumbar spine (L4 - L5 discor L5-S1) disc most common (80%) -L5-S1 most common -Cervical Spine (C5-C6 or C6-C7) distant second -thoracic spine disk injuries are unusual
Disc injuries etiology	disc injuries are usually the result of cumulative or single excessive trauma which leads to breakdown of basic disc structure
Disc injuries Mechanisms of Injury	Rotational movements w/spine in flexion -repetitive stress accumulates followed by a single or multiple instances of excessive stress causing the disc gives out
Disc Injuries Degenerative Changes	Spondylosis - disc become more fibrocartilaginous, less and less pulposus; water binding capacity decreases, -less able to stand compression -rotational forces Osteophyte formation: bony growths which narrow the spinal canal or intervertebral foramina. -common in elderly
Disc Injuries Four basic problems	-Protusion - disc bulge (usually posteriorly) with rupture of annulus fibrosus -Prolapse - only the outer fibers of the annulus remain to contain the nucleus pulposus -Extrusion - annulus fibrosus is performated. Nucleus pulposus pushes through -Sequestration - fragments of the disc outside the disc proper
Radiculopathies of disc Injury	disc put pressure on the nerves. -Sciata is common outcome of lumbar disc pathologies -L4-L5 disc usually irritates the L5 nerve root -L5-S1 disc usually irritates the L5 and S1 (or S2) nerve root
Radiculopathies of disc injury (cont'd)	Nerve roots contribute to superior gluteal, inferior gluteal and sciatic nerves -central disc lesions may irritate the entire cauda equina -cervical spine C6 and C7 nerve roots are more commonly involved
Radiculopathies of disc injury Signs and Symptoms	pain, insidious or sudden outset -sharp, burning, shooting, dull or aching -usually unilateral -distributed in low back, the SI joint area, buttocks posterior thigh, leg and foot
Radiculopathies of disc Injuries Signs and Symptoms (cont'd)	-pain increases when sitting. relieved when standing, walking or lying down -pain increases with any movement that compresses involved discs -paresthesis (pins and needles) -hypoesthesia (numbness) in mytome, dermatome, sclerotome patterns -client stands in antalgic position
Radiculopathies of disc injuries Assessment	Heel and Toe Standing inability to stand on heels indicates L5 - S1 nerve root compression inability to stand on toes indicates S1, S2 nerve root compression Positive valsava maneuver (pain upon inhalation, holding breath, bearing down) -deep tendon reflexes may be reduced or lost
Radiculopathies of disc injuries Sequellae	Overtime the muscles become wasted and flaccid. Long term compression of the nerve root may lead to permanent loss of function
Treatment for Disc injuries	-rest (sometimes complete bed rest for 3 days) -usually better for client to move w/i tolerance limits -Anti-inflammatory medications -pain relieving drugs -manipulation and mobilization (worked b doctor)
Disc injury surgeries when convservative treatment fail	-diskectomy - discs are shaved -Chymopapain - disc injected w/digestive enzymes -Laminectomy- laminae are removed to expose the disc, vertebrae are fused Rehab from surgery determined by DR. massage may help restore function
Disc Injury Massage Cautions	No local massage should ever be attempted-refer to orthopedic surgeon -Massage of paravertebrals at site of injury is contraindicated -When in doubt consult w/managing practioner to determine what is appropriate -use caution when working with someone with history of disc injuries - do not prescribe exercise for disc injuries
Disc Injury Positioning	-Avoid positioning client in the prone position -better to work supine or sidelying
Disc injury Massage Treatement Acute/Subacute	-Craniosacral techniques for dural irriation -Massage may be performed above and below site and thoughout the distribution of the nerve
Disc Injury Massage Treatment Subacute/Chronic	-As/if condition imroves - local work on the paraspinal muscles is indicated - After months tissue can bear more direct work. usu. ql, and piriformis will need work to release trigger points and fascial restrictions -in chronic - necessary to work with a more whole body approach after dealing with local issues
