Reading...
Play button
Play button
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;
236 Cards in this Set
- Front
- Back
|
Name the 5 layers of the epidermis from outside in?
|
1) stratum corneum
2) stratum lucidum 3) stratum granulosum 4) stratum spinosum 5) stratum basalis |
|
|
From superficial to deep what are the epithelial cell junctions?
|
1) zona occludens (tight junctions)
2) zona adherens (intermediate junction) 3) macula adherens (desmosome) 4) gap junctions (connexins) |
|
|
What is the zona occludins composed of? what is its function? What is another name?
|
1) claudins
2) occludins 3) prevents diffusion across paracellular space 4) other name = tight junctions |
|
|
What is the function of the zona adherens? What is another name? what proteins are found?
|
1) surrounds perimeter of zona occludens
2) intermediate junction 3) has E-cadherins that connect to actin filaments |
|
|
What is another name for the macula adherens? What are they composed of?
|
1) desmosome
2) cadherins connect to intermediate filaments 3) filaments are keratin and desmoplakin form desmosome |
|
|
gap junctions are composed of what? What anchors epithelial cells to underlying extracellular matrix? What proteins are attached to these structures?
|
1) connexins
2) hemidesmosomes 3) integrins- maintain integrity of BM and binds laminin in BM |
|
|
What is damaged in the unhappy triad?
|
1) MCL
2) ACL 3) lateral meniscus (NOT medial meniscus) |
|
|
What do the "anterior" and "posterior" refer to in ACL and PCL?
|
site of tibial attachment
|
|
|
What does a positive anterior drawer test indicate?
|
ACL tear
|
|
|
Where is the pudendal nerve block given to relieve pain in pregnancy? What is landmark for a lumbar puncture? where is McBurneys point located?
|
1) ischial spine
2) iliac crest 3) 2/3 of way from umbilicus to ASIS |
|
|
What is the motion of suprispinatus? infraspinatus? teres minor? subscapularis?
|
1) helps deltoid abduct first 15 degrees
2) laterally rotates arm 3) adducts and laterally rotates arm 4) subscapularis medially rotates arm and adducts |
|
|
where does the supraspinatus insert? infraspinatus? teres minor? subscapularis?
|
1) superior facet of the greater tubercle of the humerus
2) middle facet of the greater tubercle of the humerus. 3) lowest part of greater tubercle of humerus 4) lesser tubercle of the humerus |
|
|
A fracture of the surgical neck of the humerus will damage what nerve? What nerve roots? where are sensory deficits and what is sign?
|
1) axillary nerve
2) C5, C6 3) can also occur with dislocaton of humerus 4) sensory deficit over shoulder 5) sign is flattened deltoid |
|
|
List 2 ways damage to lower trunk of brachial plexus can occur? what is deficit called?
|
1) compression by cervical rib
2) pancoast tumor 3) result is klumpkys palsy |
|
|
which nerve is compressed in axilla with a crutch? which nerve is damaged with a midshaft humerus fracture?
|
1) radial nerve
2) radial nerve runs in spiral groove |
|
|
subluxation of the radius stretches what nerve? fracture of the hook of hamate damages what nerve? a dislocated lunate damages which nerve?
|
1) radial nerve deep branch
2) ulnar 3) median |
|
|
fracture of medial epicondyle damages which nerve? which nerve is compressed by the supracondylar fracture of the humerus? pronator teres syndrome effects what nerve?
|
1) ulnar nerve
2) median nerve 3) median nerve |
|
|
which dermatomal level is the upper shoulder? lower shoulder and later arm? lateral forearm and part of antecubital fossa? thumb? index finger?
|
1) C4
2) C5 3) C6 4) C6 5) C6 |
|
|
which dermatomal level is the middle finder and mid palm? medial forearm and part of antecubital fossa? 4th and 5th digits?
|
1) C7
2) T1 3) C8 |
|
|
what innervates the interossei and adductor pollicis? The flexor ratinaculum connects what bones?
|
1) branches of deep ulnar nerve
2) a. medially: hook of hamate and pisiform b. laterally: trapezium and scaphoid |
|
|
The median nerve provides sensory info from which part of hand?
|
1) dorsal and palmer surface of digits 2 and 3 and half 4
2) palmar surface of thumb, thenar and half of palm |
|
|
The ulnar nerve provides sensory info from which parts of the hand?
|
1) entire 5th digit and half of 4th digit on dorsal and palmer surface
2) hypothenar and medial half of dorsal hand |
|
|
What canal does the ulnar nerve run through in the hand? Waiters tip hand is also known as? It is caused by damage to what part of brachial plexus?
|
1) Guyons canal
2) Erbs palsy 3) damage to upper trunk (C5,C6) |
|
|
Total claw hand is also called? What part of brachial plexus is damaged?
|
1) klumpkes palsy
2) lower trunk (C8,T1) |
|
|
Wrist drop is caused by damage to what part of brachial plexus? Saturday night palsy is from what?
|
1) posterior cord
2) compression of radial nerve, also produces wrist drop |
|
|
Damage to musculocutaneous nerve leads to?
|
1) difficulty flexing elbow
2) sensory loss to lateral forearm |
|
|
Winged scapula is damage to what nerve? Ape hand results from? Popes blessing or claw hand is from damage to what?
|
1) long thoracic
2) median nerve damage 3) ulnar nerve |
|
|
If the clavicle fractures what protects the brachial plexus from damage?
|
1) subclavius muscle
2) The Subclavius depresses the shoulder, carrying it downward and forward. It draws the clavicle inferiorly as well as anteriorly |
|
|
the radial nerve is composed of what levels? What are motor deficits? Sensory deficits? What sign is present?
|
1) C5-C8
Motor deficits: 1) wrist extension 2) Finger extension at MCP joints 3) supination 4) thumb extension and abduction Sensory deficits: 1) posterior arm 2) dorsal hand and thumb Sign: 1) wrist drop |
|
|
the median nerve is composed of which levels? What are motor deficits after a supracondylar humerus fracture? What about with carpal tunnel syndrome?
