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Patho 3 Mus/Skel
Patho 3 Mus/Skel Barry
| Question | Answer |
|---|---|
| FRACTURES ARE DEFINED AS: | A BREAK IN THE CONTINUITY OF A BONE. |
| FRACTURES TYPICALLY OCCUR WHEN: | THE FORCE APPLIED EXCEEDS THE TENSILE OR COMPRESSIVE STRENGTH OF THE BONE. |
| THE HIGHEST INCIDENCE OF FRACTURES IS IN WHAT TWO GROUPS? | YOUNG MALES (15-24 yrs.) AND ADULTS (65 yrs AND OLDER). |
| FRACTURES IN HEALTHY <BLANK> (TIBIA, CLAVICLE AND LOWER HUMERUS) USUALLY HAPPEN IN YOUNG PERSONS AS A RESULT OF <BLANK>. | LONG BONES, TRAUMA. |
| 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. |
| 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. |
| WHAT COMMON FRACTURES IN THE ELDERLY ARE OFTEN ASSOCIATED WITH OSTEOPOROSIS? | FRACTURES OF THE UPPER FEMUR, UPPER HUMERUS, VERTEBRAE AND PELVIS. |
| THREE CLASSIFICATIONS OF FRACTURES: | PATHOLOGIC, STRESS, TRANSCHONDRAL. |
| 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. |
| EXAMPLES OF CONDITIONS THAT COULD PRECIPITATE A PATHOLOGIC FRACTURE: | TUMORS, OSTEOPOROSIS, INFECTIONS AND METABOLIC BONE DISORDERS. |
| 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. |
| TWO TYPES OF STRESS FRACTURE: | FATIGUE, INSUFFICIENCY. |
| DEFINE FATIGUE FRACTURE: | CAUSED BY ABNORMAL STRESS OR TORQUE APPLIED TO A BONE WITH NORMAL ABILITY TO DEFORM AND RECOVERY (JOGGERS, DANCERS). |
| DEFINE INSUFFICIENCY FRACTURE: | OCCURRING IN BONES LACKING NORMAL ABILITY TO DEFORM AND RECOVERY (NORMAL WEIGHT BEARING AND ACTIVITY) |
| 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). |
| ANOTHER WORD FOR TRANSCHONDRAL FRACTURE? | OSTEOCHONDRITIS DISSECANS |
| COMPLETE: | THE BONE IS BROKEN ALL THE WAY THROUGH. |
| INCOMPLETE: | INCOMPLETE: BONE DAMAGED BUT STILL IN ONE PIECE. |
| OPEN: | THE SKIN IS BROKEN. |
| CLOSED: | THE SKIN IS INTACT. |
| COMMINUTED: | BONE BREAKS INTO TWO OR MORE FRAGMENTS. |
| LINEAR: | RUNS PARALLEL TO THE LONG AXIS OF THE BONE. |
| OBLIQUE: | 45 DEGREE ANGLE TO THE SHAFT OF THE BONE. |
| SPIRAL: | ENCIRCLES THE BONE. |
| TRANSVERSE: | ACROSS THE BONE. |
| INCOMPLETE FRACTURES CAN BE OF THREE TYPES: | GREENSTICK, TORUS, BOWING. |
| GREENSTICK (A TYPE OF INCOMPLETE FRACTURE): | PERFORATES ONE CORTEX AND SPLINTERS THE SPONGY BONE (PROXIMAL DYAPHISIS OF TIBIA, RADIUS AND ULNA) |
| TORUS (A TYPE OF INCOMPLETE FRACTURE): | CORTEX BUCKLES BUT DOES NOT BREAK (OSTEOPOROSIS) |
| 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. |
| CLINICAL MANIFESTATIONS OF FRACTURE INCLUDE: | -IMPAIRED FUNCTION AND SENSATION -DEFORMITY -SWELLING -MUSCLE SPASM -TENDERNESS -PAIN |
| FRACTURE TREATMENT INVOLVES | REDUCTION AND IMMOBILIZATION. |
