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angina pectoris pathophysiology

angina pectoris pathophysiology

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Published by teddydeclines14
this pathophysiology made by the students of the Philippine Paramedical and Technical School of Cagayan de Oro City-Batch 2
this pathophysiology made by the students of the Philippine Paramedical and Technical School of Cagayan de Oro City-Batch 2

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Published by: teddydeclines14 on Oct 05, 2009
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06/04/2013

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XI. PATHOPHYSIOLOGY
Medical Diagnosis
Angina Pectoris, Unstable; Diabetes mellitus type 2 – poorly controlled; Obesity; HPN 2; Hypertensive Cardiovascular Disease(HCVD); Left Ventricular Hypertrophy (LVH); Anxiety Disorder 
Definition
Angina Pectoris, Unstable
- Unstable angina occurs when the narrowing becomes so severe that not enough blood gets through to keepthe heart functioning normally, even at rest. The atherosclerotic plaque may rupture in unstable angina, allowing blood clots to precipitate andfurther decrease the lumen of the coronary vessel. This explains why an unstable angina appears to be independent of activity. Sometimes theartery can become almost completely blocked. It may occur unpredictably at rest which may be a serious indicator of an impending heart attack.
Diabetes Mellitus type II
- occurs when the pancreas produces insufficient amounts of the hormone insulin and/or the body’s tissuesbecome resistant to normal or even high levels of insulin.
Hypertensive Cardiovascular Disease (HCVD)
- also known as hypertensive heart disease occurs due to the complication of hypertensionor high blood pressure. In this condition the workload of the heart is increased manifold and with time this causes the heart muscles to thicken. Theheart continues pumping blood against this increased pressure and over a period of time the left ventricle of the heart enlarges and this in turncauses the blood pumped by heart to reduce.
Left Ventricular Hypertrophy (LVH)
- Left ventricular hypertrophy (LVH) is the thickening of the myocardium (muscle) of the left ventricle of the heart caused by increased afterload and hypertension.
Hypertension II
- Hypertension is a chronic medical condition in which the blood pressure is elevated.
Obesity
- is a medical condition in which excess body fat has accumulated to the extent that it may have an adverse effect on health,leading to reduced life expectancy. Body mass index (BMI), which compares weight and height, is used to define a person as overweight (pre-obese) when their BMI is between 25 kg/m2 and 30 kg/m2 and obese when it is greater than 30 kg/m2.
(http://en.wikipedia.org/wiki/Obesity)
Anxiety Disorder –
The anxiety disorders are a group of mental disturbances characterized by anxiety as a central or core symptom.Anxiety is associated with a wide range of physical illnesses, medication side effects, and other psychiatric disorders.
 
29
 
Schematic Diagram
30
Predisposing
Age- 73 years oldHereditary- HPN, DMGender- femaleHx of Cholecystectomy (NMMC; 1995)Menopause (starts at age 42 years old; Menarche starts at age 13 yrs.old.)DM II (1999; usual glucose level: 140-160mg/dL; highest level: 300mg/dL)
Precipitating
>HPN (37 yrs old; usual BP 140/90; highest BP is 200/110mmHg)>Inc. serum Cholesterol level: 231mg/dL>Lack of exercise/activity>Obesity (BMI of 27 kg/m2, IBW: 48.96kg)
Increase shearing force of the arterial wall by the conditionNonspecific injury to arterial wall(endothelial injury) in thecoronary arteryDesquamation of endothelial lining andstimulation of Mast cells to produceIncrease permeability/adhesion molecules,Lipids (LDL, VLDL) and activation of plateletsOxidized LDL attracts monocytes andmacrophages to the site and plaques begin toform from cells and smooth muscle cellsMedication:>Atorvastatin Calcium (Lipitor)-80mg 1 tab OD @ HS(Antilipidemics)>Enoxaparine Sodium(Lovenox)-o.6ml SC q12(Antilipemics)>Aspirin(Aspilet EC)-80mg 1tab od(Nonopioid analgesics andantipyretics; antiplatelet)>Clopidogrel (Platexan)75mg/tab, 4tabs now, then OD(Adenosine diphosphate (ADP)receptor antagonistAtherosclerosiOcclusion and stenosis/narrowing of thecoronary artery and leads to coronaryvasoconstrictionRupture of atherosclerotic plaque(cap) and Increase adhesion of these molecules and increaseDiagnostic:Blood Chemistry:Cholesterol-231 mg/dl (0-200mg/dl) Triglycerides-191 mg/dL (0-150mg/dl)Diagnostic:CBC:Eosinophils-16.4%(0.00-6.00)Diagnostic:>X-Ray Report (Chest AP- Sitting)Impressions:Atherosclerosis thoracic aorta.> Color Flow DopplerConclusion:a)Segmental wall motion abnormalityindicative of coronary artery diseaseb)Aortic and mitral scleroses.c)Aortic regurgitation, 1+d)Mitral regurgitation, trivialSigns/ symptoms:>decreased capillary r
 
