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91 Cards in this Set

  • Front
  • Back
Simple Squamous Epithleium Disease
Arterial Endothelium Dysfunction - Tissue tear in endothelial wall causes repair process to start depositing crystal cholesterol in vessel wall (The Beginnings of Atherosclerosis)
Ciliated Columnar Epithelium Disease
Trachea Tissue from a Smoker - freezes/destroys cilia in lung tissue as well as disorganizes the columnar epithelial cells
Diseases involving overproduction of collagen fibers
Lung Fibrosis (Cystic Fibrosis)

Liver Cirrhosis

Atherosclerotic Heart Disease
Lung Fibrosis (Cystic Fibrosis) description
excess glandular secretions (like mucous)
Causes of Lung/Cystic Fibrosis
Caused by a mutation in the CTFR gene (which produces the ion channel)

This channel is important in creating sweat, digestive juices, and mucous (this is why there is high salt contentin the sweat of CF kids)
Life Span of Lung/Cystic Fibrosis Patients
Life span used to be limited to 20-30 years

It now can be possibly 40-50 years if treated properly
How Lung/Cystc Fibrosis affects the body
Obstructions and fluid in lungs causes breathing disorders and numerous infections. These result in low oxgen transport form the lungs and therefore hinder oxygen transport to the rest of the body.

Obstructions in the pancreas decrease digestive enzyme production which therefore decreases nutrient absorption. Malnutrition hinders growth so decreased nutrient absorption due to obstructions in the pancreas also hinders growth
Liver Cirrhosis description
Irreversible scarring (fiber deposition) in the liver

Excess scarring in the liver
Causes of Liver Cirrhosis
Hepatitis B, Hepatitis C, alcoholism, and as of late and more commonly obesity can cause it as well
How does Alcohol affect the liver?
Alcohol blocks the normal metabolism of protein, fats, and carbs which causes injury to the liver and therefore scarring (or cirrhosis)
How does Cirrhosis affect the bod
Cirrhosis causes edema and ascites (fluid in the periotneal space) which causes the liver to not be able to produce albumin. Albumin is the most comon protein in the blood and important for maintaining osmotic pressure, so during cirrhosis bood loses its osmotc (or sucking/pushing) pressure
increased risks and signs of cirrhosis
increased infection risk, jaundice, bruising and bleeding, portal hypertension

cirrhosis will als elevate aminotransfease enzmes like ALT, GGT, and AST (aka SGOT - largely elevated SGOT is linked to alcoholism)
How atherosclerotic heart disease is linked to cirrhosis
Atherosclerotic heart disease causes high SGOT, wich is also associated with alcoholism, so elevation of SGOT tells us that cirrhosis is a possibility
Autoimmune Disorders that affect collagen
Lupus Erythematosus
Lupus Erythematosus description
production of "auro antibodies" that target body tissues

This is a nonspecific disease that sometimes does not get diagnosed
Lupus Erythrematosus symptoms
90% of Lupus patients will experience joint and muscle pain which is caused by collage damage and destruction (collagen is a vital componenet of tendon)

Collagen damage and inflammation can occur anywhere in the body, but the most commonly affected areas are:
-Skin (rashes that result from sunlight exosure)
-articular tissue
-lungs
-blood vessels
-liver
-kidneys
-nervous system
Unique Charateristics to Lupus erythematosus
course of the disease is unpredictable with attacks and remissions

most common in women ages 18-40
Diseases of Insufficient Collagen Production
Ehlers-Danos Syndrome

Osteogenesis Imperfecta

Scurvey
Ehlers-Danos Syndrome
"Rubber man" or contortionists disease

Characterized by weakening of collagen cross link bonds
Osteogenesis Imperfecta
Brittle Bones
Scurvey
Vitamin C Deficienc

Too few hydrogen bonds occur in the formation of the collagen molecule

Causes inferior tissue formation in bones, blood vesels, skin, and teeth
"Double Jointed" vs. Ehlers-Danos Syndrome
Is inherited like Ehler-Danos Syndrome

has the same mutation as the syndrome just to a lesser degree

Double jointed is a variation of the syndrome in the genes - a small amount of extra flexibility vs extreme amount of flexibility in the syndrome
Therapy for Cystic Fibrosis
Clearance techniques for excess lung secretions

pancreatic enzyme replacement for pancreatc duct obstruction

healthy diet and exercise ( increases lung capacity, RBCs, delivery of oxygen to tissues, capillarization in muscle, and clearance of mucous)

