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BDS3: BAMS > Diseases of Human Systems > Flashcards

Diseases of Human Systems Flashcards

1
Q

what is arthritis?

A

inflammation of joints

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2
Q

what is arthrosis?

A

non-inflammatory joint disease

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3
Q

what is athralgia?

A

joint pain

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4
Q

what makes up bone?

A

o Mineralised Connective tissue
o Calcium
o Phosphate
o Vitamin D

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5
Q

what does the parathyroid hormone maintain?

A

serum calcium level

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6
Q

what does parathyroid hormone increase?

A

Increases calcium release from BONE

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7
Q

what does parathyroid hormone reduce?

A

Reduces RENAL calcium excretion

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8
Q

what is hypothyroidism?

A

low serum calcium

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9
Q

what are causes of vitamin D problem?

A

o Low Sunlight Exposure
o Poor GI Absorption
o Drug interactions
o Often a combination of factors

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10
Q

what types of drugs causes vitamin D problems?

A

 Some antiepileptic drugs
* Carbamazepine, Phenytoin

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11
Q

what is osteomalacia?

A

 Poorly mineralised osteoid matrix
 Poorly mineralised cartilage growth plate

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12
Q

what is difference between rickets and osteomalacia

A

rickets - during bone formation
osteomalacia - after bone formation

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13
Q

what is osteomalacia and rickets related to?

A

 Both related to calcium deficiency
* Serum calcium preserved at expense of bone

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14
Q

what does low dietary calcium lead to?

A

leads to reduction in plasma calcium leads to increased PTH secretion - increase in lots stuff except decrease in urinary calcium then leads to restoration of normal calcium

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15
Q

what are effects of hypocalcaemia?

A

o Muscle weakness
o Trousseau & Chvostek signs positive
 Carpal muscle spasm
 Facial twitching from VII tapping

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16
Q

what is management of calcium problems in bone?

A
  • Correct the cause
    o Malnutrition
     Control GI disease
    o Sunlight exposure
     30 mins x 5 weekly
    o Dietary Vitamin D
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17
Q

what is osteoporosis?

A

loss of mineral and matrix
- reduced bone mass

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18
Q

what systemic problem is a risk factor for osteoporosis?

A

endocrine

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19
Q

what are effects of osteoporosis?

A
  • Increased bone fracture risk
    o Height loss
    o Kyphosis & Scoliosis
    o Nerve root compression – back pain
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20
Q

what is kyphosis?

A

cervical spine tipped forward

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21
Q

what is scolisois?

A

abnormal twisting and curvature of spine

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22
Q

how to prevent osteoporosis?

A

Build maximal Peak Bone Mass
Reduce rate of Bone Mass loss

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23
Q

how to build maximal peak bone mass?

A

exercises
high dietary calcium intake

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24
Q

how to reduce rate of bone mass loss?

A

o Continue exercise and calcium intake
o Reduce hormone related effects
o Reduce drug related effects
o Consider ‘Osteoporosis Prevention’ drugs
 BISPHOSPHONATES

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25
Q

what are effects of oestrogen hormone replacement in reducing risk of osteoporosis?

A

o Reduces osteoporosis risk
o Increases breast cancer risk
o Increase endometrial cancer risk
 Patients who have NOT had a hysterectory
 Combine with a progestogen to reduce risk
o May reduce ovarian cancer risk
o Increases DVT risk

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26
Q

what are types of Multisystem vasculitic inflammatory diseases?

A
  • Systemic lupus erythematosis (SLE)
  • Systemic sclerosis (Scleroderma)
  • Sjogrens syndrome (SS)
  • Undifferentiated connective tissue disease (UCTD)
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27
Q

what are types of large vessel vasculitic diseases?

A
  • Giant cell (temporal) arteritis
  • Polymyalgia rheumatica
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28
Q

what are types of medium vessel vasculitic diseases?

A
  • Polyarteritis nodosa
  • Kawasaki disease
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29
Q

what are types of small vessel vasculitic diseases?

A
  • Wegener’s Granulomatosis
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30
Q

how to manage connective diseases?

A

 Analgesic NSAIDs (joint/muscle symptoms)
 Immune modulating treatment
* Hydroxychloroquine
* Methotrexate
* Azathioprine
* Mycophenolate

  • Biologic Medication – Cytokine inhibitors and lymphocyte depleting drugs
     Systemic steroids – prednisolone
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31
Q

what does SLE look similar to?

A

lichen planus

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32
Q

what are circulating blood autoantibodies with SLE?

A

ANA, dsDNA & Ro antibodies

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33
Q

what are dental aspects of SLE?

A
  • chronic anaemia
  • oral ulceration
    *GA risk
  • Bleeding tendency
    *thrombosytopaenia
  • renal disease
    *impaired drug metabolism
  • drug reactions
  • steroid and immunosuppresive therapy
    *possible increased malignancy risk
  • lichenoid oral reactions
  • oral pigmentation from hydroxychlorquine use
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34
Q

what does chronic anaemia causes dentally?

