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AGPC 4 > AGPC4 Final Exam > Flashcards

AGPC4 Final Exam Flashcards

1
Q

What are the expected CBC values in iron deficiency anemia?

A
  • low Hgb/Hct
  • MCV < 80 fL (average size of RBCs is reduced/microcytic anemia)
  • mean corpuscular hemoglobin concentration (MCHC - amount of Hgb per unit volume) < 33 g/dL
  • red cell distribution width (RDW) > 15% (normal is < 12% - cells are different sizes because they are produced by different processes => older cells larger than younger cells)
  • low reticulocyte count (lack of iron reduces RBC production)
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2
Q

What are the expected lab values in iron deficiency anemia?

A
  • low ferritin (normal = 200-300 ng/dL) => best indicator of iron deficiency (ferritin is a protein in cells that stores iron and allows body to use it when needed)
  • low Hgb/Hct
  • mean corpuscular volume (MCV) < 80 fL
  • red cell distribution width (RDW) > 15% (normal is < 12% - cells are different sizes because they are produced by different processes => older cells larger than younger cells)
  • low serum iron (n = 50-150 ng/dL)
  • low % transferrin saturation (n = 20-50%) => decreased in IDA because more transferrin is being produced but low levels of iron are available to bind
  • high total iron binding capacity (TIBC) (n = 25-450 ng/dL) => increases to provide more potential iron binding sites
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3
Q

What are the expected lab values in thalassemia?

A
  • severely decreased mean corpuscular volume (MCV - disproportionate to Hgb) => hallmark of thalassemia
  • low Hgb/Hct
  • normal RDW => all cells produced are small (little variation in size)
  • normal serum iron => Thalassemia does not affect iron
  • normal ferritin
  • normal transerrin saturation
  • normal TIBC
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4
Q

What are the expected lab values in thalassemia?

A
  • severely decreased mean corpuscular volume (MCV - disproportionate to Hgb) => hallmark of thalassemia
  • low Hgb/Hct
  • normal RDW
  • normal serum iron
  • normal ferritin
  • normal transerrin saturation
  • normal TIBC
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5
Q

What are the expected lab values in cobalamin (B12) deficiency anemia?

A
  • low serum B12 => hallmark of B12 deficiency anemia
  • elevated serum methylmalonic acid (MMA - substance necessary for metabolism and energy production => rises when B12 levels fall)
  • MCV > 100 fL
  • low reticulocyte count
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6
Q

What are the expected lab values in folate deficiency?

A
  • low serum folate => hallmark of folate deficiency anemia
  • normal serum methylmalonic acid
  • MCV > 100 fL
  • low reticulocyte count
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7
Q

What are the expected lab values in hemophilia?

A
  • increased PTT => hemophilia affects Factors VIII or IX - part of the intrinsic pathway
  • Factor VIII (Type A) or IX (Type B) decreased
  • normal platelet number
  • normal PT (does not affect components of the extrinsic pathway)
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8
Q

What are the expected lab values in von Willebrant Disease?

A
  • increased PTT => abnormality in platelet adhesion (causes Factor VIII to be unstable)
  • normal platelet number
  • normal PT (does not affect components of the extrinsic pathway)
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9
Q

What are the expected lab values in idiopathic thrombocytopenic purpura (ITP)?

A
  • decreased number of platelets => antibodies adhere to platelets and macrophages carry them to the spleen where they are destroyed
  • normal PTT (not a disorder of Factors)
  • normal PT (not a disorder in Factors)
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10
Q

What are the expected lab values in thrombophilia?

A
  • abnormal Protein C
  • abnormal Protein S
  • normal Factor V Leiden (level is normal - problem is mutation)
  • normal PT/INR
  • abnormal PTT
  • normal platelets
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11
Q

What is the first step in management of iron deficiency anemia?

A

determine the etiology - conduct colonoscopy to r/o occult GI bleeding

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12
Q

What is the treatment for iron deficiency anemia?

A
  • severely symptomatic PTs (myocardial ischemia) => RBC transfusion (1 pack = increase 1 g of iron)
  • all others => oral iron supplementation
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13
Q

What is the PT education for iron supplementation?

