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BDS 2 BAMS > Cardiovascular System > Flashcards

Cardiovascular System Flashcards

1
Q

name some reversible risk factors for CVD

A

obesity, exercise, smoking, diet

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2
Q

name some irreversible risk factors for CVD

A

genetics, family history, age, gender

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3
Q

what onsets of CVD are reversible

A

hypertension, hyperlipidaemia, diabetes

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4
Q

what are the two stages of prevention and what is more likely

A

primary - preventing before onset of disease

secondary - making modifications after disease eg stroke, MI, claudification, secondary is more likely

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5
Q

what stage of prevention is a dentist important in

A

primary, the dentist see’s patients for regular check ups when they are healthy, health promotion is crucial in primary prevention

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6
Q

what are the different ways to prevent disease

A

lifestyle change - exercise, stop smoking, change diet

or drugs - need to weigh up the benefit of the drug and see if it is worth the risks

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7
Q

what drugs are involved in preventing onset of diseaes

A

lipid lowering, anti-platelets, anti-coagulants

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8
Q

what drugs are involved in reducing the symptoms of disease

A

ACE inhibitors, diuretics, beta blockers

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9
Q

name an anti-platelet drug and how does it work

A

aspirin, prevents platelet aggregation. damages platelets irreversibly but these only live for a week so needs to be taken daily to catch any new ones. platelets can aggregate on blood vessel walls, making the lumen narrower and restricting blood flow, resulting in hypertension. aspirin can be used in conjunction with clopidogrel however, more used, harder it is to stop bleeding

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10
Q

name an anti-coagulant drug and how does it work

A

warfarin, blocks production of vitamin K thus stops production of vitamin K dependant clotting factors (2,7,9,10)

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11
Q

what are some problems with warfarin and what drugs cannot be used with warfarin

A

initially they cause hypercoagulation so needs to be used with herparin to stop this - patient must be hospitalised. also, can interact with so many drugs via plasma proteins which alters its bioavailability, therefore, dose might need changed regularly and patient must get INR checked regularly - should be between 2-4, cannot be used with antibiotics, NSAID and anti-fungals

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12
Q

what are the new anti-coagulant drugs

A

apixaban, more expensive but a predictable bioavailability, doesnt need constant checking or INR, can use antibiotics, local and anti-fungals but still cant use NSAID

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13
Q

name a lipid lowering drug and how does it work

A

simvastatin, prevents synthesis of cholesterol in the liver, reduces atherosclerosis, long acting drug, but cannot be used with anti-fungals

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14
Q

name a beta blocker and how does it work

A

prevents adrenaline binding to beta receptors. can be specific - just beta 1 on heart - atenolol. or non-specific, act on beta 2 in lungs and brain - makes asthma worse but can improve anxiety - propanolol.

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15
Q

why should we be cautious with patients on beta blockers

A

may be difficult for them to increase their heart rate, going from lying down to sitting up. may need an extra few minutes for blood pressure to return

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16
Q

name a diuretics and how does it work

A

furosemide, prevents reabsorption of fluid at the loop of henle. can reduce fluid retention which reduces blood pressure. but can off set electrolytes which would result in arrythmias

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17
Q

name a calcium channel blocker and how does it work

A

nifedipine, prevents smooth muscle contraction resulting in vasodilation which reduces hypertension. reduces resistance in arteries. can also act on heart to slow impulses - verapamil

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18
Q

what dental side affect is caused by calcium channel blockers

A

gingival hyperplasia

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19
Q

name an ACE inhibitor and how does it work

A

lisinopril, blocks angiotensin converting enzyme which prevents production of angiotensin 2. this is a potent vasoconstrictor. also stimulates production of aldosterone which causes fluid retention. thus blocking this reduces blood pressure

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20
Q

name a nitrate and how does it work

A

GTN, acts sub-lingually so avoids first pass metabolism, dilates veins - reduce pre load and dilates resistance arteries to reduce after load - for angina or hypertension

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21
Q

what investigations would need to be carried out if you were cautious of a patients ability to clot

A

FBC to check platelet numbers and an INR

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22
Q

why might a patient receive a blood transfusion

A

to receive clotting factors, if low RCC after trauma

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23
Q

why must blood be checked before transfusion

A

cross match the blood type ABO - A - a antigens so b antibodies, if wrong blood given, will attack the antigens on the surface of RBC