A

-oral ulceration
- GA risk

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35
Q

what does taking hydroxychloroquine do dental?

A

oral pigmentation

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36
Q

what is Antiphospholipid Antibody Syndrome (APS) characterised by?

A

o Characterised by recurrent Thrombosis
 DVT with pulmonary embolism
o Venous & arterial thrombosis

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37
Q

what do you not stop with when have Antiphospholipid Antibody Syndrome (APS)?

A

anticoagulant

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38
Q

what is sjogren’s syndrome associated with what circulating autoantibodies?

A

 ANA, Ro and La

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39
Q

what is sjogren syndrome associated with?

A

dry eyes and dry mouth

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40
Q

what is there a major involvement with in sjogren syndrome?

A

salivary glands

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41
Q

what is sicca syndrome?

A

 Dry eyes or Dry mouth

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42
Q

what is primary sjogrens?

A

 Not associated with any other disease

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43
Q

what is secondary sjogren?

A

 Associated with another Connective Tissue disease – Rheumatoid Arthiritis, SLE, etc.

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44
Q

what are oral and dental implications of sjogrens syndrome?

A

 Oral Infection
 Caries risk
 Functional loss
 Denture retention
 Sialosis
 Salivary lymphoma
* Unilateral gland size change
* usually after years

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45
Q

what is systemic sclerosis?

A

o excessive collagen deposition
o connective tissue fibrosis
o loss of elastic tissue

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46
Q

what is there a gradual onset of with systemic sclerosis?

A

 Raynoud’s phenomenon
 renal failure
 Malabsorbtion (GI involvement)

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47
Q

what are dental aspects of systemic sclerosis?

A
  • involvement of perioral tissues
  • Swallowing difficulties
  • Dental erosion
  • widening of periodontal ligament space - no mobility
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48
Q

what is the involment of the perioral tissues like with systemic sclerosis?

A
  • limited mouth opening
  • progressively poor oral access
  • limited tongue movement
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49
Q

what must you do if someone has systemic sclerosis?

A

plan treatment 10 years ahead

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50
Q

what is systemic sclerosis sometimes compounded by?

A

sjogren

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51
Q

what must you watch for if someone has systemic sclerosis?

A

watch for drug metabolism due to cardiac and renal vasculitic disease

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52
Q

what is vasculitis?

A
  • inflammation of blood vessels
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53
Q

what does infarction of tissue in vasculitis present as?

A

o May present as oral inflammatory masses
o May present as ulcers (tissue necrosis)

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54
Q

what happens in vasculitis?

A

 Vessel wall thickens with inflammation
* Narrowing of lumen reduced blood flow

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55
Q

what is usually commonly involved with giant cell arteritis?

A

temporal artery

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56
Q

what may someone with giant cell arteritis present with?

A

headache/facial pain

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57
Q

what does giant cell arteritis involve?

A

 Involves other carotid branches
* “Chewing claudication”
* Occlusion of central retinal artery (blindness)

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58
Q

what is polymalgia rheumatica?

A

 Disease of the elderly
 Pain & morning stiffness of muscles
 Non-specific systemic features
* Malaise, weight loss, profound fatigue
 Responds well to steroids

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59
Q

what are non specific systemic factors of polumyalgia rhematica?

A
  • Malaise, weight loss, profound fatigue
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60
Q

what does polymyalgia rheumatica respond well to?

A

steroids

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61
Q

what does Kawasaki disease give clinically?

A
  • Fever & lymphadenopathy
  • Crusting/cracked tongue
  • Strawberry tongue & erythematous mucosa
  • Peeling rash on hands and feet
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62
Q

what is inflammoatory condition of wegener’s granulomatosis?

A
  • Can lead to destruction of hard and soft tissues of the face and oral cavity
  • Spongy red tissue
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63
Q

what is fibyalgia?

A

 Non-specific collection of musculoskeletal symptoms
* Joint pain
* Muscle pain
* ‘functional disorders’

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64
Q

what are dental aspects of vaculitis?

A

 Steroid precautions may be needed
 May present to the dentist
* Giant cell arteritis
* Wegener’s Granulomatosis
* Kawasaki Disease

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65
Q

what are crystal arthropathies?

A

 Acute monoarthropathies
 gout

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66
Q

what is Acute monoarthropathies?

A
  • acute arthritis of a single joint
  • can be initial stage of polyarthritis
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67
Q

what is common causes of acute monoarthropathies?

A

o infection - septic arthritis
o crystal arthropathy - gout

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68
Q

what is gout?

A
  • Uric acid crystal deposition in joints
  • Significant pain from reactive inflammation
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69
Q

what is hyperuricaemia?

A

high uric acid levels

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70
Q

what enhances gout?

A

obesity and alcohol enhance?

