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BMS3052 > WEEK 2/3 CVD ATHEROSCLEROSIS, CORONARY HEART DISEASE > Flashcards

WEEK 2/3 CVD ATHEROSCLEROSIS, CORONARY HEART DISEASE Flashcards

1
Q

What is the single most important factor in cardiovascular disease?

A

Raised blood pressure.

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2
Q

Can high levels of cholesterol drive coronary heart disease (CHD)?

A
  • Yes
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3
Q

What is familial hypercholesterolaemia and what is it caused from?

A
  • This is when LDL cholesterol
    from the plasma is engulfed by macrophages on the skin to form Xanthomas
  • This also happened in the coronary arteries of patient–> plaque on artery wall –> MI (heart attack)
  • Homozygous FH inheritance
  • Had their first myocardial infarction at 8yo
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4
Q

What is the largest lipoprotein and the smallest?

A
  • Chylomicrons largest

- HDL –> smallest

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5
Q

What are the 4 different types of lipoproteins?

A
  • Chylomicrons
  • VLDL
  • LDL
  • HDL
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6
Q

Which type of Lipoprotein is the protective one?

A
  • HDL
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7
Q

What does VLDL stand for?

A
  • Very low density lipoproteins. (Triglyceride) that cannot pass through the blood vessel wall
  • It contains Apo B 100 which is a ligand for LDL reuptake
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8
Q

What is the basic role of the Apo B 100 that is found in VLDL and LDL?

A
  • It is a ligand for LDL reuptake to be recycled and reused
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9
Q

What does LDL stand for?

A
  • Low density lipoproteins (cholesterol)
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10
Q

What is another name for VLDL?

A
  • Triglyceride
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11
Q

What is another name for LDL or HDL (i.e. which class do they belong to?

A
  • Cholesterol
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12
Q

What does LDL stand for?

A
  • Low density lipoprotein
  • It can easily penetrate the vascular endothelium
  • Contains Apo-B -100
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13
Q

What is lipoprotein A formed from?

A
  • LDL and contains Apo-B-100

- It is similar to and competes with plasminogen (degrading fibrin clots-blood clots)

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14
Q

Can LDL penetrate the vascular endothelium?

A
  • Yes it can due to its size (small)

- this is NOT good

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15
Q

Is Liporprotein A, which is formed from LDL, a good or bad type of cholesterol?

A
  • It is a bad type
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16
Q

What does HDL stand for?

A
  • High density lipoproteins

- The species contain apo-A-I which is PROTECTIVE

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17
Q

Which two ways can Lipoprotein transport in the blood occur?

A
  • Exogenous pathway

- Endogenous pathway

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18
Q

What occurs in the exogenous pathways of lipoprotein transport in the blood?

A
  • There is cholesterol/triglycerides derived from the GIT
  • Pass into the intestinal lymph
  • transported as chylomicrons into the plasma
  • then hydrolysed (broken down into FAs)
  • goes into the muscle/adipose tissue
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19
Q

What occurs in the endogenous pathways of lipoprotein transport in the blood?

A
  • You have cholesterol/triglycerides that are synthesized in the LIVER
  • They are transported as VLDL and go straight to the muscle/adipose tissue
  • Then lipoprotein particles become LDL and provides cholesterol
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20
Q

What type of receptor is the LDL receptor?

A
  • A clearance receptor in liver cells
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21
Q

What sythesizes the LDL receptors?

A
  • Liver and Vascular Smooth Muscle Cells (VSMC)
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22
Q

What is the term for HDL (incorperated into apoA-1) removing excess cholesterol from cells?

A
  • Reverse cholesterol transport
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23
Q

There is a strong correlation between plasma [LDL] and _________.

A

There is a strong correlation between plasa [LDL] and atherosclerosis/CHD (cholesterol rich plaque)

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24
Q

There is a strong correlation between Lp(a) (found in plaques) and _____.

A
  • There is a strong correlation between Lp(a) and CHD (cholesterol rich plaque).
  • Reduced plasminogen favours increased thrombosis
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25
Q

With reduced plasminogen in the body because Lp(a) as outcompeted it, what does this promote?

A
  • This promotes increased thromosis which is BAD
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26
Q

There is a correlation between [HDL] and ____.

A
  • Lower CHD (cholesterol rich plaque)
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27
Q

In atherosclerosis is there early evidence of enothelial dysfunction?

