Diseases Of Human System Flashcards

(44 cards)

1
Q

What is arthritis?

A

Inflammation of the joints

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2
Q

What is arthrosis?

A

Non-inflammatory joint disease

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3
Q

What is arthralgia?

A

Joint pain

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4
Q

What is the link between bone and calcium?

A

Bone forms a store for calcium - some exchangeable
The exchangeable calcium moves from bone into ECF and calcium is absorbed from the gut into the ECF
Calcium is lost through the gut and urine
Calcium lvl has to stay at particular level for nerve and muscle function
The use of parathyroid hormone helps promote the correct location of calcium

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5
Q

What is the purpose of parathyroid hormone?

A

Maintains serum calcium levels - PTH raised if calcium levels fall
It increases calcium release from bone
It reduces renal calcium excretion

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6
Q

What is hypoparathyroidism + consequences?

A

Low levels of PTH

Leads to low serum calcium as calcium is not promoted to be released from bone

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7
Q

What is hyperparathyroidism + consequences?

A

Can be primary or secondary

Primary - usually caused due to gland dysfunction (i.e. Tumour) and results in high serum calcium as inappropriate activation of osteoclasts in bone

Secondary - caused by low serum calcium, appropriate activation of osteoclasts in bone

Both result in increased bone reabsoprtion
Appear as radiolucencies and reabsorption

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8
Q

What in the skin produces vitamin D when exposed to sunlight?

A

Cholecalciferol

This is then sent to the blood to be processed by the kidneys and liver into 1,25-dihydroxycolecalciferol

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9
Q

What is dihydroxycolecalciferol and how does it relate to bone health?

A

It is the active version of cholecalciferol after processing in the liver/kidneys and this helps calcium absorption in the gut

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10
Q

What are the sources of vitamin D?

A
Sunlight
Milk
Orange Juice
Fish (salmon)
Supplements
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11
Q

What are the problems with vitamin D?

A

Low sunlight exposure

Poor GI absorption - poor nutrition, small intestinal disease (malabsorption)

Drug Interactions - Some anti-epileptic drugs (carbamazepine, phenytoin)

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12
Q

What is osteomalacia?

A

A poorly mineralised osteoid matrix and poorly mineralised cartilage growth plate
Matrix is formed fine however, not calcified properly (normal amount of osteoid but inadequate mineralisation) - makes bone soft

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13
Q

What is osteoporosis?

A

A reduced quantity of normally mineralised bone

Loss of mineral and matrix - reduced bone mass
Mineral and matrix are in the correct form however, there is less of it therefore, correct bone mass is not achieved

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14
Q

If osteomalacia occurs bone formation, what is the common term used to name the pathology?

A

Rickets

After bone formation completion it is termed osteomalacia

Both related to calcium deficiency - serum calcium is preserved at the expense of bone calcium

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15
Q

What are the effects of osteomalacia?

A

Bone effects - “bow legs” in kids with rickets, vertebral compression in adults, bones ‘ache’ to touch

Hypocalcaemia effects - muscle weakness, carpal muscle spasm, facial twitching

Alkaline phosphatase is a measure of bone turnover and is v high when there is a problem w calcium levels

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16
Q

What is the management of osteomalacia?

A

Correct the cause - malnutrition (control GI disease), sunlight exposure (30m x5 weekly), Dietary vitamin D

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17
Q

What are risk factors of osteoporosis?

A

AGE
Female
Endocrine - oestrogen/testosterone deficiency, Cushings syndrome (increase corticosteroids in the blood)

Patient factors - inactivity, smoking, alcohol use, poor dietary calcium

Genetic - family history, race (caucasian/asian women), early menopause

Drug use - Steroids, Anti-epileptics

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18
Q

What are the consequences of osteoporosis?

A

Increased bone fracture risk - long bones (femur), vertebrae (height loss, nerve root compression - back pain)

Hip fracture

19
Q

How do you prevent osteoporosis?

A

Build maximal peak bone mass - exercise, high dietary calcium intake

Reduce rate of bone mass loss - Continue exercise and calcium intake, Reduce hormone related effects (oestrogen HRT, most effective if early menopause)

Reduce drug related effects

Consider “Osteoporosis prevention” drugs - Bisphosphonates

20
Q

What are a few common bisphosphonates?

A

Nitrogenous - Alendronate, Risedronate and Zoledronate (1x a year)

These work on osteoclasts poisoning them thus preserving bone mass

21
Q

What are SYMPTOMS of joint disease?

A

Pain
Immobility stiffness
Loss of function

22
Q

What are SIGNS of joint disease?

A

Swelling - osteophytes (bony lumps) form at the end of joints

Deformity - bones will meet differently than normal changing external appearance

Redness - indicates infection

Crepitus - Noise made by bone ends moving, associated with loss of normal cartilaginous covering of bone end

Loss of function

23
Q

What are the investigations for osteromalacia?

A
Serum calcium - Decreased
Serum phosphate - decreased
Alkaline phosphatase - v high
Plasma creatinine - high if renal cause
Plasma PTH - High if secondary hyperparathyroidism
24
Q

What are the investigations for osteoporosis?