Sciatica	-refers to neuritis (inflammation) or neuralgia (pain) associated with the sciatic nerve. client may experience symptoms in the low back. SI joint area the buttocks, hip, posterior thigh, leg and ankle foot
Sciatica Etiology	-Disc injury in L4-L5 and/or L5-S1 -SI joint dysfunction -Vertebral canal stenosis -Tumor in Lumbar or sacral region -Inflammation of nerve - due to infection or direct pressure -sitting w/poor posture -Entrapment of nerve by piriformis muscle
Sciatica Sign and symptoms	same as above
Sciatica Massage treatment	same for disc injuries
Pirformis Entrapment	-Piriformis muscle and other deep lateral rotator must be directly massaged -direct friction to the muscles @ greater trochanter -myofascial release to posterior hip & thigh, lats, posas, itb/tfl, ql, sacrotuberous ligament, erectors, flexors and adductors of hip - Tense and relax -Muscle Energy Techniques, Orthobionomy
Joint Disease Ganglion Cysts	-synovial membranes, found in hands, esp. dorsum of the wrists (rarely found on dorsum of feet,or knee) -found near or attached to joint capsules and tendon sheaths -appear as rounded swelling which gradually develops -may be quite small or large as walnut
Ganglion Cysts Etiology	-idiopathic -often history of trauma or abuse
Ganglion Cysts Incidence	-more common in women than men 3:1
Ganglion Cysts Signs and Symptoms	-swelling - raised lump -weakness in joint -pain on exertion
Ganglion cyst Sequella/Related Conditions	-Pain due to pressure on nerves. -Pain tends to be constant
Ganglion Cysts - Bible Bumps Treatment	-some disappear spontaneously -treatment s/b conservate unless movement is impeded or ganglion is resting on a nerve -Aspiration w or w/o corticosteriod injection (MD) -surgical excision (MD) -Direct compression - may break it up -thin walled- digital pressure -thick walled- heavy book (Bible)
Ganglion Cysts - Bible Bump massage treatment	-direct massage in not indicated -manipulation is sometimes helpful for reduction any irritation -fascial work may relieve some symptoms
bursitis - inflammation of bursa	bursae - small fluid filled synovial sacs located between tendons, muscles, ligaments, skin and bone. -designed to reduce friction to soft tissue structures
Bursitis etiology	-chronic overuse -Trauma -Infection - (staph usually, TB rarely) -Inflammatory arthritis- RA or gout
Bursitis sequella and related conditions	-calcification -adhesive capsulitis
Bursitis Common sites	-subacromial (subdeltoid) -olecranon - (student elbow) -trochanteric (gl max and gluteus medius, TFL) -iliopectinal (iliopsoas) ischiopgluteal (gl max & hamstrings) Prepattellar, uprapatellar
Bursitis - common sites (cont'd)	retrocalaneal -Pes anserinus -popliteal (baker's cyst) -first metatarsal head (bunion)
Bursitis - Acute (signs and symptoms)	-pain -localized tenderness -limited motion (limited severely in all directions) -swelling -warmth -redness present (superficial & infection present)
Bursitis - Chronic (signs and Symptoms	-follows previous attack of acute bursitis -multiple recurrences common -bursal wall is thickened -may be adhesions, tags, and calcareous (calcium) deposits -pain, swelling and local tenderness -lead to muscle athropy, limited ROM -pain with passive stretching over bursa -pain arch 60 - 120 should abduction for aubacromial bursitis
bursitis - Treatment	-rest -immobilization (sometimes) -high doses of NSAIDS w/narcotic analagesics -injections with corticosterioids -sometime systemic corticosterioids -infection requires antibiotics -aspiration -pendulum exercises
Bursitis - Acute Massage	ice massage
Bursitis - chronic (no sign of infection) Massage Treatment	-PROM (important at shoulder to reduce adhesive capsulitis) -stretching tissue in area -general masssage to muscle and tissue in area -friction -(subacromial and trochanteric) not too long or irritate tissue -myofascial work -exercises to strengthen if athropy is present
- Synovitis	-inflammation of synovial membrane of joint -if inflammation spreads to or begins in other joints - known as arthritis
Synovitis etiology	-trauma (if repeated my lead to chronic condition) -infection -loose bodies in joints