A
  • YES
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28
Q

Ideally, what is the ideal total cholesterol level in mmol/L?

A
  • <5.6mmol/L
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29
Q

What is the ideal value for how much LDL cholesterol one should have in their blood?

A
  • <2.5mmol/L
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30
Q

Does age become an issue with increasing cholesterol levels?

A
  • YES
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31
Q

is atherosclerosis a short or long course of progression?

A
  • Very long progression

- Decades long

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32
Q

What is a big contributor to atherosclerosis progression in terms of immune cells?

A
  • Immune cells such as leukocytes ‘sticking’ to the endothelial surface–> monocytes maturing into macrophages that engulf the lipids
  • This is vascular inflammation
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33
Q

What helps in maintaining vasodilator tone and thus an anti-thrombogenic surface?

A
  • NO that is released
  • This relaxed the smooth arterial muscle
  • The endothelial cells were key to releasing NO that would then act on smooth muscle cells to cause vasodilation
  • This means that if there are other immune cells sticking to it, so that the tissue is not available, then it cannot release NO and serious issues will occur.
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34
Q

What are two events occurring with excess oxidised LDL in the coronary artery?

A
  • Oxidised LDL induces adhesion molecule expression (VCAM, ICAM1) on endothelium
  • Oxidised LDL is phagocytosed by macrophages (these then form foam cells)
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35
Q

What are macrophages that ingest LDL called?

A
  • Foam cells
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36
Q

At what age can foam cell start to appear?

A

Can occur in the 20s.

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37
Q

Where is vascular cholesterol uptake by LDL receptors important?

A
  • Important in the liver but not in the blood vessel of the heart
  • If in the blood vessel of the heart we have atherosclerosis
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38
Q

Once monocytes are recruited into the arterial wall, what occurs?

A
  • They enter via adhesion molecules
  • They differentiate into macrophages
  • The macrophages then release inflammatory factors (cytokines etc) so then local tissue damage occurs
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39
Q

What types of antigens so DCs and macrophages present in plaque inflammation?

A
  • Oxidised LDL
  • Heat shock proteins
  • Microbes
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40
Q

What allows for T cells (particularly Th1 cells) to infiltrate the site of the coronary artery in terms of plaque formation?

A
  • Antigens such as Oxidized LDL are presented via APCs (DC or macrophage) to the T cell and causes it to differentiate into a Th1 cell and produce cytokines: IFN-y, IL-1B, IL-6, TNF-a (all the highly inflammatory cytokines)
  • This then AMPLIFIES VASCULAR INFLAMMATION
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41
Q

Are Tregs still active in vascular inflammation?

A
  • YES, they will still be producing anti inflammatory cytokines like IL-10 and TGF-b however the majority is inflammatory so this is outweighed by the inflammatory cytokines
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42
Q

What is CRP (C-reactive protein)?

A
  • Acute phase protein synthesised in the liver that can be used as a biomarker for generalised inflammation
  • This is predictive of CVD and informs on statin therapy
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43
Q

What is the mode of action for CRP?

A
  • It binds to the surface of dying cells and promotes phagocytosis
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44
Q

What is CRP stimulated by?

A
  • IL-6 from inflammatory cells
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45
Q

What can occur as a mechanism to try and stabilize the lipid core in the formation of atherosclerosis?

A
  • A fibrious cap via collagen depositing to seal it off.
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46
Q

What happens if the fibrous cap ruptures?

A
  • There can be a thrombus formation
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47
Q

Which cells are responsible for inhibiting cap fibrous cap formation?

A
  • The Th1 cell via the release of IFN-y and decreaes collagen synthesis by smooth muscle cells
  • The macrophage released MMP which degrades the collagen fibrils
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48
Q

Is the inflammasome involved in atherosclerois progression and inflamation?

A
  • YES - very complicated process
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49
Q

Which cells produce collagen?

A
  • Smooth muscle cells
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50
Q

Are there some drugs looking at inhibiting inflammatory factors to treat atherosclerosis?

A
  • YES
    e. g. IL-1b inhibition in Canakinumab BUT not approved by FDA for RISK REDUCTION (very expensive)
  • Treatment options not clear yet
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51
Q

Does plaque rupture generally come before or after thrombosis or a thrombus forming?