A
  • S/E include: nausea, constipation, heartburn, black stool
  • absorption is optimal 30 minutes before meals, but will increase gastric S/E
  • orange juice increases absorption
  • antacids, caffeine, calcium, H2 blockers, PPIs decrease absorption
  • store in locked cabinet (iron overload accounts for 30% of fatal medication overdoses in children)
  • treatment will be for 4-6 months or until ferritin level is normal
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14
Q

What is the treatment for B12 deficiency (pernicious anemia)?

A
  • parenteral (IM) therapy weekly to monthly for the rest of life
    => watch for hypokalemia
    => hematologic response is rapid (increase in reticulocyte count within 7 days) but full response takes 2 months
    => neurological changes are irreversible if deficiency has been prolonged
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15
Q

What is the treatment for folate deficiency?

A

oral folate replacement (1 mg po daily)

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16
Q

What are the signs and symptoms of B12 and folate deficiency?

A
  • common: weakness, fatigue, atrophic glossitis, stomatitis
  • unique to B12: neurological manifestations - parasthesia (first and most common), ataxia, loss of vibratory sense, + Romberg sign, dementia
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17
Q

What is the clinical presentation of anemia?

A

common to all types (severity of anemia causes symptoms, not etiology):

  • decreased O2 capacity => tiredness, exercise intolerance, poor concentration, pallor, angina
  • cardiac compensation (increased stroke volume and HR) => palpitations, dyspnea on exertion, systolic murmur
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18
Q

What are signs and symptoms unique to particular types of anemia?

A
  • IDA: pica, restless leg syndrome
  • anemia of chronic disease: s/s of chronic health conditions
  • thalassemia: within 1st year of life - severe anemia, failure to thrive, irritability, bone hyperplasia (“chipmunk face”)
  • B12: parasthesia, atrophic glossitis, stomatitis
  • folate: atrophic glossitis, stomatitis
  • hemolytic anemias: jaundice
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19
Q

What distinguishes bleeding due to platelet dysfunction from dysfunction in Factors?

A
  • primary hemostasis disorders (platelets): superficial (mucosal) bleeding, skin bleeding (petechia < 0.5 cm, purpura 0.5-1.0 cm), non-blanchable (out of the blood vessel)
  • secondary hemostasis disorders (clotting factors): deep bleeding in joints, bruises in muscles
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20
Q

What is the treatment for von Willebrant disease?

A

desmopressin (deamino-d-arginine vassopressin/DDAVP) - synthetic ADH given IV or intra-nasally => induces endothelial cells to release VWF from stores (those affected do not completely lack VWF - it is just not released)

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21
Q

What is the treatment for hemophilia?

A

clotting factor replacement (recombinant Factor VIII [type A] or IX [type B])
=> given 3X/week for life (prophylactically)
=> give additional Factors when injury occurs
=> give plasma in setting of heavy bleeding
=> analgesia and immobilization for acute hemarthrosis

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22
Q

What diseases are common to PTs with Trisomy 21 (Down Syndrome)?

A

mental retardation, leukemia, pelvic dysplasia, cardiac defects, celiac disease, obstructive sleep apnea, Alzheimer’s

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23
Q

What diseases are common to PTs with x-linked mutation (Turner Syndrome/45,X monosomy)?

A
  • premature ovarian failure, lack of breast development by age 13
  • otitis media, left-sided cardiac abnormalities, strabismus, glucose intolerance, congenital heart disease, renal abnormalities, HTN, osteoporosis, autoimmune diseases
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24
Q

What diseases are common to PTs with an extra X chromosome (Klinefelter’s/46,XXY or 47,XXY)?

A
  • hypospadias, small phallus, cryptorchidism, gynecomastia, infertility
  • osteoporosis, autoimmune disorders, Type 2 DM, autoimmune thyroiditis, breast carcinoma
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25
Q

Which common diseases have a genetic inheritance?

