Patho 3 Mus/Skel Barry
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| FRACTURES ARE DEFINED AS: | A BREAK IN THE CONTINUITY OF A BONE.
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| FRACTURES TYPICALLY OCCUR WHEN: | THE FORCE APPLIED EXCEEDS THE TENSILE OR COMPRESSIVE STRENGTH OF THE BONE.
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| THE HIGHEST INCIDENCE OF FRACTURES IS IN WHAT TWO GROUPS? | YOUNG MALES (15-24 yrs.) AND ADULTS
(65 yrs AND OLDER).
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| FRACTURES IN HEALTHY <BLANK> (TIBIA, CLAVICLE AND LOWER HUMERUS) USUALLY HAPPEN IN YOUNG PERSONS AS A RESULT OF <BLANK>. | LONG BONES, TRAUMA.
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| TRUE OR FALSE: FRACTURES OF THE HANDS AND FEET ARE USUALLY CAUSED BY TRAUMA. | FALSE. FRACTURES OF THE HANDS AND FEET ARE USUALLY CAUSED BY
ACCIDENTS IN THE WORKPLACE.
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| THE INCIDENCE OF FRACTURES OF THE UPPER FEMUR, UPPER HUMERUS, VERTEBRAE AND PELVIS IS HIGHER IN OLDER OR ELDERLY ADULTS AND OFTEN ASSOCIATED WITH WHAT? | OSTEOPOROSIS.
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| WHAT COMMON FRACTURES IN THE ELDERLY ARE OFTEN ASSOCIATED WITH OSTEOPOROSIS? | FRACTURES OF THE UPPER FEMUR, UPPER HUMERUS, VERTEBRAE AND PELVIS.
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| THREE CLASSIFICATIONS OF FRACTURES: | PATHOLOGIC, STRESS, TRANSCHONDRAL.
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| DEFINE PATHOLOGIC FRACTURE: | A BREAK AT THE SITE OF A PRE-EXISTING ABNORMAL CONDITION, BY A FORCE THAT WOULDN’T DO IT TO A NORMAL BONE.
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| EXAMPLES OF CONDITIONS THAT COULD PRECIPITATE A PATHOLOGIC FRACTURE: | TUMORS, OSTEOPOROSIS, INFECTIONS AND METABOLIC BONE DISORDERS.
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| DEFINE STRESS FRACTURE: | OCCURS IN NORMAL OR ABNORMAL BONE SUBJECTED TO REPEATED STRESS (ATHLETIC EVENTS). THE STRESS IS LESS THAN THE ONE USUALLY CAUSING THE FRACTURE.
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| TWO TYPES OF STRESS FRACTURE: | FATIGUE, INSUFFICIENCY.
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| DEFINE FATIGUE FRACTURE: | CAUSED BY ABNORMAL STRESS OR TORQUE APPLIED TO A BONE WITH NORMAL ABILITY TO DEFORM AND RECOVERY (JOGGERS, DANCERS).
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| DEFINE INSUFFICIENCY FRACTURE: | OCCURRING IN BONES LACKING NORMAL ABILITY TO DEFORM AND RECOVERY (NORMAL WEIGHT BEARING AND ACTIVITY)
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| DEFINE TRANSCHONDRAL FRACTURE: | FRAGMENTATION AND SEPARATION OF A PORTION OF THE ARTICULAR CARTILAGE THAT COVERS THE END OF A BONE AT A JOINT (HEAD OF THE FEMUR, ANKLE, PATELLA, ELBOW, WRIST).
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| ANOTHER WORD FOR TRANSCHONDRAL FRACTURE? | OSTEOCHONDRITIS DISSECANS
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| COMPLETE: | THE BONE IS BROKEN ALL THE WAY THROUGH.
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| INCOMPLETE: | INCOMPLETE: BONE DAMAGED BUT STILL IN ONE PIECE.
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| OPEN: | THE SKIN IS BROKEN.
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| CLOSED: | THE SKIN IS INTACT.
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| COMMINUTED: | BONE BREAKS INTO TWO OR MORE FRAGMENTS.
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| LINEAR: | RUNS PARALLEL TO THE LONG AXIS OF THE BONE.
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| OBLIQUE: | 45 DEGREE ANGLE TO THE SHAFT OF THE BONE.
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| SPIRAL: | ENCIRCLES THE BONE.
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| TRANSVERSE: | ACROSS THE BONE.
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| INCOMPLETE FRACTURES CAN BE OF THREE TYPES: | GREENSTICK, TORUS, BOWING.