A
  • It comes BEFORE the thrombus forms

- Plaque contents burst through the ruptured cap into the lumen in mins-hrs

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52
Q

Can thrombus/infarction occur throughout the whole body?

A
  • YES

- But the outcomes are dependent on the location of the tissue injury

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53
Q

What are the symptoms associated with DVT (this has nothing to do with atherosclerosis!)?

A
  • Sharp pain when foot is flexed
  • tenderness and swelling in the leg
  • Fever and rapid heart beat
  • Sudden unexplained cough and joint pain
  • Leg may become red and warm to touch
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54
Q

What are examples of acute presentation in terms of coronary heart disease (e.g. Acute coronary syndrome)?

A
  • Angina–> radiating chest pain
  • Acute myocardial infarction (AMI- heart attack)
  • Others
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55
Q

What are examples of chronic coronary heart diseases?

A
  • Stable angina

- Heart failure

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56
Q

What are two immediate treatments for life threatening events?

A
  1. Revascularization

2. Drugs

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57
Q

What is involved in revascularization for the treatment of life threatening events?

A
  • A Percutaneous coronary intervention (PCI)/angioplasty usually with stents.
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58
Q

What is one type of drug that has a narrow therapeutic window, that we can use for the immediate treatment of life threatening events?

A
  • Tissue palsminogen activator (recombinant tPA- rtPA)
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59
Q

What are two chronic drug treatments for atherosclerosis used for Prevention?

A
  1. Reducing the lipid/plaque/inflammation burden.(e.g. Lipid-lowering drugs–] statins and newbies PCSK9)
  2. Many other drugs help with CHD Burden (by decreasing the workload)
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60
Q

What are the three different types of hyperlipidaemia (dyslipidemia)?

A
  • Cholesterol (hypercholesrerolaemia)
  • Trigylcerides (hypertriglyceridaemia)
  • Both (mixed)
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61
Q

What are the causes of CVD related hyperlipidaemia?

A
  • Genetic e.g. FH (Familial hypercholersterolemia)–> defect in the LDL receptor
  • Dietary excess
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62
Q

What types of diseases can hyperlipidaemia be secondary to?

A
  • Diabetes mellitus

- Alcoholism, Obstructive liver disease, drugs

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63
Q

What type of feedback inhibition occurs with the LDL receptor in the synthesis of cholesterol?

A
  • When the intracellular cholesterol content increases, there is NEGATIVE regulation that occurs
  • Decrease in the productionof HMG CoA Reductase which decreases its synthesis in the hepatic cells
  • Decrease in the LDL receptors
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64
Q

What are some things that you must consider in the treatment of hyperlipidaemia?

A
  • CV status and risk factors
  • If it is secondary to other diseases such as diabetes or hypertension, in which case you would treat those first
  • You must consider lifestyle modification BEFORE any drug treatment.
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65
Q

What are two drugs used to treat hypercholesterolemia?

A
  • Statins

- PCSK9 inhibitors

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66
Q

What is the main mechanism of action for statins in the liver?

A
  • They inhibit the intracellular formation of cholesterol in the liver
  • ‘HMG-CoA reductase inhibitors’ –> competitive enzyme inhibitor
    e. g. Simvastatin (Zocor), Pravastatin (Pravachol), Atovastatin (Liptor)
  • Re
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67
Q

Have statins been shown to work well in large scale clinical trials?

A
  • YES
68
Q

Do statins reduce the exogenous or endogenous cholesterol ?

A
  • They reduce the endogenous synthesis of cholesterol in hepatocytes –> this promotes increased increased expression of LDL receptors on hepatocytes. –> so disrupting the feedback regulation
  • This leads to increased plasma clearance (LDL)
69
Q

What are 3 clinical uses of statins?

A
  • Primary prevention in cardiovascular disease. (high risk with elevated cholesterol)
  • High risk of chd (cholesterol rich plaque). (with/without elevated cholesterol)
  • Secondary prevention of myocardial infarction and stroke. (symptomatic)
70
Q

What are three side effects of statins?

A

GI disturbance. Diabetes risk. Memory loss

71
Q

Do patients with lower CRP levels after statin therapy have better outcomes?

A
  • Yes these patients have better outcomes than those who don’t as these people had a better reduction in inflammation (which is what CRP indicates)
72
Q

Do statins and other drugs increase or decrease thwe LDL receptor expression?

