Cardiovascular System Flashcards
name some reversible risk factors for CVD
obesity, exercise, smoking, diet
name some irreversible risk factors for CVD
genetics, family history, age, gender
what onsets of CVD are reversible
hypertension, hyperlipidaemia, diabetes
what are the two stages of prevention and what is more likely
primary - preventing before onset of disease
secondary - making modifications after disease eg stroke, MI, claudification, secondary is more likely
what stage of prevention is a dentist important in
primary, the dentist see’s patients for regular check ups when they are healthy, health promotion is crucial in primary prevention
what are the different ways to prevent disease
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
what drugs are involved in preventing onset of diseaes
lipid lowering, anti-platelets, anti-coagulants
what drugs are involved in reducing the symptoms of disease
ACE inhibitors, diuretics, beta blockers
name an anti-platelet drug and how does it work
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
name an anti-coagulant drug and how does it work
warfarin, blocks production of vitamin K thus stops production of vitamin K dependant clotting factors (2,7,9,10)
what are some problems with warfarin and what drugs cannot be used with warfarin
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
what are the new anti-coagulant drugs
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
name a lipid lowering drug and how does it work
simvastatin, prevents synthesis of cholesterol in the liver, reduces atherosclerosis, long acting drug, but cannot be used with anti-fungals
name a beta blocker and how does it work
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.
why should we be cautious with patients on beta blockers
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
name a diuretics and how does it work
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
name a calcium channel blocker and how does it work
nifedipine, prevents smooth muscle contraction resulting in vasodilation which reduces hypertension. reduces resistance in arteries. can also act on heart to slow impulses - verapamil
what dental side affect is caused by calcium channel blockers
gingival hyperplasia
name an ACE inhibitor and how does it work
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
name a nitrate and how does it work
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
what investigations would need to be carried out if you were cautious of a patients ability to clot
FBC to check platelet numbers and an INR
why might a patient receive a blood transfusion
to receive clotting factors, if low RCC after trauma
why must blood be checked before transfusion
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
why are some complications of blood transfusions
heart failure due to increased volume, wrong blood type given resulting in jaundice, fever and possible death
define ischaemia
narrowing of a blood vessel, reducing the oxygen delivery to that area
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
give examples of ischaemic disease
angina pectoralis, transient ischaemic attack in brain
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
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
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
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
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
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
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
what is the difference between ischaemia and infarction
infarction the vessel is completely occluded, no blood flow at all to the area
how can infarction occur
on a vessel already with atherosclerotic plaque, the endothelial lining is damaged so platelets aggregate and completely occlude the vessel
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
what are some symptoms of MI
pale, nauseous, severe pain which radiates
what investigations would you undertake if someone was having an MI
ECG - check for ST segment elevation, biomarkers - troponin, creatine kinase
what treatment might a patient undergo after an MI
thrombolysis, CABG, angioplasty
what medication might a patient be on after an MI
aspirin, clopdirogrel, GTN, nifidepine, verapamil, lisinopril, furosemide, warfarin
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
what cells come from the myeloid cell line
RBC, platelets, monocytes and granulocytes
what cells come from the lymphoid cell line
B cells, T cells and Natural killer cells
how do haemo malignancies come about
genetic mutation, normally translocation - oncogene switched on or tumour suppressor gene switched off
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
what are some characteristics of cancer
uncontrolled proliferation, turn off apoptosis, loss of normal function and products
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
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
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
what is hodgkin lymphoma
painless adenopathy, good prognosis, dont know what has caused it
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
how can monoclonal antibodies be used for treatment
target antigens on cancer cells directly, no other cell types damaged
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
what is anaemia
lack of haemaglobin
name different ways anaemia can occur
lack of production - problem with bone marrow or haemantics - loss of blood, bleeding - increased demand, pregnancy
what are the haemantics
constituents of haem in haemaglobin - iron, vitamin b12, folic acid
how might you investigate anaemia
fbc - rbc numbers - if bone marrow production problem
hmt - haemantic count to see if problem there
what would be found if it was a bone marrow problem
normal cells being produced but low numbers
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
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
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
how might iron be lost
unexplained bleeding - gi ulcers or polyps
where can we source vitamin b12
we cannot make b12, we rely on animals making it and us ingesting it, dairy products and meat
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
where can we source folic acid
green leafy veg, oranges
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
why is folic acid important in pregnancy
a deficiency can result in neural tube defects - failed closure - spina bifida
how might the globin chain result in anaemia
genetic disorder thalassaemia or sickle cell anaemia
what is thalassaemia
genetic disorder of globin chain, alpha or beta, low RBC
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
what is sickle cell anaemia
problem with the shape of the haemaglobin, result in blocking the vessel and preventing blood flow
what is mcv
mean cell volume - size of red blood cells
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
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
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
what would the treatment of anaemia be
treat the cause, replace haemantics or give blood transfusion
what oral conditions are associated with anaemia
recurrent oral ulcers and fungal infections