Drugs:
-Ibuprofen (slows rate of decline of pulmonary function)
-Corticosteroids (decrease inflammation in lungs, joints, and vasculature)
-Antibiotics (to treat and reduce the incidence of lung infections
*Rotation of drugs prevent development of resistance

Immunoglobulin (antibody) experimental research (currently in human trials hase)
Therapy for Lupus
Drugs
-Disase Modifying Anit-Rheumatic Drugs (DMARDs) (Decrease flare ups)
-NSAIDs
-Corticosteroids and other immunosuppresants
-Hydroxychoroquine (decreases inflammation and activation of inflammation causing dendritic cells, also used as an antimalarial drug)
-Experimental Drugs (inhibits stimulation of antibody production)

Autograft bone marrow stem cell infusion has been very promising in reducing symptoms

Ultraviolet Radiation Therapy (Phase 2 clinical trials)
Human Trials Phases
Phase 1 - 10 or 20 people in study, low doses, used to pick up onte effect of the drug

Phase 2 - Raise number of people in study and vary the doses people are taking, trying to discover adverse affects as well as starting to look for signs of efficacy

Phase 3 - Proving the efficacy of the drug, multiple sites administer drug and compare this new treatment to od treatments and compare results

Phase 4 - Post marketing surveillance, studying long term effects
Bone Diseases
Pagets Disease
Osteoporosis
Osteopenia
Osteomyelitis
Osteoarthritis
Rheumatoid Arthritis
Pagets Disease Description
enlarged deformed bones
Symptoms of Pagets Disease
Pain, pinched nerves

Pinched nerves also cause tingling and numbness, leg bowing, hip and knee pain
How Pagets Disease affects the body
Increased bone reabsorption and deposition rates (overactivity of osteoblasts and osteoclasts cause inefficent bones)

This causes weak bones, bone pain, increased fracture risk, and arthritis
Characteristics of Pagets Disease
Affects about 1% of adults

rarely diagnosed in people under 40 years of age
Osteoporosis Description
decreased bone density which increases fracture disposition

2.5 standard deviations below the mean bone density of young people

Doesn't measure relative to what your bone density originally was, its just a preset number for all people
Osteopenia Description
bone loss bu not as seere as osteoporosis

1.5 standard deviatins below the mean bone density of young people
How Osteoporosis affects the body
decrease in bone resorption in the presence of bone metabolism

decrease both cortical (thick) and trabecular (porous) bone density, although it affects cortical bone more
Characteristics of Osteoporosis
Women start losing bone density about age 40

Men start losing bone density about age 60

Over 28 million people in the US have osteoporosis (80% of these are women)

Many women experience up to a 20% decrease in cone mas by 5 to 7 years after menopause

1 in 2 women and 1 in 4 men over age 50 will have an osteoporosis related fracture in their lifetime
Common fracture sites with osteoporosis
thoracic vertebra, distal radius (close to wrist), FEMUR NECK (hip fracture)

Bone density is highest in your 20s
Why are osteoporosis drugs used to treat Pagets disease
use osteoporosis drugs to buld bone density and decrease turnover rate and increase bone strength
Causes of Osteoporosis
Prolonged treatment with corticosteroids

anorexia nervosa

inadequate diet, especially during pregnancy and breast feeding

Amenorrhea causes an increase in estrogen metabolism disturbaces and results in bone loss (usually osteopenia)
Treatments for Osteoporosis
Estrogn replacement (for postmenopausal women) or EVISTA (selective estrogen receptor modulator that decreases bone resorption)

Calcium supplementation

Vitamin D Supplementation

Biphosphonate drugs (also called diphosphonates) - decrease osteoclast activity (this is also used to treat bone cancer andother bone weakening diseases)

Calcitonin (calcimar or miacalcin) - increases osteoblast activity

PTH analog (teriparatide) - increases osteoblast activity because intermittent exposure to PTH will increase osteoblast activity more than osteoclast activity

Weight bearing exercise can increase bone mineral density and decrease falls
Osteomyelitis description
bone inflammation and destruction
Causes of osteomyelitis
caused by bacteria and fungi spreading from oter infection sites
Symptoms of Osteomyelitis
fever
localized wamth and swelling
localized pain
Treatment of osteomyelitis
antibiotics
Osteoarthritis Description
degenerative changes in cartilage and bone

Loss of articular cartilage (due to proteoglycan loss which causes water loss and decreases compliance of cartilage) in hands, hips, and knees
Symptoms of Osteoarthritis
Roughening, pitting, and destruction of hyaline cartilage causes an increase in joint stiffness

