Cardiovasuclar Disease treatment and management Flashcards

1
Q

What are the three essential parts of the circularity system?

A

The circular system consists of the blood a liquid containing suspended cells which carries substance around the body

The heart a muscular pump which provides the force needed to move blood around the body

The blood vessels, the tubes through which the blood travels to through and from the tissues

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2
Q

Define cardiovascular disease and what does it include?

A

Cardiovascular disease compromises all diseases of the heart and circular system including heart disease/27% of all deaths in the UK in 2014 were CVD related 69,000 would due to coronary and 39,000 a stroke

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3
Q

List and explain three layers of blood vessels giving all of their names and relative locations within the blood vessels?

A

Blood vessels are made up of three layers the intima which is also referred to as the Tunica or endothelium which is the centre most layer it is a single layer of specialised multifunctional end Afilia cells which sense changes in blood pressure, oxygen tension and blood flow under normal circumstances. They prevent blood clotting and line the entire circular system from the heart to capillaries.

The media or Tunica media is the middle layer which is compromise of mainly smooth muscle reinforced by elastic tissue and there’s more prominent in arteries less so in veins and is responsible for vasodilation and vasoconstriction the closer a blood vessel is to the heart the more elastic tissue in order to cope with the pressure of systolic pressure

The outer layer is the adventitia and his compromise mainly of collagen which provides strength. This layer is most prominent in veins. The adventitia have small blood vessels which penetrate into the media to supply it with blood.

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4
Q

Explain the importance of endothelial cells in the control of blood pressure

A

Endothelial cells produce endothelium derived relaxing factor (EDRF) the most prominent of which is nitric oxide (NO) nitric oxide place a key in relaxing blood vessels but there are other chemical electric contributes too

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5
Q

Describe and explain arteriosclerosis.

A

Arterial sclerosis is the vascular changes identified with aging. These changes are inconsequential before the age of 40 but I’m more common after the age of 70.

The important changes are a progressive fibrous thickening of the intima and the fibro scarring of the muscular or elastic media

The effect of this is a reduction in strength elasticity of the vessel wall with progressive dilation of the aorta and coronary arteries. It is a major contributor to cardiac cerebral colonic Renal ischaemia in the elder population.

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6
Q

Explain atherosclerosis

A

Atheroma describes infiltration of fatty material in the intima which results in atheromatous plaque.

The consequences are an impaired blood flow, thrombus (blood clot) and aneurysm information which is balloon or bulge that is filled with blood in the wall of a blood vessel

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7
Q

Describe the pathogenesis of atherosclerosis

A

The The pathogenesis has been debated however the consensus is it starts with the deposition of cholesterol and other soluble lipids in the arterial intima-media the atheroma hardens to become atheromatous plaque.

The plaque causes a regular blood flow although this is not initially significant clinically until it reaches around 50% blockage where symptoms are experienced.

This is due to the plaque stopping the endothelium from functioning correctly resulting in endothelial injury.

Plaque and endothelial injury encourage thrombus (clot) formation.

Plug also weekends the wall of the artery through loss of elastic and smooth muscle from the media and the pressure of the blood may cause a local bulge in the blood vessel and aneurysm

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8
Q

List the effects of atherosclerosis

A

Deposition of cholesterol in the arterial, intimate and media hardens becomes plaque which can cause endothelial injury which supports the rhombus formation and a loss of elastic and smooth muscle from the media which may cause increased pressure due to narrowing arteries and reduce size of the lumen thus formation may eventually block the lumen completely resulting in tissue death.

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9
Q

Describe risk factors with atherosclerosis and complications

A

It is unusual for females to have this before menopause however both sexes experience hypertension hyperlipidaemia diabetes and these are important risk factors in the incidents as well as age

Complications include stroke, carotid atheroma resulting in an ischaemic attack (mini stroke), angina pectoris (chest pain), heart attack or myocardial infraction. Aortic aneurysm, gangrene, peripheral vascular disease

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10
Q

List risk factors of cardiovascular disease that are modifiable

A

Modifiable risk factor.

Smoking
High blood pressure
Diabetes
Obesity
Physical
Excessive alcohol
Poor diet

Smokers can have the risk of heart attack within five years of quitting
Physical activity, you can have the risk of heart attack
High blood pressure reduction by 5MMHG can reduce the risk of heart attack by 16%
Overweight reduction of cholesterol can also reduce risk of heart attack

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11
Q

List the non-modifiable risk factors of cardiovascular disease

A

Genetics family history of disease
Age with more age comes high risk
Ethnic background, some ethnic groups have been shown to higher rates of cardiovascular disease disease
Gender Men also have a higher risk of heart attack
Previous history of Angina diabetes or previous heart attack

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12
Q

Explain how to calculate cardiovascular health risk and how it is scored

A

Healthcare providers use a number of risk calculators including Framingham risk score, joint British societies 2 guidelines and QRISK2.

These has taken into account the patient’s age gender blood pressure diabetes if the patient smokes or has a family history of CVD and their cholesterol level.

Current guidelines say that you should be assessed if you meet the following :

Aged 40 to 84
Have Familia history of CVD
Have type two diabetes

The test measures fasting blood test to check the lipid profile and glucose level

Measuring blood pressure and weight

Finding out if the patient smokes
Finding out about a family history

The assessment score is given as a percentage chance of contracting cardiovascular disease within 10 years. A high risk is anything over 20% moderate risk is 10 to 20% low risk is less than 10%

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13
Q

What is the difference between dyslipaemia and hyperlipidaemia?

A

Dyslipaemia encompasses both raised and reduced lipid levels whereas hyperlipidaemia only 1st to raise lipid levels, e.g. cholesterol or triglycerides

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14
Q

What is hyperlipidaemia classified into?

A

Hypercholesteraemia increased cholesterol, including total and LDL cholesterol

Hypertriglyceridemia increase triglyceride

Mixed combined hyperlipidaemia increased in both cholesterol and lipidaemia

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15
Q

Most hyperlipidaemia are primary but give examples in which they can be secondary to other diseases

A

Thyroid disease nephrotic syndrome/renal disease, obesity and alcohol abuse

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16
Q

What is the cause of primary hyperlipidaemia mainly?

A

Primary hyperlipidaemia is mainly genetic which can be familiar or non-Familia Familia hypercholesteraemia is a genetic defect in LDL receptors in the liver while nonfamilial involves the intersect between genetics and lifestyle issues

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17
Q

Explain lipids importance within the body

A

Lipids are important for metabolic functions within the body such as cell membranes and pre-curses to compound such as steroid hormones and bile salts

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18
Q

What are the most common lipids founder in the body?

A

Neutral fats e.g triglycerides, phospholipids and steroids (cholesterol)

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19
Q

What allows lipids to move around the body and why do they need this structure? Give examples of these structures.

A

Lipo proteins or proteins that allow lipids to be transported in the blood as lipids are nonpolar and don’t dissolve.

Examples of these approach are low density lier proteins, LDL and high density life proteins which aid in carrying cholesterol and are measured within clinical practice

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20
Q

Why and how are HDL and LDL measured in clinical practice?

A

In clinical practice a lipid profile is done to understand a patient risk of coronary heart disease. The lipid profile includes total cholesterol which is all the cholesterol carried by the HDL and the LDL as well as triglycerides HDL cholesterol on its own LDL cholesterol on its own and total cholesterol to HDL ratio is completed.

If a patient has a high level of both triglycerides and blood cholesterol, they run a greater risk of coronary heart disease. The risk is particularly high if they have low levels of HDL cholesterol and high levels of LDL cholesterol.