|
1) C6-C8 and T1
Motor deficits proximal: 1) opposition of thumb 2) lateral finger flexion 3) wrist flexion Motor deficits distal: 1) opposition of thumb |
|
|
Median nerve Sensory deficits with a supracondylar humerus fracture are? what about with carpal tunnel syndrome?
|
Sensory deficits proximal:
1) dorsal and palmer aspects of lateral 3.5 fingers and thenar Sensory deficits distal: 1) dorsal and palmer aspects of lateral 3.5 fingers |
|
|
what sign is present with a supracondylar humerus fracture as opposed to carpal tunnel syndrome?
|
1) ape hand with proximal fracture
2) ulnar deviation of wrist upon wrist flexion with carpal tunnel syndrome |
|
|
The ulnar nerve is composed of what nerve levels? what are motor deficits of a medial epicondyle humerus fracture versus a fracture of hook of hamate?
|
1) C8 and T1
Proxiaml fracture: 1) medial finger flexion 2) wrist flexion 3) abduction and adduction of fingers (interossei) 4) adduction of thumb 5) extension of 4th and 5th digits (lumbricals) Distal fracture: 1) abduction and adduction of fingers (interossei) 2) adduction of thumb 3) extension of 4th and 5th digits (lumbricals) |
|
|
What is the sensory deficit with ulnar nerve palsy?
|
Sensory deficits:
1) medial 1.5 fingers 2) hypothenar eminance Proximal fracture sign: 1) radial deviation upon wrist flexion Distal fracture sign: 1) ulnar claw hand, aka popes blessing or hand of benediction |
|
|
Musculocutaneous is composed of which nerve roots? How is it injured? What motor deficit is present? what sensory deficit?
|
1) C5-C7
2) upper trunk compression 3) flexion of forearm 4) lateral forearm |
|
|
What are findings in erb-duchennes palsy?
|
1) waiter's tip = upper trunk of brachial plexus C5-C6
Findings: 1) limb hangs at side 2) medially rotated 3) forearm pronated |
|
|
what are findings in klumpkes palsy?
|
1) atrophy of thenar and hypothenar eminences
2) atrophy of interosseous muscles 3) sensory deficits on medial side of forearm and hand 4) disappearance of radial pulse upon moving head toward the side of palsy (Adsons test) |
|
|
What causes the median nerve claw? Note this is not ape claw! How does it present?
|
1) distal median nerve lesion after branch containing C5-C7 branches off and feeds forearm flexors
2) loss of lateral lumbricals 3) 2nd and 3rd digits are clawed Note: ape hand has loss of oppens pollicis muscle causing loss of thumb abduction |
|
|
which muscles does the radial nerve supply?
|
1) brachioradialis
2) extensors of wrists and fingers 3) supinator 4) triceps |
|
|
How is the obturator nerve damaged? What is the motor deficit? Sensory deficit?
|
1) anterior hip dislocation
2) thigh adduction 3) medial thigh |
|
|
How is the femoral nerve damaged? What is motor deficit? sensory deficit?
|
1) pelvic fracture
2) thigh flexion and leg extension 3) anterior thigh and medial leg |
|
|
How is the common peroneal nerve damaged? What is the motor deficit? What is the sensory deficit?
|
1) trauma to lateral aspect of leg or fibula neck fracture
2) foot eversion and dorsiflexion and toe extension 3) anterolateral leg and dorsal aspect of foot |
|
|
How is the tibial nerve damaged? what is the motor deficit? sensory deficit?
|
1) knee trauma
2) foot inversion, plantarflexion, toe flexion 3) sole of foot |
|
|
How is the superior gluteal muscle damaged? what is motor deficit? sensory deficit?
|
1) posterior hip dislocation or polio
2) thigh abduction (+trendelenberg from glut medius weakness) 3) none |
|
|
How is the inferior gluteal nerve damaged? What is the motor deficit? sensory deficit?
|
1) posterior hip dislocation
2) can't jump, climb stairs, or rise from seated position 3) none |
|
|
Which muscles comprise the thenar eminence? hypothenar? what is function of both?
|
Thenar:
1) opponens pollicis 2) abductor pollicis brevis 3) flexor pollicis brevis Hypothenar: 1) opponens digiti minimi 2) abductor digiti minimi 3) flexor digiti minimi Function: 1) oppose 2) abduct 3) flex (OAF) |
|
|
What is the function of the dorsal interosseous muscles? Palmer interosseous muscles? Lumbricals?
|
1) abduct fingers
2) adduct fingers 3) flex at MCP joint |
|
|
When an action potential travels down the T-tubule of a skeletal muscle what are the events that follow?
|
1) depolarization of voltage sensitive dihydropyridine receptor which is coupled to ryanodine receptor on SR
2) conformational change occurs and Ca is released from SR 3) Ca2+ binds troponin C which moves tropomyosin out the myosin-binding groove on actin filaments 4) myosin head releases ADP and is displaced on actin filament (power stroke) 5) contraction results in shortening of H zone and I band |
|
|
Which structures of sarcomere do NOT shorten during muscle contraction? Which do shorten?
|
1) A band never shortens
2) H zone, I band |
|
|
The sarcomere runs from what to what? the Z line is composed of what? Triangular structures of M line are what?
|
1) I band to I band
2) actin 3) myosin |
|
|
Where is the dihydropyridine recpetor located? What about ryanodine receptor?
|
1) T-tubule membrane
2) SR |
|
|
What are the 4 stages of the skeletal and cardiac muscle contraction?
|
1) cocked state = myosin head bound to ADP and phosphate
2) myosin binds actin (cross-bridge) = Ca2+ bound to troponin C displaces tropomyosin 3) release of phosphate (power stroke) = after power stroke ADP is released 4) released state = myosin and actin separate when ATP binds myosin head Note that lack of ATP causes rigor mortis |
|
|
What is the entire process for smooth muscle contraction?
|
1) action potential and membrane depolarization
2) VG Ca2+ channels open 3) increased Ca2+ in cytoplasm 4) Ca2+ binds calmodulin 5) activates myosin light chain kinase 6) kinase phosphorylates myosin 7) myosin-P then binds actin forming cross-bridge and contraction 8) myosin light chain phosphatase removes P 9) get relaxation |
|
|
What is endochondral ossification? How does it occur?