Synovitis - Sequella and Related Conditions- chronic	-capsule becomes thickened, vascular and roughened -portions of capsule my break off and form loose bodies in joints- leading to chronic inflammation in joint space, fibrosis -ligaments become lax -muscles may atrophy -joint instability -arthritis
Synovitis Signs and Symptoms	-pain- (dull and aching at rest, intensifies with movement) -swelling (exudation of clear, serous synovial fluid) -may be bleeding at joint -joint held in open packed (midrange/neutralized) position when effusion is extensive -dull aching pain -stiffness and limited ROM due to adhesions (fibrous ankylosis) fibrous buildup
Synovitis - Subacute Massage Treatment	-PROM -AROM Effleurage above the inflamed joint -reduce swelling (begin proximal and move toward joint as swelling resolves) -finger kneading around joint (tolerated) vigorous massage around joint to improve circulation -Exercise - strengthen muscles
Synovitis - Chronic Massage Treatment	-vibration of joint w/traction -gentle tapotment to joint capsule -deep friction -heat, contrast bathing -passive stretching, moist heat
Frozen Shoulder (FS) Adhesive Capsulitis	clinical syndrome associated with pain and restricted AROM and PROM of the shoulder and scapulothoracic joints -self limiting disorder -resolves with time, leaving some residual loss of movement (10-15 %) -best treatment - avoid long term immobilization -promptly treat any condition any condition that results in reduced usage
FS Etiology	-idiopathic (most common) -unidentified stimulus, substantial tissue change in the capsules are different from those due to immobilization
FS (secondary)	-develops after trauma -surgery -rib fracture -upper limb immobilization -infection -cancer, arthritis, cervical disc disease -chronic inflammatory condition -long-term intravenous infusion
FS Incidence	-Primary occurs between 40 and 70 years -more common in non-dominant arm -female to male ration 2:1 -more likely: -insulin dependent diabetics than regular population
FS/ Adhesive Capulitis Pathological changes	-capsular attachments approximate and forshorten -low grade inflammatory response develops in capsules, synovial lining, rotator cuff tendons -adhesions form in overlying tendons -joint capsule disc drawn tightly and humeral head, becomes attached to bone -rotator cuff becomes contracted an in elastic
Three stages of Frozen shoulder (each last approx. 6 months) -Freezing -Frozen -Thawing	-Freezing stage -painful inflammatory stage -characterized by: -constant shoulder pin - muscle spasm -actual fibrosis at joint developing -motion restriction due to inflammation, muscle spasms -
Frozen Shoulder/Adhesive Capulitis Freezing stage Signs and Symptoms	-insidious onset -pain in midrange, constant pain, worse at night -empty end feel -capsular pattern (lateral rotation most limited) -reversal of normal scapulohumeral rhythm -movement of scapula on the thorax is often reduced by half -sensations and reflexes are normal
FS/Adhesive Capulitis Frozen Stage Signs and Symptoms	-pain is not constant now -resting pain decreases -dull ache during movement -Passive ROM painful at end range only -Resisted isometric contractions are often painless -no painful arc -point tenderness at bicipital grove -disuse atrophy of cuff muscles, deltods
FS/Adhesive Capulitis Thawing Stage Signs and Symptoms	-motion slowly increases -return to functional activities -often some residual reduction in ROM
FS/Adhesive Capulitis Treatment (General)	-persisent shoulder joint restrictions treated by manipulation under anesthesia (controversial) -best to continue w/conservative treatment -manipulation contraindicated if osteoporosis, shoulder dislocation, prolonged steroid use or fracture is part of the history -surgery is a last resort
FS/Adhesive Capulitis Treatment - Freezing stage	-anti-inflammatory and analgesics to allow movement into the pain -pendulum exercise w/ or w/o wrist weights -PROM and AROM into the pain to prevent adhesion formation
FS/Adhesive Capulitis Treatment -Frozen stage	-Moist heat -PROM -Passive stretching w/moist heat -Cold application for 5-10 mts. -massage to work hypertonic, contracted muscles and adhesions friction to cuff tendons, TP work -wand exercises
FS/Adesive Capulitis Treatment -Thawing Stage	- continue as in frozen stage -add resisted exercises to strengthen muscles as movement returns -shoulder mobilization exercises and wand exercises continue