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21
Q

What word increased blood levels of LDL cholesterol or reduce levels of HDL tell you about a persons predisposition?

A

The patient has a higher risk of atherosclerosis and has also been associated to death from coronary disease. Alternatively it has been established that lowering LDL cholesterol may reduce the progression of coronary atherosclerosis and may even induce regression evidence shows that lowering total cholesterol by 20 to 25% is effective in both primary and secondary prevention of clinical manifestations and it’s associated with a 22% reduction of risk of CV events rate.

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22
Q

What is the recommended treatment for patients with a high risk of coronary death associated with lipid regulation or hyperlipidaemia?

A

Statins have been shown to reduce myocardial infraction coronary death and overall mortality although they should be combined with advice on die and lifestyle measures to reduce coronary risk

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23
Q

Explain the importance of cholesterol

A

Cholesterol although seen as dietary bad actually plays a crucial role as it is important steroid molecule found in cell membrane abundant in the brain and also needed to synthesise vitamin D oestrogen, testosterone and cortisol. It is also a glucocorticoid hormone which increases blood sugar through gluconeogenesis plus bile salts.

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24
Q

How is cholesterol taken into the body and how does it function?

A

Cholesterol is a fat substance which comes from diet, e.g. eggs, liver and kidney however it is also made internally in the liver

Cholesterol is transported in lipoproteins with LDL containing the highest proportion of cholesterol. Its function is to deliver cholesterol to cells that have LDL receptors including the liver and the arterial wall.

HDL are made in the liver but collect cholesterol from peripheral tissues, including the arterial wall to then be secreted as bile through a process called reverse cholesterol transport

