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Rheumatology Flashcards

(51 cards)

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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

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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

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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

Study These Flashcards
A

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

24
Q

Seronegative spondyloarthropathy

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A

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

25
Diseases associated with AS
weightloss, fatigure, chest pain, enthesitis, anemia, anterior uveities, aortitis, IBS, heart block
26
Schobers test
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
AS radiological findings
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
Management of AS pharmaceutical
- 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
Psoriatic arthritis background and pathophysiology
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
Types of psoritatic arthritis
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
Diagnosis of PA
blood test for rheumatoid factor and anti-citrullination; absent in PA x-ray for erosin and pencil in cup
32
Treatment PA
NSAIDs Immunomodulatory drugs TNF inhibitors IL12 and 23 inhibitor
33
Systemic lupus erythematous
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
Pathogensis of SLE
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
RIsk factors SLE
siblins, women of childbearing age, UV over exposure, EBV, drug induced, high oestrogen, OCP, pregnancy
36
Clinical presentation of SLE
``` 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
Diagnosis of SLE
``` 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
Management
MILD TO MOD: reduced enviro triggers, NSAIDs, low dose corticosteroids, antimalarias SEVEVER: corticosteroids, immunosuppresants,
39
Gout
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
Pathogenesis of gout
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
Risk factors gout
genetis, renal disease, use of diuretics or salicyate, hypertensionand CHD , high purine diet : shellfish, lobster, bacon, turke, beer, ham
42
STage 1 gout
Asymptomatic hyperuricaemia | No treatment other than lifestyle modifications
43
Stage 2 gout
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
Stage 3 gout
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
Stage 4 gout
Chronic tophaceous gout and chronic gouty arthritis uric acid levels are high over many years Permanent joint destruction
46
Diagnosis gout
synovial fluid aspirate Elevated serum uric acid X-ray: punched out erosions, tophi and visible joint effusion
47
Management of gout
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
CPPD
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
CPPD clinical features
``` 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
Diagnosis of CPPD
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
Managment fo CPPD
NSAIDs Cortisone into joint: prevents further inflammation oral corticosteroids

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