|
1) longitudinal bone growth
2) cartilaginous model 3) later replaced with woven and lamellar bone |
|
|
Which bones are formed from membraneous ossification? How?
|
1) flat bones of skull and face, also axial skeleton
2) woven bone formed directly without cartilage model and later becomes lamellar bone |
|
|
Is longitudinal bone growth or membraneous bone growth effected in achondroplasia?
|
1) both
2) Longitudinal = short limbs 3) membraneous = larger than normal head and skull |
|
|
What is inactivated in achondroplasia? what are mutations associated with? How is lifespan and fertility effected?
|
1) AD though >85% seen to be sporadic
2) mutated FGFR3 which inhibits chondrocyte proliferation 3) associated with increased paternal age 4) normal lifespan and fertility |
|
|
What is primarily effected in osteoporosis? How is mineralization effected?
|
reduction primarily in trabecular (spongy) bone mass in spite of normal bone mineralization
|
|
|
Who does type I osteoporosis occur in? What is it due to?
|
1) postmenopausal women
2) due to low estrogen 3) estrogen prophylaxis is controversial |
|
|
Who does type II osteoporosis occur in? what drugs are contraindicated in osteoporosis in general?
|
1) senile osteoporosis
2) affects men and women >70 3) glucocorticoids |
|
|
what are common presenting features of osteoporsis?
|
1) vertebral fractures:
a. acute back pain b. loss of height c. kyphosis 2) femoral neck fracture 3) distal radius (colles) fracture |
|
|
What is prophylaxis and treatment of osteoporosis?
|
Prophylaxis:
1) exercise and calcium before 30 Treatment: 1) estrogen and/or calcitonin 2) bisphosphonates 3) pulsatile PTH for severe cases |
|
|
Osteopetrosis is also known as? How is it characterized?
|
1) marble bone disease
2) failure of normal bone resorption resulting in thick dense bones that are prone to fracture |
|
|
What is cell is defective in osteopetrosis? How are serum Ca2+, phosphate, AP effected?
|
1) defective osteoclasts
2) calcium, phosphate, and AP are all NORMAL |
|
|
What is the genetic deficiency in osteopetrosis? How is blood cell production impacted? What do X-rays show? what sensory and motor deficits can occur?
|
1) carbonic anhydrase II
2) narrowing of marrow cavity leads to pancytopenia 3) Erlenmyer flask bones that flare out 4) cranial nerve impingement and palsies |
|
|
What is wrong in osteomalacia and rickets? What is deficient?
|
1) defective mineralization/calcifaction of osteoid causing soft bones
2) vitamin D deficiency |
|
|
How are Ca2+, PTH, AP and phosphate effected in osteomalacia/rickets?
|
1) decreased calcium
2) increased PTH 3) decreased phosphate 4) AP normal |
|
|
Osteitis fibrosa cystica is also known as? What causes it?
|
1) von Recklinghausen disease of bone
2) hyperparathyroidism |
|
|
What are characterisitic findings in osteitis fibrosa cystica? how are Ca2+, phophate, PTH and AP effected?
|
1) brown tumors = cystic spaces lined by osteoclasts filled with fibrous stroma and sometimes blood
2) high Ca2+, low phosphorous, high AP, high PTH |
|
|
Pagets disease is also called? Who gets it? What cells are overactive?
|
1) osteitis deformans
2) people over 40 and women more than men 3) increased osteblastic and osteoclastic activity results in abnormal bone architecture |
|
|
What is a possible cause for pagets disease of bone? How are calcium, phosphorous, PTH and AP effected? what can it progress to?
|
1) paramyxovirus
2) noraml Ca2+, phosphorous, PTH and increased AP 3) osteogenic sarcoma |
|
|
How do the bones appear in Paget's disease of bone? How is heart effected?
|
1) mosaic bone pattern
2) long bone chalk-stick fractures 3) indirectly by arteriovenous shunts leading to high output cardiac failure |
|
|
A 70 year old woman has notice that her hat size has increased and she has had hearing loss. Blood analysis shows high AP. what is diagnosis?
|
1) pagets disease of bone
2) hearing loss from narrowing of foramina |
|
|
What occurs polyostotic fibrous dysplasia?
|
1) bone is replaced by fibroblasts, collagen and irregular bony trabeculae
2) multiple bones effected |
|
|
McCune-Albright syndrome is a form of what bone disease? How does it present?
|
1) polyostotic fibrous dysplasia
2) multiple unilateral bone lesions 3) endocrine abnormalities (precocious puberty) 4) cafe-au-lait spots resembling coast of main |
|
|
What is osteoma associated with? What happens with the tumor? where does it often occur?
|
1) Gardner's syndrome
2) new piece of bone grows on another piece of bone 3) often occurs in the skull |
|
|
How is osteoid osteoma characterized? Who does it generally occur in?
|
1) interlacing trabeculae of woven bone surrounded by osteoblasts
2) <2cm and found in proximal tibia and femur 3) men <25 |
|
|
How is osteoblastoma characterized?
|
1) interlacing trabeculae of woven bone surrounded by osteoblasts similar to osteoid osteoma but larger and found in vertebral column
|
|
|
Giant cell tumor is also called? where does it commonly occur? In what age group?
|
1) osteoclastoma
2) epiphyseal end of long bones especially in distal femur and proximal tibia 3) women more than men 20-40 |
|
|
What are characteristic diagnostic findings of a giant cell tumor?
|
1) double bubble or soap bubble on x-ray
2) spindle-shaped cells with multinucleated giant cells |
|
|
what is the most common benign bone tumor? what else is it called? where does it occur and how does it present?
|
1) osteochondroma = exostosis
2) mature bone with a cartilagenous cap in the metaphysis in long bones |
|
|
Who does osteochondroma occur more in? What can it rarely transform into?
|
1) men <25
2) chondrosarcoma |
|
|
Where do endochondromas occur? Compare it to where condrosarcomas occur?