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25
Explain the process of reverse cholesterol transport and how it protects against hyperlipidaemia in arteries (anti-aerogenic function)
Reverse cholesterol transport is a process for HDL removes excess cholesterol from peripheral tissues like arteries and transports it back to the liver deliver them processes and excrete cholesterol and bile to protect against buildup in arteries. Later the secreted bile is reabsorbed back into the liver through enter hepatic circulation contributing to the total blood cholesterol level OCT is one of the ways HDL may exert it’s too atherogenic function regulatory systems balancing dietary cholesterol absorption, liver production and clearance maintain cholesterol levels in the blood
26
Explain Familia hypercholesteraemia
Familial hypercholesterolemia (FH) is an autosomal dominant genetic disorder characterized by elevated levels of low-density lipoprotein (LDL) cholesterol from birth. It results from mutations in genes involved in LDL receptor function, such as LDLR, APOB, or PCSK9. These mutations impair the ability of cells, particularly liver cells, to remove LDL cholesterol from the bloodstream, leading to its accumulation.
27
What is the link between lipids and Atheroma and how can the link be used in a healthy diet?
Atheroma the deposition of lipids within the arterial walls happens when LDL is oxidised and taken up by the cells of the Connery artery walls beginning the process of narrowing the lumen on the other hand. HDL cholesterol removes cholesterol from circulation through reverse cholesterol transport and eventually a taro hepatic circulation affecting the total blood cholesterol level. These two molecules work to regulate each other and the level of LDL in the blood tends to rise in HDL falls with the amount of saturated fats that are consumed conversely unsaturated fats have a good effect as they lower LDL levels healthy diet include unsaturated fats e.g. olive nut oils Instead of saturated fats, red meat hard cheese
28
Explain how blood cholesterol is calculated and what targets we have for the Millimole per litre measurements
Total cholesterol triglycerides and HDL are measured whilst LDL needs to be calculated with friedwald formula although LDL cannot be calculated if the triglycerides are larger than 4.5 millmole per litre (mmol/l) . Clinically total cholesterol level targets should be below 5MMOL/L and LDL levels under 3MMOL/L However, in secondary prevention of CVD the clinicians a.m. is to keep the LDL cholesterol to 2 instead of the usual 3MMOL/L or 2.6 non-HDL cholesterol levels Usually a collection requires multiple blood samples due to the variability of blood cholesterol in different times the day and different days. The average blood cholesterol of England is 5.5 which is high in comparison to place like China is 4.5.
29
What are the nice guidelines following for modification of lifestyle and prevention of cvd
Lifestyle modification Lydia physical activity weight management alcohol consumption decreased and smoking cessation Therapeutically the advice include statins specifically atorvastatin according to patient’s risk global and other lipid lowering medication
30
Name the recommended statin as well as its function
Atorvastatin is a medicine from the statin family, and it works by lowering the amount of “bad” cholesterol (LDL) in your blood. It targets your liver, which is where most cholesterol is made. Scientifically, it blocks an enzyme called HMG-CoA reductase, which your body needs to produce cholesterol. By shutting this enzyme down, your liver slows cholesterol production and starts pulling LDL cholesterol out of your blood instead. At the same time, atorvastatin also helps increase the “good” cholesterol (HDL) a bit and can lower triglycerides. All this reduces the risk of clogged arteries, heart attacks, and strokes.
31
How do statins benefit anticoagulation?
2. Improved Endothelial Function: They improve the health of the endothelium (the inner lining of blood vessels), which produces nitric oxide. Nitric oxide relaxes blood vessels and reduces the stickiness of platelets, lowering the risk of clot formation. 3. Reduced Platelet Activation: Statins decrease the activation and aggregation (clumping) of platelets, which are key players in clot formation. Less platelet activity means a lower chance of thrombosis. 4. Fibrinolysis Promotion: They boost the body’s ability to break down clots by increasing the production of tissue plasminogen activator (tPA) and reducing plasminogen activator inhibitor-1 (PAI-1). 5. Stabilizing Plaques: Statins make atherosclerotic plaques more stable, meaning they’re less likely to rupture. Plaque rupture is a major trigger for thrombosis.
32
Explain the mechanism of how statins work
Statins competitively inhibit the enzyme HMG CoA reductive an important enzyme for cholesterol synthesis in the liver. When synthesis of cholesterol is lowered within the liver the liver attempts to increase its uptake of cholesterol via compensatory increase of LDL receptors. This causes an increase in uptake of LDL cholesterol from the circulation and lowers LDL cholesterol and total cholesterol concentrations. Fibre or more effective for reducing triglycerides however as statins have a moderate effect on triglycerides
33
Who should statins be considered for?
Statins should be to considered for all patients, including elderly, high CVD risk arterial disease or diabetes. Statins are also used as a primary prevention for patients that have not had enough event yet but a high risk although cholesterol concentration alone does not accurately predict coronary events you should take into account as well as other factors just smoking hypertension diabetes to estimate risk
34
What should the target for statin treatment be in terms of cholesterol concentration?
Statin treatment should be adjusted for target total cholesterol of 5MMOL/L or a reduction of 20 to 30% if that produces a lower concentration in terms of LDL cholesterol the target should be below 3MMOL or a reduction of about 30% if that produces a little concentration
35
Which group should exercise caution with statins?
Starting should be used in caution with people with the history of liver disease or high alcohol intake hypothyroidism should be managed adequately before starting treatment of stands as statins additionally active liver disease, pregnancy and breastfeeding should be considered
36
What are the common side effects of statins?
Gastrointestinal cramps, pain, flatulence nausea, dyspepsia headaches, muscle pain raised creatine kinase the muscle pain is often over reported and one of the main reasons patients wish to stop the medication
37
What are bile acid sequestraints
1. Binding Bile Acids in the Gut: • Bile acids are made in the liver from cholesterol and stored in the gallbladder. When you eat, bile acids are released into the intestine to help digest fats. • Bile acid sequestrants (like cholestyramine, colestipol, or colesevelam) bind to bile acids in the intestines, forming a complex that cannot be reabsorbed. 2. Preventing Reabsorption: • Normally, about 95% of bile acids are reabsorbed in the intestines and sent back to the liver to be reused. • By binding to bile acids, BAS prevent their reabsorption. This means the bile acids are excreted in the stool instead. 3. Forcing the Liver to Use More Cholesterol: • To replace the lost bile acids, the liver pulls LDL cholesterol from the blood to make new bile acids. • This reduces the overall amount of LDL cholesterol circulating in the bloodstream, lowering cholesterol levels.
38
Name the substances that act as an ion exchange bile acid resin and how they reduce LDL cholesterol plus side effects
Colestyramine and colestipol are bile acid sequestrants (BAS) that work as anion exchange resins to reduce LDL cholesterol levels. Colestyramine and colestipol reduce LDL cholesterol by stopping bile acids from being recycled. This forces the liver to make more bile acids using cholesterol from the blood. To do this, the liver pulls in more LDL cholesterol by increasing LDL receptors, which lowers the amount of LDL in the bloodstream. Colestryamine is used to treat hyperlipidaemia and primary prevention of coronary heart disease in men age 35 to 59 with primary hypercholesteraemia colestipol hyperlipaemia, especially in patients who have not responded adequate to diet or other measures
39
Explain nicotinic acid and it’s role in hyper lipidaemia
Nicotinic acid, also known as niacin (a form of vitamin B3), is a lipid-lowering therapy used to manage hyperlipidemia (high cholesterol and triglycerides). It improves lipid profiles by targeting multiple pathways when given is levels above vitamin requirements How Nicotinic Acid/Niacin Works in Hyperlipidemia 1. Inhibits Lipolysis in Fat Cells • Niacin blocks the enzyme hormone-sensitive lipase in adipose tissue, reducing the breakdown of stored fat into free fatty acids. • With fewer free fatty acids reaching the liver, the production of VLDL (very low-density lipoprotein) decreases. Since LDL cholesterol is formed from VLDL, this leads to lower LDL cholesterol levels. 2. Increases HDL Cholesterol • Niacin increases HDL cholesterol (the “good” cholesterol) by slowing its breakdown in the liver. • Higher HDL levels help remove excess cholesterol from blood and tissues, reducing the risk of atherosclerosis. 3. Lowers Triglycerides • By decreasing the liver’s production of VLDL, Alternatively acipimox is a nicotinic acid derivative designed with few side effects other than the nicotinic acid products
40
What are the drawbacks of nicotinic acid?
Because the dose needed is about 100 times more than the recommended diet allowance for niacin and can potentially be toxic. It has to be taken under a doctor supervision and never self prescribed and can contribute to liver disease peptic ulcer arterial bleeding and there’s no longer available within the UK apart from acipimox it’s derivative with less side effects
41
State the effect on LDL and triglycerides in terms of percentage that nicotinic acid produces as well as the potential side effects