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71
Q

gout is less common in women until when?

A

menopause then equalises?

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72
Q

what are symptoms of gout?

A

o acute inflammation of SINGLE joint
o usually great toe
o usually a precipitating event
 trauma, surgery, illness, diet/alcohol excess
o rapid onset - hours
o NSAIDs to treat

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73
Q

what are dental aspects of gout?

A

o avoid aspirin
 interferes with uric acid removal
o drug treatments may give oral ulceration (allopurinol)

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74
Q

what happens to aspirin in gout?

A

o avoid aspirin
 interferes with uric acid removal

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75
Q

what drug treatments may give oral ulceration?

A

allopurinol

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76
Q

what are symptoms of osteoarthris?

A
  • pain - improve with rest worse with acitivty
  • brief morning stiffness
  • slowly progressive over years
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77
Q

what is treatment of osteooarthritis?

A
  • nothing alters disease progression!
  • Pain improved by
    o increasing muscle strength around the joint
    o weight loss
    o walking aids
  • role of NSAIDs
  • Prosthetic replacement for PAIN
  • Joint replacement
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78
Q

what is dental aspects of osteoarthrtis?

A
  • TMJ can be involved
    o symptoms RARE!
  • Difficulty in accessing care
  • chronic NSAID use
    o oral ulceration possible
    o bleeding tendency - anti-platelet
  • Joint replacements - AB prophylaxis?
    o Usually not needed
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79
Q

what is rheumatoid arthritis?

A

o Initially a disease of the synovium with gradual inflammatory joint destruction

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80
Q

what are diff patterns of joint involvement?

A

 Sero-positive RA
* rheumatoid factor present
 Sero-negative RA
* rheumatoid factor NOT present

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81
Q

what is there a slow onset to in rheumatoid arthrtiis?

A
  • initially hands and feet
  • proximal spread
  • potentially ALL synovial structures
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82
Q

what are early signs of RA?

A

 symmetrical synovitis of MCP joints
 symmetrical synovitis of PIP joints
 symmetrical synovitis of wrist joints

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83
Q

what are late signs of RA?

A

 ulnar deviation of fingers at MCP joints
 hyperextension of PIP joints
 “Z” deformity of thumb
 subluxation of the wrist
 loss of abduction and external rotation of shoulders
 flexion of elbows and knees
 deformity of the feet & ankles

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84
Q

what shows up on radiographs with RA?

A
  • erosions, loss of joint space, deformity
  • joint destruction & secondary osteoarthritis
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85
Q

what are treatment options of RA?

A
  • physiotherapy
  • occupational therapy
  • drug therapy
  • Surgery
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86
Q

what is aim of physio therapy?

A

o Aim to keep the patient active for as long as possible!
o active and passive exercises
 to maintain muscle activity
* to improve joint stability
o to maintain joint position

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87
Q

what is occupational therapy?

A

o maximising the residual function
o providing aids to independent living
o assessment & alteration of home

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88
Q

what are 2 types of disease modifying drugs?

A
  • hydroxychloroquine, methotrexate,
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89
Q

what are dental aspects of RA?

A
  • disability from disease
  • sjogrens
  • joint replacements
  • drug effects
  • chronic anaemia - GA problems
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90
Q

what does methroxate cuase orally?

A

oral ulceration

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91
Q

what is effects of Sero-negative Spondyloarthritides?

A
  • Disabling progressive lack of axial movement
  • symmetrical other joint involvement – e.g.hips
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92
Q

what does Sero-negative Spondyloarthritides result?

A

o low back pain
o limited back and neck movement – turning spine restricted
o limited chest expansion – breathing compromised
o cervical spine tipped forward (Kyphosis)
 movements restricted

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93
Q

what are dental aspects of sero-negative Spondyloarthritides?

A
  • GA hazardous
    o limited mouth opening
    o limited neck flexion
  • TMJ involvement possible, but rare except in Psoriatic Arthritis
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94
Q

tmj involvement in connective disease is rare except in what?

A

psoriatic arthritis

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95
Q

what is stroke?

A

“acute focal neurological deficit resulting from cerebrovascular disease and lasting more than 24hrs or causing earlier death”

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96
Q

stroke is death of brain tissue from what?

A

hypoxia

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97
Q

what happens when there is no local cerebral blood flow?

A

 Infarction of tissue
 Haemorrhage into the brain tissue

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98
Q

what is transient ischaemic attack?

A
  • Localised loss of brain function
    o Ischaemic event – not haemorrhage
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99
Q

how long does it take to recover from TIA?

A
  • FULL recovery within 24hrs
    o Most recover in 30mins
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100
Q

in stroke what does FAST stand for?

A

facial drooping, arm weakness, speech difficulty and time

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101
Q

what are risks for stroke?

A

 HYPERTENSION
 SMOKING
 Alcohol
 ISCHAEMIC HEART DISEASE
 Atrial Fibrillation
 Diabetes Mellitus

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102
Q

when is there greatest risk for stroke in hypertension?