A

Radiography - Plain, MRI, Arthrography

Blood - C-reactive protein, Rheumatoid factors (RF), Extractable nuclear antigens (ENA’s), ANA

Arthroscopy and biopsy

25
What is acute monoathropathies?
Acute arthritis of a single joint Common causes involve infection (septic arthritis), crystal arthropathy (gout) - uric acid crystals deposited in joint which cause irritation to the joint surface - this causes swelling and inflammation Can be an initial stage of polyarthritis
26
What is gout?
Uric acid crystals deposition in joints Significant pain from reactive inflammation Hyperuricaemia - high uric acid levels
27
What are the dental aspects of gout?
Avoid aspirin - interferes with uric acid removal Drug treatments may give oral ulceration (allopurinol)
28
What are the causes of gout?
Drug induced - thiazide diuretics Genetic predisposition Nucleic acid breakdown - Chemotherapy cancer treatment Tumour related - Myeloma Obesity and alcohol endurance
29
What are the symptoms associated with gout?
Acute inflammation of single joint Usually great toe Usually a precipitating event - trauma, surgery, illness, diet/alcohol excess Rapid onset - hours NSAIDs used to treat
30
What is osteoarthritis?
Degenerative joint disease Weight bearing joints/joint damage - predominantly hips and knees Not wear and tear - cartilage repair dysfunction
31
What are the symptoms of osteoarthritis?
PAIN - improves w rest, worse with activity Brief morning stiffness Slowly progressive over years
32
What are the signs of osteoarthritis?
Radiographs - loss of joint space and subchondral sclerosis (thickening of bone under cartilagenous layer), Osteophyte lipping at joint edge, radiographs may show ASYMPTOMATIC changes Joint swelling and deformity
33
What is the treatment for osteoarthritis?
Nothing alters disease progression Pain can be improved by - increasing muscle strength around the joint - weight loss - walking aids Role of NSAIDs Prosthetic replacement for PAIN not function
34
What are the dental implications of osteoarthritis?
TMJ can be involved - symptoms rare Difficulty in accessing care Chronic NSAID use - oral ulceration possible, bleeding tendency - anti-platelet Joint replacements - AB prophylaxis? - usually not needed
35
What is rheumatoid arthritis?
Initially a disease of the synovium with gradual inflammatory joint destruction Different patterns of joint involvement - Sero-positive RA (RF present) - Sero-negative RA (RF not present)
36
What are the symptoms of RA?
Slow onset - initially hands/feet, proximal spread, potentially involving all synovial structures SYMMETRICAL polyarthritis Occ. onset with SYSTEMIC symptoms - Fever, weight loss, anaemia
37
What are the early signs of RA?
Symmetrical synovitis of Metacarpal pharyngeal joints Symmetrical synovitis of PIP joints Symmetrical synovitis of wrist joints These cause joint stiffness, swelling and pain - eventually lead to destruction of the joint
38
What are the late signs of RA?
Ulnar deviation of fingers at MCP joints Hyperextension of PIP joints - "swan-neck" deformity "Z" deformity of thumb - Hyperflexion of MCP - Hyperextension of IP joint
39
What are the consequences of RA on patients hands?
Less possible for pts to grip and use their hand effectively which may affect OH
40
What investigations would you carry out for rheumatoid arthritis?
Radiographs - To see erosions, loss of joint space, deformity, joint destruction and secondary osteoarthritis Blood - Normochromic, normocytic anaemia - due to failure of RBC stimulation
41
What is the treatment of Rheumatoid Arthritis?
Aim is to improve the quality of life Combination of: - Physiotherapy - maintain patients function and actions for as long as possible - Occupational therapy - Maintain patients function and actions for as long as possible - Drug therapy - Slow down the disease and ease of pain - Surgery - can be helpful with joint stability that has been lost
42
In terms of RA, what drug therapy is used?
for most cases: Analgesics - Paracetamol, Cocodamol NSAIDs Disease modifying drugs - Hydroxychloroquine, methotrexate (slow down immune process and damage to joints) For moderate/severe cases: Immune modulators - Azathioprine, Steroids - Oral Prednisolone
43
What are the dental implications of RA?
Disability from the disease - reduced dexterity, access to care Sjogrens syndrome - Association of connective tissue disease - the dry eyes/mouth Joint replacement - Multiple - Large/small joints Drug effects - Bleeding (NSAIDs/Sulphasalazine) Infection risk (steroids, immune modulators), Oral lichenoid reactions (gold, sulphasalazine, hydroxycholoroquine) Oral Ulceration (methotrexate) Oral Pigmentation (hydroxychloroquine) Chronic anaemia - GA problems
44
Where is a common area for ligaments to rupture with Rheumatoid Arthritis?
Damage to the ligaments in the neck particularly the ligaments connecting the skull base to the upper cercival vertebrae With RA it is easier for these ligaments to rupture and the bone of the dens impinging into the space of the spinal cord causing spinal damage