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24
Q

why are some complications of blood transfusions

A

heart failure due to increased volume, wrong blood type given resulting in jaundice, fever and possible death

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25
Q

define ischaemia

A

narrowing of a blood vessel, reducing the oxygen delivery to that area

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26
Q

how does ischaemia occur

A

build up of lipid in blood, becomes deposited on blood vessel walls, forms an atherosclerotic plaque on the blood vessel, resulting in narrowing of the lumen and reducing blood flow

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27
Q

give examples of ischaemic disease

A

angina pectoralis, transient ischaemic attack in brain

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28
Q

how does angina occur

A

heart receives blood supply from coronary arteries, these have no collateral supply or anastomses. when the heart contracts and the valves open, the coronary arteries are shut off, they only receive blood supply during diastole, therefore, if the coronary arteries have atherosclerosis and the heart is working harder (less time in diastole) it receives less oxygen than it requires

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29
Q

what is the difference between classical and unstable angina

A

classical - onset with increase in demand of heart eg exercise, unstable - happens randomly, no extra pressure on heart

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30
Q

what are signs and symptoms of angina

A

symptoms - chest pain, may radiate down back and jaw, nausea, shortness of breath, angiography - blockage in coronary artery

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31
Q

how can angina be treated

A

modifying risk factors - stop smoking, reduce diet, gradually increase exercise
drugs - statins, nitrates to reduce pre load, calcium channel blockers, ACE inhibitors
surgery - angioplasty, thrombolysis or CABG

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32
Q

what is an angioplasty

A

when the surgeon enters through arteries in leg into the heart - has a balloon and stent, at the plaque in coronary artery, inflates the balloon and breaks off plaque, then inserts a stent to keep artery open, not too invasive but not very long lasting and doesnt treat the cause

33
Q

what is a CABG

A

coronary artery bypass graft, taking a vein from the leg and placing it in the heart so the affected coronary artery is bypassed and no blood flows through here

34
Q

what are some disadvantages and advantages to CABG

A

adv - restores blood flow

disadv - not attacking cause, very invasive, patient might have a heart attack during surgery, veins replacing artery

35
Q

what is the difference between ischaemia and infarction

A

infarction the vessel is completely occluded, no blood flow at all to the area

36
Q

how can infarction occur

A

on a vessel already with atherosclerotic plaque, the endothelial lining is damaged so platelets aggregate and completely occlude the vessel

37
Q

what is the problem with unstable angina and MI

A

difficult to differentiate, have to check biomarkers - troponin is released in MI due to muscle damage, this indicates MI, until then, treat both as MI

38
Q

what are some symptoms of MI

A

pale, nauseous, severe pain which radiates

39
Q

what investigations would you undertake if someone was having an MI

A

ECG - check for ST segment elevation, biomarkers - troponin, creatine kinase

40
Q

what treatment might a patient undergo after an MI

A

thrombolysis, CABG, angioplasty

41
Q

what medication might a patient be on after an MI

A

aspirin, clopdirogrel, GTN, nifidepine, verapamil, lisinopril, furosemide, warfarin

42
Q

what other types of infarcation and ischaemia is there

A

Claudication and lower limb infarction - poor wound healing, gangrene, amputation
transient ischaemic attack or stroke - normally caused by an embolism, brain has good collateral blood supply

43
Q

what cells come from the myeloid cell line

A

RBC, platelets, monocytes and granulocytes

44
Q

what cells come from the lymphoid cell line

A

B cells, T cells and Natural killer cells

45
Q

how do haemo malignancies come about

A

genetic mutation, normally translocation - oncogene switched on or tumour suppressor gene switched off

46
Q

what is clonal proliferation

A

one cell type has a mutation resulting in it becoming immortal, every cell to then derive from this has the same mutation, tumour from one cell type - not always true

47
Q

what are some characteristics of cancer

A

uncontrolled proliferation, turn off apoptosis, loss of normal function and products

48
Q

what is the difference between acute and chronic cancer and give examples

A

acute - get very sick very quickly, very aggressive form of disease - acute lymphoblastic leukaemia
chronic - happens over a period of time, normally picked up on routine blood test, dont realise they have it - chronic lymphocytic leukaemia

49
Q

give some examples of signs and symptoms of leukaemia

A

anaemia - bone marrow only producing cancer cells, tired, pale, breathless
prone to infections that normally wouldn’t effect the healthy - lack of normal WBC’s
bleeding - lack of platelets
lumps at neck - so many cells they infiltrate into tissues, lymph nodes but not lymphoma