A 10 to 20% decrease in LDL is expected and a 20 to 50 decrease in triglycerides whereas a 15 to 35 HDL increase In terms of side-effects flu flushes are common as it widen blood vessels but most patients develop tolerance to this as well as a variety of gastrointestinal symptoms such as nausea, indigestion, gas, liver problems, gout, high blood sugar increase as the dose is increased
42
What is the medication for hypertriglyceridemia and how do they effect LDL AND HDL
Fibrates • Examples: Gemfibrozil • How They Work: Activate PPAR-alpha receptors, which increase the breakdown of triglycerides in the liver and reduce VLDL production. • Effect: Lower triglycerides by 30–50% and may slightly increase HDL cholesterol small effect on LDL 2. Omega-3 Fatty Acid Supplements Made up of Omega-3 acid ethyl Esters - used with diet and statins Omega three marine triglycerides - very high triglycerides level intervention • How They Work: Reduce triglyceride synthesis in the liver and promote breakdown. • Effect: Can lower triglycerides by 20–50%. • Note: alternative to fibrates It is usually taken twice a day 30 minutes before meals side-effects can be diarrhoea, nausea stomach pain, gas, and heartburn Ezetimibe • How It Works: Reduces cholesterol absorption in the intestine, indirectly lowering VLDL and triglycerides. • Effect: Modest triglyceride-lowering effect (10–15%).
43
Explain ezetimibe
Ezetimibe inhibit the intestinal absorption of cholesterol and it is licensed as an add-on therapy when an individual is changing diet for primary hyper core ER in combination with a statin or it can be prescribed alone is used in patient with a Familia hypercholesteraemia in combination with a statin
44
Explain omega-3 fatty acid compounds
These compounds are made up of omega-3 acid ethyl Esters and omega-3 marine triglycerides the compounds reduce triglycerides and work as an alternative to vibrates and can also be using addition to statins in a patient with mixed hyperlipidaemia who have been on statin treatment and has not worked adequately Omega three Marine triglycerides are used as an adjunct for her very high hyper triglyceridemia Omega-3 acid ethyl Esther’s use as an adjunct to die and statins for hypertriglycerides a secondary prevention in those who had recent myocardial infraction
45
Talk about side effects of using a combination of therapies to treat hyperlipidaemia
Often with severe hyperlipidaemia a combination of statins fibrate nicotinic acids are used however this should be under expert supervision as the consequences can be deadly for example Rhabdomyolysis - muscle breakdown which ends up having protein such as myoglobin in the bloodstream which can affect the kidneys This particularly means that gemfibrozil should not be used in concordance with statins
46
Define hypertension and explain why is responsible for between 10 to 20% of all deaths worldwide.
Hypertension is described as sustained raised blood pressure in excess level levels of upper limits of normal Hypertension is indirectly or directly responsible for so many debts due to the detrimental effects. High blood pressure has on the arterial system particularly the coronary and cerebral circulation is Hypertension is the main cause of stroke along with smoking and high blood cholesterol and one of the main three reasons of coronary heart disease Dangerously hypertension is often left undiagnosed as it can be asymptomatic however when it is diagnosed is often found alongside other cardiovascular risk factors and other diseases such as diabetes
47
Define blood pressure scientifically and clinically and explain the difference differences
Blood pressure scientifically is the force exerted on the walls of the blood vessels Clinically blood pressure refers to blood pressure in the arteries taken when a person is relaxed and either sitting or lying down and it expressed as systolic blood pressure SBP over diastolic blood pressure DPD
48
Define systolic blood pressure and diastolic blood pressure
SBP refers to the blood pressure when the ventricles are contracting and blood pressure is at the highest point healthy values are 120 MMHG and should be below 140 DPD refers to the blood pressure when the ventricles are relaxing and blood pressure is added to the lowest healthy values are around 80 MHG and should be below 90
49
What is a normal healthy blood pressure?
120/80mmHG This refers to 120 systolic pressure over 80 diastolic pressure
50
Explain the concept of pulse pressure
Pulse pressure refers to difference between the systolic and diastolic readings for example for a normal blood pressure of 120/80 the post pressure would be 40 MMHG
51
Explain cardiac output and how it’s used to determine blood pressure
Cardiac output is a combination of the rate the heartbeats the amount of blood injected with each contraction known as a stroke volume and the resistance to cardiac output based on blood vessel, contraction and relaxation Blood pressure = cardiac output x peripheral resistance Small arteries arterials are especially important in terminal the persons blood pressure and vasoconstriction of these vessels will lead to an increase in blood pressure Blood pressure is controlled but electrically and chemically two systems interacting for maximum control
52
Explain how the nervous system affects blood pressure
The sympathetic system is excitatory and the parasympathetic system is inhibitory. Importantly, the sympathetic nervous system, please a crucial role in blood pressure by increasing the heart rate and controlling the size of blood vessels During substantial haemorrhage, blood pressure is detected by barorecptors (pressure receptors) which caused the release of adrenaline and no adrenaline which increased the heart rate as well as cause peripheral resistance this increasing the blood pressure
53
What are the three significant tissue receptors involved in electrical control of blood pressure?
Alpha one our receptors found in the smooth muscle of blood vessels stimulation leads to vasoconstruction in increasing peripheral resistance and blood pressure Beta one these receptors are found mainly in the heart stimulation leads to increased heart rate increase cardiac output and increase blood pressure Beta two found mainly in smooth muscle of blood vessels supplying the heart and the smooth muscle of the bronchi stimulation increased vasodilation
54
Explain how renin angiotensin system affects blood pressure
In the event of blood loss and decreased blood pressure Presoreceptors within the kidney release an enzyme called Renin Renn converts plasma protein called angiotensinogen to angiotensin 1 which travels to the long way it has acted upon by angiotensin converting enzyme to form angiotensin 2 Angiotensin two is a potent vasoconstrictor causing an immediate and local increase in blood pressure additionally angiotension to travel to the adrenal gland where it releases aldosterone from the adrenal cortex Alderstone increases permeability of renal tubes to sodium in this context due to diffusion where sodium goes water will follow resulting in a net increase of volume and resulting increase in blood pressure A negative feedback loop where angiotensin to inhibits the release of running keeps the system balanced. Additionally rise is slower but longer lasting compared to the nervous control.
55
Explain the difference between secondary hypertension and essential idiopathic or primary hypertension
Essential idiopathic or primary hypertension is where there is no identified viable cause of hypertension this is the case for 90 to 95% of cases Secondary hypertension is where physicians have an identify cause for the hypertension. This usually requires more investigation common causes of secondary hypertension or pregnancy combined contraceptive pill, renal disease endocrine disorders. Physicians define hypertension as borderline mild, moderate and severe and this can determine if intervention is needed based on the benefits of treatment being clear
56
Explain the pathogenesis of hypertension in primary hypertension and secondary hypertension
The mechanism for primary hypertension is unknown but it is assumed that genetic acceptability excessive sympathetic nervous system activity, high salt intake and abnormalities in the ras system play apart The mechanism for secondary hypertension can be caused by chronic renal failure, renal arteries stenosis, acute glomeronephrotitis, adrenal tumours Cushing syndrome drugs corticosteroids non-steroid anti-inflammatory drugs oral contraceptives Although many of the mechanisms are kidney relayed, it’s worth stating that high blood pressure hypertension can damage the renal function
57
Explain chronic hypertension
Chronic hypertension occurs when cardiac output is normal and peripheral resistance is increased due to resistance vessels small arteries and arterioles structural changes including wall thickness and reduction of lumen diameter leading to maintained elevated blood pressure
58
What is the most important risk factor to stroke?
High blood pressure is the most important factor of a stroke about 70 to 80% of strokes are thromboses of atherosclerotic cerebral blood vessels. - blockages of blood vessels in the brain the rest of Leeds Strokes can cause anything from sudden death to impaired motor skills depending on their location High blood pressure is also serious but transischemic attacks which are essentially mini strokes less than 24 hours
59
What is the relationship between heart disease and high blood pressure?
High blood pressure means the heart has to work harder as the heart is a muscle. It can develop an increase in size to deal with increased workload particularly the left ventricle. This can be recorded through an ECG of left ventricular height hypertrophy. High blood pressure also increases the risk of congestive heart failure when the heart cannot pardon and fluid accumulates fluid buildup in the left part of the fluid buildup in the lungs resulting in breathlessness and oedema if the right side heart is affected fluid buildup and lower limbs resulting in the oedema of the feet ankles and legs
60
How do we treat hypertension?