A
  • They all INCREASE THE LDL R EXPRESSION
73
Q

What is PCSK9?

A
  • It is a circulating serine protease enzymes that binds to LDL receptors
  • It facilitates lysosomal degradation
  • this leads to a DECREASE in the LDL receptor recycling
  • It reduces LDL clearance which leads to elevating circulating LDL
74
Q

Are there gain of function and loss of function mutations revealed in patients with high and low LDL respectively?

A
  • YES
75
Q

Has there been succcess in PCSK9 inhibitors?-

A
  • YES
  • People who were on statins but still had a high LDL cholesterol level compared to patients on the inhibitor
  • Those on the inhibitor resulted in a significant decrease in LDL levels
76
Q

What form are the PCSK9 inhibitors?

A
  • Monoclonal antibodies
77
Q

Is there a drug to treat FH?

A
  • YES PCSK9 inhibitor with a good diet and exercise
78
Q

What is PCSK9 inhbitor used to treat?

A
  • FH (with diet and exercise)
  • High CVD risk patients
  • statin intolerant patients
79
Q

What is the downside of PCSK9 inhibitors?-

A

COST $$$

80
Q

Do you usually die from hypertension?

A
  • NO

- You usually die from other comorbidiries but this is a cause of many issues e.g. heart attack

81
Q

What two branches come off Coronary heart disease?

A
  • Acute presentation

- Chronic disease

82
Q

What is another name for coronary heart disease?

A

Ischaemic heart disease or coronary artery disease.

83
Q

What is the name for an acute presentation of coronary heart disease?

A
  • Acute Coronary Syndrome (ACS)
84
Q

What does ACS (Acute Coronary Syndrome) comprise of?

A
  • Angina (radiating chest pain)
  • Acute myocardial infarction (AMI; heart attack)
  • Others
85
Q

What does the chronic coronary artery disease comprise of?

A
  • Stable angina

- Heart failure

86
Q

Does the location of the infarct determine the severity of it?

A
  • YES where you have the atherosclerosis and blockages determines the severity
  • e.g. left anterior descending artery obstruction leads to sudden death
87
Q

Which layer of the heart muscle is vulnerable to ischaemia?

A
  • The sub-endocardial zone
  • This is because passive diffusion occurs on the left ventricle and because the coronary arteries are small calibre, this can lead to limiting flow if there is any narrowing of these
88
Q

What is the location of the coronary arteries and when do they fill?

A
  • They sit above the aortic valve and fill during diastole
89
Q

Are the coronary artieries external to the myocardium?

A
  • YES
90
Q

Does muscle hyperytrophy occur in the heart muscle? (i.e. do the vessels get stretched)?

A
  • YES
91
Q

What is the sub-endocardial zone a balance of in the heart?

A
  • It is a balance of the coronary artery supply versus the diffusion from the left ventricle
  • So the coronary artery must supply the blood and it then must diffuse (via passive diffusion) in to the left ventricular muscle (sub-endo zone)
92
Q

Is actute coronary syndrome black or white, or a spectrum?

A
  • A spectrum ranging from normal, to angina, to ACS, to right at the other extreme with myocardial infarction
93
Q

What is ACS defined as by the ACS guidelines?

A
  • Any condition causing sudden, reduced blood flow to the heart. Includes the type of chest pressure that you feel during the heart attack, or pressure in your chest while you’re at rest or doing light physical activity (unstable angina). Cardiac arrest could be the first sign!
94
Q

According to the ACS guidelines what is a leading symptom that initiates a diagnostic and therapeutic Cascade in patients with suspected ACS?

A
  • Chest pain
95
Q

In patients with suspected ACS with chest pain as the leading symptom, which two groups of people can be differentiated based on the ECG?

A
  1. patients with acute chest pain and persistent (>20mins) ST-segremnt elevation
  2. Patients with acute chest pain but NO persistent ST segment elevation
96
Q

Out of the two groups of people with ACS, which one is the most at risk?

A
  • The one with a persistent S-T segment elevation

- This is because it is likely a blockage in the LV wall

97
Q

What does the classification of patients with acute chest pain and ST elevation reflect in the heart and what do they ultimately develop (for people with suspected ACS) ?