50
Q

what is the non-hodkin lymphoma

A

when b and t cells proliferate due to an external factor - H pylori or autoimmune disease, can treat the cancer but wont go away until actual cause is treated

51
Q

what is hodgkin lymphoma

A

painless adenopathy, good prognosis, dont know what has caused it

52
Q

what are the concepts of treatment of leukaemia

A

induction - chemotherapy to kill cancer cells
remission - complete treatment but have it at a low level to keep things at bay and prevent it coming back
maintenance - taking medication to prevent cancer cells
relapse - when cancer cells come back, maybe in a hard to reach area, need another round of treatment

53
Q

how can monoclonal antibodies be used for treatment

A

target antigens on cancer cells directly, no other cell types damaged

54
Q

how can bone marrow transplant be used for treatment

A

completely remove patients bone marrow and replace with donor match or family match, starting fresh, however, if it doesnt work, left with nothing

55
Q

what is anaemia

A

lack of haemaglobin

56
Q

name different ways anaemia can occur

A

lack of production - problem with bone marrow or haemantics - loss of blood, bleeding - increased demand, pregnancy

57
Q

what are the haemantics

A

constituents of haem in haemaglobin - iron, vitamin b12, folic acid

58
Q

how might you investigate anaemia

A

fbc - rbc numbers - if bone marrow production problem

hmt - haemantic count to see if problem there

59
Q

what would be found if it was a bone marrow problem

A

normal cells being produced but low numbers

60
Q

how can we get iron into our body and what are the diff types

A

diet - red meat and green leafy veg, can be haem or non-haem. our body can absorb haem - from red meat. if non-haem needs to be transformed into haem in stomach before absorption in the small intestine

61
Q

what might be the cause of iron deficiency

A

lack of in diet, stomach acid unable to convert non-haem to haem, coeliac disease, unable to absorb

62
Q

how do we measure iron in blood

A

check levels of ferritin, this is what iron is stored in cells as and the level of ferritin in blood is directly proportional to levels stored in cells

63
Q

how might iron be lost

A

unexplained bleeding - gi ulcers or polyps

64
Q

where can we source vitamin b12

A

we cannot make b12, we rely on animals making it and us ingesting it, dairy products and meat

65
Q

what is required for vitamin b12 absorption and what type of anaemia is this if it is not there

A

intrinsic factor from parietal cells in stomach, pernicious anaemia

66
Q

where can we source folic acid

A

green leafy veg, oranges

67
Q

if a patient has low levels of folic acid and ferritin, what might we suspect

A

coeliac disease, both absorbed at jejenum so a deficiency of both indicates that absorption is the problem

68
Q

why is folic acid important in pregnancy

A

a deficiency can result in neural tube defects - failed closure - spina bifida

69
Q

how might the globin chain result in anaemia

A

genetic disorder thalassaemia or sickle cell anaemia

70
Q

what is thalassaemia

A

genetic disorder of globin chain, alpha or beta, low RBC

71
Q

what problems are seen in patients with thalassaemia

A

over production of RBC to counteract lack of oxygen, result in more removal of rbc and iron - splenomegalgy and cirrhosis

72
Q

what is sickle cell anaemia

A

problem with the shape of the haemaglobin, result in blocking the vessel and preventing blood flow

73
Q

what is mcv

A

mean cell volume - size of red blood cells

74
Q

how can mcv be used to detect anaemia

A

microcytic - small, not enough in it, Fe deficiency or thalassaemia
macrocytic - problem with shrinkage, vitamin b12 or folic acid deficiency
hypochromic - paler, less haemaglobin so less red

75
Q

what are reticulocytes

A

rbc’s that have been released into bloodstream before fully matured, indicates there has been a loss of blood and cells been released to increase numbers

76
Q

what investigations would be undertaken to find cause of anaemia

A

fbc - check rbc number
hmc - check for deficiencies
faecal sample - check for unexplained bleeding
endoscopy - gastric ulcers and coeliac disease
bone marrow sample

77
Q

what would the treatment of anaemia be

A

treat the cause, replace haemantics or give blood transfusion

78
Q

what oral conditions are associated with anaemia

A

recurrent oral ulcers and fungal infections

BDS 2 BAMS (12 decks)

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