Ischaemic Heart Disease Case Study Biology Essay

Identify 4 hazard factors that make Mrs Gray a likely campaigner for ischemic bosom disease. Explain how each of these hazard factors can lend to the development of ischemic bosom disease.

Ischaemic bosom disease besides known as coronary arteria disease is characterised by loss of O and foods to myocardium due to deficient coronary blood flow ( Copstead & A ; Banasik, 2010 ) . In United States, approximately 250,000 people die every twelvemonth due to ischemic bosom disease ( McCann, 2009 ) . Risk factors of ischemic bosom disease are categorised as modifiable and non-modifiable hazard factors. In the instance of Mrs. Judy Gray, the four major hazard factors that make her a campaigner for ischemic bosom disease are:

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Non-modifiable hazard factors:

Advanced age and adult females post menopausal- Mrs. Gray is 55 old ages old and she is post menopausal. Harmonizing to McCance, Huether, Brashers, and Rote ( 2010 ) , aging and station menopausal adult females are major hazard factors of ischaemic bosom disease. Due to degenerative alterations in the bosom and blood vass, individuals aged 40 and above are at hazard to develop coronary arteria disease. Post menopausal adult females are besides at hazard due to reduced oestrogen degree, decreased HDL ( high denseness lipoprotein ) , and increased LDL ( low denseness lipoprotein ) . These contribute to the development of coronary artery disease, which is the chief cause of coronary arteria disease ( Copstead & A ; Banasik, 2010 ) .

Family History- Mrs. Gray ‘s male parent had a coronary arteria beltway at the age of 57. Her aunt and uncle died in their 30 ‘s due to unexplained bosom failure. Harmonizing to McCann ( 2009 ) , that research grounds confirmed that 250 cistrons are link to bosom diseases and coronary arteria disease. Some cistrons linked to coronary arteria disease are low-density lipoprotein ( LDL ) receptor and apolipoprotein B-100. A mutant of low-density lipoprotein ( LDL ) receptor contribute to familial hypercholesteremia and apolipoprotein B-100 causes LDL to remain longer in the plasma that consequence to really high LDL degrees ( McCann, 2009 ) .

Modifiable hazard factors:

c. ) Hypertension- Mrs. Gray has a history of high blood pressure. Harmonizing to Phibbs ( 2007 ) , a individual with high blood pressure increases the hazard of coronary arteria disease about 200 % . Due to abnormally high force per unit area within the vas, the cells in the liner of the coronary arterias are frequently damaged. The damaged endothelial liner speeds up the narrowing of the arterias. Cells Begin to devolve and organize multitudes of fat called atheromas. These atheromas cause a obstruction to the flow of blood through the vass ensuing to coronary artery disease ( Hurst, 2008 ) .

d. ) Hypercholesterolemia- the cholesterin degree of Mrs. Gray was 4.5 mmol/L ; nevertheless, the ratio of her good cholesterin ( HDL ) to bad cholesterin ( LDL ) was lower than desirable significance she has high degree of LDL ( bad cholesterin ) . High degree of LDL amendss endothelium and causes accretion of fatty plaques on endothelial liner and proliferation of smooth musculus cells that contribute to the development of coronary arteria disease ( Copstead & A ; Banasik, 2010 ) .

2. ) Discuss the pathogenesis of myocardial infarction. Associate your treatment to Mrs Gray.