Lifestyle changes such as losing weight exercise less salt alcohol consumption healthy diet fresh fruit vegetables Medicines such as diuretics beta blockers, alpha blockers, calcium blockers Ace inhibitors angiotensin to antagonists Many of the medicines are taken sequently until the required reduction of blood plasma pressure is achieved
61
Explain how the main types of diuretics work
Diuretics are the oldest class of hypertensive diuretics act on the kidney increase the excretion of sodium and water a process referred to as diuresis which causes a decrease in blood volume therefore blood pressure Thaizide diuretics moderately potent and inhibit sodium reabsorption in the distal convoluted tubular. They act in 12 to 24 hours one to 2 hours of oral administration. A low dose is used to treat hypertension and producers are maximal blood pressure lowering effect with little biochemical disturbance. Loop diuretics powerful diuretics used in pulmonary oedema which is buildup of fluid in the lung and diuretic resistant oedema inhibit reabsorption from ascendingly of Henle. Strong side effects low potassium enlarged prostrate urinary retention Potassium-sparing diuretics weak diuretics cause retention of potassium therefore can be used with thaizide as better alternatives than potassium supplements
62
What type of medicine is thiazide and name some of the specific medicine?
Thigh is a diuretic which is moderately potent and inhibit sodium reabsorption in the distal convoluted loop and acts within one or two hours of oral administration. Low-dose is used to treat hypertension to reach a maximal effect of lowering blood pressure with little biochemical disturbance. Types of thighs eyes are bendroflumethiazide , chlortalidone, metolazone, indapamide
63
What type of medicine is loop diuretic
Loop diuretics are primary used to treat pulmonary oedema due to left ventricular failure, chronic heart failure and diuretic diuretic resistant oedema and I usually combined with thaizide. Inhibit reabsorption from ascending loop of loop of Henley very strong with side effects such as low potassium enlarged prostrate unitary retention Drug names furosemide, bumetanide, torasemide
64
What type of medicine is potassium-sparing diuretics and give names of specific medicine types?
Amiloride and triamterene are weak diuretics that cause the retention of potassium and can be more effective than giving potassium supplement when a patient is going through thaizide or loop diuretics
65
Explain beta blockers and how they work.
Beta blockers block beta one receptors in the heart, which will reduce heart rate to reduce blood pressure. The mechanism is less clear, however, it’s theorised to be related to running secretion and a decrease in peripheral resistance
66
Why is it important to choose between lipid soluble and water soluble data blockers and give some beta blocker names?
Water soluble beta blockers cannot enter the brain which is less likely to cause sleep disturbances and nightmares. Additionally, they are excreted by the kidneys and accumulate in renal impairment. Beta blockers usually have to be given two or three times a day due to relatively short duration however modify view these formulations can be administered once daily for hypertension Propranolol, exprenolol, pindolol, sotalol
67
How do alpha blockers work and what do they do Give some names?
Alpha blockers can be used to treat hypertension by blocking alpha receptors in the heart which will cause vasodilation reducing blood pressure through peripheral resistance Prazosin Doxazosin Terazosin
68
How do you calcium channel blockers work? Given examples.
Calcium channel blockers interview with the entry of calcium ions into the heart calcium ions are important in vascular and smooth muscle contraction. This blocking calcium reduces contraction through reduction of electrical impulses. The end result is relaxation therefore vasodilation. Almodipine Felodipine Nicardipine Verapamil Diltiazem
69
What are the important diffrences between these 2 groups Almodipine Felodipine Nicardipine Verapamil Diltiazem
All of these groups are examples of calcium blockers, however Verapamil Diltiazem should not be used in case of heart failure as they may further depress the cardiac function
70
Explain ace inhibitors and their effect on hypertension
Ace inhibitors or angiotensin converting enzyme inhibitors prevent angiotensin one from being converted to angiotensin too, which is an important vasoconstrictor leading to the release of aldosterone and increased pressures By inhibiting this means lowering both blood volume and blood pressure Asian inhibit is often the initial and medicine for treatment of hypertension in younger concussion patients and insulin dependent diabetes with nephropathy. It leads to rapid falls in blood pressure. If the patient is receiving diuretic therapy the first dose should be preferably given at bedtime.
71
Give examples of ace inhibitors
Captopril, cilazapril , enalapril, fosinopril
72
Explain the key differences between ace inhibitors and angiotension to receptor antagonists and why we use one of the other
Ace inhibitors inhibit angiotensin one being converted into angiotensin too, which stops the vasoconstriction affect caused by aldosterone. And to receptor antagonist do the similar job, however they do not inhibit the breakdown of Bradykinin and other kinins Which stops the persistent cough that comes with ace inhibitors and can be used as an alternative if the patient stops in ace inhibitors due to cough
73
Give examples of angiotensin to receptor antagonists and Ace receptors
Angiotensin 2 receptor Losartan Valsartan Candesartan Eprosartan Ace Lisinopril • Enalapril • Ramipril • Captopril
74
Explain how the cardiac muscle has the ability to beat rhythmically without any electrical or chemical stimulus
The heartbeat is governed by a special area of cardiac muscle called the sinoatrial nude which is found in the right atrium close to where the superior vena cava enters the heart because this is the starting point of the heartbeat. The essay notice is referred to as the pacemaker region.
75
Explain the step-by-step process of heart contraction and electrical impulse
A contraction impulse starting from the sinoatrial mood spreads rapidly to both walls of the atria causing them to pump blood into the ventricles The electrical impulse passes to the HU of ventricular node located in the lower right atrium after a brief pause then transmit the impulse to the walls of the ventricles through a thin band of conducting fibres called atrial ventricular bundle or bundle of his. The short pauses is to delay between atrial and ventricular contractions. The bundle of his/AV bundle splits into two right and left branch the split into a smaller fire is called purkinje fibres which conduct electrical impulse throughout the ventricles causing contraction After this diet, a time of rest issues with blood coming back to the heart from the large veins
76
Explain how an electrocardiogram works and what the patient would experience
An ECG or electrocardiogram is a painless procedure which can be measured while the patient is at resting or during exercise. In order to perform it 12 self-adhesive electrodes are attached to the skin arm and legs and chest in specific positions. Electrical activity in the heart is recorded and digital readout or paper printout is taken. It should take less than a minute. A typical ECG trace appears which is a series of waves
77
Explain an ECG trace
The P wave begins the trace and represents atrial depolarisation or the electrical impulse leaves the SA node and spreads the atria to the AV node The QRS complex represents ventricular depolarisation. The electrical impulse spreads throughout the right and left ventricles and has a lot larger impulse than the P wave as the ventricles are a lot larger. The P to all interval tells us how long the impulse takes to travel from the sinoatrial node to the H2O ventricular node and it is a good estimate of atria ventricular node function Finally, the tea wave represents ventricular depolarisation or the refractory period QTT interval is measured from the beginning of the QRS complex on the end of the T wave prolonged QT interval is a risk for ventricular tachyarrhythmias
78
What is atrial fibrillation?
When the heart contracts are very high rate and in an irregular way
79
What is bradycardia?
When the heart beats more slowly than normal
80
What is ventricular tachycardia?
An abnormally fast ventricular berate meaning the heart does not work efficiently
81
What is ventricular fibrillation?
A rapid and disorganised rhythm of heartbeats that leads to loss of consciousness and sudden death if not treated properly
82
What is supra ventricular tachycardia?
A heart rhythm disorder with periods of abnormally fast heart rate
83
Explain atrial fibrillation and give some of the associated diseases as well as causes and how the ECG would look
H2 fibrillation occurs when abnormal electrical impulses occur near the sign of atrial node, overriding its function meaning it can no longer control the rhythm of the heart the atria contract randomly and sometimes too quickly reducing the efficiency of the heart pump On an ECG HU fibrillation would look like a random and disorganised P wave followed by a QRS which looks normal followed by a random after that The disease is more common with pre-existing heart conditions, hypertension ethereal sclerosis, heart valve disease, congenital heart disease cardiomyopathy It can be triggered through excessive alcohol, high caffeine, obesity, illegal drugs
84
What are the three types of atrial fibrillation?
Paroxysmal atrial fibrillation - this comes and goes usually stops in 48 hours Persistent atrial fibrillation – this lasts longer than seven days or less when treat Permanent atrial fibrillation this is present all the time and then no more attempts to restore normal heart rhythm
85
If a patient is going through atrial fibrillation, what is one of the main concerns and how do we treat this?