A
  • von Willebrant disease (autosomal dominant - non-X-linked, requires only 1 defective gene => 50% risk each pregnancy)
  • hemophilia (X-linked recessive => 50% of sons affected, 0% of daughters affected - but daughters can be carriers)
  • Thalassemia (autosomal recessive - non-X-linked, requires 2 defective genes => 25% risk each pregnancy)
  • sickle cell disease (autosomal recessive - non-X-linked, requires 2 defective genes (25% of pregnancies affected, 50% risk for carrier status)
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26
Q

What is the genetic counseling for a PT who is a carrier for an autosomal recessive trait?

A
  • manifestation of the disease only occurs when a child inherits 2 copies of the defective gene
    => if the PT’s partner does not carry any defective genes, none of their children will have the disease but there is a 25% risk with each pregnancy of passing along carrier status
    => if both parents are carriers, 50% of pregnancies risk carrier status and 25% risk full-blown disease
    => if partner has full blown disease, 50% of pregnancies risk carrier status and 50% risk full-blown disease
27
Q

Which laboratory findings support a diagnosis of rheumatoid arthritis?

A
  • elevated erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) => inflammatory markers
  • (+) rheumatoid factor
  • (+) anti-CCP (antibodies to cyclic citrulinated peptide)
28
Q

Which laboratory findings support a diagnosis of systemic lupus erythematous?

A
  • anti-nuclear antibody (ANA - antibodies against one’s own DNA) => hallmark of SLE
  • anti-dsDNA (antibodies against double stranded DNA) => very specific to SLE (used to cofirm the diagnosis if ANA is +)
29
Q

What are the differential x-ray findings in rheumatoid versus osteoarthritis?

A
  • RA: spares the distal interphalangeal joints, soft tissue swelling, bone erosions, joint narrowing, ulnar deviation, swan neck deformity
  • OA: joint space narrowing, osteophytes (NO bone erosions), Heberden’s nodes (more distal), Bouchard’s nodes (proximal)
30
Q

What is the differences between Heberden’s and Bouchard’s nodes?

A

both due to osteophytes in finger joints but Bouchard’s are found in more proximal joints while Heberden’s are in more distal joints (B before H)

31
Q

What is the treatment for rheumatoid arthritis?

A

goals are to:

(1) improve symptoms: NSAIDS +/- steroids (steroids for PTs with renal disease), symptomatic control for breakthrough pain
(2) stop disease progression (disease modifying antirheumatic drugs): methotrexate (1st line), tumor necrosis factor (TNF) inhibitors (adalimubab/Humira, infliximab/Ramicade)

32
Q

What are the side effects, monitoring requirements, etc. of methotrexate?

A
  • PO weekly (inexpensive)
  • folate antagonist => need folate supplements (contraindicated in pregnancy)
  • hepatotoxic/bone marrow suppression => excreted from kidneys (monitor liver enzymes, CBC, and renal function)
    => screen for viral hepatitis prior to initiation
33
Q

What are the side effects, monitoring requirements, etc. of TNF inhibitors?

A
  • IV or SubQ injections (expensive)
  • can be used in combination with methotrexate
  • inhibits only one specific protein of inflammation (more precise mechanism of action/fewer side effects)
    => screen for TB prior to initiation - TNF acts as glue for TB granulomas (can reactivate latent TB and fungal or bacteria infections)
34
Q

What is the treatment for osteoarthritis?

A
  • weight loss
  • regular exercise to improve joint ROM and muscle strength
  • acetaminophen (1st line) => < 3 g/day (topical or oral NSAIDs)
  • intra-articular injections (no more than 3-4/year)
  • surgery only for serious disability
    => nutritional products (glucosamine and chondroitin sulfate have no good evidence of efficacy)
35
Q

What is the treatment for SLE?

A
  • for acute exacerbations: corticosteroids (IV or PO in high doses)
  • for maintenance (to prevent exacerbations and treat symptoms): sun screen (UV light can cause rashes and trigger flares), hydroxycholoroquine/Plaquenil (for skin rashes and arthritis)
  • cytotoxic drugs for severe cases of lupus nephritis
36
Q

What are the side effects, monitoring requirements, etc. of hydroxycholoroquine/Plaquenil?