Mrs. Gray has developed myocardial infarction due to predisposing factors such as aging, station menopausal, household history of bosom disease and high blood pressure and hypercholesteremia. These hazard factors contribute to the development of coronary artery disease which is the major cause of myocardial infarction. Normally, the coronary arterias supply blood flow sufficient to the myocardium to run into oxygen demand ( McCance et al. , 2010 ) . When the endothelial cell bed of the coronary arterias are injured due to predisposing factors, the white blood cells, thrombocytes, lipoids and fibrins converge at the damaged site. Hence, doing the occupant macrophages or foam cells to constellate at the injured liner and absorb oxidised cholesterin which accordingly form into a mass of fat or atheroma. This atheroma narrows the arterial lms ( Turer & A ; Hill, 2010 ) . Due to gradual narrowing of arterial lms, the collateral circulation develops which attempt to counterbalance myocardial perfusion distal to the obstructor ( Port & A ; Matfin, 2009 ) . Then myocardial metamorphosis displacement from aerophilic to anaerobic that consequence to the increased lactic acid production which activate the nervus stoping, therefore doing hurting and referred hurting to Mrs. Gray. Then myocardial cells die due to insufficient O that causes lessening in myocardial contractility, cardiac end product and diminish arterial force per unit area. Hypoperfusion stimulates baroreceptors which cause stimulation of sympathetic receptors. The release of adrenaline and nor epinephrine increases the bosom rate, peripheral vasoconstriction and myocardial O demand. Then ventricular arrhythmias develop with elevated cardiac troponin, CK-MB, and lactate dehydrogenase. Due to self-generated depolarization and repolarisation of myocardial cells, the electrical conductivity system is affected by hurt, infarct and ischaemia. Left ventricle impair its ability to pump blood due to extended harm, doing blood to endorse up into the left atrium and eventually in the pneumonic venas and capillaries of Mrs. Gray ( McCann, 2005 ) .

3. ) Explain the underlying pathophysiology of both ST lift in Mrs Gray ‘s ECG recording and the altered degrees of Troponin. Discuss the relevancy of these consequences in the diagnosing and intervention of Mrs Gray ‘s status.

Mrs. Gray had chest hurting and her EKG ( ECG ) consequence shows ST section lift. This indicates that there is a decreased blood supply due to 100 % occlusion of the anterior descending coronary arteria that causes myocardial ischaemia and cell hurt ( McCann, 2005 ) . ST section lift leads to allow intervention to Mrs. Gray which includes BalIoon angioplasty and stent. In fact, ischemic decease of myocardial tissue is the chief cause of the ST-segment lift on the ECG reading of Mrs. Gray ( Cohen, Roubin, & A ; Kuepper, 2007 ) . Within several proceedingss of myocardial infarction alterations of cell constructions occur like mitochondrial puffiness and animal starch depletion. This will be reversible if blood flow is restored instantly, nevertheless, irreversible mortification occur when there is terrible ischaemia in 20 to 40 proceedingss. ST lift myocardial infarction ( STEMI ) causes multiple structural alterations in the cardiac map of Mrs. Gray. This includes progressive alterations in ventricular size, form and thickness, early wall cutting, mending, hypertrophy and dilation of both infarcted and non-infarcted countries ( Porth & A ; Matfin, 2009 ) .

Blood trial was drawn from Mrs. Gray 2 hours post oncoming of symptoms and revealed Troponin T at 0.2 mcg/L. Normal scope of Troponin within first 3 hours station oncoming is 0 to 0.2 mcg/L ( Wood, Froelicher, Motser & A ; Bridges, 2005 ) . After 6 hours, it was repeated and revealed abnormally high degree of Troponin T at 1.1 mcg/L. Cardiac Troponins are the most specific laboratory trial to observe myocardial infarction ( Bukkapatman, Robinson, Turnipseed, Tancredi, Amsterdam, Srivatsa, 2010 ) . Normally, Troponin I and Troponin T are present in myocardium and become elevated within 3 hours after the oncoming of symptoms of myocardial infarction ( Porth & A ; Matfin, 2009 ) .Due to myocardial cell decease, troponin becomes elevated. Myocardial cell contains isoforms, a cardiac protein. These isoforms become elevated when there is escape from fatally injured cells that have lost plasma membrane unity ( Copstead & A ; Banasik, 2010 ) .

4. ) Describe the actions of GTN and morphia and explicate why these 2 drugs were given to Mrs Gray.