|
1) benign cartilaginous neoplasm in intramedullary cavity of bone
2) usually distal extremities 3) chondrosarcomas occur in proximal areas like pelvis, spine, scapula, humerus, tibia and femur |
|
|
Osteosarcoma is also called? This is the second most common primary malignant bone tumor. what is first?
|
1) osteogenic sarcoma
2) multiple myeloma |
|
|
What age group is most effected by osteosarcoma? what bones are effected?
|
1) men 10-20
2) metaphysis of long bones, often distal femur, proximal tibia |
|
|
What are predisposing factors to osteogenic sarcoma?
|
1) Pagets disease of bone
2) bone infarcts 3) radiation 4) familial RETINOBLASTOMA |
|
|
Codmans triangle is seen on x-ray of distal femur. What is disease? what other sign may be seen? what is prognosis?
|
1) osteogenic sarcoma
2) sunburst pattern (from elevation of periosteum) 3) poor |
|
|
Who does ewings sarcoma occur in? What do cells look like? How does bone appear?
|
1) boys <15
2) anaplastic small blue cells 3) onion skin appearance of bone |
|
|
Where does Ewings sarcoma occur? What are genetics?
|
1) diaphysis of long bones, pelvis, scapula, ribs
2) 11;22 translocation |
|
|
Chondrosarcoma is benign or malignant? who is it common in? Where is it located? What disease may person previously have had? How does it appear with bone marrow cavity?
|
1) malignant
2) men 30-60 3) pelvis, spine, scapula, humerus, tibia, femur 4) osteosarcoma is risk factor 5) expansitile glistening mass within medullary cavity |
|
|
Which bone tumors primarily occur at epiphysis? which predominate at metaphysis?
|
1) giant cells tumor
2) osteochondroma and osteosarcoma 3) osteoid osteoma and ewing sarcoma 4) endochondroma and chondrosarcoma |
|
|
What are findings in osteoarthritis?
|
1) wear and tear of joints with destruction of articular cartilage
2) subchondral cysts 3) sclerosis 4) osteophytes (bone spurs) 5) eburnation (polished ivory like appearance) 6) heberdens nodes (DIPs) 7) bouchards (PIP) |
|
|
Is osteoarthritis inflammatory or noninflammatory? When is pain worse? What happens if it occurs in knees?
|
1) non-inflammatory
2) pain with weight-bearing and at end of day 3) if in knees cartilage loss begins medially and person becomes bow-legged |
|
|
How does rheumatoid arthritis effect the joints?
|
1) pannus formation in MCP and PIP
2) subcutaneous rheumatoid nodules 3) ulnar deviation 4) subluxation 5) bakers cyst |
|
|
Are the DIPs involved in RA or osteoarthritis? microscopically how do rheumatoid nodules look?
|
1) DIPs (heberdens nodes) are in osteoarthritis
2) fibrinoid necrosis surrounded by palisading histiocytes |
|
|
Who does RA effect more? What type of hypersensitivity?
|
1) women>men
2) type III |
|
|
RF is positive in how often in RA? What is RF? What is most specific antibody but less sensitive than RF?
|
1) 80%
2) anti-IgG antibody (binds Fc portion) 3) anti-CCP (anti-cyclic citrullinated protein antibodies) |
|
|
What genetic association is there with RA? What is the classic presentation of RA?
|
1) HLA-DR4
2) morning stiffness >30min improved with use 3) symmetric joint involvement 4) systemic symptoms a. fever b. fatigue c. pleuritis d. pericarditis |
|
|
What 3 finger abnormalities occur in RA?
|
1) Boutonnieres = (PIP hyperflexion with DIP hyperextension).
2) Swan-neck = (DIP hyperflexion with PIP hyperextension) 3) Z-thumb deformity |
|
|
What is the classic triad of Sjogrens syndrome?
|
1) xeropthalmia = dry eyes, conjunctivitis, sand in eyes
2) xerostomia = dry mouth, dysphagia 3) arthritis |
|
|
Which gland is enlarged in sjogrens? What is there increased risk of developing?
|
1) parotid gland
2) increased risk of B cell lymphoma and dental caries |
|
|
What autoantibodies are found in Sjogrens?
|
1) anti-ribonucleoprotein
2) SS-A (Ro) 3) SS-B (La) |
|
|
Who does Sjogrens primarily affect? What is it associated with?
|
1) females 40-60
2) RA |
|
|
What is sicca syndrome? How are the joints effected?
|
1) dry eyes
2) dry mouth 3) nasal and vaginal dryness 4) chronic bronchitis 5) reflux esophagitis 6) NO arthritis |
|
|
Does gout cause symmetric or asymmetric joint inflammation? How do the joints present clinically?
|
1) assymetric distribution
2) joints are swollen, painful, and red |
|
|
What is the classic manifestation of gout? where do tophi form in gout?
|
1) painful MTP joint of big toe (called podagra)
2) external ear, olecranon bursa, or Achilles tendon |
|
|
What can precipitate acute attacks of gout?
|
1) large meal
2) alcohol consumption |
|
|
how does alcohol consumption precipitate gout?
|
1) alcohol metabolites compete for same excretion sites in kidney as uric acid, causing decreased uric acid secretion and subsequent buildup in blood
|
|
|
What conditions or diseases precipitate monosodium urate crystals in joints?
|
hyperuricemia due to:
1) Lesch-Nyhan 2) PRPP excess 3) decreased excretion of uric acid (thiazides) 4) increased cell turnover (chemotherapy) 5) von Gierkes disease |
|
|
Are most cases of gout due to overproduction or undersecretion of uric acid? How are the crystals characterized in gout? Who is gout more common in?
|
1) 90% underexcretion and 10% overproduction
2) negatively birefringement = yellow crystals when under parallel light 4) Crystals are needle shaped 3) men |
|
|
What is pseudogout? How do crystals appear?
|
1) calcium pyrophosphate cyrstals deposited in joint space
2) basophilic rhomboid crystals that are weakly positively birefringent |
|
|
What joints are effected by pseudogout? Who is affected most? What is prophylaxis for pseudogout?