A
  • Reflects an acute total coronary occlusion

- They ultimately develop ST-elevation myocardial infarction (STEMI)

98
Q

In more general terms, what is the main treatment for those with suspected ACS involving persistent chest pain and elevated ST segment?

A
  • It involves immediate re-perfusion by percutaneous coronary intervention (angioplasty/stent) or fibrinolytic therapy
99
Q

What are the 6 different types of ECG that can occur in patients with suspected ACS?

A
  1. Transient ST-segment elevation
  2. Persistent or transient ST-segment depression
  3. T-wave inversion
  4. Flat T waves
  5. Pseudo-normalization of T waves
  6. NORMAL ECG
100
Q

What occurs in NSTEMI in terms of vessels?

A
  • There is a partial vessel occlusion

- Partial thickness infarct

101
Q

What occurs in STEMI in terms of vessels?

A
  • Complete vessel occlusion

- Full thickness infarct

102
Q

What can be associated with NSTEMI or STEMI?

A
  • Thrombus formation

- e.g. occlusive thrombus for STEMI and mural thrombus with variable obstruction

103
Q

According to the AMI guidelines, what is the definition of myocardial infarction?

A
  • Acute myocardial infarction (AMI) defines cardiomyocyte necrosis in a clinical setting consistent with acute myocardial ischaemia.
104
Q

What two things do you have to have to diagnose acute MI?

A
  1. Detection of an increase and/or decrease in high sensitivity cardiac troponin
  2. At least one of the following:
    - Symptoms of ischaemia
    - New or presumed new, significant ST-T wave changes or left bundle branch block on 12-lead ECG
    - Development of pathological Q wave on ECG
    - Imaging evidence of new or presumed new loss of viable myocardium or regional wall motion abnormality
    - Intracoronary thrombus detected on angiography or autopsy
105
Q

What are the two worse biomarkers to use for a heart attack indication?

A
  • Myoglobin

- CK (Creatine Kinase)

106
Q

What is some information about myoglobin in terms of heart attacks?

A
  • Can be a biomarker (but not as good as troponin)
  • Heme containing protein in heart and skeletal muscle - early release into the blood after AMI (1-2 hours, short lived)
  • Detected in the blood after AMI AND skeletal muscle injury
107
Q

What are the downsides of using myoglobin as a biomaker for acute MI?

A
  • Short lived - only 1-2 hours in blood

- NON specific - released after cardiac OR skeletal muscle damage

108
Q

What is some information about CK as a biomarker for AMI?

A
  • It is found in heart and skeletal muscle
  • Exists as a dimer and 3 isoforms (BB, MM, and MB)
  • MB is quite heart specific thus the best option
109
Q

Which biomarker is the gold standard for AMI?

A
  • Cardiac Troponin (cTn)
110
Q

Are the cTn-T or cTn-I isoforms of cardiac troponin both cardiac specific?

A
  • YES
111
Q

How long can troponin be detected in the blood after a heart attack?

A
  • 4-10 hours after AMI, they peak at 12-48 houts and it is abnormal for 4-10 days (can help with diagnoses for delayed presentations)
112
Q

Will someone who presents to an emerency department late and is having/had an AMI be able to have treatment still?

A
  • YES

- This is due to its long half life in blood

113
Q

What is another important class of biomarkers for AMI?

A
  • NPs (Natriuretic peptides)
114
Q

What are NPs released by?

A
  • Atrial distension (pressure- ANP) and LV stretch/stress (BNP)
115
Q

Are NPs mainly vasodilators or constricters?

A
  • Vasodilators!
116
Q

What do the biomarkers NP inhibit?

A
  • Inhibit Ang II mediated NA+ water reabsorption
117
Q

What types of NPs are biomarkers for heart failure?

A
  • BNP and NT-proBNP (N-terminal breakdown product)
118
Q

Which section of the heart is the biomarker BNP (NPs) found usually?

A
  • ventricle mainly
119
Q

What are some causes of AMI?

A
  • Coronary artery occlusion plaque build up (with our without a rupture)
  • Aortic valve problems.
    . Coronary artery aneurysms.
  • Electrical failure (Arrhythmias)
  • Illicit drugs
  • Anticancer drugs
120
Q

What are the causes of acute myocardial infarction similar to?

A
  • Similar causes to heart failure chronic phase.
121
Q

What is the ruptured atheromatous morphology associated with?