A

If DIASTOLIC >110mm Hg then a x15 risk compared to diastolic <80mm Hg

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103
Q

what are causes of stroke?

A

 Ischaemic stroke – uncertain
 Intracranial Bleed
 Embolic Stroke
 Atheroma of cerebral vessels

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104
Q

what happens with an intracranial bleed?

A

aneurysm rupture

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105
Q

what is embolic stroke?

A
  • Embolism from left side of heart
    o Atrial fibrillation
    o Heart valve disease
    o Recent MI
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Perfectly
106
Q

where do atheroma’s happen?

A
  • Carotid bifurcation
  • Internal carotid artery
  • Vertebral artery
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107
Q

in prevention of stroke what is antiplatelet action?

A

secondary prevention only

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108
Q

what is used in antiplatelet action for stroke?

A
  • Aspirin
  • Dipyridamole
  • Clopidogrel
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109
Q

when are anticoagulants used in stroke?

A

when there is an embolic risk - AF, LV thrombus

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110
Q

what do you need to differentiate when you investigate stroke?

A
  • INFARCT
  • BLEED
  • Subarachnoid Haemorrhage
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111
Q

what is best investigation of visualising brain circulation?

A

o MRA (MR angiography)

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112
Q

what risk factors should you assess in stroke?

A
  • Carotid ultrasound
  • Cardiac ultrasound (LV thrombus)
  • ECG (arrhythmias)
  • Blood pressure
  • Diabetes screen
  • Thrombophilia screen (young patients)
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113
Q

why do you assess for cardiac ultrasound?

A

for LV thrombus

114
Q

when do you assess for thrombophilia screen

A

in younger patients

115
Q

what is the effect of stroke?

A

 Loss of functional brain tissue
* immediate nerve cell death
* Nerve cell ischaemia in penumbra around infarction
o Will die if not protected

 Gradual or rapid loss of function
* Stroke may ‘evolve’ over minutes or hours

 Inflammation in tissue surrounding the infarct/bleed
* Recovery of some function with time

116
Q

what happens to tissue surrounding infarct/bleed?

A

inflammation

117
Q

what happens when there is a loss of functional brain tissue in stroke?

A
  • immediate nerve cell death
  • Nerve cell ischaemia in penumbra around infarction
    o Will die if not protected
118
Q

what are complications of stroke?

A

 Motor function loss
 Sensory loss
 Cognitive impairment

119
Q

what happens to motor function loss in stroke?

A
  • Cranial nerve or somatic (opposite side!)
  • Autonomic in brainstem lesions
  • Dysphonia
  • Swallowing
    o Aspiration of food & saliva
    o Pneumonia and death
120
Q

what happens in sensory loss in stroke?

A
  • Cranial nerve or somatic (opposite side!)
  • Body perception
    o Neglect
    o Phantom limbs
121
Q

what happens in cognitive impairment for complication of stroke?

A
  • Appreciation – special sensation
  • Processing
    o understanding of information
    o Speech and language
     Dysphasia, dyslexia,dysgraphia & dyscalculia
  • Memory impairment
  • Emotional lability and depression
122
Q

what are the treatments in acute phase of stroke?

A

o Reduce damage
o Remove haematoma
o Prevent future risk

123
Q

during acute phase of stroke how do you reduce damage?

A

 Penumbra region – survivable ischaemia
* Calcium channel blockers (Nimodipine)
 Improve blood flow/oxygenation
* Thrombolysis possible within 3hrs (alteplase)
* Maintain perfusion pressure to brain tissue
 Normoglycaemia - hyper/hypo harmful

124
Q

what do you do for treatment of penumbra region to reduce damage in acute phase of stroke treatment?

A
  • Calcium channel blockers (Nimodipine)
125
Q

how do you improve blood flow in acute phase of stroke treatment?

A
  • Thrombolysis possible within 3hrs (alteplase)
  • Maintain perfusion pressure to brain tissue
126
Q

what do you remove heamatoma from in acute phase of stroke treatment?

A

 Subarachnoid haemorrhage only

127
Q

how do you prevent future risk in acute phase of stroke treatment?

A

 Aspirin 300mg daily
 Anticoagulation if indicated (delay 2 weeks)
* Atrial Fibrillation
* Left ventricular thrombus

128
Q

how much aspirin do you give to prevent future risk of stroke in acute phase treatment?

A

300mg

129
Q

what do you do if anticoagulation is indicated in acute phase of stroke treatment?

A

delay 2 weeks

130
Q

when is anticoagulation is indicated in acute phase of stroke treatment?

A
  • Atrial Fibrillation
  • Left ventricular thrombus
131
Q

what is given during treatment of chronic phase of stroke treatment?

A

 Immobility support
 Speech and language therapy
 Occupational therapy

132
Q

what are dental aspects of stroke?