Temporomandibular Joint syndrome	dysfunction of the temporomandibular joint characterized by clicking, locking and pain in the joint
TMJ Syndrome Incidence	-commonly occurs in patients between 20 and 40 -more common in women than men
TMJ Syndrome Etiologie	-Myofascial Trigger Point in the temporalis, masseter, medial and lateral pterygoids, suprahyoids, anterior cervicals, SCM, scalenes. -Arthritis of the TMJ (osteoarthritis or rhematoid) -mechanical dysfunction (often due to hypermobility) -Malocclusion (uneven bite) -Bruxism (clenching teeth) Trauma -vascular problems -unilateral mastication
TMJ Syndrome Phases	-early incoordination phase -later limitation phase
TMJ Sydrome Signs and Symptoms (unilateral usually, but may be bilateral) Incoordination phase	-clinking in the joint -muscular tenderness -dull aching pain perarticular area -pain on movement in joint, as in chewing -spasm of the masticatory muscles -decreased mobility -recurrent subluxation or dislocation -hypermobility on one side, hypomobility on the other side Tinnitis
TMJ Syndrome Signs and Symptoms Limitation Phase	-mandibular catching or locking -spasm and contracture of the muscles -possible degenerative changes of the joint, the condyle, articular disc
TMJ Syndrome Treatment	-exercises to improve strength of suprahyoid mucle and to improve balance between all muscles acting at that joint -malocclusion plates -stress reduction techniques -manipulation -tirgger point injection at lateral pterygoid
TMJ Syndrome Massage Treatment	-deep friction massage at the capsule of the joint -trigger point work-mastication muscles -tense and relax -passive stretching -Myofascial release to temporalis, masseter, facial muscles and scalp
Arthritis -Osteoarthritis -rheumatoid -gout -lyme -systemic lupus erythematosus -ankylosing spondlyitis	inflammation of the joints -refers to many different joint diseases -in some cases arthrictic inflammation is secondary to trauma or degeneration -systemic autoimmune process
Rheumatism	-acute chronic condition characterized by: -inflammation -soreness -stiffnes of muscles and pain in joints and associated structures
Ankylosis	immobility of the joint
Bony Ankylosis	abnormal union of he bones at the joint
Fibrous Ankylosis	ankylosis due to fibrous bands within the joint
infectious Arthritis/ aka Bacterial Arthritis, Septic Arthritis	lyme arthritis falls under this category
infectious Arthritis Etiology	-infection by pathogen, usually bacterial(gonorrhoeae, staph, borrelia burgdorferii) -can be fungal or viral -infected by direct penetration from neighboring bone or blood
Infectious Arthritis Pathological tissue Changes	-usually one joint involved (sometimes more) -range mild synovitis to severe arthritis -when severe, joint destroyed 7-10 days -necrosis of bone and other joint structures -purulent exudate filling synovial cavity
Infectious Arthritis Sequellae/Related Conditions	-fibrous ankylosis is common -w/extensive damage-bony ankylosis will develop
Infectious Arthritis signs and symptoms	-inflammation (extreme exudation) -pain -muscle spasms -loss of function -fever and leukocytosis (wBC count up) -Systemic complaints - malaise, fatigue
Infectious Arthritis Assessment	-empty end feel -capsular pattern
Capsular pattern Definition	inflammation in joint causes pain, passive stretching causes pain and limited ROM is also found in a specific pattern. This pattern is always similar for that paticular joint. each joint has different and instantly recogniable capsular pattern
Infectious Arthritis treatment	-antibiotics and anti inflammatories -rest and elevation
infectious Arthritis Massage Treatment	-once infection resolved: -treat ankylosis and extra articular fibrosis with: -myofascial -trigger point -strengthening and stretching
Lyme Arthritis	acute migratory polyarthalgia with fever, headache, fatigue and skin lesions. -sub type of infectious arthritis because of etiolog
Lyme Arthritis etiology Signs and Symptoms -early stage -late stage	Etiology: - tick bite and infection w/ Borrelia burgdoferi Signs and symptoms -early stage: -bulls-eye rash -late stage -intermitten monarthritis or ligoarthritis (one of few joint affected) -knees often involve (swollen, hot)