May result in formation of osteophytes (bone spurs) or nodes (Bouchard's nodes)
How des osteoarthritis affect the body
IL1beta (stimulates destruction of bone) and TNFalpha from chondrocytes causes a decrease in collagen production and and increase in catabolism of articular cartilage
Who is usually diagnosed with osteoarthritis?
80% to 90% of people over age 65 have some evidence of osteoarthritis
Cause of osteoarthritis
heredity (50% to 65%), infection endocrine disorders, joint injury, OVERUSE

Fracture of ligament injury causes bad joint alignment and instability which increases "wear and tear"
Treatments of Osteoarthrits
Exercise - helps maintain ROM, healthy cartilage, strengthens muscle stabilizing the joint, and reduse pain (Immobilization worses the disease by reducing blood flow and reduce muscle strength)

Weight loss for osteoarthritis in weight bearing joints

NSAIDs and COX2 inhibitors for pain

Injections of hyaluronic acid or new artificial injectible materials

Corticosteroid injections may be useful when inflammation is present (acute inflammation of the joint)

Joint replacement (when conservative therapy fails)

"Tissue engineering" to regenerate cartilage has had some success, but is more of a future treatment than present

Glucosamine and chondroitin supplements, but definitive meta analysis says no real benefit
Rheumatoid Arthritis Description
Autoimmune inflammaory disease that affects the joints
Possible causes of Rheumatoid Arthritis
may be related to genetic factors, environment triggering autoimmune response, or infectious agents such as viruses, bacteria, and fungi
How Rheumatoid Arthritis affects the body
Rheumatoid factor (autoantibody) plus globulins make up immune complexes which activate the compliment system which causes INFLAMMATION

Involves synocial membranes of joints (most common manifestation) - inflammtion leads to swelling and thickening of synovial membrane (increasing ESR or erythrocyte sedimentary rate which is an indicator of inflammation)
Characteristics of Rheumatoid Arthritis
usually occurs between ages 25 and 55 and affects mostly young to middle aged females - may fluctuate substantially in severity

60% of RA patients are unable to work 10 years after disease onset

Most research suggests that life span is reduced five to ten years
Symptoms of Rheumatoid Arthritis
Heart - endocarditis, pericarditis, CHF, valvular fibrosis, MI (RA and other autoimmune patients have a raised risk for CHD)

Lungs - fibrosis and pleural effusion

Kidneys - amyloidosis (deposition of insoluble proteins in organ tissue)

GI Tract - anemia resulting from chronic disease and constant NSAID use (most RA patients are anemic)

Fibrin deposition (fibrosis) and necrosis are also present
Sclerotic Tissue
damaged tissue
Treatments for Rheumatoid Arthritis
NO CURE (just managing symptoms like decreasing pain)

NSAIDs
COX2 inhibitors
Corticosteroids
DMARDs
Exercise to maintain joint stability
Surgery (synovectomy or joint replacement)
Gene therapy (injection of genes tat produces desired protein bia a vector aka carious types of viruses)
DMARDs in Rheumatoid Arthritis
Disease Modifying Anti-Rheumatic Drugs

Methotrexate
-decreases TNF, neutrophils, histamine, lymphocyte number and function
-decrease growth of certain cells in blood, skin, GI Tract and immune system
-cytotoxic and inhibits metabolism causing decreased immune function
-developed in 1940s as chemotherapy for leukemia

Sulfasalazine - decreases immune function
Hydroxychloroquine (PLAQUENIL) - an antimalarial drug

Gold Salt injections
Major Difference between Rheumatoid Arthritis and Osteoarthritis
RA - Autoimmune disease
OA - degenerative disease/overuse injury
Nerve Diseases
Multiple Sclerosis
Parkinson's
Multiple Sclerosis Description
an autoimmune disease in which auto-reactive T cells cross the blood-brain barrier and attack the myelin sheath leading to a cascade of inflammation

The result is demyelination, acute axonal transection, gliosis and subsequent axonal degeneration
What are the most common types of Multiple Sclerosis?
Of the 4 types of multiple sclerosis the 2 most common are:
primary progressive (12.5%)relapsing-remitting (85%)
What are the causes of Multiple Sclerosis?
-autoimmune factors (exact antigen not identified)
-virus triggers (not proven)
-possible genetic predsposition
-various forms of physical trauma
Sympoms of Multiple Sclerosis
weakness, numbness ("pins and needles"), lossof balance, loss of coordination, bowel and bladder dysfunction, muscle spasticity, optic nerve neuritis
What is the nature of the symptoms of multiple sclerosis?
Symptoms are episodic
Therapies for Multiple Sclerosis
Immunomodulator drugs (decrease inflammatory effects of lymphocytes)
-inhibits cytokines which decreases inflammation and the number of episodes
-inteferon beta (1a and 1b) - AVONEX, BETASERON,REBIF First line drugs
-Glatimar Acetate - COPAXONE second line drug

