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BDS 2 BAMS > Cardiovascular 2 > Flashcards

Cardiovascular 2 Flashcards

1
Q

what is the most important risk factor in atherosclerosis

A

hyperlipidaemia

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2
Q

what are the 2 processes in atherosclerosis that result in disease

A

chronic inflammation and healing

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3
Q

describe chronic inflammation in atherosclerosis

A

high cholesterol damages the endothelial cells on blood vessels. these then increase their permeability to allow lipid and monocytes to move into the tunica intima. macrophages then engulf the lipid but cannot do anything with it. instead it forms foam cells

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4
Q

describe healing in atherosclerosis

A

cytokines then move to the site of inflammation, cause proliferation of smooth muscle, this then forms a fibrous cap over the foam cells. this is now known as an atheroma

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5
Q

how can chronic periodontitis be related to hypertension

A

the inflammatory markers produced in perio disease migrate to the liver and can increase systemic inflammation which increases atherosclerosis production

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6
Q

give an example of a chronic coronary condition

A

ventricular hypertrophy - caused by hypertension, pump has to pump harder against more resistance, heart muscle increases in size as myocytes proliferate, size of chamber decreases in size and blood flow to heart remains the same, becomes ischaemic

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7
Q

what kinds of valvular disease

A

insufficiency - failure to close

stenosis - failure to open

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8
Q

why might a blood vessel tumour appear in the elderly

A

haemangioma - hamartoma is congenital, bengin but as the mucosa thins with age it becomes apparent

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9
Q

what causes kaposi sarcoma and who is more vulnerable

A

human herpes virus 8, immunocompromised people especially HIV positive patients

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10
Q

what defines hypertension

A

raised blood pressure, higher than 140/90, take 3 measurements with 15 mins of rest between

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11
Q

what are some risk factors for hypertension

A

age - less elasticity, gender, genetics, obesity and diabetes

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12
Q

what is the result of hypertension

A

increased atherosclerosis, increases risk of heart problems, stroke and dvt. also can result in renal failure

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13
Q

what are the types of hypertension

A

essential - unsure of cause
renal - caused by renal stenosis, low blood flow to kidney, increases renin secretion to increase fluid retention
endocrine - tumour on adrenal gland, pressing on kidney and increasing cortisol secretion - increasing fluid resorption

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14
Q

what are the signs and symptoms of hypertension

A

usually none, may have a headache or TIA

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15
Q

what investigations can be done

A

urine sample - check electrolytes for reabsorption in kidney, check blood for creatinine, urea and cholesterol

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16
Q

how is hypertension treated

A

elderly - diuretics and calcium channel blockers

young - beta blockers and ACE inhibitors

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17
Q

what is heart failure defined as

A

heart unable to meet demands of body

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18
Q

what is the difference between high output and low output heart failure

A

high - when heart cant meet demands as demands are increasing, low - when heart cant meet basic demands

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19
Q

how can heart failure and hypertension be linked

A

heart failure - body thinks body has lost blood due to reduced output, increases blood pressure to counteract, this then makes heart failure worse

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20
Q

what might cause heart failure

A

damage to heart muscle - angina or MI
pressure overload - aortic stenosis, hypertension
arrythmias - atrial fibrillation, drugs - beta blockers, corticosteroids and anti-cancer drugs

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21
Q

what are the symptoms and signs for heart failure

A

depends on what side is effected
left - tachycardia, low HR, breathless, low bp
right - liver and gastrointestinal problems, oedema and ascites - increased venous pressure

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22
Q

how can heart failure be treated

A

reduce hypertension, treat valve disease or arythmias, positive ionotropes - digoxin

23
Q

what is valve stenosis

A

blockage of heart valve, unable to open fully, backs up left ventricle which can affect pulmonary system

24
Q

what is valve insufficiency

A

failure to close valves, get back flow into ventricle

25
Q

what is the effect of valve disease

A

reduced cardiac output

26
Q

what causes valve disease

A

heart muscle damage, mi or ischaemia, aortic aneurysm, cant cover full width, rheumatic disease, congenital

27
Q

what is rheumatic disease

A

host produces antibodies against streptocci infection. these antibodies can attack the heart valves, lead to calcification of valves. infections can be caused by dental treatment or infections

28
Q

how can valve disease be investigated

A

ultrasound, see the blood flow in real time, can see direction of travel of blood

29
Q

what kind of heart valves can be used for replacement

A

porcine - pig valves, similar to human, but only last 10 years, dont need to be on anticoagulants, better for elderly or young children
mechanical - everyone else, needs to be on anticoagulants for life but can last a long time