A
  • retinal damage (rare but irreversible) => perform fundoscopic exam by specialist prior to initiation and annually
37
Q

What is the treatment for acute gout?

A
  • NSAIDs +/- colchicine (reduced dosage or avoid in PTs with renal disease)
  • steroids (if poor response to initial therapy)
38
Q

What is preventive therapy for gout attacks?

A
  • reduce alcohol intake (especially beer), avoid high purine foods (red meat, organ meats, seafood)
  • urate lowering therapy if > 2 attacks/year (start slow and titrate to uric acid level < 6 mg/dl - uric acid crystals form at > 6 mg/dl):
    => drugs to decrease production of uric acid: allopurinol, febuxostat/Uloric
    => drug to increase excretion of uric acid from kidneys: probenecid
39
Q

What are the side effects, monitoring requirements, etc. of urate lowering therapy?

A
  • drugs to decrease uric acid production (allopurinol and febuxostat/Uloric): for prevention => do NOT give during acute attack
  • drug to increase renal excretion of uric acid (probenecid): for prevention => contraindicated in renal insufficiency, nephrolithiasis
40
Q

What are the signs and symptoms of an acute gout attack?

A
  • sudden onset of exquisite joint pain (wakes from sleep)
  • usually affects great toe
  • redness, warmth, swelling, tenderness
  • elevated serum uric acid level
  • x-ray normal during early stages
  • elevated CRP/ESR
  • aspiration of synovial fluids (is diagnostic) => WBCs 5,000-50,000, 75% neutrophils, needle-shaped crystals (have to bring PT in daily if aspiration is deferred)
41
Q

What labs are used to diagnose lupus nephritis?

A
  • creatinine/GFR
  • urinalysis for protein (albuminuria) and RBC => cannot do urine dip because dip only detects microalbuminuria
  • 24-hour urine collection for urine protein or spot urine protein to creatinine ratio (perform if urinalysis is + for protein or RBCs)
  • renal biopsy is definitive diagnosis
42
Q

What is lupus nephritis?

A

deposition of immune complexes/proteins in glomerular capillary membrane

43
Q

What are the differences in joint appearance in inflammatory versus degenerative arthritis?

A
  • inflammatory (RA, SLE, gout, septic arthritis): joint effusion (soft joint, swelling, bogginess), tenderness, redness, warmth
  • degenerative (OA): bony crepitus, mild tenderness, hard/bony joint enlargement, NO redness/warmth/soft effusion
44
Q

Which joints are involved in RA, SLE, and OA?

A
  • RA: polyarticular/symmetric/small joints - wrist and hands (spares distal interphalangeal joints)
  • OA: monoarticular - weight bearing joints (knees most common, hips, lower spine)
  • SLE: polyarticular/symmetric/small joints - wrist and hands (does NOT spare distal interphalangeal joints)
45
Q

What is the distinction between Osgood-Schlatter disease and slipped capital femoral epiphysis?

A
  • OSD: pain and swelling of tibial tubercle - exacerbated by activity/relieved by rest, occurs in young athletes (9 to 14 years old) who have undergone a growth spurt
  • SCFE: chronic or intermittent pain in the hip or knee exacerbated by activity, no Hx of trauma, occurs in obese children (12 to 14 years old), limited ROM, leg may be externally rotated => risk for necrosis - avoid weight bearing until seen by orthopedist (requires surgery)
46
Q

What is the distinction between Morton’s neuroma and plantar fasciitis?

A
  • Morton’s: burning pain in the ball of the foot, “walking on pebbles,” numbness between 3rd and 4th toes, common in women who wear high heels with narrow toe box, (+) squeeze metatarsal joints test
  • plantar fasciitis: chronic heel (plantar surface) pain with first few steps in the morning or after periods of inactivity, common in runners and PTs with inappropriate footwear, (+) heel tenderness
47
Q

What is the distinction between a rotator cuff tear and rotator cuff tendonitis?