One of the main concerns that each fibrillation is risk of stroke due to blood clots forming In order to mitigate the risk of stroke anticoagulant are used Types of anticoagulant include heparins of which there are two types low molecular weight heparins and unfractionated heparin which indirectly act as the Rubin inhibitors by bonding to complexes such as antithrombin and inactive thrombin Warfarin is a more long-term medicine and is an oral vitamin K antagonist. There is however an increased risk of bleeding dosage should be measured by the international normalised ratio Apixaban and rivaroxaban are factor Xa inhibitors to prevent thesis with nonvalvular atrial fibrillation Dabigatran is a direct thrombin inhibitor?
86
How do you beta blockers act as anti-arrhythmic medicines?
Bitter blockers slow the rate of discharge of the SA node and increase the refractory period of the AV node thereby bringing a heart rhythm under control
87
Describe the differences in the use of beta blockers versus amiodarone
Amiodarone cannot be used in the long-term, but it acts similar to beta blockers in increasing the factory period and slowing conduction of electrical impulses
88
During arithmetic, what medicines are used to control the rate at which the heart beats?
Beta blockers, calcium channels and digoxin Calcium channels through interfering with the entry of calcium ions affecting the conduction system of the heart beta blockers slow the rate of discharge of the SA node and increase for factory period to digoxin slows the conduction in the AV node and increases their factory.
89
What is electrical cardio version and what is the recommended drug to go along with it?
Electrical cardioversion is manual control of the heart through two catheters inserted into the heart via a vein in the groin and a small electrode pad applied to the chest controlled electric shock tries to restore normal rhythm In patients who have had atrial fibrillation, for more than two days blood clots are high risk so warfarin is given for 3 to 4 weeks before cardio version and at least four weeks afterwards to minimise stroke risk
90
Explain how a catheter ablation works.
A catheter is led through the veins to the area of abnormality energy source such as high frequency radio waves the generate heat is transmitted through the catheter to destroy the tissue on it performed in a general anaesthetic
91
Explain how a pacemaker works
A pacemaker is a minor surgical procedure performed under local anaesthetic that involves a battery operated device that ensures the heartbeat regularly being surgically implanted below the collarbone Leads are fed into the heart and positioned where the electrical stimulation is needed. The electrical stimulation is controlled by the implanted pacemaker device very useful for bradycardia but can also be using other types of arrhythmias.
92
Define bradycardia and explain some potential causes
Bradycardia is defined as a heart rate of less than 60 bpm although pretty cardio can occur normal heart function for example during sleep or very Fit people can have a low resting heart rate which is referred to a sinus bradycardia However, it’s really called a can occurred you to slow firing at the SA node or poor transmission of electrical impulses through the heart or side effects of medications
93
Describe the two main types of bradycardia and the degrees
Sick sinus syndrome is where the SA node fails and irregular heartbeat takes place patients may experience brachycardia and tachycardia heartbeats which swaps back-and-forth and can lead to dizziness weakness and is seen in the elderly The second type is heart block. This occurs when electrical impulses are slowed or blocked from the atria through to the AV node and there are multiple grades of this hard work. 1st° impulses are slow but not stopped rarely causes any symptoms Type one 2nd° electrical impulses are delayed to a greater effect until a heartbeat is skipped entirely than the cycle repeats itself. This causes dizziness and other symptoms and a pacemaker may be required. Type II second-degree heart block is when some of the electrical impulses from the SA are unable to reach the ventricles. This occurs as a result of underlying disease may require pacemaker. 3rd° is a complete block no electrical impulses reach the ventricles
94
Explain ventricular tachycardia and it’s potential progression and effects
Ventricular tachycardia occurs when electrical impulses arise in the ventricles rather than the atrium causing abnormal heart rate and symptoms can be weakness dizziness chest pain, shortness of breath or collapse There are several types of VT and it can lead to ventricular fibrillation. It can be monomorphic regular rhythm or originating from a single focus with a similar QRS complex or polymorphic a regular rhythm variations and QRS complexes. Can also be sustained greater than 30 seconds of duration or non-sustained less than 30 seconds in duration One minute
95
Explain ventricular fibrillation
Ventricular fibrillation is where electrical impulses are fired from multiple sites in the ventricles in a very fascinating irregular way meaning of the blood is unable to be pumped around the body and the patient is in a prompt state of emergency and will likely die without treatment
96
If a patient is going through ventricular tachycardia or ventricular fibrillation, how should they be treated if they have no pulse?
A defibrillator which is a large electric shot given by two pads on the chest should be administered followed by airway management e.g. oxygen and anti-arrhythmic therapy such as amiodarone Nice recommends an implantable cardioverter defibrillator a device which gives the heart a large electric shock of dangerous heart rhythm is detected High risk patients should have something like this in place if they have previously had a cardiac arrest VT or VF have sustained VT without treatable cause. Additionally, people with familial cardiac condition such as lung QT syndrome or undergo surgical repair for congenital heart disease.
97
Explain supraventricular tachycardia and who is most susceptible
SVT is commonly found in young healthy people and it occurs when the electrical impulse does not fade out with the normal heartbeat but continues to move a rapid circle within the conduction system. It occurs because an additional electric pathway that forms a short circuit within the heart.
98
What are the two causes of super ventricular tachycardia and their treatments?
SVT is caused by abnormalities of impulse conduction this is referred to you as re-entrant tachycardias alternatively disorders of impulse initiation automatic tachycardias Two most common types of re-entrant SVT AV nodal re-entry tachycardia is the most common form caused by the presence of two distinct conducting pathways in the AV note Alternatively AV re-entry tachycardia is caused by accessory pathways connecting the atria and ventricles line outside the AV note Treatments or cardio version, calcium channel blockers, beta blockers, ablation of accessory pathway identification of triggers and underlying disease
99
Explain angina and what type of muscle is implicated in the disease?
Angina is pain or discomfort or feeling of pressure in the chest that is caused by an inadequate blood supply (ischaemia). The coronary arteries provide oxygen for coronary muscles however due to things such as atherosclerosis the myocardium becomes a vulnerable to poor distribution of blood supply. Unfortunately, the myocardium cannot take up more oxygen from existing blood supply as it is close to Maximo and the only way to increase the blood supply is dilation of the arteries. Myocardial ischaemia is temporary which would feel like a spasm or temporary pain in the chest however if the ischaemia is more severe and prolonged due to a blockage of arteries such as promise formation then there will be death in the affected area of tissue and potentially a myocardial infraction
100
Give alternate reasons why Angie may take place if the cause is not ischaemia
Eight aortic stenosis, which is an obstruction in the aortic valve that separates the left ventricle from the aorta causing the left ventricle to work harder Hyperthyroidism excessive reproduction of thyroid homo cause an increase in heart rate and therefore increased myocardial oxygen demand Coronary spasm, temporary restriction of one or more of the coronary arteries
101
Talk about the symptom characteristics of angina pectoral such as location character relation to exercise and duration
Location and Pictoria is most often felt behind the middle or upper thirds of the sternum but can also present in other areas however the sternum is usually involved. Both sides of the chest however more common the left also the neck and lower jaw both arms but may only affect the upper arm but can reach the The elbow wrist and fingers Character sensations are reported ranging from discomfort to intense pain and has been described as heaviness squeezing cushion choking. I’m throwing sometimes shortness of breath is also reported. Relation to exercise is common and is often provoked by walking particularly uphill and can also be more readily provoked after a heavy meal or cold weather some patients even have nocturnal and Gina, which prevents them from sleeping and wakes them up potentially due to emotions, excitement and dreams Duration usually last between one to 3 minutes and is rarely ever less than 30 seconds or more than 15 minutes although a vague sense of discomfort may assist after the pain
102
What is the difference between stable and unstable angina
Stable angina can be predicted in the patient knows what will bring on symptoms. Symptoms are short lived and relieved by seizing the activity or using short acting nitrates. However unstable angina can be developed suddenly or progress from stable angina and occurs even at risk and the pain is more prolonged to frequent and severe
103
What is used to treat stable angina?
Nitrates calcium channel blockers, potassium channel activators beta blockers revascularisation, Similar drugs are used to those used to treat hypertension
104
Explain how nitrate can be used to treat angina pectoral and give the two types of nitrates used