efill of 5secs>RR: 26 cpm; tachypneic>dyspnea>use of accessory muscles tobreathe Increase demand for oxygen and glucose in thetissues and leads to diminished myocardialoxygenation, Cellular hypoxia and
 
altered cell
 
Interventions:>O2 therapy via nasalcannula at 2L/minDecreased myocardialcontractilityDiagnostic:Clinical Chemistry:Decreased Calcium8.3 mg/dl(8.4 – 10.2 mg/dl)Decreas
 
ed left ventricularIncreasedpreloadDecreased
 
CardiacOutputSigns/symptoms:>bradycardia;PR: 49-59bpmSigns/symptoms:>Jugular veindistention(JVD) at 8cmnotedIn
 
terventions:NPO (Sept.4-5,2009) exceptP.O medsStimulation of sympatheticnervous system to stimulateadrenal medullaIncrease re
 
lease of norepinephrine and
 
IncreaseoxygenneedsIncreased afterInterventions:>O2 therapy vianasal cannula at2L/min>Elevated HOB
 
Signs/symptoms:>Cold,Clammy skin>prolonged/decreasedcapillary refillof 5 seconds>increasedBP of 170/110mmHgPeripheralvasoconstriction anddecreased blood flowto the kidnes
 
Diagnostic:Clinical Chemistry:Urea nitrogen-22mg/dl (7-17mg/dL)Altered repolarization
 
of the myocardium that canlead to decreasedcardiac oututDiagnostic:>ECG tracing:
 
ST-depression & T waveinversion>ClinicalChemistry:Hypokalemia3.0 mmoL/L(3.5- 5.1Anaerobic metabolismcaused by increaseddemand for O2 & glucose
 
in the tissues/hoxiaIncrease Lactic Acid productionwith kinins, potassium ions,
 
prostaglandinsStimulation of cardiac sensory nerveendings to transmit to the central nervous
 
system to cause painUnstable Angina
 
Medication:>Amlodipine Besylate (Norvasc)-50mg 1 tab OD (Calcium-channelblockers; Antianginals)>Nitroglycerin (Glyceryl Trinitrate)-10mg Patch(Nitrates/Vasodilators;Antianginals)>Isosorbide Mononitrate (Imdur)30mg 1 tab OD(Nitrates/Vasodilators;Antianginals)>Aspirin(Aspilet EC) 80mg 1tabod (Nonopioid analgesics)>Diazepam (Valium)-5mg 1 tabBID (Anxiolytics)> Metoprolol Tartrate (Toprol-XL)Signs/ symptoms:Right& left subcostalmargin chest pain-5-6/10pain scale; pain occureven during exertion orat rest; heaviness andtightness of chest withdyspnea; pain radiatesup to the neck and chin;guarding behavior, facialgrimace; tachycarsia of 130-150bpm; mild
 
Interventions:>Obtained a 12 lead ECG asprescribed>Administered O2 inhalation via nasalcannula at 2L/min>Advised to perform deep breathingexercises and used of pursed-lipbreathing technique>maintained relaxing environment
 
Coronary Ischemia and Ischemiaof tissue in the region supplied bythe arteryIncreased Heart
 
Signs/ symptoms:>tachycardia;PR:130-150bpm>palpitationsSigns/ symptoms:Dysrhythmias(bradycardia;PR:49-59bpm; tachycardia;PR 130-150bpm);palpitations; dizziness
 
Medication:> Metoprolol Tartrate(Toprol-XL) 50mg 1tabBID (beta-adrenergicblockers,Anti-dysrhythmics)>Spironoloctone(Aldactone) 25mg 1tab OD(Potassium Sparing
 
31
Renin (released from kidneys) tosplit off angiotensinogen to formMedication:>Losartan Potassium(Cozaar)-100mg 1tab OD(Angiotensin II antagonists)>Captopril(Capoten)-25mg ½tab BID (Angiotensin IIantagonists)Angiotensin II stimulatesadrenal cortex releasealdosteroneSodium retention bykidneys and promotes anincreased plas
 
maosmotic ressureAntidiuretic hormone
 
released fromhypothalamus to increasereabsorption of water by
 
Angiotensin-converting enzyme (ACE)removes and converts Angiotensin I intoAngiotensin II which promotes

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hi? will you please help me to rearrange it?? please??so much thanks ! :)
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Thanks Teddy, this will help me prepare my report. I appreciate it!
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