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Radiology > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Bone growth stimulators

A

Vit D- for Ca2+ absorption
Oestrogen and progesterone- inhibit bone resorption
Calcintonin- Opposes PTH

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2
Q

Bone resorption stimulators

A

Parathyroid hormone- Controls Ca2+ in your blood,

Thyroid hormone and interleukin 1- affect osteoclasts leading to resorption

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3
Q

Smoking and alcohol on osteoporosis

A

Suppression of thyroid hormone and vitamin D and affects Ca2+ absorption

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4
Q

Calcium reccomendations

A

1000mg for men 50-70

13000mg for women >50 and men >70

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5
Q

Corticosteroids and osteoporosis

A

decrease Ca2+ intestinal absorption, increased Ca2+ renal excretion,

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6
Q

Drugs that affect osteoporosis

A

Corticosteroids, anti-eptileptics, prostate and Breast cancer hormone replacement, heparin,

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7
Q

Treatment of osteoporosis

A

Biophosphonates- fosamax: increase osteoclast apoptosis,
Selective oestrogen receptor modulators (SERMs): acts on bone like normal oestrogen
HRT: normalise oestrogen levels, slows bone loss, increased CVD risk though

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8
Q

Osteomyelitis inflammatory phase

A

Phase 1:

acute inflammation and exudate into the bone, increase lymphocytes, intraosseus pressure

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9
Q

Osteomyelitis Suppartion phase

A

Phase 2:
Pus formation after 48-72 hours, as pressure increases it travels through Volkmann canals, bursts through perisoteum , and spreds into soft tissues and joints (septic arthritis)

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10
Q

Osteomyelitis necrosis phase

A

Phase 3:
Intraosseus pressure impairs endosteal blood supply. leads to periosteal stripping and formation of sequestrum: segment of dead bone with no blood supply and surrounded by pus

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11
Q

Osteomyeltis formation of new bone phase

A

Phase 4: 10-14 days

periosteum forms new bone allowing involucrum to surround sequestrum

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12
Q

Diagnosing osteomyelitis

A

Rasied ESR, biopsy, x-ray, MRI, radionucleide scan

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13
Q

Pathophysiology of osteoarthritis

A

when matrix degeneration ezymes are overexpressed leading to loss of collagen and proteoglycans in the cartilage.

Matrix metalloprotineases, colagenase and protease are secreted which leads to stimulatio of IL1. This all leads to breakdown of proteglycans and collagen causing breaking and cracking of cartilage (joint mice). MOre pressure on the bone leads to osteophytes and thickening of synovium

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14
Q

Normal healthy cartilage

A

Has chondrocytes and ECM which:
decrease friction
Resist tension via type II collagen
Resist compression via proteglycans

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15
Q

OA vs RA

A

OA is assymetrical
RA affects MCP and PIP
OA affects DIP and PIP

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16
Q

Macrophage role in the RA joint

A

macrophages release IL1 and IL6, stimulation of fibroblasts and synoviovytes.

These then proliferate and release RANKLand proteases
Proteases break down cartilage and RANKL+ cytokineases cause osteoclast activation

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17
Q

T cells role in the RA joint

A

make up 50% of synovial cells
Promote inflammation and release IL17
Promote macrophage activity and fibroblast and RANKL ex expression

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18
Q

Plasma cells in RA

A

5% of cells in synovium. release cytokines and antibodie

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19
Q

SYnovial fluid role in RA

A

has neutrophiles which release ROS and proteases which leads to bone adn cartilage erosion

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20
Q

Porphyromonas ginigivalis

A

Potenital casue of RA
a bacteria that causes the modification of autoantigens leading to an immune response. amino acid arginine becomes citrulline

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21
Q

Infection leading to RA

A

Infection > cytokine release and inflam > citrillination of autoantigens > seem foreigen and recognised by antigen presenting cells > immune response initiaed > antigen presenting cells activate Cd4 T cells > activate B cells in germinal layer of lymph node > production of plasma cells > production of antibodies> CD4 T, antibodies and Plasma cells migrate to joint

22
Q

Antibodies involved in RA

A

pl factor- IgM antibody target igG antibodies to form an immune complex that can deposite in synovial tissue

Anti-citrullinated protein antibody- they take fibrin and fillarin and target citrillinicated proteins: specific to RA

23
Q

Extra-aeticular invovlement RA

A

anemia, fatigue, depression, osteopoeina, insulin resistance in muscles, infection, thrombus

24
Q

Seronegative spondyloarthropathy

A

group of diseases related to HLA B27 gene includes AS, PA and reactive arthritis

25
Q

Diseases associated with AS

A

weightloss, fatigure, chest pain, enthesitis, anemia, anterior uveities, aortitis, IBS, heart block

26
Q

Schobers test

A

assesses mobility of LS
locate l5 and mark a point 5cm below and 10cm above. Get pt to bend forward, and meeasure distance between points, if it is < 20cm then there is lumbar restriction

27
Q

AS radiological findings

A

Bamboo spine: late stages, squaring of vertebral bodies
Subchondral sclerosis
Subchondral erosion
Syndesmophytes (bony growth from where ligament attaches)
Ossification (ligaments start to turn into bone)
Fusion of facet, SIJ and costovertebral joints