Lyme Arthritis Disease course Treatment	Disease course -arthritis may persist for more than 6 months -may recur for several years Treatment -antibiotics, anti-inflammatories
Osteoarthritis(OA) aka Degenerative Joint Disease Hypertrophic Arthritis	-not inflammatory in nature -degenerative process -effective older men and women (over 60)
OA Osteoarthritis Degenerative Joint Disease Hypertrophic arthritis Incidence Etiology	-Incidence - men and women over 60 - universal Etiology: -degeneration - wear and tear - can be secondary to trauma or surgery
OA Degenerative Joint disease Hypertrophic Arthritis Pathological Changes	-articular cartliage begins to degenerate (cause unknown) -weakend cartliage wears away -underlying bone exposed -eburnation (bone becomes polished by friction) -osteophytes (bone spurs) -osteophytes irritate joint capsules -capsules become inflammed, thicken and fringed, leading to fibrous ankylosis
OA Degenerative Joint Disease Hypertrophic Arthritis Signs and Symptoms	-gradual onset -aching joints -stiffness in morning or after inactivity -stiffness resolves after activity (early stage) -pain increase w/activity and decreases w/rest -joint tenderness -creaking (crepitus) grinding noise -osteophyte formation -thickened capsule, proliferation of other joint soft tissue
OA Degenerative Joint disease Hypertrophic Arthritis Involved Joints	Hands - DIP's and PIP's, first carpometacarpal joint -Bouchard's nodes -bump on either side of pIP -Heberden's nodes - bump on either side of DIPS -cervical and lumbar posterior interveterbral joints -hips -knees -ankles -first tarsometatarsal joint -SI joint
OA Sequella/related conditions	-in cervical or lumbar spine may lead to disc herniation and radiculopathy -in hip causes gradual loss of ROM progressing to total -in knee may lead to erosion of medial cartilage causing lax capsule
OA - Treatment	NSAIDS (long term uses causes gastritis, peptic ulcers, liver and kidney toxicity and anemia) -intraarticular injections when inflammation is present -glucosamine sulfate, chondroitin sulfate, sea cucumber -joint replacement surgically -limit caffine, nicotine, alcohol -daily stretching -rest balanced w/exercise
OA Massage treatment	-AROM and PROM -general massage -avoid inflammed joints -paraffin baths
(RA) Rheumatoid Arthritis Atrophic Arthritis	chronic syndrome -non specific symetrical inflammation of peripheral joints -categorized as systemic autoimmune disease -manifest primarily in joints
RA Atrophic Arthritis Etiology	Etiology -idiopathic -genetic predisposition -viral and bacterial causes suspected by not proven
RA Atrophic Arthritis Incidence	-1% of population effected -women 2-3 times more likely than men -onset usually 25-50 years
RA Atrophic Arthritis Pathological changes	-immune complex deposited in joints (antibodies attach to antigens to destroy them) -new antibodies produce Rheumatoid factor -lymphocytes migrate to joint space -synovial lining thickening -fibrin deposited and fibrosis develops -pannus (hyperplastic synovium) covers and erodes joint surfaces
RA Atrophic arthritis Signs and Symptoms	-onset insidious -course is episodic -recurrent -progressive
RA Atrophic Arthritis Early stages	-fatigue, weakness, weight loss -paresthesias of hands, feet, low grade fever -vague aching and stiffness in joints -appears in multiple joints in symmetrical pattern -tenderness in involved joints -stiffness lasting longer than 30 minutes after inactivity
RA Atrophic Arthritis Later stages	-synovial thickening (pannus) -red skin over joints -deformities -flexion contractures -butonniere deformity -swan neck deformit -ulnar deviation of fingers -bouchard's nodes crippling pain, muscular aches
RA Atrophic Arthritis Joints commonly involved	-Hand: PIP and MP joints -wrist, elbow, metatarsophlangeals, knee, ankles
RA Atrophic Arthritis Treatment	-Rest, sometimes complete bed rest -splinting -NSAIDS, especially salicylates (asprin) -corticosteroids, quinine, sulfur drugs -intramuscular gold salt injections -avoidance of stimulants- alcohol, food allergies -surgery to repair damaged joints
RA Atrophic Arthritis Sequella/related conditons	-total joint destruction and bony ankylosis -carpal tunnel syndrome -periarticular osteoporosis
