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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
define ischaemia
narrowing of a blood vessel, reducing the oxygen delivery to that area
26
how does ischaemia occur
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
27
give examples of ischaemic disease
angina pectoralis, transient ischaemic attack in brain
28
how does angina occur
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
29
what is the difference between classical and unstable angina
classical - onset with increase in demand of heart eg exercise, unstable - happens randomly, no extra pressure on heart
30
what are signs and symptoms of angina
symptoms - chest pain, may radiate down back and jaw, nausea, shortness of breath, angiography - blockage in coronary artery
31
how can angina be treated
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
32
what is an angioplasty
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
what is a CABG
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
what are some disadvantages and advantages to CABG
adv - restores blood flow | disadv - not attacking cause, very invasive, patient might have a heart attack during surgery, veins replacing artery
35
what is the difference between ischaemia and infarction
infarction the vessel is completely occluded, no blood flow at all to the area
36
how can infarction occur
on a vessel already with atherosclerotic plaque, the endothelial lining is damaged so platelets aggregate and completely occlude the vessel
37
what is the problem with unstable angina and MI
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
what are some symptoms of MI
pale, nauseous, severe pain which radiates
39
what investigations would you undertake if someone was having an MI
ECG - check for ST segment elevation, biomarkers - troponin, creatine kinase
40
what treatment might a patient undergo after an MI
thrombolysis, CABG, angioplasty
41
what medication might a patient be on after an MI
aspirin, clopdirogrel, GTN, nifidepine, verapamil, lisinopril, furosemide, warfarin
42
what other types of infarcation and ischaemia is there
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
what cells come from the myeloid cell line
RBC, platelets, monocytes and granulocytes
44
what cells come from the lymphoid cell line
B cells, T cells and Natural killer cells
45
how do haemo malignancies come about
genetic mutation, normally translocation - oncogene switched on or tumour suppressor gene switched off
46
what is clonal proliferation
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
what are some characteristics of cancer
uncontrolled proliferation, turn off apoptosis, loss of normal function and products
48
what is the difference between acute and chronic cancer and give examples
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
give some examples of signs and symptoms of leukaemia
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
what is the non-hodkin lymphoma
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
what is hodgkin lymphoma
painless adenopathy, good prognosis, dont know what has caused it
52
what are the concepts of treatment of leukaemia
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
how can monoclonal antibodies be used for treatment
target antigens on cancer cells directly, no other cell types damaged
54
how can bone marrow transplant be used for treatment
completely remove patients bone marrow and replace with donor match or family match, starting fresh, however, if it doesnt work, left with nothing
55
what is anaemia
lack of haemaglobin
56
name different ways anaemia can occur
lack of production - problem with bone marrow or haemantics - loss of blood, bleeding - increased demand, pregnancy
57
what are the haemantics
constituents of haem in haemaglobin - iron, vitamin b12, folic acid
58
how might you investigate anaemia
fbc - rbc numbers - if bone marrow production problem | hmt - haemantic count to see if problem there
59
what would be found if it was a bone marrow problem
normal cells being produced but low numbers
60
how can we get iron into our body and what are the diff types
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
what might be the cause of iron deficiency
lack of in diet, stomach acid unable to convert non-haem to haem, coeliac disease, unable to absorb
62
how do we measure iron in blood
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
how might iron be lost
unexplained bleeding - gi ulcers or polyps
64
where can we source vitamin b12
we cannot make b12, we rely on animals making it and us ingesting it, dairy products and meat
65
what is required for vitamin b12 absorption and what type of anaemia is this if it is not there
intrinsic factor from parietal cells in stomach, pernicious anaemia
66
where can we source folic acid
green leafy veg, oranges
67
if a patient has low levels of folic acid and ferritin, what might we suspect
coeliac disease, both absorbed at jejenum so a deficiency of both indicates that absorption is the problem
68
why is folic acid important in pregnancy
a deficiency can result in neural tube defects - failed closure - spina bifida
69
how might the globin chain result in anaemia
genetic disorder thalassaemia or sickle cell anaemia
70
what is thalassaemia
genetic disorder of globin chain, alpha or beta, low RBC
71
what problems are seen in patients with thalassaemia
over production of RBC to counteract lack of oxygen, result in more removal of rbc and iron - splenomegalgy and cirrhosis
72
what is sickle cell anaemia
problem with the shape of the haemaglobin, result in blocking the vessel and preventing blood flow
73
what is mcv
mean cell volume - size of red blood cells
74
how can mcv be used to detect anaemia
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
what are reticulocytes
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
what investigations would be undertaken to find cause of anaemia
fbc - check rbc number hmc - check for deficiencies faecal sample - check for unexplained bleeding endoscopy - gastric ulcers and coeliac disease bone marrow sample
77
what would the treatment of anaemia be
treat the cause, replace haemantics or give blood transfusion
78
what oral conditions are associated with anaemia
recurrent oral ulcers and fungal infections

BDS 2 BAMS (12 decks)

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