A

 Impaired mobility & dexterity

 Communication difficulties
* Dysphonia, dysarthria
* cognitive difficulties

 Risk of Cardiac Emergencies
* MI
* Further stroke

 Loss of protective reflexes
* Aspiration
* Managing saliva
o ?anticholinergic drugs help

 Loss of sensory information
* Difficulty in adaption to new oral environment
e.g. new dentures

 ‘Stroke pain’
* CNS generated pain perception

133
Q

what is epilepsy associated with and what does it lead to?

A
  • Epilepsy is associated with reduced GABA levels in the brain
  • This leads to abnormal cell-cell message propagation
134
Q

what are the types of generalised epilespy?

A

 Tonic/clonic
 Absence (petit mal)
 myoclonic/atonic

135
Q

what are types partial epilepsy?

A

 simple partial
 complex partial
 simple sensory

136
Q

what are epilepsy triggers?

A

o Idiopathic
o Trauma - head injury
o CNS disease
o Social

137
Q

what is tonic clonic seizures?

A

 prodromal aura
 loss of consciousness/continence
 initial tonic (stiff)
 clonic - (contraction/relaxation)
 post-ictal drowsiness

138
Q

what does status epilepticus mean?

A

recurrent seizures

139
Q

how long do petit mal seizures last?

A

5-15 seconds

140
Q

what happens with a petit mal seizure?

A

 loss of awareness – eyelids flutter, vacant stare, stops activity, loss of response

141
Q

when do petit mal seizures usually happen?

A

 CHILDHOOD usually
 Can be multiple attacks in a single day

142
Q

what must you do if someone is having a tonic clonic seizure?

A

 INJURY - protect where possible
* remove objects from the mouth IF POSSIBLE
 Asphyxia
* USE SUPPLEMENTAL OXYGEN
* GUEDEL airway IF POSSIBLE
* SUCTION any secretions

143
Q

what are precipitators of tonic clonic seizures>

A

 withdrawal/poor medication compliance
 epileptogenic drugs
* some GA agents
* alcohol
* tricyclics & SSRIs
 fatigue/stress
 Infection
 Menstruation

144
Q

what are partial seizures?

A

o Motor localised to ONE region of the brain
o may move/spread to other motor areas

145
Q

how do you treat epilepsy preventatively?

A

 Anticonvulsant drugs
* Tonic –clonic
o Valproate, Carbamazapine, Phenytoin, Gabapentin, Phenobarbitone, Lamotrigine
* Absence
o Levitiracetam

146
Q

how do you emergency treat epilepsy?

A

 most require SUPPORTIVE treatment ONLY if UNCONSCIOUS - Airway & Oxygen
 Status epilepticus requires BENZODIAZEPINES

147
Q

what does status epilepticus require?

A

BENZODIAZEPINES

148
Q

what are epilepsy drugs give GABA reception actions?

A

 Valproate
* Gaba transaminase inhibitor
 Benzodiazepines
* GABAA receptor action on Cl- enhanced

149
Q

what are epilepsy drugs give sodium channel actions?

A

 Carbamazepine
* Stabilises
 Phenytoin
* ? Unsure of action

150
Q

when is surgery for epilepsy used?

A

o Removal of focal neurological lesions
 Brain tumours (benign)
o Focal seizures
 Identifiable point of origin within the brain
 Not well controlled by medication

151
Q

what are dental aspects of epilepsy? in terms of fits?

A

o Complications of fits
 oral soft tissue injury
 dental injury/fracture

152
Q

what are dental aspects of epilepsy? in terms of epilepsy treatment?

A

 gingival hyperplasia (phenytoin)
 bleeding tendency (valproate)
 folate deficiency (rare)

153
Q

what causes gingival hyperplasia with epilepsy treatment?

A

phenytoin

154
Q

what causes bleeding tendency with epilepsy treatment?

A

valproate

155
Q

what must you know when treating someone with epilepsy?

A

emergency care

156
Q

how do you assess risk of fit for someone with epilepsy?

A

 good & bad phases
 ask when last three fits took place
 ask about compliance with medication
 ask about changes in medication

157
Q

what is multiple sclerosis?

A

 CNS lesions only
* DEMYELINATION of Axons

progressive functional loss

158
Q

what are symptoms of MS?

A
  • muscle weakness
  • visual disturbance
  • paraesthesia
  • autonomic dysfunction
  • dysarthria
  • pain
  • balance/hearing loss
159
Q

what are signs of MS?

A
  • muscle weakness
  • spasticity
  • altered reflexes
  • tremor
  • optic atrophy
  • proprioreceptive loss
  • loss of touch
160
Q

what CSF analysis do you do to investigate MS?

A
  • CSF analysis
    o reduced lymphocytes
    o increased IgG protein
161
Q

what happens when someone has MS?