A
  • tear: pain and weakness on abduction, (+) open can test, (+) drop arm test
  • tendonitis: pain with overhead activities (+) Neer’s test, (+) Hawkins test, painful arc syndrome
48
Q

What is the distinction between lateral and median epicondylitis?

A
  • lateral (tennis elbow): pain in the lateral aspect of the elbow with wrist extension (backhand stroke, forceful gripping) => have PT hyperextend wrist against resistance (hand up in STOP position)
  • median (golfer’s elbow): pain over the median aspect of the elbow with wrist flexion (lifting, forceful gripping) => have PT flex the wrist against resistance
49
Q

What is the treatment for acute soft tissue injury?

A
  • RICE: rest, ice, compression, elevation (first 2-3 days + short course of NSAIDs)
  • when pain and swelling subside, physical therapy recommended to prevent chronic instability and recurrent injury
50
Q

What is the treatment for chronic tissue injury?

A
  • relative rest (avoid activities that aggravate pain)
  • pain control (NSAIDs - even though there is no inflammation)
  • physical therapy (stretching and muscular strengthening)
  • corticosteroid injections (if no response after treatment for 6 weeks)
  • surgery - if no response to conservative therapy (last resort)
51
Q

What are the Ottawa rules for ankle x-rays?

A

conduct an ankle x-ray only if there is pain in the malleolar zone and any of the following apply:

  • bone tenderness in the posterior edge or tip of the lateral malleolus
  • bone tenderness in the posterior edge or tip of the medial malleolus
  • inability to bear weight
52
Q

What are the Ottawa rules for foot x-rays?

A

conduct a foot x-ray only if there is pain in the mid-foot zone and any of the following apply:

  • bone tenderness in the base of the 5th metatarsal
  • bone tenderness in the navicular bone (top of mid-foot)
  • inability to bear weight
53
Q

What is Neer’s sign?

A

raise PT’s arm with scapula immobilized (compresses head of humerous against acromion) => (+) = pain - rotator cuff tendonitis

54
Q

What is Hawkin’s sign?

A

flex PT’s shoulder and elbow to 90 degrees with palm down and rotate arm internally (compresses greater tuberosity against acromion) => (+) = pain - rotator cuff tendonitis

55
Q

What is the Drop Arm sign?

A

ask PT to fully abduct arm to shoulder level and lower slowly or hold abducted arm against resistance => (+) = inability to hold arm fully abducted - rotator cuff tear

56
Q

What is the Empty Can test?

A

elevate arm to 90 degrees and rotate internally asking PT to resist as you place downward pressure on arm => (+) = inability to hold arm at 90 degrees/shoulder level - rotator cuff tear

57
Q

What is Finkelstein’s test?

A

ask PT to grasp thumb against the palm and move wrist toward midline in ulnar deviation (stretches thumb extensor tendon) => (+) = pain over thumb extensor - de Quervain’s tenosynovitis

58
Q

What is Tinel’s sign?

A

tap lightly over the course of the median nerve => (+) = numbness/pain in the median nerve distribution (1st to 3rd fingers) - carpal tunnel syndrome

59
Q

What is Phalen’s sign?

A

ask PT to hold the wrist in flexion for 60 seconds (compresses median nerve) => (+) = numbness/pain in the median nerve distribution (1st to 3rd fingers) - carpal tunnel syndrome

60
Q

What is McMurray’s test?

A

place PT supine and flex knee - extend knee in rotational movement => (+) = click or tenderness over the joint - meniscus tear

61
Q

What is Lachman’s test?

A

place knee in 15 degrees of flexion and pull tibia forward => (+) = laxity of the joint (no firm endpoint) - ACL tear

62
Q

What is the anterior drawer test?

A

PT supine and knees in 90 degrees of flexion with feet immobilized - pull tibia forward => (+) = laxity of the joint (no firm endpoint) - ACL tear

63
Q

What is the posterior drawer test?

A

PT supine and knees in 90 degrees of flexion with feet immobilized - push tibia posteriorly => (+) = laxity of the joint (no firm endpoint) - PCL tear

AGPC 4 (22 decks)

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