RA Atrophic Arthritis Massage treatment	-ROM, caution w/PROM especially during flare up -General massage for mucular aches an possible atrophy -exercise during remission
Systemic Lupus Erytheatosus (SLE)	-chronic inflammatory connective tissue disorder -can involve any order system -usually involves joints, skin, kidneys, blood vessel walls, CNS -autoimmune disease
SLE Etiology Incidence	Etiology -idiopathic Incidence: -500,000 people in US -female: male 9:1
SLE Signs and symptoms	-articular sign in 90% of patients -may be confused with RA -usually non-destructive and non-erosive -other muscloskeletal signs: tenosynovities ruture of infrapatellar, Archilles Tendon, avascular necrosis of femoral head
SLE Treatment Massage Treatment	Treatement - NSAID and antimalarials -coriticosteroids in severe cases Massage Treatment -massage okay, don't work swollen joints
Ankylosing Spondylitis (aka) Marie-Strumpell Disease	-system rheumatic disorder -characterized by inflammation of axial skeleton & proximal joints (esp. SI joint and lumbar spine)
Ankylosing Spondylitis Marie Strumpell Disease Etiology Incidence	Etiology: - idiopathic -genetic component -possible autoimmune mechanism Incidence: - Men: women 3:1 - begins between 20 and 40 years of age
Ankylosing Spondylitis Marie Strumpell disease Signs and symptoms	-back pain, (esp. SI joint and L-spine) (worse at night) -morning stiffness relieved by activity -diminished chest expansion -low grade fever, fatigue, anorexia, weight loss, anemia -flexed position eases pain -radiculopathies, cauda equina syndrome
Cauda equina syndrome	-nerve roots are compressed and paralyzed cutting off sensation and movement -nerve roots that control function of: -bladder and bowels are especially vunerable to damage -if not treated can result in permanent paralysis, impaired bladder and/or bowel control -loss of sexual sensation
Ankylosing Sponkylitis Marie Strumpell disease Sequella/Related Conditions	-Iritis (inflammation of iris) -angina (vascular dysfunction) -pericarditis -respiratory conditions similar to TB
Ankylosing Spondylitis Marie Stumpell Disease Treatments	NSAIDS -gold injections -exercise
Ankylosing Spondylitis Marie Stumpell Disease Massage treatment	-Massage for parvertebral muscle spasm -release flexors of trunk -PROM -Postrual re-education
Gout aka Gouty Arthritis	-arthritis caused by: -monsodium urate crystals in joint characterized by: -hyperuricemia (too much uric acid) -WBC attack crystals, release chemicals - mediators of of inflammation causing arthritis
Gout aka Gouty Arthritis Etiology	hyperuircemia caused by: -decreased renal clearance of uric acid -increased purine synthesis due to genetic enzyme abnormalities -eating food high in purine (beer, yeast, organ meat legumes, etc) -high alcohol intake -seconart to other disease or drugs
Gout aka Gouty Arthritis Signs and symptoms	Early Stage -actue onset, often at night -usually begins in one joint, spreads -pain increases, eventually becomes excruiating -MP joint of great toe, (most common) -overlying skin is red, shiny, warm, or purplish -fever, tachycardia (rapid heart beat), malaise, chills, and leukocytosis may occur
Gout aka Gouty Arthritis Signs and symptoms Later stages	-local signs regress, normal joint function returns -time between attacks decreases -as disease progresses -tophi (urate deposits) occur: in the walls of bursae, tendon sheaths, subcutaneous
Gout aka Gouty Arthritis Sequella and Related Conditions	-untreated, chronic joint symptoms leading to erosive joint deformity -renal disease and death if not managed
Gout aka Gouty Arthritis Treatment	-Rest -NSAIDS -Colchicine for acute inflammation, alopurinol for reducing prine concentrations -pain medications -antioxidants -Drink 3 liters of water per day -joint aspiration and injections w/corticosterioids
gout aka Gouty Arthritis Massage Treatment	-massage contraindicated during acute attacks -during asymptomatic periods massage can be used to resolve tophi -PROM, AROM -paraffin baths

Share This Flashcard Set

Set the Language

Pathology I - Red Blood Cell Disorders

Add to Folders

Upgrade to Cram Premium

Card Range To Study

621 Cards in this Set