28
Q

Management of AS pharmaceutical

A
  • NSAIDs: ibruoprofen and naproxen, if not relief after 2-4 weeks of max dosage then switch NSAIDs
  • Steroids during flares: oral, intramuscular slow release, or into joint
  • TNFa mediation- monoclonal antibodies or anti-TNFa
  • monoclonal antibodies for IL7
29
Q

Psoriatic arthritis background and pathophysiology

A

T cell mediateed attack on joints in people with psoriasis.

self- antigens are seen as foreign- release of cytokines and TNFa and inflammation- keratinocytes and fibroblasts proliferate- formation of psoriatic plaque-

T cells can also activate osteobalsts and osteoclasts leading to erosion and ossification

30
Q

Types of psoritatic arthritis

A

Oligoarticular: asymmetrical, <5 joints
polyarticular: resemble RA, > 5 joints,
Spondylarhtiris: affects spine and SIJ
DIP predmominant: dactylitis, joint and bone deformintes
Arthritis mutlians: bone eroision with telescopic digits opera glass hands

31
Q

Diagnosis of PA

A

blood test for rheumatoid factor and anti-citrullination; absent in PA
x-ray for erosin and pencil in cup

32
Q

Treatment PA

A

NSAIDs
Immunomodulatory drugs
TNF inhibitors
IL12 and 23 inhibitor

33
Q

Systemic lupus erythematous

A

SLE with joint manifestations or discoid lupus: more skin less joint and organ

An autoimmune disease that has multi-system involement
CT disease, over production of auto-antibodies

34
Q

Pathogensis of SLE

A

Results from recurrent activation of the immune system of T and B cells from genetic or environmental disorders
Cascade of inflammation that deposits into the tissues

35
Q

RIsk factors SLE

A

siblins, women of childbearing age, UV over exposure, EBV, drug induced, high oestrogen, OCP, pregnancy

36
Q

Clinical presentation of SLE

A 
Malar butterfly rash, photosentsitve
Discoid rash:  raised scaly lesion 
Alopecia
hives
raynauds
bilateral and symmetrical arthritis, joint destruction, 
Renal nephritis
anemia, leukopoenia, thrombocytopoenia,
Non-specific ss
37
Q

Diagnosis of SLE

A 
antinuclear antibodies, 98% sensitive
double stranded DNA
ENA antibodies
raised ESR or CRP
Direct coombs test: detects autoimmune haemoltyic anaemia becasue it breask down RBCs
38
Q

Management

A

MILD TO MOD: reduced enviro triggers, NSAIDs, low dose corticosteroids, antimalarias
SEVEVER: corticosteroids, immunosuppresants,

39
Q

Gout

A

Monosodium urate crystal disorder: abnormality on uric acid metabolism that results in hyperuricaemia and urate crystal deposition in joitns, soft tissue and urinary tract

40
Q

Pathogenesis of gout

A

Purines come together to make xanthine. xanthine oxidase converts xanthine into uric acid. we are unable to break down uric acid so we must expel it, usually xanithine via kidneys. If unable to expel it all there is a build up of the crystals which and this activates macro-hages and phagocytes creating an acute inflammatory response

41
Q

Risk factors gout

A

genetis, renal disease, use of diuretics or salicyate, hypertensionand CHD , high purine diet : shellfish, lobster, bacon, turke, beer, ham

42
Q

STage 1 gout

A

Asymptomatic hyperuricaemia

No treatment other than lifestyle modifications

43
Q

Stage 2 gout

A

Acute gouty arthritis
Acute attack of severe pain, usually in great toe, in early hours of morning and wakes patient
skin is red, hot, shiny, tender
subsides in 3-10 days without treatmetn

44
Q

Stage 3 gout

A

Intercritical gout
Time between attacks
Low to no pain
Low level inflammtaion causing joint destruction
Aggressive lifestyle and medication here to prevent chronic gout
Tophi: stone like deposits of monosodium urate in ST, bone, synovium, joints

45
Q

Stage 4 gout

A

Chronic tophaceous gout and chronic gouty arthritis
uric acid levels are high over many years
Permanent joint destruction

46
Q

Diagnosis gout

A

synovial fluid aspirate
Elevated serum uric acid
X-ray: punched out erosions, tophi and visible joint effusion

47
Q

Management of gout

A

NSAIDs acute attack
lifestyle modificatios
corticosteroids for chronic
Allopurinol- xanthine oxidase inhibitor- stops the conversion of xanthine to uric acid
used as prophyalxis and treatmetn
can cause rash, nausea, vomitting, suppress bone marrow

48
Q

CPPD

A

calcium phyrophosphate deposition disease
disease of crystal depostion is ST and joits
most common cuase of chondrocalcinosis
main theory is an excess of pyrophosphate production in cartilage which results in calcium pyrophosphate deposition
disease > 65
OA, joint trauma and metabolic disease are risk factors

49
Q

CPPD clinical features

A 
acute attacks that mimic gout
synovitis w tenderness and swelling
knee most common, 2nd 3rd MCP, wrist and shoulder
fever malaise
No joint destruction
50
Q

Diagnosis of CPPD

A

Synovial fluid analysys: rhomboid shape rather than rod shaped like gout
X-ray: chondrocalcinosis: hyperwhite line along cartialeg, joint space narrowing, subchondral new bone, no joint destruction

51
Q

Managment fo CPPD

A

NSAIDs
Cortisone into joint: prevents further inflammation
oral corticosteroids

Radiology (9 decks)

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