30
Q

what is tachycardia

A

increase of heart rate, atrial fibrillation

31
Q

what is bradycardia

A

decrease of heart rate, induced by drugs eg beta blockers

32
Q

what is ventricular fibrillation

A

still have electrical impulse but ventricle muscle is not contracting regularly, in MI or electrocuted, can be defibrillated reset SA node and heart muscle

33
Q

what is atrial fibrillation

A

qrs complex is happening, bit irregular but no p wave, treated by anticoagulants

34
Q

why might implanted pacemakers be used

A

in patients with bradycardia, sets a base line for electrical impulse for SA node, if it falls beneath this, pacemaker will pick it up and start firing, prevents heart rate getting so low than output results in unconsciousness

35
Q

how might a dentist recognise heart failure

A

peripheral oedema if right side, on digoxin or if left side heart might be breathless lying back

36
Q

describe infective endocarditis

A

streptococcus viridans into blood stream, can colonise cardiac valves (commonly mitral), causes vegetation, enlargement and surface abnormalities, this results in haemodynamic changes and turbulent flow, results in platelet aggregation - further vegetation of valve and heart muscle - heart valve and muscle damage

37
Q

what patients are at risk of infective endocarditis

A

those who have had it before, those with congenital cardiac problems and those with valve replacement - porcine or mechanical

38
Q

how did the guidelines for patients change regarding IE

A

used to be anyone remotely at risk would receive antibiotic prophylaxis for dental treatment - if had rheumatic fever or any cardiac problems - CABG, angioplasty - now it is more specific and less people get it

39
Q

what changed with the 2016 NICE guidlines regarding IE

A

routinely - AP shouldn’t be given routinely, more up to the dentist and the physician if the patient should be given AP prior to treatment

40
Q

what dental treatments are a risk for IE

A

anything manipulating dento-gingival junction - restorations are okay unless matrix band required, periodontal treatment, extractions are risk, endodontics should be okay

41
Q

what should the focus be more for dentists to reduce risk of IE

A

reduce requirement for treatment - preventative measures, oral hygiene instructions, reduce bacteria in mouth

42
Q

what are some disorders of haemophillia

A

haemophillia A - lack of factor VIII, sex linked recessive
haemophilia B - lack of factor IX, sex linked recessive
von wille brand disease - lack of factor VIII plus lack of platelet aggregation - autosomal dominant

43
Q

what is the effect of a haemophilia disorder

A

inability to clot, prolonged bleeding time, risk of haemorrage

44
Q

how is haemophilia A treated

A

carriers or mild disease - transexamic acid - slows down the break down of clot, DDAVP - vasopressin pulling factor 8 off of epithelial cells
moderate to severe - requires recombinant factor 8

45
Q

how is haemophilia B treated

A

cannot use DDAVP as this is a factor 9 problem, all spectrums have to have recombinant factor for treatment, can use transexamic acid also

46
Q

how is von wille brand disease treated

A

DDVAP and transexamic acid, more severe can receive recombinant factor 8

47
Q

how are patients with bleeding disorders treated for dental

A

mild or carriers - minor oral surgery, periodontal treatment, extraction - requires hospital. local anaesthetic - buccal infiltration, intra ligamentary or intra papillary can be done in GDP but treatments requires IDB or lingual infiltration require hospital
moderate and severe - require hospital for everything, unless edentulous and only prosthodontics required - can be done in GDP

48
Q

give examples of thrombophilia

A

congenital - protein c or s deficiency, anti thrombin 3
acquired - oral contraceptive pill, surgery, immobility after surgery, smoking, cancer
normally have a congenital problem without knowing, acquired on top

49
Q

what is the consequence of thrombophilia

A

embolism, can block arteries - result in DVT or stroke or pulmonary embolism

50
Q

how can you get for a palatelet problem

A

FBC - check platelet numbers

51
Q

what can be done to check liver function in a patient with liver disease and what treatment can be given

A

pro thrombin time - PTT - checked in INR, should be 1. anything higher than this suggest lack of function. if liver disease, lacking many clotting factors, better to give fresh frozen plasma - replace all clotting factors

52
Q

what is drug induced coagulopathy and what patients might experience this

A

inability to clot blood due to medication, normally on medication for atrial fibrillation, valve replacement, DVT or heart valve disease

53
Q

what are the treatment guidelines for those on warfarin

A

check INR 48 hours prior to treatment but as close as possible, should be between 2-4. treat early in morning, aid homeostasis - vasoconstrictor with LA, sutures, pressure, if using LA avoid IDB if you can, can give it if required, provide good post op instructions including emergency contact

BDS 2 BAMS (12 decks)

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