A
  • Relapsing and remitting type - acute exacerbations and periods of respite
    o Damage builds up with each episode
162
Q

what will many people develop with MS?

A

secondary progressive

163
Q

what is primary progressive type of MS?

A
  • Primary progressive type – slow steady progressive deterioration
    o Cumulative neurological damage
164
Q

how do you manage MS symptoms?

A

o antibiotics, antispasmodics, analgesia, steroids
o physiotherapy & occupational therapy

165
Q

what is disease modifying therapies of MS?

A

o Disease modifying therapies – may also slow some progressive forms
 Cladribine
 Siponomod
 Ocrelizumab

166
Q

what are dental aspects of MS?

A
  • limited mobility & psychological disorders
  • treat under LA
  • orofacial motor & sensory disturbance
  • Chronic orofacial pain possible
  • Enhanced TRIGEMINAL NEURALGIA risk
167
Q

what must you suspect in younger patients of MS?

A
  • orofacial motor & sensory disturbance
  • Enhanced TRIGEMINAL NEURALGIA risk
168
Q

what is motor nuerone disease?

A

 degeneration in the spinal cord
* corticospinal tracts/anterior horns
 bulbar motor nuclei

169
Q

when happens to people with motor neurone disease?

A

 patients aged 30-60yrs
* death with 3 years of diagnosis

170
Q

what happens to motor function of motor neurone disease?

A

 Progressive loss of motor function
* limbs
* intercostal
* diaphragm
* motor cranial nerves VII – XII

171
Q

what is death due to in motor neurone disease?

A
  • ventilation failure
  • aspiration pneumonia (swallowing/cough)
172
Q

what is treatment of motor neurone disease?

A
  • Physiotherapy & occupational therapy
  • Riluzole
    o some get 6-9 months life extension
  • Aspiration prevention
    o PEG tube feed
    o Reduce salivation
173
Q

what is purpose of riluzole in MND treatment?

A

o some get 6-9 months life extension

174
Q

how do you prevent aspiration in MND?

A

o PEG tube feed
o Reduce salivation

175
Q

what are dental aspects of MND?

A
  • difficulty in acceptance of dental care
    o muscle weakness of head & neck
  • realistic treatment planning
  • drooling & swallowing difficulties
176
Q

what is cause of parkinson’s?

A
  • Degeneration of dopaminergic neurones in the basal ganglia of the brain (substantia nigra)
    o Shortage of Dopamine results in difficulty of message passaging from ‘thinking’ to ‘doing’ brain
    o Underlying reason for this is unclear
177
Q

what are clinical signs of parkinsons?

A
  • BRADYKINESIA
  • RIGIDITY
  • TREMOR
178
Q

what is bradykinesia?

A

o Slow movement, and slow initiation of movement

179
Q

what is rigidity?

A

increased muscle tone

180
Q

what is tremor in MND?

A

o slow amplitude
o Can progress to on/off movement disorder – often after treatment

181
Q

what are clinical observations of parkinsons?

A
  • Manifestation
  • Impaired gait and falls
  • Impaired use of upper limbs
  • Mask-like face
  • Swallowing problems
182
Q

what is physical support treatment of parkinsons?

A

physiotherapy and Occupational therapy

These work to maintain function at as high a level for as long as possible

183
Q

what is medical treatment of parkinsons?

A

o Dopamine
 Levadopa

o Dopamine analogues
 Tablets – Promipexole, Selegiline
 Injection – apomorphine - subcutaneous
 Infusion – duodopa – directly into the gut

184
Q

what is dopamine analogues?

A

 Tablets – Promipexole, Selegiline
 Injection – apomorphine - subcutaneous
 Infusion – duodopa – directly into the gut

185
Q

what is surgical treatment of parkinsons?

A
  • Stereotactic surgery
    o Deep brain stimulation
  • Stem cell transplant?
186
Q

what does anticholinergic effects of drugs do dentally?

A

dry mouth

187
Q

what are dental aspects of parkinsons?

A
  • Difficulty accepting treatment
    o Tremor at rest of body
    o Often facial tremor reduces on purposeful movements e.g. mouth opening
  • Dry mouth
    o Anticholinergic effects of the drugs
  • Drug interactions?
188
Q

what does increased oestorgen and porgestorone do in pregnancy?

A

 act on kidney to increase Renin secretion
 Increased salt & water retention
 Increased plasma volume by 45%

189
Q

what does the increase in plasma volume in pregnancy do?

A
  • Dilution effect makes Hb fall from 15-12g/dL
  • Protects against haemorrhage at birth
190
Q

in pregnancy the lower oesophageal sphincter relaxes causing what?

A

With increase abdominal pressure gives increased GORD

191
Q

what does increase in hormonal changes do during pregnancy?

A

reduce insulin sensitivity so diabetes

192
Q

what happens haematologically when pregnant?