Matrix or potent vasodilators and give the principle benefit of reduction of venous return which reduces left ventricular work reducing chest pain however may result in flushing and headaches Glycyl trinitrate is one of the most effective drugs for rapid for rapid relief of stable angina it’s affects us 20 to 30 minutes and it’s taken sublingually under the term or can be prolonged by using a modified release and transdermal preparations but tolerance may develop. It can also be taken through an aerosol spray if people find it difficult to take under the tongue or intravenous infusion or transoral application. Alternatively isosorbide dinitrate is also taken sublingually under the tongue or through modified release but is more stable preparation for those that require in frequent doses. The effects are slower onset but the duration of action is longer up to 12 hours and affects can vary due to production of active metabolite such as a source a source isosorbide mononitrate Patients on long acting transdermal nitrates readily develop tolerance which can be reduced by reduction of blood nitrate concentrations to low for 48 hours each day usually maintains effectiveness
105
How do calcium blockers affect angina pectoral?
Calcium channel blockers interview the entry of calcium irons into the heart and myocardial cells within the specialised conducting system of the heart and smooth muscle. Thus myocardial contraction may be reduced to reducing the electrical impulses within the heart and so the pain associated with Angie is relieved.
106
Which potassium channel activates are used in angina
Nicorandil is indicated in prevention and a long-term of Angie and it has similar effect to other anti-drugs controlling symptoms but there is little evidence for efficacy and combination with other anti drugs
107
How are beta blockers used to treat angina
Beta blockers block the beta Andrew receptors in the heart peripheral of vascular bronchi and pancreas liver and taking twice daily or once depending how strong the beta blockers are and they slow the heart and can depress the myocardium although this should be monitored in patient with unstable heart failure or stable heart failure As beta blockers reduce cardiac work, they can be used to improve exercise tolerance and relieve symptoms of angina as well as three hypertension
108
Explain revascularastion and give the two types of methods
Coronary artery bypass craft CABG or percutaneous coronary intervention PCI should be considered for people with stable Angie who are not reacting to optimal medical treatment and if coronary lesions are severe enough and treatable CABD is a surgical procedure in which a healthy blood vessel is harvested from the body usually the legs ungrafted to the blocked artery giving a bypass route for blood to flow PCI is a non-surgical procedure where a catheter is passed through with a balloon tip that started to the affected artery once in place the balloon is inflated to compress the plaque against the walls and sometimes a small mass tubes placed to keep the artery open
109
Explain acute coronary syndrome and the three types of acute cardiac events that are associated with it
Acute coronary syndrome is the name given to the three types of cardiac events that are associated with sudden rapture of plaque inside the coronary artery The three types of events are unstable angina, non-ST segment elevation myocardial infraction and ST segment elevation myocardial infraction
110
Explain the link between atherosclerosis unstable angina and non-segment elevation myocardial infraction
Atherosclerosis plaque suddenly breaking inside the coronary artery increases the risk of NSTEMI and can be a precursor for myocardial infraction due to consequence formation of thrombi. It is also related closely to unstable angina. How was the rupture may lead to some myocardial necrosis? This type of infraction does not cause ST elevation on an electrocardiogram however chemical markers in blood trooping in one trooping in T and creatine can indicate damage has occur occurred
111
What is the recommended treatment for unstable angina and non-ST segment elevation myocardial infraction?
Initial treatment of oral anti-platelet therapy aspirin and antithrombin therapy heparin/Fondaparinux Intravenous Glyco protein IIb/IIIa inhibitors eptifibatide or tirofiban for patients who have an intermediate or high risk of adverse cardiovascular event Maintenance therapy to prevent cardiovascular episodes Antiplatelet therapy as indicated clopidogrel, ticagrelor Antithrombin therapy as indicated bivalirudin Revascularisation if needed/possible CABD/PCI
112
Explain how aspirin act as an anti-platelet therapy
Aspirin inhibits production of throne boxing air which is involved in the binding of platelets to seal damaged blood vessels. These platelet patches can become too large and effect flow in the heart. Low dose of aspirin are used long-term to prevent heart attacks but in the case of suspected heart attack high dose 300 mg can be taken to reduce risk of cardiac tissue death
113
Explain glycoprotein IIb/IIIA INHIBITS platelet formation and the medicines involved in treatment
Glycoprotein IIb/IIa inhibitors such as eptifibatide and tirofiban reversibly inhibit platelet aggregation by preventing binding to fibrinogen and other adhesive leggings The inhibitor is given in addition to aspirin and unfractionated heparin in management of unstable vagina or NSTEMI who are high risk of subsequent myocardial infraction or death Abciximab isn’t an inhibit to use for patients undergoing PCI who are not suitable for eptifibatide
114
Explain the use of clopidogrel
Clopidogrel is an anti-platelet drug that inhibits platelet aggregation by irreversibly modifying the platelet adenosine phosphate receptor and his licensed in combination with aspirin for the treatment of unstable angina and NSTEMI and his recommended 12 months post ACS
115
Explain the use of ticagrelor, prasugrel and clopidogrel
These are all ADP receptor inhibitors that are used in anti-platelet therapies Ticagrelor is an oral reversible antagonist of ADP receptor that inhibits platelet aggregation and thrombus formation from atherosclerosis disease Clopidogrel inhibit platelet aggregation by irreversible modification of the ADP receptor this blocking aggregation effects of ADP and is used in combination with aspirin for treatment of unstable angina and NSTEMI is recommended 12 months post ACS Prasugrel is an ADP inhibitor which inhibits platelets recommended for use with aspirin and with acute coronary syndrome who are undergoing percutaneous coronary intervention?
116
Explain and list three antithrombic therapies
Heparin which come into forms low molecular weight heparin and unfractionated heparin or indirect thrombin inhibitors which form complexes with antithrombin inactive thrombin clotting factor LMWH is administered subcutaneously to patients with unstable angina or NSTEMI if if an angiograph is expected within 24 hours Fondaparinux is a synthetic Penta saccharide that binds to antithrombin with greater affinity than heparin and increases the ability of antithrombin to inactivate cutting factor XA and his administer subcutaneously to patients with low bleeding risk unless they have an angiography in 24 hours then happens are more necessary Bivalirudin is an analog of hirudin which is secreted by leeches and has an anticoagulant to affect this natural inhibit has ability to lies thrown by an inhibit thrombin without interacting with any of the serum proteins. Heparin only acts on soluble thrombin whereas this is able to lyse thrombi. This can be considered as an alternative combination of heparin plus glycoprotein IIB/IIIA if the patient is not already on Fondaparinux or GPIIB/IIIA and angiography isn’t scheduled within 24 hours. It can be given intravenously
117
What is the main difference between non-ST segment elevation myocardial infraction and ST segment elevation myocardial infraction?
ST segment elevation myocardial infraction is the most serious of the ACS is and requires urgent medical attention and it is caused by the prolonged blocked blood supply to the heart which needs to thrombosis and myocardial ischaemia and irreversible necrosis of the heart muscle that affects a large area of the heart and can be seen on the ECG as the ST segment elevation or the left bundle branch block. Biomarkers such as troops TNI and creatine kindness or at least due to the myocardial fraction. Non-ST segment elevation myocardial infraction is the less serious version of this and you cannot see it affects on an ECG however the bio marks such as provenance Tea and I and creatine are still involved
118
What treatment is therefore ST segment elevation myocardial infraction?
PCI also known as an angioplasty the surgical procedure where a catheter is passed along the coronary arteries with a balloon on the end and the blue thread to the affected artery and inflated pushing the atherosclerosis plaque to open the artery wall to restore the blood flow to the artery a small stent a small mist tube is sometimes used to place the Conry to help it. Keep open Medicine wise anti-platelet therapy aspirin bivaliruden and copied Dora should be given prior to PCI. Fibrinolysis is used to act as thrombolytics by activating plasminogen to form plasma which degrades fibrin and breaks up the thrombus fibrinolytics can restore blood flow administered within 12 hours of symptom onset.
119
Name 4 thrombolytic medicines
Streptokinase Alteplase Reteplase Renecteplase
120
Explain cardio myopathy and give the four main types
Cardio myopathy are disorders where the heart muscle is abnormal in the absence of coronary heart disease, hypertension problems, and problems with the heart valves Dilated cardiomyopathy is the most common and as well left or both ventricles and large and the heart muscle becomes weakened and unable to contract is normal 35% hereditary Hypertrophic cardio myopathy second most common where cardiac muscle thickens resulting in reduced filling of the ventricles about 50% of cases are genetic Restrictive cardio myopathy the heart is unable to relax between contractions and there’s not genetic Arrhythmmogenic rate of ventricular cardiomyopathy a form in which the right ventricular muscle is replaced with fibro fatty tissue 30% or genetic Symptoms can be mild or severe and end up in palpitations, shortness of breath, chest pain and collapse in case of sudden death