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| GREENSTICK (A TYPE OF INCOMPLETE FRACTURE): | PERFORATES ONE CORTEX AND SPLINTERS THE SPONGY BONE (PROXIMAL DYAPHISIS OF TIBIA, RADIUS AND ULNA)
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| TORUS (A TYPE OF INCOMPLETE FRACTURE): | CORTEX BUCKLES BUT DOES NOT BREAK (OSTEOPOROSIS)
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| BOWING (A TYPE OF INCOMPLETE FRACTURE): | LONGITUDINAL FORCE APPLIED. COMMON IN RADIUS-ULNA AND TIBIA FIBULA. ONE BONE SUFFERS COMPLETE FRACTURE AND THE OTHER BOWS.
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| CLINICAL MANIFESTATIONS OF FRACTURE INCLUDE: | -IMPAIRED FUNCTION AND SENSATION
-DEFORMITY
-SWELLING
-MUSCLE SPASM
-TENDERNESS
-PAIN
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| FRACTURE TREATMENT INVOLVES | REDUCTION AND IMMOBILIZATION.
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| WHAT IS REDUCTION? | REALIGNING THE BONE FRAGMENTS CLOSE TO THEIR ANATOMICAL POSITION, WHICH SOMETIMES MUST BE OPEN (SURGICAL)
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| WHAT IS IMMOBILIZATION? | HOLDING THE ALREADY REDUCED BONE FRAGMENTS IN PLACE BY USING SPLINTS AND PLASTER CASTS.
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| ARTHROPATHIES: | A GROUP OF DISEASES AFFECTING THE JOINTS.
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| HOW ARE ARTHROPATHIES CATEGORIZED? | INFLAMMATORY AND NON-INFLAMMATORY.
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| NON-INFLAMMATORY ARTHROPATHIES: | NO SYNOVIAL MEMB.
INFLAMMATION, SYSTEMIC SIGNS AND
SYMPT. OR ABNORMAL SYNOVIAL FLUID.
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| INFLAMMATORY ARTHROPATHIES (ARTHRITIS): | :
--INFLAMMATORY DAMAGE OR
DESTRUCTION IN THE SYNOVIAL
ARTICULAR CARTILAGE OR MEMB.
--SYSTEMIC SIGNS OF INFLAMMATION
(FEVER, LEUKOCYTOSIS, ANOREXIA).
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| WHAT IS THE MOST PREVALENT NON-INFLAMMATORY JOINT DISEASE? | OSTEOARTHRITIS
(DEGENERATIVE JOINT DISEASE)
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| OSTEOARTHRITIS (DEGENERATIVE JOINT DISEASE) IS THE MOST PREVALENT NON-INFLAMMATORY JOINT DIS. CHARACTERIZED BY: | DEGENERATION AND LOSS OF ARTICULAR CARTILAGE IN SYNOVIAL JOINTS.
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| SOME CASES OF OSTEOARTHRITIS RESULT FROM JOINT STRESS, CONGENITAL ABNORMALITIES OR JOINT INSTABILITY CAUSED BY TRAUMA AND ARE KNOWN AS... | SECONDARY.
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| WHAT ARE CONDITIONS THAT CAUSE SECONDARY OSTEOARTHRITIS? | RESULT FROM JOINT STRESS, CONGENITAL ABNORMALITIES OR JOINT INSTABILITY CAUSED BY TRAUMA.
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| THE <BLANK> OR <BLANK> TYPE OF OA IS NOT ASSOCIATED TO ANY OF THESE RISK FACTORS AND IS THE MOST COMMON TYPE OF NON-INFLAMMATORY JOINT DISEASE.. | PRIMARY OR IDIOPATHIC.
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| THE PATHOLOGICAL CHARACTERISTICS ARE THE SAME FOR BOTH PRIMARY AND SECONDARY OA AND INCLUDE: | --EROSION AT THE ARTICULAR
CARTILAGE.
--SCLEROSIS OF BONE UNDERNEATH
THE CARTILAGE.
--FORMATION OF BONE SPURS
(OSTEOPHYTES).
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| CLINICAL MANIFESTATIONS OF OA INCLUDE: | --PAIN (PREDOMINANT SYMPTOM)
--STIFFNESS
--SWELLING OR ENLARGEMENT
--TENDERNESS
--LIMITED RANGE OF MOTION
--MUSCLE WASTING
--PARTIAL DISLOCATION
--DEFORMITY
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| DIAGNOSIS OF OA IS ESTABLISHED BY: | CLINICAL EXAM, SIMPLE BONE X-RAY, CAT-SCAN, MRI AND ARTHROSCOPY.
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| CONSERVATIVE TREATMENT FOR OA: | REST, ANALGESIC AND INFLAMMATORY DRUG THERAPY, WEIGHT LOSS IF OBESITY.
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| SURGICAL TREATMENT FOR OA: | USED TO IMPROVE JOINT MOV., CORRECT DEFORMITY OR CREATE A NEW JOINT WITH ARTIFICIAL IMPLANTS.