Mrs. Gray experienced chest hurting, when the ambulance officers arrived, they gave Nitrolingual Pump Spray ( GTN ) under her tongue.GTN is a signifier of nitrates which is the drug of pick for forestalling and alleviating acute angina ( McCann, 2005 ) . Nitrates have direct loosen uping consequence on vascular smooth musculus and causes vasodilation ( Lehne, 2007 ) . Nitrate Acts of the Apostless by distending blood vas so that less blood will returns in the bosom. This will cut down the volume of blood in the ventricle at the terminal of diastole or the preload. By diminishing the preload, nitrates cut down the ventricular wall tenseness and ventricular size ensuing to cut down bosom ‘s work load and oxygen demand of the bosom ( Lehne, 2007 ) .

Since Mrs. Gray ‘s chest hurting was non relieve with GTN, she was given morphine 2.5 milligram via intravenously. Morphine is narcotic agonist that reduces the thorax hurting by adhering opioid receptors within the peripheral nervous system and cardinal nervous system ( Schrefer, 2005 ) . Morphine Acts of the Apostless by miming the effects of endomorphines and produces curative effects of analgesia. It besides acts by distending venas in the fringe and cut downing cardiac preload and afterload ( McCann, 2005 ) .

5. ) Explain the mechanism of action of any 2 of the drugs Mrs Gray was prescribed on discharge. Discourse the patient instruction you will give to Mrs Gray in relation to these drugs.

Upon discharge Mrs. Gray was prescribed Betaloc 2.5 mg daily. Bataloc is beta-adrenergic adversary 1 that is known for long term bar of angina. Beta-adrenergic antagonist Acts of the Apostless by barricading beta-1 receptor in the bosom, forestalling noradrenaline and adrenaline from suppressing beta receptor site ( McCann, 2005 ) . By barricading beta receptor, Betaloc decreases bosom rate, decreases myocardial contractility, decreases oxygen demand of the bosom and reduces myocardial ischaemia badness to Mrs. Gray ( Lehne, 2007 ) . Instruct Mrs. Gray that before taking Betaloc, buttocks foremost her pulsation, cheque for the quality and abnormality and withhold the drug if bradycardia is present. Ask her to take the drug with repast to forestall gastro enteric disturbance. Ask Mrs. Gray to detect for the side effects of the drug which includes diarrhea, sickness, purging, weariness, and decreased sexual map. Instruct her to take blood force per unit area often while taking the drug to supervise marks of hypotension and shortness of breath. And if she missed a dosage, take the following agenda dosage and ne’er duplicate the dosage ( Schrefer, 2005 ) .

Another drug that was prescribed to Mrs. Gray is Crestor 5 milligram one time daily. Since the ratio of cholesterin degree of HDL ( good cholesterin ) to LDL ( bad cholesterin ) of Mrs. Gray was lower than desirable intending the more LDL in her plasma and less HDL, the greater hazard of developing coronary bosom disease ( Lehne, 2007 ) . High degree of LDL contributes to the development of coronary bosom disease, in contrast, high degree of HDL reduces the hazard of coronary bosom disease ( Lehne, 2007 ) . Crestor ( Rosuvastatin ) is a signifier of 3-hydroxy-3-methylglutaryl coenzyme A ( HMG-CoA ) reductase inhibitors or besides known as lipid-lowering medicine that lowers the cholesterin degree associated with LDL ( Lehne, 2007 ) . Crestor ( Rosuvastatin ) acts by suppressing the hepatic HMG-CoA reductase, an enzyme that is responsible for the transition of HMG-CoA to mevalonate. In response to the suppression of cholesterin synthesis, the heptocytes causes to synthesis more LDL receptor, taking more LDL ( bad cholesterin ) from the blood ( Lehne, 2007 ) . Ask Mrs. Gray to supervise her cholesterin and triglyceride degree on a regular basis to look into for the curative response of the drug. State her that concern, diarrhea, sickness, indigestion and epigastric hurt are the occasional side effects of the drug. Instruct her that cholesterol-lowering diet is really of import as portion of her intervention ( Schrefer, 2005 ) .


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