A

 increased production of RC, WC, Platelets
 20% increase in RC mass
 Increased platelet consumption makes platelets normal to low

 Increased WC makes diagnosing infections difficult

193
Q

when pregnant the vascular smooth muscle relaxes so what happens?

A

 Reduced peripheral resistance
 Reduced systolic and diastolic blood pressure
 Compensatory increase in heart rate by 25%

194
Q

what happens to the coagulation screens when pregnant?

A

 Clotting factor production increases
 Fibrinolysis increases
 Increased system sensitivity with increased DVT risk

195
Q

when does development start in pregnancy

A

week 4

196
Q

what does the zygote become?

A

embryo

197
Q

when does embryonic circulation start?

A

o Week 6 – start of embryonic circulation
 Weeks 6-10 embryonic development & growth

198
Q

what happens week 10 in pregnancy?

A

 Foetus 10-14 weeks – features and limbs become developed and active!

199
Q

what is highest in first trimester?

A

miscarriage

200
Q

when is 2nd trimester?

A

14 weeks

201
Q

what happens 18 weeks pregnant?

A

toe and fingers formed

202
Q

when is final development of vision and senses when pregnant?

A

20-26

203
Q

when is 3rd trimester?

A

week 27

204
Q

what is birth testing?

A

 Physical examination
 Hearing test
 Blood spot

205
Q

what is blood spot for?

A
  • Phenylketonuria - PKU
  • Hypothyroidism
  • Cystic Fibrosis
  • Sickle cell disease
206
Q

what is blood spot for?

A
  • Phenylketonuria - PKU
  • Hypothyroidism
  • Cystic Fibrosis
  • Sickle cell disease
207
Q

what does APGAR score stand for?

A

activity, pulse, grimace, appearance and respiration

208
Q

what is dentistry during pregnancy?

A

 Cost of dental care
 Drugs in pregnancy
 Pregnancy gingivitis
 Periodontal health in pregnancy
 Position of mother

209
Q

in babies what happens month 1?

A

raise head

210
Q

in babies what happens month 2?

A

smile and rolls

211
Q

in babies what happens month 3?

A

eyes follow

212
Q

in babies what happens month 4?

A

sits supported

213
Q

in babies what happens month 5?

A

stands held

214
Q

in babies what happens month 6?

A

sits little support

215
Q

in babies what happens month 7?

A

sits without support

216
Q

in babies what happens month 8?

A

sits steadily

217
Q

in babies what happens month 9?

A

stand short time

218
Q

in babies what happens month 10?

A

pull self up

219
Q

in babies what happens month 11?

A

walk holding furniture

220
Q

in babies what happens month 12?

A

walk one hand held

221
Q

in babies what happens month 15?

A

walks self

222
Q

in babies what happens month 18 months?

A

say 6 words

223
Q

in babies what happens 2 years?

A

able run

224
Q

in babies what happens 3 years?

A

can repeat 2 numbers in a row

225
Q

in babies what happens 4 years?

A

repeat 6 word sentence

226
Q

in babies what happens 5 years?

A

can follow 3 commands

227
Q

what act is Concerned purely with management & treatment of psychiatric disorders?

A

mental health act (scotland) 2003

228
Q

how long is emergency detention?

A

72 hours

229
Q

how long is short term detention?

A

28 days

230
Q

how long is compulsory treatment order?

A

6 months

231
Q

how long is detention by a doctor?

A

2 hours

232
Q

what is application of mental health act 2003?

A

 That the person has a mental disorder.
 Medical treatment is available which could stop their condition getting worse, or help treat some of their symptoms.
 If that medical treatment was not provided, there would be a significant risk to the person or to others.
 Because of the person’s mental disorder, his/her ability to make decisions about medical treatment is significantly impaired.
 That the use of compulsory powers is necessary.

233
Q

what is neurosis and psychosis/

A

o Neurosis
 Contact retained with reality
o Psychosis
 Contact lost with reality

234
Q

what is Generalised anxiety disorder?

A

 free-floating anxiety in many/all situations

235
Q

what is phobic anxiety?

A

 intense anxiety / panic in specific situations

236
Q

what is panic disorder?

A

 unpredictable extreme anxiety

237
Q

what are anxiolytic drugs?

A

o Alcohol
o Benzodiazepines
o Antidepressants – with anxiolytic features

238
Q

what are types of benzodiapines?

A

 diazepam, midazolam, temazepam, lorazepam

239
Q

what are types of antidepressants?

A

 Tricyclic (noradrenaline & 5HT)
* Amitriptyline, Dosulepin, Nortriptyline, Imipramine

 Mirtazepine

 SSRI (Selective Serotonin Reuptake Inhibitors – 5HT)
* Fluoxetine, Sertraline, Citalopram

240
Q

what is bipolar 1?

A

mania

241
Q

what is bipolar 2?

A
  • Cyclothymia
  • Hypomania
242
Q

what is mania and hypomania symptoms?