|
1) large joints like the knee
2) people >50 3) both sexes equally 4) colchicine |
|
|
How do gout crystals appear when parallel to light and perpendicular to light? What about pseudogout?
|
Gout:
1) parallel = yellow crystals 2) perpendicular = blue Pseudogout: 1) parallel = blue crystals 2) perpendicular = yellow |
|
|
What are 3 cocci that cause septic arthritis?
|
1) S aureus
2) streptococcus 3) N gonorrhoae |
|
|
How does gonococcal arthritis present?
|
1) monoarticular
2) migratory arthritis with asymmetrical pattern 3) joint is swollen, red and painful |
|
|
What are chronic causes of infectious arthritis?
|
1) TB from dissemination
2) lyme disease |
|
|
What are examples of seronegative spondyloarthropathies? Why are they considered seronegative? What is the genetic association?
|
1) All are seronegative because they cause arthritis but are RF negative
2) HLA-B27 (gene that codes for MHC I) Diseases: 1) ankylosing spondylitis 2) reactive arthritis (reiters syndrome) 3) psoriatic arthritis 4) inflammatory bowel disease |
|
|
Who are seronegative spondyloarthropathies more common in? What does HLA-B27 code for?
|
1) men
2) gene for HLA MHC I |
|
|
In akylosing spondylitis what parts of body are effected?
|
1) chronic inflammatory disease of spine and SI joints
a. leads to fusion 2) uveitis 3) aortitic regurgitation |
|
|
What is the classic triad of reactive arthritis? What is another name?
|
Reiters syndrome
1) conjunctivitis and anterior uveitis 2) urethritis 3) arthritis |
|
|
How does psoriatic arthritis present? is it symmetric? What is finding in fingers? What is seen on x-ray?
|
1) joint pain and stiffness associated with psoriasis
a. asymmetric patchy involvment 2) dactylitis = sausage fingers 3) pencil in a cup deformity (only in 1/3 of patients with psoriasis |
|
|
Bamboo spine is seen in who? dactylitis is seen in who? pencil in a cup deformity is seen in who?
|
1) ankylosing spondylitis
2) psoriatic arthritis 3) psoriatic arthritis |
|
|
SLE occurs in who? which race?
|
1) 90% in females
2) black women more affected and have severe form |
|
|
What are general presenting symptoms of SLE? how is the heart effected? vascular system? pulmonary? kidneys? skin?
|
General:
1) fever 2) fatigue 3) weight loss Specific: 1) nonbacterial verrucous endocarditis 2) hilar adenopathy 3) Raynauds phenomena 4) wire-loop lesions in kidney from immune deposition 5) Malar and discoid rash 6) serositis 7) photosensitivity 8) mucosisitis (oropharyngeal ulcers) |
|
|
What is death usually from in SLE? What type of lesion and syndrome develop in this organ?
|
1) death from chronic renal failure
2) wire-loop lesions in kidney from immune complexes 3) develop nephritic syndrome |
|
|
Someone with SLE can test positive for what? Why?
|
1) syphilis via the RPR/VDRL test
2) due to antiphospholipid antibodies which cross react with cardiolipin |
|
|
What antibodies are detected in SLE? which are sensitive and specific? Which determine a poor prognosis?
|
1) ANA = sensitive but not specific
2) anti-dsDNA = very specific and poor prognosis 3) anti-smith antibodies = very specific but not prognostic |
|
|
What is the antibody for drug induced lupus?
|
antihistone
|
|
|
A 20 year old black female presents with oropharyngeal ulcers, arthritis and photosensitivity. What do you suspect?
|
SLE
|
|
|
ANA is positive in what diseases?
|
1) SLE
2) sjogrens and sicca 3) scleroderma 4) polymyositis 5) dermatomyositis 6) RA 7) JRA 8) MCT disease |
|
|
How is sarcoidosis characterized? 5 things
|
1) gammaglobulinemia
2) RA 3) ACE increased 4) Interstitial fibrosis 5) noncaseating granulomas |
|
|
Who is sarcoidosis more common in? How does it effect the lungs?
|
1) black females
2) restrictive lung disease 3) B/L hilar lymphadenopathy |
|
|
How does sarcoidosis effect the skin? What nerve is effected? How are the eye and parotid gland effected?
|
1) erythema nodosum
2) Bells palsy CN VII 3) epithelial granulomas 4) uveoparotitis |
|
|
What do the epithelial granulomas of sarcoidosis contain? Why is there hypercalcemia? How is sarcoidosis treated?
|
1) Schaumann bodies and asteroid bodies
2) epitheliod macrophages contain 1alpha-hydroxylase 3) steroids |
|
|
What are symptoms of polymyalgia rheumatica?
|
1) pain and stiffness in shoulders and hips
2) fever 3) malaise 4) weight loss |
|
|
Is there muscle weakness in polymylalgia rheumatica? Who does it occur in? what is it associated with?
|
1) no muscle weakness
2) people >50 3) temporal arteritis |
|
|
What are lab findings in polymyalgia rheumatica? How is it treated?
|
1) increased ESR and normal CK
2) Prednisone |
|
|
What are symptoms of polymyositis? what cell is predominately involved? how is it diagnosed?
|
1) progressive symmetric muscle weakness
a. involves shoulders usually 2) CD8+ injury of myofibers 3) muscle biopsy of inflammation is diagnostic |
|
|
What are symptoms of dermatomyositis?
|
1) proximal muscle weakness like polymyositis
2) malar rash (similar to SLE) 3) HELIOTROPE rash (shawl and face rash) 4) gottrons papules 5) mechanics hands |
|
|
What is there increased risk of in dermatomyositis? what antibodies are detected? What are lab findings?
|
1) increased risk of malignancy
2) increased CK 3) increased aldolase 4) positive ANA 5) anti-Jo-1 |
|
|
Gottrons papules are seen on a patient and there is a malar rash with shoulder weakness. What is disease?
