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98 Cards in this Set

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Indomethacin
Gout treatment
Works FAST
Side-effects: GI & CNS
NSAIDS for Gout
Indomethacin
Ibuprofen
Colchicine
Gout
Prevents tubulin polymerization -> prevents leukocyte migration & phagocytosis
Side effects: **GI (diarrhea)**, hair loss, bone marrow depression
2nd line to NSAIDS
Allopurinol
Inhibits formation of uric acid by inhibiting xanthine oxidase (XO)
Its metabolite also inhibits XO
Allopurinol Pharmacokinetics
Cleared by kidneys (know GFR!)
Long 1/2-life
Converted to an active metabolite
Allopurinol Side Effects
Mainly allergic (especially with ampicillin)
Exacerbation of disease with initial treatment (give colchicine or NSAIDS before starting)
Febuxostat
Similar to allopurinol
Better for patients with renal insufficiency
Uricosurics
Work in renal tubules to a decrease in uric acid re absorption
Use high doses
Probenecid
Blocks Uric Acid reabsorption
Don't use if urine flow is low
Don't use if patients excrete large amounts of uric acid already
Sulfinpyrazone
Blocks uric acid reabsorption
Side effects: GI
Choices for control of gout and prevent joint changes
1st: Allopurinol
2nd: Probenecid
3rd: Sulfinpyrazone
NSAIDS Properties
Analgesia
Antipyresis
Anti-inflammatory
Anti-platelet
NSAIDS MOA
Inhibits COX enzymes -> inhibition of prostaglandin synthesis
COX 1
Present all of the time
Protective/Maintenance
Location: Stomach, Intestine, Kidney, Platelet
COX 2
Inducible
Pro-inflammatory function
Bring prostaglanins to inflammatory sites -> macrophages
Aspirin
Non-selective COX inhibitor (irreversible)
Relieves mild pain
Interferes with hypothalamus -> reduce fever
Diflunisal
Flourinated derivative or salicylate
Non-selective COX inhibitor
No anti-pyretic affect
Median Nerve Motor
Flexors of forearm
Thenar emminence
1st two lumbricals
Median Never Sensory
Anterior palm digits 1, 2, 3, & 1/2 of 4
Thoracic Outlet compression (3 ways)
Elevated 1st rib
Compression by clavicle
Pec minor pulling coracoid process inferiorly
Ulnar Nerve Motor
2 muscles of anterior forearm compartment -> Flexor carpi ulnaris & Flexor digitorum profundus (ulnar head)
Intrinsic muscles of hand
Ulnar Nerve Sensory
Anterior and posterior 1/2 of 4 and 5 digits
Musculocutaneous Nerve Motor
Flexors of elbow (anterior arm compartment)
Musculocutaneous Nerve Sensory
Lateral forearm
Axillary Nerve Motor
Deltoid
Teres Minor
Flexes, extends, & aBducts shoulder
Radial Nerve Motor
Posterior arm compartment
Posterior forearm compartment
Anconius & supinator
Erb Duchenne Palsy
Superior trunk damage
Proximal arm problems
Waiter's Tip Sign
Fall on head
Klumpke Paralysis
Inferior trunk damage
Stretch arm from above
Distal (hand) problems
Superior Gluteal Never Motor & function
Gluteus medius & minimus
Tensor Fascia Lata
ABducts lower limb
Resists pelvic tilt during normal gait
Trendelenberg Sign
Stand on 1 foot and hip drops on that side
=Superior Gluteal Nerve Palsy
Inferior Gluteal Nerve Motor & function
Gluteus maximus
Extend hip (climbing stairs and getting up from a chair)
Femoral Nerve Motor & Function
Anterior thigh
Psoas
Iliacus
Flex hip and extend knee
Femoral Nerve Sensory
Medial thigh, leg, and heel (via saphenous nerve)
Obturator Nerve Motor
ADductors in medial compartment of thigh
Obturator Nerve Sensory
Medial thigh
Sciatic Nerve Branches
Tibial
Common Fibular
Tibial Nerve Motor in the thigh
Hamstrings
Common Fibular Nerve Motor in the thigh
Short head biceps femoris
Tibial Nerve Motor (lower leg) & Function
Deep and superficial posterior compartments of leg
Plantar flexion
Inversion
Toe flexion
Common Fibular Branches
Superficial Fibular
Deep Fibular
Superficial Fibular Nerve Motor & Function
Lateral lower leg
Eversion
Deep Fibular Nerve Motor & Function
Dorsiflexion
Toe extension
Muscle Spindle Fibers
Provide info on tension
Adjust tone to prevent injury
Relaxes antagonist muscle
Golgi Tendon Organs
Cause stretched muscle to relax
Contract antagonist
Prevents a muscle tear
UMN Lesion
Weakness
Increased tone
Increased reflex
LMN Lesion
Weakness
Atrophy
Fasiculations
Decreased reflex
Decreased tone
Most common manifestation of SLE
Polyarthralagia or arthritis
Rheumatoid Factor
Produced by B-cells of synovium
IgG or IgM Ab against Fc region of IgG
Citrullinated Peptides
Key in the diagnosis of rheumatoid arthritis
Where does Rheumatoid Arthritis typically begin?
Small joints of hands, wrists, ankles, knees, elbows, and shoulders
Joints in fingers affected by Rheumatoid Arthritis
PIP
MCP
NOT DIP
Subcutaneous Nodules on extensors surface of forearm?