A

 Increased productivity & feeling of wellbeing
 Reduced need for sleep
 Gradual reduction in social functioning and occupational functioning
 Increase in reckless behaviour
 Followed by period of depression

243
Q

what is drug treatment of mood disorders?

A

 Antidepressant
 Mood stabilising

244
Q

how long does drug treatment of mood disorder last?

A

2 years

245
Q

what are acute phase antidepressants?

A

 Selective Serotonin Reuptake inhibitor (SSRI)
 Venalfaxine/Mirtazepine
 Tricyclic antidepressants (TCA)
 Monoamine oxidase inhibitor (MAOI)

246
Q

what are mood stabilising drugs>

A

 Lithium
 Carbamazepine
 Valproate
 Lamotrigine

247
Q

what are side effects in tricylic antidepressants?

A

dry mouth, sedation, weight gain

248
Q

what are cuations in tricylic antidepressants?

A

glaucoma, prostatism

249
Q

what are SSRIs?

A

o prozac’ type drugs
 fluoxetine, paroxetine, fluvoxamine
 citalopram, sertraline

250
Q

what are SSRIs side effects?

A

 Acute anxiety disorders
 some patients similar to TCA - sedation, dry mouth
 gastrointestinal upset

251
Q

what are interactions of MAOIs?

A

 indirect acting sympathomimetic amines (e.g ephedrine)
* enhanced vasoconstrictor effect
* cold & cough remedies
 foodstuffs - tyramine containing, alcohol/low alcohol
bovril/oxo/marmite, cheese, herring, beans

252
Q

when on lithium what is avoided?

A

 avoid NSAID, METRONIDAZOLE

253
Q

what is lithium?

A

K+ subsitute

254
Q

what is direct drug effect of anti depressants in dentistry?

A

 dry mouth – caries (lithium)
 sedation
 facial dyskinesias

255
Q

what are drug effects of psychoses?

A

 dry mouth
 drug interactions
 dyskinesias - tonic or dystonia (tardive)

256
Q

what are drug therapy of schizophrenia?

A
  • Oral or depot IM injection - compliance, frequency of requirement
  • Dopamine antagonist drugs - cause ‘extrapyramindal’ side effects, dry mouth and sedation
  • Atypical Antispychotics – less likely to cause extrapyramidal side effects
257
Q

what are antipsychotic drugs?

A

o Butryrophenones
o Phenothiazines
o Thioxanthenes

258
Q

what are extrapyramidal side effects of antipsychotics?

A

o Akathisia
o Dystonia
o Parkinsonism
o Tardive dyskinesia

259
Q

what is akathsia?

A

 feeling of restlessness, making it hard to sit down or hold still
 Symptoms include tapping your fingers, rocking, and crossing and uncrossing your legs

260
Q

what is dystonia?

A

 muscles involuntarily contract and contort leading to painful positions or movements

261
Q

what is parkonism?

A

 the same symptoms as someone with Parkinson’s disease, but your symptoms are caused by medications, not by the disease
 may include tremor, slower thought processes, slower movements, rigid muscles, difficulty speaking, and facial stiffness.

262
Q

what is tardive dyskinesia?

A

 uncontrollable facial movements such as sucking or chewing, lip-smacking, sticking your tongue out or blinking your eyes repeatedly
 Do not go away if medicine is stopped

263
Q

how do you treat extrapyramidal symptoms?

A

o Use an ‘atypical’ antipsychotic instead
o Beta-adrenergic Blockers (non-selective)
o Anticholinergics

264
Q

what are common beta blockers?

A

 Propranolol
 Metropolol

265
Q

what are common antichloinergics?

A

 Procyclidine
 Benztropine
 Diphenhydramine
 Pramipexole

266
Q

what are oral effects of anorexia?

A

 don’t eat - oral effects of malnutrition
* ulcers, dry mouth, infections, bleeding

267
Q

what are oral effects of bulimia?

A

 dental erosion & oesophageal stricture
o Comfort eating

268
Q

what is sialosis and where does it usually happen?

A

enlargement of salivary glands and usually the parotid gland

269
Q

what is ischaemia?

A

inadequate blood supply to part body

270
Q

what is infarction?

A

tissue death of that part due to inadequate blood supply

271
Q

what is aneurysm?

A

bulging of the blood vessel

272
Q

what is atheroma?

A

fatty material build up in arteries

273
Q

what is dysphonia?

A

abnormal voice

274
Q

what is dysarthria?

A

difficulty speaking because of facial muscle weakness

275
Q

what is hyperplasia?

A

enlargement of organ

276
Q

what is lability?

A

rapid exaggerated changes in mood

277
Q

what is dyspesia?

A

ingestion

278
Q

what is cylcothymia?

A

periods of feeling low and periods of extreme happiness

279
Q

what is hypomania?

A

periods of over active high energy

280
Q

what is dykinesisa?

A

involuntary movements

BDS3: BAMS (8 decks)

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