A
  • Association with ACS and mortality.

- This is because the thrombi is forming and occluding the vessel.

122
Q

What is the fibrous plaque morphology associated with?

A
  • Associated with a healed disrupted plaque; Stenotic, fibrous, causing stable ischaemic syndromes, e.g. ‘demand’ angina (like with exercise, increased activity)
123
Q

Why is there potential for cardiac rupture in week post-MI?

A
  • Because the heart has been weakened overall (fibrous tissue replaces the cardiomyocytes which cannot regenerate)
124
Q

What are the symptoms of angina pectoris and do females present differently?

A

Pain, severe, crushing, substantial, May radiate. (may come on when you are exerting yourself)
- Females often do present differently (lots of nausea, vomiting, back/jaw pain)

125
Q

What are the causes of angina pectoris?

A

Coronary artery disease karma coronary vasospasm.

- I.e. imbalance: . Myocardial O2 demand is greater than the O2 supply.

126
Q

When is urgent medical attention required for in terms of angina?

A
  • For worsening angina (unstable angina)

- Chest pain lasting more than a few minutes.

127
Q

What are three types of angina?

A
  1. Chronic, stable angina
  2. Unstable angina
  3. Variant (vasospastic angina)
128
Q

Out of the three main types of angina, which one presents with no atherosclerosis?

A
  • The variant vasospastic one –> this is the spasm of the coronary artery and can occur in the morning. 5HT is thought to be involved
129
Q

What is chronic, stable angina caused by?

A
  • Caused by ‘demand’ e.g. exercise, stress-test etc. and there is usually a lot of atherosclerosis
130
Q

What is unstable angina caused by?

A
  • this can be due to thrombi formation and is UNPREDICTABLE

- This is the classic ACS and there is probably some atherosclerosis

131
Q

What are the risk factors for angina?

A

Hypertension, cholesterol, smoking etc.

132
Q

What is angina precipitated by?

A

Exertion, cold, stress, large meals…

133
Q

In general terms, what are the drug treatments for angina?

A
  • Acutely relieved by rest and or nitro vasodilators
134
Q

What is the pharmacological treatment for unstable angina?

A
  • tPA
135
Q

What are three types of drug treatments for chronic stable angina?

A
  • nitro vasodilators
  • B1 adrenoceptor antagonists
  • Ca2+ channel antagonists
136
Q

In generaly terms, what are the mechanisms for the treatment of stable angina?

A
  • increased coronary reperfusion to increase the oxygen supply
  • Decreasing the metabolic demand
  • A combination of both of these
137
Q

What are the surgical treatments for anigna?

A

-Angioplasty/stents/CABG

138
Q

What types of risk factors can be modified for the treatment of angina?

A
  • Smoking, obesity, hypertension, hyperlipidemia, diabetes
139
Q

In general terms, NO is a good ____ and ____ agent.

A
  • NO is a good vasodilator and thrombogenic agent
140
Q

What is the mechanism of action of nitrates in angina?

A
  • Venous dilation reduces venous pressure and pre-load, with consequent fall in cardiac oxygen consumption.
  • Arterial dilation reduces peripheral resistance and afterload with consequent following cardiac oxygen consumption.
  • Coronary dilation for example variant angina
141
Q

Is there an effect of NO in cardiac / skeletal muscle?

A
  • No! Only in the vascular smooth muscle cells
142
Q

In what situations should NO (nitrates) be given for angina?

A
  • For the treatment of acute attack of angina
  • For immediate prophylaxis.
  • Given chronically for stable angina (often as a patch.)
143
Q

What are two limitations for nitrates given for the treatment of angina?

A
  • A decrease in blood pressure is associated with a reflex tachycardia. From a Barro-reflex effect
  • There is a tendency to increase cardiac oxygen consumption.
144
Q

What type of metabolism are the nitrates in the treatment of angina?

A
  • They go through a large hepatic first pass metabolism.
  • GTN is a prodrug
  • given sublingually or transdermally
145
Q

What are the adverse effects of nitrates for the treatment of angina?

A

Hypotension (fainting)
Tachycardia
. Headache
. Flushing

146
Q

Which other drug should nitrates not be combined with and what is the reason for this?