Immunosuppressants (decrease inflammatory effects of lymphocytes, decrease inflammation) - third line drug
-Mixantrone, Cyclophosphamide, Methylprednisone, ACTH
-Danger of infecton from copromised immune system

Natalizumab - TYSABRI - precents activate lymphocytes from crossin blood-brain barrier

Weakness Therapies: dopamiergic drugs - similar to those for Parkinson's patients, exercise (WATER EXERCISE AND SWIMMING MOST BENEFICIAL)

Spacticity Therapies: reflex inhibitors (example is alpha2 agonists that inhibit spinl motor neurons), muscle relaxer drugs

Incontinence Therapies: muscarinic acetylcholine receptors antagonists (relaxes bladder detressor muscle), antidiuretic hormone analogs

Tremmor Therapies: anticonvulsant drugs

Visual Problem Theraies: corticosteroids to reduce ocular inflammation
Parkinson's Description
loss of production of the neurotransmitter dopamine in the basal ganglia (loss of 80% of dopamine producing cells) causes a disruption of balance between dopamine and Acetylcholine an therefore decreases volntary movement control
Causes of Parkinson's Disease
-free radical damage (theory)
-toxins (theory)
-age related decrease in dopamine producing neurons
-genetic predisposition
-repeated head trauma (boxing)
-illegal drug use
-hydrocephalus (CSF accumulation in venricle of the brain)
-encephalitis (most often viral - inflammation of white and gray brain matter)
Symptoms of Parkinson's Disease
resting tremor - "pill rolling" motion (70%)

bradykinesia (inability to generate movement)

Rigidity

postural instability

difficulty rising from sitting position

shuffling gait
Therapy for Parkinson's Disease
Levodopa: increase dopamine levels in the brain (the current gold standard of treatment)

Stem Cells: Increase dopamine neurons (Parkinson's is likey to be the first disease "cured" by stem cells)

Caechol-O-methylransferase inhibitors: inhibits levodopa's peripheral metabolism and causes more levodopa to be available for transport across blood-brain barrier

Dopamine Agonists: stimulate post-synaptic dopamine receptors

Monoamine Oxidase B Inhiitors: slow dopamine neuron degeneration

Embryonic tissue transplantation: not very successful so far

DBS Surgery: brain "pacemaker" sends electrons to parts of the brain (promising)
Muscle Diseases
Fibromyalgia
Muscular Dystrophy
Fibromyalga Description
chronic non-inflammatory pain in muscles and connecive tissues
Characteritics of Fibromyalgia
affects over 6 million Americans
Most people who have it are women 20-50 years old
Theoretical Causes of Fibromyalgia
Thyroid problems
Overgrowth of yeast bacteria
trauma
stress
hormone malfunction
infection
immune system dysfunction
autonomic nervous ystem malfunction
abnormal spinal cord pain processing
decreased gray brain matter density
dopaminergic neurotransmission in the brain
Symptoms of Fibromyalgia
"aching"
"unrefreshed by sleep"
GI problems
fatigue
anxiety and depression
"decreased energy"
presence of pain trigger points
What characteristic do all the symptoms of Fibromyalgia share?
All tend to be chronic, better one day and worse the next
Fibromyalgia s often associated with what other co-morbid conditions?
Anxiety
Migraine headache
depression
sleep disturbances
irritable bowel syndrome
restless leg syndrome
TMJ Syndrom
Chronic Fatigue Syndrome
How do you diagnose fibromyalgia?
Process of exclusion, if its not all these other things it has to be fibromyalgia
Therapy for fibromyalgia
stress reduction
exercise
growth hormone therapy
psychiatric help
acupuncture
NSAIDs
tricyclic antidepressants
muscle rlaxants of the cyclobenarine family
opiods
SSRI's
SNRI's
anticonvulsants
Muscular dystrophy description
an inherited disorer characerized by progressive proximal muscle weakness with destruction of muscle fiber and replacement with connective tissue
Common characteristics of Muscuar Dystrpohy (not symptoms)
diagnosed between 2 and 5
wheelchair by 10 or 12
eath in the 20's
blood creatine kinase is elevated (indicator of muscle damage)
some are mildly mentally challenged
Causes of Muscular Dystrophy
genetic related absence of dystrophin, a muscle membrane protein
Initial Symptoms of Muscular Dystrophy
"waddling" gait
falls
difficulty standing
difficulty climbing or descending stairs