Rheumatoid Arthritis
Diagnostic Criteria of Rheumatoid Arthritis
Morning stiffness
Arthritis in 3 or more joints
Arthritis of hand joints
Symmetric
Rheumatoid nodules
Serum Rheumatoid Factor (RF)
Radiologic changes
Felty's syndrome
Association of rheumatoid arthritis, splenomegaly, & neutropenia
Develops in patients with high titer rheumatoid factor, nodules, and HLA-DR4
TNF Alpha (in Rheumatoid Arthritis)
Activates inflammatory mechanisms
Stimulates endothelial cells
Cells breakdown surrounding matrix
Juvenille Rheumatoid (Idiopathic) Arthritis
<16 years old
1 or more joint
Both cellular and humoral immune abnormalities
Ankylosing Spondylitis
Chronic inflammation of sacroiliac joints, vertebrae, entheses
HLA-B27+
No RF
X-Linked (usually younger men)
Always stiff in morning
**Inflammation in eye**
Reactive Arthritis (Reiter's)
Arthritis, urethritis, & conjunctivitis
Usually affects males
Asymmetric
Usually lower extremity joints
Thought to be an immune response to an infection somewhere else in the body
HLA-B27 + (80%)
Myasthenia Gravis
Ab's against post-synaptic acetylcholine receptors at NMJ
Muscle Weakness
Myastenia Gravis is often associated with?
Thymomas
Thymic hyperplasia
What do all types of polymyositis & dermatomyositis have in common?
Skeletal muscle that is damaged by lymphocytic inflammation
polymyositis & dermatomyositis immunologic features
ANA +
Ab against cytoplasmic antigens
CD8+ T-cells and macrophage infiltration of involved muscle
Pro-inflammatory and cytotoxic cytokine production
Proximal muscle weakness
Think polymyositis & dermatomyositis
Heliotrope rash
dermatomyositis
Eyelids
Gottron's sign
dermatomyositis
Knuckles
Diagnostic criteria of polymyositis & dermatomyositis
Proximal muscle weakness
Biopsy evidence
Elevated muscle enzymes (CCK)
Anaerobes Usually Lack
Superoxide dismutase
Coverts O2- to O2 + H2O2
Clinical findings suggestive of anaerobes
Foul smell
Necrotic tissue with gas
Black discoloration
Predominate anatomical sites for anaerobic infection
Mouth
GI
Bacteroides fragilis
Gram - rod
Growth stimulated by bile
Think abdominal -> GI abscess
Pelvic inflammatory disease
Think below waste
Prevotella (Bacteriodes) melaninogenicus
Gram - coccobacilli
Oral and brain abscesses
Think above waist
Above waist infection think
Prevotella (Bacteriodes) melaninogenicus
Below waist infection think
Bacteroides fragilis
Tx of anaerobic infection
Debridement and drainage
Metronidazole or clindamycin
Fusobacterium nucleatum
Thin gram - rods
Fusiform shaped
Head, neck, & chest infections
Vincent's angina aka trench mouth
Fusobacterium nucleatum
Gram + spore formers
Most pathology due to toxins
Unable to infect healthy tissue
Will not produce toxin at high Eh
Clostridium perfringens
Normal habitat is GI and soil
Causes cellulitis & gas gangrene
Alpha toxin -> degrades mammalian cell membranes
Alpha toxin
Think Colstridium perfringens
Myonecrosis
Gas gangrene
Clostridium perfringens
Follows trauma/lack of circulation
Gram + box car-like rods
Zonal hemolysis
Clostridium perfingens -> gas gangrene
Clostridium tetani
Virulence factor -> tetanospasmin
Gram + rod
Terminal spores
Tetanospasmin
Clostridium tetani
Suppresses release of inhibitory NT's -> signals are unopposed and muscles are constantly stimulated
Clostridium botulinum
Toxin produces release of acetylcholine from alpha-motor neuron
No signals to muscle = flaccid paralysis
Clostridium difficile
Causes pseduomembraneous colitis
Enterotoxin (Toxin A) -> fluid production and mucosal damage
Cytotoxin(Toxin B) -> Kills mucosal cells
pseduomembraneous colitis
Clostridium difficile
Usually caused by selection via antibiotic treatment
Necrotizing Fasciitis Features
Extensive tissue destruction
Thrombosis of vessels
Bacteria spread through fascial planes
Differentiating necrotizing fasciitis vs cellulitis
**PAIN**
High fever
Toxic appearance
Type 1 Necrotizing Fasciitis
Mixed infections
Diabetes, ab surgery, perineal infection
Resembles gas gangrene
Unpleasant odor
Involved muscle still reacts to stimulation
Type 2 Necrotizing Fasciitis
Group A Strept
Rapid progression
Type 1 Necrotizing Fasciitis Diagnostic aids
Culture usually mixed
Anaerobic strept, group A strept, S. aureus
Increased leukocytes (left shift)
Increased ESR
Increased CCK
Gangrene with/without gas
With -> Clostridium
Without -> Strept pyogenes
Aeromonas hydrophilia myonecrosis
Motile Gram - rods
Live in fresh water
Oxidase positive
Rapid progression following penetrating trauma in freshwater environment
Tx -> Fluoroquinolone
Clinical Findings with Necrotizing Fasciitis
Lots of pain
Pt appears ill with rapid pulse and falling BP
Shock and renal failure may follow shortly
Rapid process and often fatal
Spontaneous, non-traumatic gas gangrene
Clostridium septicum
Usually associated with colon cancer, diverticulitis, or GI surgery
Neisseria Characteristics
Gram -
Diplicocci (coffee bean shape)
Oxidase positive
Clinical features of infectious arthritis
90% are mono-articular
Knee is most common, followed by hip
Swollen hot painful joint
Joints most susceptible to infection?
Previously damaged -> Increase adhesion factors