| WHAT IS REDUCTION? | REALIGNING THE BONE FRAGMENTS CLOSE TO THEIR ANATOMICAL POSITION, WHICH SOMETIMES MUST BE OPEN (SURGICAL) |
| WHAT IS IMMOBILIZATION? | HOLDING THE ALREADY REDUCED BONE FRAGMENTS IN PLACE BY USING SPLINTS AND PLASTER CASTS. |
| ARTHROPATHIES: | A GROUP OF DISEASES AFFECTING THE JOINTS. |
| HOW ARE ARTHROPATHIES CATEGORIZED? | INFLAMMATORY AND NON-INFLAMMATORY. |
| NON-INFLAMMATORY ARTHROPATHIES: | NO SYNOVIAL MEMB. INFLAMMATION, SYSTEMIC SIGNS AND SYMPT. OR ABNORMAL SYNOVIAL FLUID. |
| INFLAMMATORY ARTHROPATHIES (ARTHRITIS): | : --INFLAMMATORY DAMAGE OR DESTRUCTION IN THE SYNOVIAL ARTICULAR CARTILAGE OR MEMB. --SYSTEMIC SIGNS OF INFLAMMATION (FEVER, LEUKOCYTOSIS, ANOREXIA). |
| WHAT IS THE MOST PREVALENT NON-INFLAMMATORY JOINT DISEASE? | OSTEOARTHRITIS (DEGENERATIVE JOINT DISEASE) |
| OSTEOARTHRITIS (DEGENERATIVE JOINT DISEASE) IS THE MOST PREVALENT NON-INFLAMMATORY JOINT DIS. CHARACTERIZED BY: | DEGENERATION AND LOSS OF ARTICULAR CARTILAGE IN SYNOVIAL JOINTS. |
| SOME CASES OF OSTEOARTHRITIS RESULT FROM JOINT STRESS, CONGENITAL ABNORMALITIES OR JOINT INSTABILITY CAUSED BY TRAUMA AND ARE KNOWN AS... | SECONDARY. |
| WHAT ARE CONDITIONS THAT CAUSE SECONDARY OSTEOARTHRITIS? | RESULT FROM JOINT STRESS, CONGENITAL ABNORMALITIES OR JOINT INSTABILITY CAUSED BY TRAUMA. |
| 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. |
| 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). |
| CLINICAL MANIFESTATIONS OF OA INCLUDE: | --PAIN (PREDOMINANT SYMPTOM) --STIFFNESS --SWELLING OR ENLARGEMENT --TENDERNESS --LIMITED RANGE OF MOTION --MUSCLE WASTING --PARTIAL DISLOCATION --DEFORMITY |
| DIAGNOSIS OF OA IS ESTABLISHED BY: | CLINICAL EXAM, SIMPLE BONE X-RAY, CAT-SCAN, MRI AND ARTHROSCOPY. |
| CONSERVATIVE TREATMENT FOR OA: | REST, ANALGESIC AND INFLAMMATORY DRUG THERAPY, WEIGHT LOSS IF OBESITY. |
| SURGICAL TREATMENT FOR OA: | USED TO IMPROVE JOINT MOV., CORRECT DEFORMITY OR CREATE A NEW JOINT WITH ARTIFICIAL IMPLANTS. |
| THE INFLAMMATORY JOINT DISEASE (ARTHRITIS) PRESENTS: | --INFLAMMATORY DAMAGE OR DESTRUCTION IN THE SYNOVIAL ARTICULAR CARTILAGE OR MEMB. --SYSTEMIC SIGNS OF INFLAMMATION (FEVER, LEUKOCYTOSIS, ANOREXIA). |
| INFLAMMATORY JOINT DISEASE CAN BE INFECTIOUS WITH INVASION HAPPENING... | THROUGH A TRAUMATIC OR SURGICAL WOUND, CONTAMINATED NEEDLE OR BLOODSTREAM (FROM SEPTIC FOCI). |
| 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). |
| 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. |
| MOST COMMON JOINTS AFFECTED BY RH? | FINGERS, FEET, WRISTS, ELBOWS, ANKLES AND KNEES. |
| RA LEADS TO DEFORMITY WHICH LEADS TO... | LOSS OF FUNCTION. |
| WHAT COHORT MORE FREQUENTLY SUFFERS FROM RA? | WOMEN. |
| 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. |