all of these difficulties in locomotion cause muscle wastig, contractures (any condition that affects mobility or ROM of a joint and usually involves fiber depostion in skin, fascia, muscle, or joint capsul), cardiac involvement, respiratory muscle weakness with complications (such as respiratory infections)
Therapy for Muscular Dstrophy Patients
daily steroids produce long term symptom improvement, exercise should be continud as long as possible, surgery may be done to release contractures, pneumonia vaccine (prophylactic), physical therapy to delay development of contractures
Factors thought to contribute to fatigue and subsequent exercise induced muscle cramps
Exercising in hot, humi environments (due to dehydration and electrolyte deficiencies such as hyponatrmia/kalemia/calcaemia/magneasmia)

Overexertion (fatigue)causing muscle hypoxia

Disturbances in carbohydrate (hypoglycemia), fat, or protein metabolism

Nutritional deficiences inadequate amounts of elerolytes, vitamins b1 (thiamine), B% (pantothenic acid)
Why is pantothenic acid (or vitamin B5) important for exercise and reduction of Exercise Induced Muscle Cramps?
Pantothenic Acid is the backbone for Coenzyme A, which is used in the Krebs byble as acetyl coenzyme A, and is therefore important for enery production

It is also strongly correlated to strength gain without hypertrophy when in excess because it increases the amount of ATP available for use
Hypothesized Cramp Mechanisms supported by recent literature
Fatigue causes and increase in spindle firing rate and a decrease in GTO firing rte causing an increase in alpha motor neuron activity

Overproduction of reflex alpha motor neuron activity n a shortened muscle causes cramps
Factors thought to Contribute to Idiopathic Leg Cramps (although noconsensus on exact etiology)
Metabolic disturbance (hyponatremia, hypo/hyperkalaemia, hypocalcaemia, hypomagnesia, hypoglycaemia)
Chronic or severe acute diarrhea
Pregnancy, especially in late months
Cirrhosis of the liver (difficult digestion and electrolyte imbalance indirectly, decrease i albumin which maintains osmotic pressure and the bod cant regulate fluids down to the issue level)
Renal dialysis, possibly owing to plasma volume contraction
Thyroid disease (hyperthyroid myopathy and hypothyroidism)
Havy alcohol ingestion may induce severe muscle cramps
Lead tosicity
Disorders of the lower motor neurons (amyotrophic lateral ssclerosis ALS, MS, polyneuopathies involving the motor neurons, recovered poliomyelitis, peripheral nerve injury, and root compression)
Describe Hyperthyroid myopathy and hypothyroidism with symptoms and treatments
Hypertyroid Myopathy: autoimmune disease whose smptoms include palpitations, heatintolerance, weight loss, and nail looseness. It is treated with drugs to interfere with thyroid hormone production and radioactive iodine.

Hypothyroidism: weaknessand painful muscle spasms, decrease in protein and carbohydrate metabolism. Symptoms inclue fatigue, weakness, weight gain, coarse dry hair, dry skin. Treatment is Levothyroxine.
Treatment for cramps
Stretching - activation of GTO helps relax the muscle
Movement - walking allows muscle spindles to rese
Mssage
Cold application -reduces alpha motor neuron activity
transcutaneous electrical nerve stimulation
Quinine - (antimalaria, antipyretic, an analgesic drug) - used for chronic cramping and works by decreasingthe excitability of the motor end plate and increasing the refractory period of skeletal muscle
How do you help prevent cramps?
Stretching
Correction of muscle weaknesses and strength imbalances
Conditioning to prevent onset of fatigue
Strength training - reduce spindle sensitivty whih causes a decrease in reflex alpha motor neuron activity
Proper nutrition before and durig event (replacement of fluid and energy substrate decreases fatigue)
Common drugs that might cause or increase the risk for cramps
Beta blockers and Calcium channel blockers (these two are used for heart disease), beta agonists 2 (for kids with asthma), THORAZINE (for psychosis)

DANOZOL (corticosteroid fo endometriosis), LITHIUM, PREDNISONE, LASIX
Why is Gatorade not all that freat for regular exercisers or preventing cramps?
rare you dont get enough sodium in your diet so things like fatorade are not beneficial for the normal people, especially kids

May be useful after extremely intense or long bouts oexrcise where electrolytes may be depleted (marathons, two a day practices, etc)