121
How do we treat cardio myopathy?
Ace inhibitors diuretics beta blockers to treat heart failure Amiodarone to treat arrhythmia warfarin to prevent blood clots and stroke Cardio version pacemaker implanted cardio converter defibrillators to prevent serious arrhythmia Surgery and heart transplant in severe patients
122
What is heart failure and how are the three main ways we classify it?
Heart failure is categorised by the heart not being able to pump enough blood around the body at the correct pressure symptoms can be breathlessness fatigue, and ankle swelling which can develop quickly referred to as acute heart failure or more gradually chronic heart failure Heart failure is classified in three main ways Is it the right or left ventricle that’s predominantly affected? Is the defect in left ventricular function systolic or diastolic? According to injection fraction Heart failure with preserved ejection fraction hot failure normal ejection fraction HFNEF patients have heart failure but do not have any evidence of left of ventricular systolic dysfunction Heart function with left ventricular systolic function is also called systolic heart failure
123
What are the risk factors for heart failure?
Hypertension, coronary heart disease, cardiomyopathy atrial fibrillation, heart valve, disease, damage or problems at heart valves Secondary anaemia, thyroid gland issues and high pressure in the lungs may also be a risk
124
How to treat heart failure
Depending on the type of heart failure for example HFPEF or heart failure normal ejection fraction is treated by management of underlying conditions e.g. hypertension diabetes ischaemia heart disease However LVSD or left ventricular systolic dysfunction where the ejection fraction is not normal treatment it is administered in the following steps if symptoms persisted Ace inhibitors and beta blockers are first line Aldo antagonist angiotensin to receptor antagonists or hydralazine plus a nitrate or second line Then digoxin Cardio version pacemaker implanted cardioversion defibrillator Lastly, left ventricular assisted device for patients awaiting a heart transplant Patience should also be given lifestyle advice
125
What what is an ischaemic stroke?
What Blitz supply is stopped to the brain due to a blood clot over 80% of cases are due to blood clots
126
What is a haemorrhagic stroke?
A blood vessel supplying the brain bursts and bleeds into the brain intracerebral haemorrhage
127
What is a transient ischaemic attack TIA?
A transit ischaemic attack is a related condition which the supply of the blood to the brain is temporarily interrupted and can often be a warning sign of a stroke
128
What are the risk factors for stroke?
Hypertension hypocholesteraemia which increases the risk of atherosclerosis Diabetes excess glucose in the blood can damage the arteries Atrial fibrillation can cause blood clots Age 75% of people of strokes are over 65 ethnicity south Asian African Caribbean people are high risk of stroke Family history of heart disease or diabetes History of strokes or TIA or heart attack lifestyle factor Medicines given to prevent blood clots such as warfarin increases risk of haemorrhage Aneurysms
129
What are the symptoms of stroke or TIA transient ischaemia attack?
Fast is used to identify strokes F refers to face may have dropped in one side, unable to smile or move their mouth eyes may have dropped A patient may not be able to lift one or both arms because of weakness and numbness S speech may be slurred Tea time urgent medical help is required if symptoms are evident TIA has the same symptoms however only lasting for a few minutes or a few hours but then disappearing again completely
130
how to treat a stroke
First steps is brain imaging to determine the cause of the stroke or TIA whether it’s ischaemic or haemorrhagic Ischaemic stroke within three hours of symptom onset administer Alteplase which is a thrombolytic medication to breakdown thrombus Followed by aspirin and anticoagulant heparin initially than warfarin long-term For haemorrhagic return clotting levels to normal with a combination of prothrombin complex concentrate and intravenous vitamin C In some cases, fatty deposits may require surgery to remove from the cord arteries or repair damage caused by haemorrhagic stroke
131
How to treat transient schema attacks or TIA
Administer aspirin immediately Assess their risk of stroke Start preventative measures as soon as possible, such as lower blood pressure or cholesterol
132
What is a thrombus, thrombosis and an embolism?
A thrombus is a blood clot and thrombosis is its formation of the clot. An embolism is a clot breaking free
133
What is a Venous Thromboembolism ; a Pulmonary embolism and what are the symptoms and risk factors
A VTE is a condition where a thrombus forums in a vein, it commonly occurs in the deep leg veins ( deep vein thrombosis) and can lead to chronic pain, swelling, ulceration. Occurs in the legs commonly A pulmonary embolism occurs in the pulmonary artery and stops blood from getting to the lungs Risk factors - immobility History of VTE Family thrombosis history Medical conditions Blood vessel damage Obesity Pregnancy’
134
What does a patient take first heparin or warfin and which is better for long term
Heparin is always taken first and warfin for long term use
135
How to treat Venous thromboembolism
Anticoagulant such as herarin then warfarin for 3-6 months to break down clot Compression socks for swelling and to prevent ulceration and raise legs to allow blood flow to upper body
136
What is arterial thrombosis its symptoms and its treatment
It is where blood clots forum in arteries leading to obstruction of major organs It can lead to heart attack Stroke Peripheral arterial disease - blood flow in legs It is treated through thrombolytic medications such as thrombolytic medication alteplase. Surgery is also effective CABD, PCI
137
What is the increased risk associated with HIV infection?
Increased risk of developing coronary heart disease or myocarditis/pericarditis ## Footnote HIV (human immunodeficiency virus) can lead to serious cardiovascular issues.
138
Define myocarditis.
Inflammation of the heart muscle (myocardium) ## Footnote Myocarditis can be caused by viruses, such as parvovirus B19.
139
What are common symptoms of myocarditis?
Chest pain, heart failure, sudden death ## Footnote Symptoms can vary from mild to severe.
140
What indicates a bleak outlook for a patient with myocarditis?
Losing left ventricular function ## Footnote This is a critical indicator of prognosis.
141
How is myocarditis treated?
Managing symptoms as they emerge ## Footnote There is no specific cure for myocarditis.
142
Define pericarditis.
Inflammation of the pericardial sac surrounding the heart ## Footnote This condition can sometimes be due to viral infection.
143
Name a few viruses that can cause pericarditis.
* HIV virus * Influenza * Mumps virus ## Footnote There are many other viruses that may also cause pericarditis.
144
What is a common issue with infectious pericarditis?
The cause is often not identified ## Footnote Despite being common, pinpointing the exact virus can be challenging.
145
What bacteria is associated with the development of atherosclerotic plaques?
Chlamydia pneumoniae ## Footnote Treatment includes antibiotics.
146
What role does Helicobacter pylori play in heart disease?
Implicated as a causative agent for ischaemic heart disease ## Footnote The exact mechanism remains unclear.
147
How might Helicobacter pylori contribute to heart disease?
* Promoting an immune response * Linked with plaque formation and platelet aggregation ## Footnote These connections require further investigation.
148
What did a 2009 study find regarding Cytomegalovirus (CMV)?
A link between CMV and high blood pressure in mice ## Footnote Suggests CMV infection in blood vessels may contribute to atherosclerosis.
149
What is periodontitis?
An inflammatory disease affecting the periodontium ## Footnote It progressively erodes the bone around the teeth.
150
What can untreated periodontitis lead to?
Loss of teeth ## Footnote It can also increase overall body inflammation.
151
What inflammatory mediator is raised in periodontitis?
Interleukin ## Footnote This mediator is linked to increased risks of serious cardiovascular events.
152
How is periodontitis treated?
Anti-inflammatory medications ## Footnote Treatment aims to reduce inflammation and prevent further damage.
153
What gastrointestinal side effects may result from the use of certain medications?
Constipation, diarrhoea, nausea, vomiting, gastrointestinal discomfort ## Footnote These side effects can vary in severity among users.
154
What are bile acid sequestrants?
Medications that help lower cholesterol levels in the body ## Footnote Examples include Colestyramine and Colestipol.
155
What is the indication for the use of bile acid sequestrants?
Hyperlipidaemia, primary prevention of coronary heart disease in men aged 35-59 years with primary hypercholesterolaemia who have not responded to diet and other measures ## Footnote They are particularly effective in patients who have not adequately responded to dietary changes.
156
What is Nicotinic acid also known as?
Niacin ## Footnote It is a water-soluble B vitamin.
157
What effect does Nicotinic acid have on lipid profiles?
Lowers total cholesterol, LDL cholesterol, triglyceride levels; raises HDL-cholesterol levels ## Footnote This effect is observed when given in doses above the vitamin requirement.
158
What are the two types of Nicotinic acid formulations?
Immediate release and modified release ## Footnote Each type has different pharmacokinetic properties.
159
What condition is Nicotinic acid useful in treating?
Patients with both hypertriglyceridaemia and low HDL-cholesterol levels ## Footnote It is particularly beneficial for improving lipid profiles in these patients.
160
What are the two Bile acid seqestrants giving medicine names
Colestyramine and Colestipol