Crighton Flashcards

1
Q

What are examples of the immune systems second line of defence?

A

Phagocytes (natural killer cells, granulocytes, macrophages)

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2
Q

What are examples of the immune systems third line of defence?

A

Antibodies

Lymphocytes (t cells, B cells)

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3
Q

What are examples of acquired and genetic immunodeficiency?

A

Acquired - viral (HIV), cancer chemotherapy, therapeutic immunosuppression (drugs - steroids, organ transplant)
Genetic - thymic aplasia, neutrophil deficiencies

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4
Q

What are the causes of neutrophil deficiency?

A

Congenital, bone marrow depression, drugs, autoimmune, viral

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5
Q

What are the effects of PMN (granulocytes) deficiency?

A
Pyogenic infection (skin infections, URTI eg pneumococcal infections, urinary and renal infections)
Fungal infections - candida
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6
Q

What are the primary and secondary causes of lymphocyte deficiency?

A

Primary - congenital (thymus)

Secondary - acquired (drugs, radiation)

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7
Q

What are examples of the immune systems first line of defence?

A

Skin, mucous membranes, enzymes, natural microbial flora, complement proteins

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8
Q

What is the main aetiology of strokes?

A

Infarction 85%, haemorrhage 10%, subarachnoid haemorrhage 5%, venous thrombosis

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9
Q

What is the epidemiology of a stroke, including lifetime risk of a stroke?

A

2 per 1000/year
Male>female
Increasing incidence with age (0.5/1000 age 50, 15/1000 age 80)
1 in 6

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10
Q

What are the risk factors for stroke?

A

Hypertension (if diastolic >110mmHg, then 15x more at risk)

Smoking, alcohol, ischaemia heart disease, atrial fib, diabetes mellitus

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11
Q

What is the aetiology of stroke?

A

Ischaemic stroke - uncertain
Intracranial bleed - aneurysm rupture
Embolic stroke - embolism from left side of heart, (atrial fib, heart valve disease, recent MI), atheroma of cerebral vessels (carotid bifurcation, ICA, vertebral a.)
Venous thrombosis - OCP use, polycythaemia, thrombophilia

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12
Q

What are the prevention methods for stroke?

A

Reduce risk factors (smoking, diabetes control, control hypertension)
Antiplatlet action (secondary prevention only - aspirin, dipyramidole, clopidogrel)
Anticoagulants if embolic risk
Carotid endarterectomy - severe stenosis, previous TIAs,

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13
Q

What investigations can be used for stroke?

A

Need to differentiate between infraction, bleed, subarachnoid haemorrhage
Imaging - CT scan (rapid, easy access, poor for ischaemic stroke), MRI scan (difficult to obtain quickly, better at visualising early changes of damage), MRA (best for visualising brain circulation), digital subtraction angiography (if MRA unavailable)
Assess risk factors - carotid ultrasound, ECG, BP, diabetic screening, thrombophilia screening (in young pts)

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14
Q

What is the management for strokes?

A

Acute phase - reduce damage - penumbra region (Ca channel blockers eg Nimodipine), improve blood flow/oxygenation (thrombolysis possible within 3hrs, maintain perfusion pressure to brain, ensure normoglycaemia)
Remove haematoma (subarachnoid haemorrhage only)
Prevent future risk - aspirin 300mg daily, anticoagulation if indicated (eg atrial fib., left ventricular thrombus)
Chronic phase - nursing and rehab - immobility support (prevent bed sores, physiotherapist to prevent contracture); speech and language therapy; occupational therapy

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15
Q

What are the dental aspects of stroke?

A

Impaired mobility and dexterity (attendance, OH)
Communication difficulties (dysphonia, dysarthria, cognitive difficulties)
Risk of cardiac emergencies - MI, further stroke
Loss of protective reflexes - aspiration, managing saliva (anticholinergic drugs help)
Loss of sensory info. - difficulty adapting to new oral environment eg new denture
‘Stroke pain’ - CNS generated pain perception

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16
Q

What is the pathophysiology of epilepsy?

A

Associated with reduced GABA levels in brain -> leads to abnormal cell-cell message propagation

17
Q

What are the different classifications of epilepsy?

A

Generalised - tonic/clonic, absence (petit mal), myoclonic/atonic
Partial - simple partial, complex partial, simple sensory

18
Q

What is the aetiology of epilepsy?

A

Idiopathic (most common cause)
Trauma (head injury)
CNS disease - tumour, stroke, CJD, meningitis, encephalitis
Social - late nights, alcohol, hypoglycaemia, flashing lights
HYPERTHERMIA

19
Q

What is the management for strokes?

A

Acute phase - reduce damage - penumbra region (Ca channel blockers eg Nimodipine), improve blood flow/oxygenation (thrombolysis possible within 3hrs, maintain perfusion pressure to brain, ensure normoglycaemia)
Remove haematoma (subarachnoid haemorrhage only)
Prevent future risk - aspirin 300mg daily, anticoagulation if indicated (eg atrial fib., left ventricular thrombus)
Chronic phase - nursing and rehab - immobility support (prevent bed sores, physiotherapist to prevent contracture); speech and language therapy; occupational therapy

20
Q

What are the dental aspects of stroke?

A

Impaired mobility and dexterity (attendance, OH)
Communication difficulties (dysphonia, dysarthria, cognitive difficulties)
Risk of cardiac emergencies - MI, further stroke
Loss of protective reflexes - aspiration, managing saliva (anticholinergic drugs help)
Loss of sensory info. - difficulty adapting to new oral environment eg new denture
‘Stroke pain’ - CNS generated pain perception

21
Q

What is the pathophysiology of epilepsy?

A

Associated with reduced GABA levels in brain -> leads to abnormal cell-cell message propagation

22
Q

What are the different classifications of epilepsy?

A

Generalised - tonic/clonic, absence (petit mal), myoclonic/atonic
Partial - simple partial, complex partial, simple sensory

23
Q

What is the aetiology of epilepsy?

A

Idiopathic (most common cause)
Trauma (head injury)
CNS disease - tumour, stroke, CJD, meningitis, encephalitis
Social - late nights, alcohol, hypoglycaemia, flashing lights
HYPERTHERMIA

24
Q

What is the difference between tonic/clonic seizures and petit mal seizures? How would you risk assess these patients?

A
Tonic/clonic - pt loses consciousness, muscles stiffen, and jerking movements can be seen (initial tonic - stiff, then clonic - contraction/relaxation)
Petit mal (absence) - brief spells of unconsciousness without loss of posture, last about 5-15secs, childhood
Risk assessment - ask when last 3 fits were, ask about compliance with medication, ask about changes in medication
25
Q

What oral effects may tonic/clonic epileptic pts have?

A

Medication - phenytoin causes hyperplasia, valproate has a bleeding tendency
Trauma - complication of fit, oral soft tissue injury, dental injury/fracture