A

Sildenafil (Viagra)

  • This can lead to collapse or death.
  • Sildenafil inhibits PDE which stops the conversion of cGMP to GMP. This leads to a build up of cGMP and accelerates the formation of myosin light chain stimulation which leads to relaxation
  • So you don’t want a large amount of relaxation
147
Q

Can a patient develop tolerance to nitrates?

A
  • Yes, after continual exposure.
148
Q

What is a method to prevent nitrate tolerance?

A
  • A nitrate free period e.g. nitrate free for 8 hours per 24 hours of using transdermal patches reduces the tolerance
149
Q

What are the clinical signs / symptoms of left heart failure?

A
  • Dysponea (shortness of breath)
  • Shortness of breath lying flat
  • Oemema
  • Back pressure to pulmonary circulation
  • Tachycardia
150
Q

What are the clinical signs/ symptoms of right heart failure?

A
  • Back pressure to systemic circulation
  • Oedema
  • JVP elevation (jugular vein pressure)
  • Hepatomegaly
151
Q

Is heart failure biventricular?

A

Yes yes

152
Q

What can be the causes of heart failure?

A
  • Lung condition
  • Pulmonary hypertension
  • Hypertension
  • HEART CONDITION: Valves, Ischaemia, Arrhythmia, Cardiomyopathy, CHD, atherosclerosis
  • Other co-morbidities such as renal failure and diabetes
  • Decreased exercise tolerance
153
Q

Are the two types of heart failure (cardiac remodelling)?

A
  • Acute heart failure

- Chronic heart failure

154
Q

Can a cat heart failure be precipitated by an event for example trauma or AMI?

A
  • Yes
155
Q

The main focus for chronic heart failure?

A

Long-term management is the main focus.

156
Q

What are two events that can occur in chronic heart failure?

A
  • Systolic dysfunction- impaired contraction = HF with a REDUCED ejection fraction (HFrEF)
  • Diastolic dysfunction- contraction okay but impaired filling –> HF with PRESERVED ejection fraction (HFpEF)
157
Q

What is HFrEF?

A
  • Heart failure with reduced ejection fraction
  • Systolic dysfunction, impaired contraction
  • Dilated heart
158
Q

What is HFpEF?

A
  • Heart failure with PRESERVED ejection fraction
  • diastolic dysfunction (contaction okay but impaired filling) –> not too bad at rest
  • Hypertrophied heart
159
Q

In which groups is the prevalence of HFpEF increasing at an alarming rate and what is it associated with?

A
  • Older population
  • Females
  • Diabetics
  • Associated with fibrosis and the most difficult to treat
160
Q

What occurs in ventricular remodelling in diastolic and systolic heat failure?

A
  • There can be a hypertrophied heart or a dilated heart
161
Q

What occurs in a hypertrophied heart as a result of ventricular remodelling due to heart failure?

A
  • Preserved CO (contraction)
  • Relaxation (diastole) impaired
  • Decrease in cardiac output in exercise
    e.g. hypertension
    HFpEF
162
Q

What occurs in a dilated heart as a result of heart failure?

A
  • Depressed CO (ej fraction)
  • Change in geometry (dilation)
  • e.g. dilated cardiomyopathy
    HFrEF
163
Q

What are the end results for compensation due to decreased CO in heart failure?

A
  • Increase in Cardiac output (CO) by increasing the force and rate of contraction and increasing preload, and after load.
  • Remodelling occurs
164
Q

Do the compensatory mechanisms for trying to increase CO in heart failure (which causes reduced CO) make the cardiac state better or worse?

A
  • They make it WORSE !
  • the decreased CO leads to increased NA, Ang II and ET. This leads to increased afterload which DECREASES ejection fraction (EF) which leads to a further decrease in CO
  • This is a viscious cycle that keeps on repeating until the CO is extremely reduced hence heart failure
165
Q

Drugs commonly used to treat heart failure and hypertension?

A
  • ABCD drugs
166
Q

What are the ABCD drugs used to treat heart failure and hypertension?

A

Angiotensin converting enzyme inhibitors and angiotensin antagonists
Beta blockers
Calcium channel blockers (but NOT for HF)
Diuretics (thiazides, loop, K+ sparing)

167
Q

Treatment for heart failure?

A
  • Lifestyle changes (weight, sodium, diet; exercise)

- Decrease in cardiac workload via Angiotensin inhbition, Diuretics and beta blokcers

BMS3052 (14 decks)

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