| RA DIAGNOSIS IS ESTABLISHED BY: | PHYSICAL EXAM, X-RAY OF THE JOINT AND SEROLOGIC TESTS FOR RHEUMATOID FACTOR AND CIRCULATING IMMUNE COMPLEXES. |
| RA TREATMENT? | CONSERVATIVE: REST, HOT AND COLD PACKS, CORTICOSTEROIDS, PHYSICAL THERAPY, ANTINEOPLASTIC DRUGS, ANTI-INFLAMMATORY DRUGS (ORALLY OR INJECTED INTO THE JOINT), SURGICAL. |
| THE MUSCULAR DYSTROPHIES ARE A GROUP OF FAMILIAL DISORDERS WHICH CAUSE... | DEGENERATION OF SKELETAL MUSCLE FIBERS. |
| 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. |
| FIVE MAIN TYPES OF MUSCULAR DYSTROPHIES: | --PSEUDOHYPERTROPHIC (DUCHENNE) --FACIOSCAPULOHUMERAL --LIMB GIRDLE --OCULOPHARYNGEAL --MYOTONIC MUSCULAR |
| CLINICAL FINDINGS AND GENETIC INHERITANCE PATTERNS ARE CONSISTENT FOR EACH TYPE OF MUSCULAR DYSTROPHY BUT THE PHYSIOLOGY IS... | ABOUT THE SAME FOR ALL TYPES. |
| PHYSIOLOGY OF MUSCULAR DYSTROPHIES: | NECROSIS AND PHAGOCYTOSIS OF MUSC. CELLS AND EARLY FRAGMENTATION AND DISSOLUTION OF MYOFILAMENTS. |
| 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). |
| 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. |
| MOST COMMON OF THE MUSCULAR DYSTROPHIES: | DUCHENNE MUSCULAR DYSTROPHY. |
| DUCHENNE MUSCULAR DYSTROPHY IS THE MOST COMMON OF THE MUSCULAR DYSTROPHIES, DESCRIBED AS A... | PSEUDOHYPERTROPHIC MUSC. PARALYSIS. |
| CLASSIC DUCHENNE OCCURS ONLY IN <BLANK>, WITH HALF THE CASES SHOWING <BLANK> INHERITANCE. | BOYS, X-LINKED. |
| DUCHENNE MUSCULAR DYSTROPHY PATIENTS LACK <BLANK>, CAUSING CELL DEATH AND FIBER NECROSIS? | DYSTROPHIN. |
| 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. |
| 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. |
| IN DUCHENNES MUSCULAR DYSTROPHY, WEAKNESS ALWAYS BEGINS IN THE... | PELVIC GIRDLE. |
| IN DUCHENNES MUSCULAR DYSTROPHY, <BLANK> IS EVIDENCED IN 80 PERCENT OF THE CASES. | CALF MUSCLE HYPERTROPHY. |
| IN DUCHENNES MUSCULAR DYSTROPHY, CONTRACTURES AND WASTING OF MUSCLES CONTRIBUTE TO... | MUSC. ATROPHY AND DEFORMITY OF THE SKELETON. |
| PATIENTS WITH DUCHENNES MUSCULAR DYSTROPHY SUFFER: | -PULMONARY COMPLICATIONS -CARDIAC FAILURE -MENTAL RETARDATION -SMOOTH MUSC. DYSFUNCTION |
| 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. |
| IN CHILDREN WITH DUCHENNE MUSCULAR DYSTROPHY, SMOOTH MUSCLE DYSFUNCTION MAY CAUSE... | MEGACOLON, VOLVULUS, MALABSORPTION SYND. AND CRAMPING PAIN IN THE GI TRACT. |
| DIAGNOSIS OF DUCHENNE MUSCULAR DYSTROPHY IS CONFIRMED BY: | -ELECTROMYOGRAPHY (EMG), -MEASUREMENT OF SERUM ENZYMES (CPK INCREASED MORE THAN 10 TIMES) -MUSCLE BIOPSY. |
| WHAT DOES CPK STAND FOR? | CREATINE PHOSPHOKINASE. |
| 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. |
| 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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