|
1) dermatomyositis
2) also have heliotrope rash (shawl and face rash) |
|
|
What is the most common neuromuscular junction disorder? What are antibodies directed toward? What are symptoms and treatment?
|
1) MG
2) anti-AChR 3) cause ptosis, diplopia and generalized weakness 4) reverse symptoms with AChE inhibitors |
|
|
What is pathologic process in Lambert-Eaton? Where is weakness? Can AChE inhibitors be used?
|
1) autoantibodies to presynaptic Ca2+ channel blockers
2) results in decreased ACh release 3) proximal muscle weakness 4) no reversal with AChE inhibitors |
|
|
What is lambert-eaton syndrome associated with? when do symptoms improve?
|
1) paraneoplastic diseases like small cell cancer
2) improve with muscle use |
|
|
A smoker of 48 years come to clinic. Central chest mass is noted on x-ray. He has proximal muscle weakness that improves with activity. What does he have?
|
1) small cell cancer with paraneoplastic syndrome causing Lambert-Eaton
|
|
|
What are findings in MCT disease?
|
1) Raynauds phenomena
2) Fatigue 3) arthralgias 4) myalgias 5) esophageal hypomotility |
|
|
What are autoantibodies found in MCT disease?
|
1) ANA
2) anti-U1RNP |
|
|
what is scleroderma in general? How does skin appear? what are involved organs?
|
1) excessive fibrosis and collagen deposition throughout body
2) skin is puffy and taut without wrinkles 3) sclerosis of other organs: a. renal b. pulmonary c. cardiovascular d. GI |
|
|
Who does scleroderma occur in mostly? How is the diffuse form of scleroderma characterized?
|
1) 75% female
2) a. widespread skin involvement b. rapid progression c. early visceral involvement 3) anti-Scl-70 antibody (anti-DNA topoisomerase I antibody) |
|
|
What happens in CREST syndrome?
|
1) Calcinosis
2) Raynauds phenomenon 3) Esophageal dysmotility 4) Sclerodactyly 5) Telangectasia |
|
|
How is CREST different from the diffuse form of scleroderma?
|
1) CREST has limited skin involvement often confined to fingers and face
2) more benign 3) has antiCentromere antibody |
|
|
How are lipomas characterized? How are liposarcomas characterized?
|
1) soft, encapsulated, benign and easily excised and cured
2) malignant large fat tumor that tends to recur unless deeply excised |
|
|
How is a rhabdomyoma characterized? how is a rhabdomyosarcoma characterized?
|
1) benign tumor of striated muscle (skeletal or cardiac)
2) malignant tumor of skeletal muscle that is most often in head or neck |
|
|
What is rhabdomyoma associated with? What is the most common soft tissue tumor of children?
|
1) tuberous sclerosis
2) rhabdomyosarcoma |
|
|
describe a macule and disease it occurs with? patch? papule?
|
1) flat discoloration <1cm = tinea versicolor
2) macule >1cm 3) elevated skin lesion <1cm = acne vulgaris |
|
|
Describe a plaque and condition it occurs in? vesicle? wheal?
|
1) papule >1cm = psoriasis
2) small fluid containing blister = chickenpox 3) transient vesicle = Hives |
|
|
Describe a bulla and condition it occurs in? keloid? pustule?
|
1) large fluid containing blister = bullous pemphigoid
2) irregular, raised lesion from scar hypertrophy = T pertenue (yaws) 3) blister containing pus |
|
|
Describe hyperkeratosis and a condition it is seen in? parakeratosis? crust?
|
1) thickened stratum corneum = psoriasis
2) hyperkeratosis with retention of nuclei in stratum corneum = psoriasis 3) dried exudates from vesicle, bulla or pustule = impetigo |
|
|
Describe acantholysis and a condition it is seen in? acanthosis?
|
1) separation of epidermal cells = pemphigus vulgaris
2) epidermal hyperplasia (increased spinosum) |
|
|
How are verrucae described? what is another name?
|
1) warts
2) soft tan-colored, cauliflowered lesions 3) epidermal hyperplasia 4) hyperkeratosis 5) koilocytosis |
|
|
verruca vulgaris is common where? condylomata accuminatum occur where and from what?
|
1) hands and feet
2) genital from HPV |
|
|
What is nevocellular nevus? How are urticaria characterized?
|
1) common benign mole
2) hives a. intensely pruritic wheals that form after mast cell degranulation |
|
|
Ephelis is what? How are melanocytes effected?
|
1) freckle
2) normal number of melanocytes 3) increased melanin pigment |
|
|
A pruritic eruption commonly on skin flexures could be what? what could it be associated with?
|
1) atopic dermatitis (eczema)
2) asthma and allergic rhinitis |
|
|
How is allergic contact dermatitis characterized?
|
1) Type IV hypersensivity
2) lesion at site of contact |
|
|
What are features of psoriasis?
|
1) papules or plaques with silvery scaling, especially on knees and elbows
2) acanthosis with parakeratotic scaling (nuclei still in stratum corneum) |
|
|
How are the layers of the epidermis effected in psoriasis?
|
1) increased stratum spinosum
2) decreased stratum granulsom |
|
|
What is Auspitz sign? What disease is it associated with? What are other signs that may be present?
|
1) seen in psoriasis
2) Auspitz = bleeding spots when scales are scraped off 3) nail pitting and psoriatic arthritis are also seen |
|
|
What are features of seborrheic keratosis epithelium?
|
1) Flat
2) Greasy 3) pigmented squamous epithelial proliferation with keratin filled cysts (horn cysts) |
|
|
Where does seborrheic keratosis appear on body? How does it look? Who is it common in?
|
1) lesions on head, neck, trunk, extremities
2) skin looks "pasted on" 3) common benign neoplasm in older people |
|
|
Leser-Trelat sign is seen in what disease? What are features of sign? What does it indicate?
|
1) Seborrheic keratosis
2) sudden appearance of multiple seborrheic keratoses 3) indicates underlying malignancy possibly of GI or lymphoid |
|
|
What are causes of albinism?
|
1) normal melanocyte number with decreased melanin production from decreased tyrosinase activity (common)
2) failure of neuralcrest cell migration (less common) |
|
|
What is vitiligo? is it from decreased melanocytes or just decreased melanin production?