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| THE INFLAMMATORY JOINT DISEASE (ARTHRITIS) PRESENTS: | --INFLAMMATORY DAMAGE OR
DESTRUCTION IN THE SYNOVIAL
ARTICULAR CARTILAGE OR MEMB.
--SYSTEMIC SIGNS OF INFLAMMATION
(FEVER, LEUKOCYTOSIS, ANOREXIA).
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| INFLAMMATORY JOINT DISEASE CAN BE INFECTIOUS WITH INVASION HAPPENING... | THROUGH A TRAUMATIC OR SURGICAL WOUND, CONTAMINATED NEEDLE OR BLOODSTREAM (FROM SEPTIC FOCI).
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| INFLAMMATORY JOINT DISEASE CAN BE NON-INFECTIOUS (MOST COMMON) RESULTING FROM... | NON-INFECTIOUS (THE MOST COMMON) RESULTING FROM IMMUNE REACTIONS (RHEUMATOID ARTHRITIS AND ANKYLOSING SPONDYLITIS) OR DEPOSITION OF CRYSTALS OF URATE IN AND AROUND THE JOINT (GOUTY ARTHRITIS).
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| TRUE OR FALSE: RHEUMATOID ARTHRITIS IS A LOCALIZED AUTOIMMUNE DISEASE WHICH CAUSES CHRONIC INFLAMMATION OF CONNECTIVE TISSUE, PRIMARILY IN THE JOINTS. | FALSE. RHEUMATOID ARTHRITIS IS A SYSTEMIC AUTOIMMUNE DISEASE WHICH CAUSES CHRONIC INFLAMMATION OF
CONNECTIVE TISSUE, PRIMARILY IN THE JOINTS.
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| MOST COMMON JOINTS AFFECTED BY RH? | FINGERS, FEET, WRISTS, ELBOWS, ANKLES AND KNEES.
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| RA LEADS TO DEFORMITY WHICH LEADS TO... | LOSS OF FUNCTION.
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| WHAT COHORT MORE FREQUENTLY SUFFERS FROM RA? | WOMEN.
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| CLINICAL MANIFESTATIONS OF RA INCLUDE: | FEVER, FATIGUE, WEAKNESS, ANOREXIA, WEIGHT LOSS AND GENERALIZED ACHING AND STIFFNESS AS WELL AS PAINFUL, TENDER AND STIFF JOINTS, GRADUALLY LEADING TO DEFORMITY WHICH IS RESPONSIBLE FOR THE PHYSICAL LIMITATIONS.
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| RA DIAGNOSIS IS ESTABLISHED BY: | PHYSICAL EXAM, X-RAY OF THE JOINT AND SEROLOGIC TESTS FOR RHEUMATOID FACTOR AND CIRCULATING IMMUNE COMPLEXES.
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| RA TREATMENT? | CONSERVATIVE: REST, HOT AND COLD PACKS, CORTICOSTEROIDS, PHYSICAL THERAPY, ANTINEOPLASTIC DRUGS, ANTI-INFLAMMATORY DRUGS (ORALLY OR INJECTED INTO THE JOINT), SURGICAL.
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| THE MUSCULAR DYSTROPHIES ARE A GROUP OF FAMILIAL DISORDERS WHICH CAUSE... | DEGENERATION OF SKELETAL MUSCLE FIBERS.
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| THE MUSCULAR DYSTROPHIES ARE THE MOST PREVALENT OF THE MUSCULAR DISEASES IN CHILDHOOD AND ARE CHARACTERIZED BY: | PROGRESSIVE, SYMMETRIC WEAKNESS AND WASTING OF SKELETAL MUSCLE GROUPS WITH INCREASING DISABILITY AND DEFORMITY.
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| FIVE MAIN TYPES OF MUSCULAR DYSTROPHIES: | --PSEUDOHYPERTROPHIC (DUCHENNE)
--FACIOSCAPULOHUMERAL
--LIMB GIRDLE
--OCULOPHARYNGEAL
--MYOTONIC MUSCULAR
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| CLINICAL FINDINGS AND GENETIC INHERITANCE PATTERNS ARE CONSISTENT FOR EACH TYPE OF MUSCULAR DYSTROPHY BUT THE PHYSIOLOGY IS... | ABOUT THE SAME FOR ALL TYPES.
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| PHYSIOLOGY OF MUSCULAR DYSTROPHIES: | NECROSIS AND PHAGOCYTOSIS OF MUSC. CELLS AND EARLY FRAGMENTATION AND DISSOLUTION OF MYOFILAMENTS.
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| WHAT HAPPENS TO MUSCLE FIBERS IN MUSCULAR DYSTROPHIES? | THE MUSCLE FIBERS MAY BE SWOLLEN, SOME OF THEM HYPERTHROPHIC AND OTHERS ATROPHIC AND EVENTUALLY REPLACED BY FAT (FATTY INFILTRATION) AND CONNECTIVE TISSUE (FIBROSIS).