|
1) irregular areas of complete depigmentation
2) decreased melanocytes |
|
|
Melasma is seen in what?
|
Hyperpigmentation due to:
1) pregnancy (mask of pregnancy) 2) OCP |
|
|
How does impetigo present? What are causes? is it contagious?
|
1) very superficial skin infection
2) honey-colored crusting 3) S aureus, S pyogenes 4) highly contagious |
|
|
how does cellulitis present? What is cause?
|
1) acute, painful spreading infection of dermis and subcutaneous tissue
2) S pyogenes and S aureus |
|
|
How is necrotizing fascitis characterized? What causes? what is also known as?
|
1) deep tissue injury
2) anearobic bacteria and S pyogenes 3) results in crepitus from methane and CO2 production 4) Flesh eating bacteria |
|
|
Staph scalded skin syndrome causes destruction where? who does it occur in? How does it present?
|
1) exotoxin destroying keratinocyte attachments in stratum granulosum only
2) newborns and children have fever, generalized red rash with sloughing of upper layers of epidermis |
|
|
How does hairy leukoplakia present? What causes?
|
1) White, painless plaques on the tongue that cannot be scraped off
2) EBV |
|
|
what is attacked in pephigus vulgaris? what pattern is seen with immunflouresence?
|
1) IgG attacks desmosomes (anti-epithelial cell antibody)
2) antibodies are around epidermis in a reticular or netlike pattern |
|
|
Nikolsky's sign is present in what disorder? What type of skin dysfunction is observed?
|
1) pemphigus vulgaris
2) sign is separation of epidermis with stroking of skin 3) acantholysis is seen = intraepidermal bullae involving skin and oral mucosa |
|
|
How is the immunoflouresence pattern different between pemphigous vulgaris and bullous pemphigoid? Which skin protein is attacked in each?
|
1) PV = reticular or netlike pattern
2) BP = linear pattern 3) PV = antibody to desomosome 4) BP = antibody to hemidesomosome |
|
|
How is bullus pemphigoid characterized pathologically?
|
1) IgG against hemidesmosome
2) epidermal basement membrane resulting in bullae 3) bullae on skin and oral mucosa |
|
|
What cell type is seen in blisters of bullous pemphigoid? How is the less severe form characterized? What pattern is seen with immunoflouresence?
|
1) eosinophils
2) bullae on skin but spares oral mucosa 3) linear pattern |
|
|
Dermatitis herpetiformis is associated with what? What is pathogenesis?
|
1) celiacs disease
2) IgA deposits at tips of papillae 3) pruitic papules and vesicles |
|
|
Erythema multiforme is associated with what?
|
Infections:
1) mycoplasma pneumoniae 2) HSV Drugs: 1) sulfa drugs 2) Beta-lactams 3) phenytoin Cancers Autoimmune diseases |
|
|
How does erythema multiforme present?
|
1) macules
2) papules 3) vesicles 4) target lesions - red papules with a red center |
|
|
How is steven-johnson syndrome characterized? Does it have a high mortality rate? what is a more severe form of it called?
|
1) fever
2) bulla 3) necrosis 4) sloughing of skin 5) high mortality 6) Toxic epidermal necrolysis |
|
|
How is Lichen planus characterized? Where does skin damage occur? What is it associated with?
|
1) Pruitic, Purple, Polygonal Papules
2) Sawtooth infiltrate of lymphocytes at dermal-epidermal junction 3) associated with Hep C |
|
|
What is actinic keratosis? How is it characterized? What is there a risk of developing?
|
1) premalignant lesions caused by sun exposure
2) small, rough, red-brown papules 3) cutaneous horn 4) carcinoma is proportion to degree of dysplasia |
|
|
A cutaneous horn is a feature of what disorder and horn cysts are a feature of which disorder?
|
1) cutaneous horn = actinic keratosis
2) horn cyst = seborrheic keratosis |
|
|
How is acanthosis nigricans characterized? What diseases cause it?
|
1) hyperplasia of stratum spinosum
Associated diseases: 1) hyperinsulinemia from Cushings or diabetes 2) visceral malignancy |
|
|
Where does erythema nodosum present?
|
1) inflammatory lesions of subcutaneous fat usually on anterior shins
Associations: 1) coccidioidomycosis 2) histoplasmosis 3) TB 4) leprosy 5) streptococcal infections 6) sarcoidosis |
|
|
How is pityriasis characterized? How is it treated?
|
1) herald patch initially followed by christmas tree distribution
2) multiple papular eruptions 3) remits spontaneously |
|
|
When is a strawberry hemangioma seen?
|
1) first few weeks of life
2) grows rapidly then regresses spontaneously by 5-8 |
|
|
When are cherry hemiangiomas seen?
|
1) people 30-40
2) does not regress like strawberry hemangioma of infant |
|
|
Squamous cell carcinoma of skin is very common. What is it associated with? where do they commonly appear? Do they invade and metastisize?
|
1) associated with sunlight and arsenic exposure and draining sinuses
2) commonly occur on hands and face 3) locally invasive but rarely metastisize |
|
|
how does squamous cell carcinoma present? What is a precursor skin lesion?
|
1) ulcerative red lesion
2) keratin pearls under microscope 3) actinic keratosis |
|
|
What is a variant of squamous cell carcinoma? How does it progress?
|
1) keratoacanthoma
2) grows rapidly in 4-6 weeks 3) regresses spontaneously (4-8 weeks) |
|
|
where is basal cell carcinoma most common? Is it locally invasive or metastatic?
|
1) sun-exposed areas
2) locally invasive almost never metastisizes |
|
|
What are gross and microscopic features of basal cell carcinoma?
|
1) rolled edges with central ulceration
2) pearly papules commonly with telangectasias 3) palisading nuclei |
|
|
What serum marker is used for melanoma? Who does it primarily occur in? What correlates with metastisis of tumor?
|
1) S-100
2) sun exposed fair skin people in particular 3) DEPTH correlates with metastisis |
|
|
What is precursor to melanoma? How does melanoma appear grossly?
|
1) dysplastic nevus (atypical mole)
2) dark lesion with irregular borders |
|
|
Which leukotriene attracts neutrophils? Which cause bronchonstriction and what other functions do these have?
|
1) neutrophils = LTB4
2) bronchonstriction = LTC4, D4, E4 a. these 3 also cause vasoconstriction, contraction of smooth muscle, increased vascular permeability |
|
|
What is the effect of PGI2?
|
1) inhibits platelet aggregation
2) vasodilation 3) decreased uterine tone |
|
|
Do corticosteroids effect the synthesis of leukotrienes or prostacyclins, prostaglandins and thromboxanes? What else do they effect?
|
1) all by inhibiting phospholipase A2
2) protein synthesis of COX enzymes |
|
|
What is the function of phospholipase A2? What drug inhibits lipoxygenase?
|
1) remove arachidonic acid from membrane lipid phosphatidylinositol
2) Zileuton |
|
|
What are effects of PGE2?
|
1) decreased vascular tone
2) increased pain 3) increased uterine contraction 4) increased body temp |
|
|
What is the function of TXA2?
|
1) increase platelet aggregation
2) vasoconstriction |
|
|
What is the MOA of aspirin?
|
1) irreversibly inhibits COX with covalent bond
2) decreases thromboxanes and prostaglandins |
|
|
Clinically how is aspirin used based on dose?
|
1) low dose (<300mg/day) = antiplatelet
2) intermediate dose (300-2400mg/day)= antipyretic and analgesic 3) High dose (2400-4000mg/day) = anti-inflammatory |
|
|
What are toxic effects of aspirin?
|
1) GI upset
Chronic use: 1) acute renal failure 2) interstitial nephritis 3) upper GI bleed Note: causes Reyes syndrome in children with viral infection |
|
|
What are examples of NSAIDs? What is the there MOA?
|
1) ibuprofen
2) naproxen 3) indomethicin 4) ketorolac MOA = reversibly inhibit COX1 and COX2 |
|
|
Clinically what are NSAIDs used for? Which is used to close a PDA?
|
1) anitpyretic
2) analgesic 3) anti-inflammatory 4) indomethacin for PDA Note: these do note have anti-platelet effect |
|
|
What are toxic effects of taking NSAIDs?
|
1) renal damage
2) fluid retention 3) aplastic anemia 4) GI distress 5) ulcers |
|
|
What is a COX2 inhibitor? is it reversible or irreversible? Where is COX2 found? What symptoms does it help reduce?
|
1) celecoxib
2) COX2 = inflammatory cells, vascular endothelium 3) inflammation and pain |
|
|
celecoxib has benefit of not causing what in GI tract like NSAIDs? What diseases is it used to treat?
|
1) ulcers because COX1 is found in GI tract
2) RA and osteoarthritis |
|
|
What are toxicities of COX2 inhibitors?
|
1) increased thrombosis
2) sulfa allergy 3) lower incidence of GI ulcers |
|
|
What is the MOA of acetaminophen? Where in body does it primarily act?
|
1) reversible COX inhibitor
2) works mostly in CNS and is inactivated peripherally |
|
|
Clinically what is acetaminophen used for?
|
1) antipyretic
2) analgesic 3) lacks anti-inflammatory 4) used instead of aspirin to prevent Reyes |
|
|
What are toxic effects of acetaminophen? What is antidote for toxicity?
|
1) hepatic necrosis
2) deplete glutathione forming toxic tissue adducts in liver 3) antidote is N-acetylcysteine |
|
|
Which NSAID is given that has no anti-inflammatory response? Which is given if fa person needs antiplatelet effects?
|
1) acetaminophen
2) aspirin |
|
|
Which drugs are bisphosphonates?
|
1) etidronate
2) pamidronate 3) alendronate 4) risedronate |
|
|
What is the MOA of bisphosphonates?
|
1) inhibit osteoclastic activity
2) reduce formation and resorption of hydroxyapeptite |
|
|
Clinically what are bisphosphonates given for?
|
1) malignancy associated with hypercalcemia
2) Pagets disease of bone 3) postmenopausal osteoporosis |
|
|
What are toxic effects of bisphosphonates?
|
1) corrosive esophagitis
2) nausea 3) diarrhea |
|
|
What drug is used to treat acute gout? What is its MOA? What is another drug that is less toxic and often used in acute gout?
|
1) colchicine
2) binds and stabilizes tubulin to inhibit polymerization in leukocytes impairing chemotaxis and degranulation 3) indomethacin |
|
|
when is probenicid given? What is its MOA? What drug can be increased if given at same time?
|
1) chronic gout
2) inhibits reabsorption of uric acid in PCT a. also inhibits secretion of penicillin |
|
|
What diseases is allopurinol given for?
|
1) chronic gout, lymphoma and leukemia
2) inhibits xanthine oxidase a. which decreases xanthine to uric acid b. |
|
|
How does allopurinol help in lymphoma and leukemias? Which drugs are increased if taken at same time?
|
1) prevents tumor lysis associated urate nephropathy
2) azathioprine and 6-MP both of which are metabolized by xanthine oxidase |
|
|
Why should salicylates never be given in gout patients?
|
1) all but high doses depress uric acid clearance
2) even at 5-6g/day still have a minor effect on uricosuric activity |
|
|
Which two drugs should not be given for acute gout?
|
1) probenicid
2) allopurinol |
|
|
What is the MOA of etanercept?
|
1) fake form of TNF receptor that binds TNF in blood
Uses: 1) RA 2) psoriasis 3) ankylosising spondylitis |
|
|
What is the MOA of infliximab?
|
1) anti-TNF antibody
Uses: 1) crohns disease 2) RA 3) ankylosing spondylitis |
|
|
What is the MOA of adalimunab? What are its uses?
|
1) binds directly to TNF-alpha
Uses: 1) RA 2) psoriasis 3) ankylosising spondylitis |
|
|
low dose salicylates and diuretics effect uric acid elimination from kidney how?
|
prevent tubular secretion
|