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| IF YOU OBSERVED UNDER THE MICROSCOPE A MUSCLE SAMPLE FROM A PATIENT WITH A MUSCULAR DYSTROPHY YOU WOULD SEE.. | THE INVOLVED MUSCLE FIBERS ARE RANDOMLY DISTRIBUTED, WITH NO DISTINCT PATTERN.
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| MOST COMMON OF THE MUSCULAR DYSTROPHIES: | DUCHENNE MUSCULAR DYSTROPHY.
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| DUCHENNE MUSCULAR DYSTROPHY IS THE MOST COMMON OF THE MUSCULAR DYSTROPHIES, DESCRIBED AS A... | PSEUDOHYPERTROPHIC MUSC. PARALYSIS.
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| CLASSIC DUCHENNE OCCURS ONLY IN <BLANK>, WITH HALF THE CASES SHOWING <BLANK> INHERITANCE. | BOYS, X-LINKED.
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| DUCHENNE MUSCULAR DYSTROPHY PATIENTS LACK <BLANK>, CAUSING CELL DEATH AND FIBER NECROSIS? | DYSTROPHIN.
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| CLINICAL MANIFESTATIONS OF DUCHENNE MUSCULAR DYSTROPHY? | THE DIS. IS USUALLY IDENTIFIED IN CHILDREN OF ABOUT 3 YRS OF AGE. SHOWING SLOW MOTOR DEVELOPMENT WITH PROGRESSIVE WEAKNESS AND
MUSC. WASTE.
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| MOTOR DEVELOPMENT PROBLEMS IN CHILDREN WITH DUCHENNE MUSCULAR DYSTROPHY? | SITTING, STANDING AND WALKING ARE DELAYED AND THE CHILD IS CLUMSY, FALLS FREQUENTLY AND HAS PROBLEMS CLIMBING STAIRS.
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| IN DUCHENNES MUSCULAR DYSTROPHY, WEAKNESS ALWAYS BEGINS IN THE... | PELVIC GIRDLE.
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| IN DUCHENNES MUSCULAR DYSTROPHY, <BLANK> IS EVIDENCED IN 80 PERCENT OF THE CASES. | CALF MUSCLE HYPERTROPHY.
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| IN DUCHENNES MUSCULAR DYSTROPHY, CONTRACTURES AND WASTING OF MUSCLES CONTRIBUTE TO... | MUSC. ATROPHY AND DEFORMITY OF THE SKELETON.
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| PATIENTS WITH DUCHENNES MUSCULAR DYSTROPHY SUFFER: | -PULMONARY COMPLICATIONS
-CARDIAC FAILURE
-MENTAL RETARDATION
-SMOOTH MUSC. DYSFUNCTION
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| PERCENTAGE OF CHILDREN WITH DUCHENNE MUSCULAR DYSTROPHY WHO HAVE CARDIAC FAILURE, PERCENTAGE WHO HAVE SOME CARDIAC INVOLVEMENT: | 50 PERCENT OF CHILDREN WITH CARDIAC FAILURE; SOME CARDIAC INVOLVEMENT IN UP TO 95 PERCENT OF THE CHILDREN.
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| IN CHILDREN WITH DUCHENNE MUSCULAR DYSTROPHY, SMOOTH MUSCLE DYSFUNCTION MAY CAUSE... | MEGACOLON, VOLVULUS, MALABSORPTION SYND. AND CRAMPING PAIN IN THE GI TRACT.
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| DIAGNOSIS OF DUCHENNE MUSCULAR DYSTROPHY IS CONFIRMED BY: | -ELECTROMYOGRAPHY (EMG),
-MEASUREMENT OF SERUM ENZYMES (CPK INCREASED MORE THAN 10 TIMES)
-MUSCLE BIOPSY.
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| WHAT DOES CPK STAND FOR? | CREATINE PHOSPHOKINASE.
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| WHAT DO WE DO FOR CHILDREN WITH DUCHENNE MUSCULAR DYSTROPHY? | THERE’S NO EFFECTIVE TREATMENT FOR THE DISEASE AND MAINTAINING FUNCTION IN UNAFFECTED MUSC. GROUPS FOR AS LONG AS POSSIBLE IS THE MAIN GOAL.
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| WHAT PERCENTAGE OF CHILDREN WITH DUCHENNE MUSCULAR DYSTROPHY REACH ADULTHOOD? WHAT DO THEY USUALLY DIE FROM? | ONLY 25% OF AFFECTED CHILDREN REACH THE AGE OF 21 YEARS, WITH
DEATH USUALLY RESULTING FROM
RESP. OR CARDIAC MUSCLE WEAKNESS.
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