Showing posts with label week 1 - paper 3 - IHD. Show all posts
Showing posts with label week 1 - paper 3 - IHD. Show all posts

Diabetes and IHD

Posted In: . By PBL Group A

Relationship between diabetes and blood pressure

Having diabetes increases risk of developing high BP
- High blood glucose levels over time --> increased deposits of fatty materials on the insides of the blood vessel walls --> Affect blood flow, increasing the chance of clogging and hardening of blood vessels (atherosclerosis)--> high BP--> untreated- can lead to blood vessel damage, stroke, heart failure, heart attack, or kidney failure.

Statistically, having diabetes means:
• You're 2 to 4 times as likely to have a heart attack or stroke as is someone without diabetes.
• You're > likely to die of a heart attack than you'd be if you did not have diabetes.
• Your risk of sudden death from a heart attack is the same as that of someone who has already had a heart attack.

Role of diabetes in clinical presentation of IHD
1) In diabetic patients, myocardial ischemia due to coronary atherosclerosis is typically asymptomatic-->reflect abnormalities in the perception of pain related to autonomic neuropathy.
2) They are more likely to develop thrombus and more vulnerable to plaque rupture--> due to the prothrombotic and procoagulant state with which diabetes
3) Clinical presentation of IHD: Angina
- diabetes--> coronary atherosclerosis--> reduce blood flow to the heart--> symptoms often appear at times when we are stressed, exercising or climbing stairs-as heart tries to pump faster to meet O2 demands, narrowed arteries struggle to keep, heart deprived of O2-->pain

 

Pathophysiology of IHD

Posted In: . By PBL Group A




Abbreviation/definition;
• CHD = coronary heart disease
• IHD = ischemic heart disease
• ACS = acute coronary syndrome
• MI = myocardial infarction

• Ischemia = to suppress or withhold blood flow



Why ischemia happens?
• Increase oxygen demand --> high metabolic demand
• Decrease oxygen supply --> narrowing

Cholesterol and Triglyceride transport



Colour of boxes represents:
• Yellow contains cholesterol
• Blue contains triglyceride
• White contains both cholesterol and triglyceride
* Red arrow represents explanation of CHD

Hypothesis of plaque formation:
• Injury to the endothelial vessel layer, due to:
o Smoking
o Immune mechanism
o Mechanical stress --> hypertension
o Turbulent flow

Determinant of plaques vulnerability to rupture:
• Size of lipid core and stability and thickness of fibrous cap
• Presence of inflammation with plaque degradation
• Lack of smooth muscle cells with impaired healing and plaque stabilization


Site of atherosclerosis in order of frequency
1. abdominal aorta and iliac arteries
2. proximal coronary arteries
3. thoracic aorta, femoral and popliteal arteries
4. internal carotid arteries
5. vertebral basilar and middle cerebral arteries

Lipoprotein

1. chylomicrons - synthesize in intestine and transport dietary;
• triglygeride (adipose and skeletal muscle tissue)
• cholesterol (taken up by liver to form VLDL or secreted by bile)

2. LDL ;
• Main carrier of cholesterol
• LDL is mainly removed by receptor dependent pathway (mainly hepatocytes
• Also remove by non-receptor-dependent mechanism (scavenger cells)
o Can result in formation of foam cells

3. HDL ;
• Reverse transport of cholesterol; ie transport cholesterol from peripheral tissues to the liver to be excreted

 

General Aetiology of IHD
IHD happens when the blood supply to the myocardium via the coronary arteries is cut. This in effect causes the lack of much needed oxygen and nutrients for the heart muscles to function properly.


Epidemiology of IHD
Ischemic heart disease (IHD) was the commonest cause of cardiovascular mortality and accounted for 2,556 deaths in 2002 with a further 896 deaths due to heart failure of ischemic origin. Despite improvement in health services and facilities, mortality due to IHD has been rising steadily since census began in 1990. Nationally IHD probably accounts for 20-30% of all-cause mortality annually.
The true incidence of IHD and IHD-related deaths in Malaysia is unknown. All the data presented thus far relates only to the 122 MOH hospitals. Data on IHD cases and deaths at the 7 University and other non-MOH Government hospitals, and 211 private hospitals is unavailable although it is suspected the number may be double the figures from MOH hospitals only. This means that there may have been over 110,000 admissions and over 7,500 deaths directly caused by IHD in Malaysia in 2002. And this number is increasing every year.

Risk Factors and Epidemiologic Relevance for IHD
IHD is the result of interaction between polygenic, lifestyle, and environmental factors:
Family history
Several regions of the human genome have been shown to be associated with either IHD or hypertension. A family history of IHD is a strong risk factor for MI and acts synergistically with other risk factors below. Family history is significant if a male relative suffered a IHD event before 55yrs, or a female relative before 65yrs.

Age
The older you get, the stiffer
your arteries become. Risk of death from IHD doubles with every 8 years of age
with the death rates for women the same as for men 10 years younger.


Gender
Estrogen production in
menstruating females is a protective factor (Lowers LDL levels while increasing
HDL levels in the bloodstream). Rates of IHD-related death are 3-4x greater in
men than in women across countries with differing levels of disease. Same risk
factors for women as for men but absolute risk is less.

Socio-economic status
IHD is 2x more
common among the poor. Related to many factors including diet, smoking,
exercise, alcohol.

Ethnicity
There is a higher
incidence of IHD in patients from India and Pakistan and a lower incidence in
patients originating from Africa and West Indies.

Diet and cholesterol
A high fat diet
increases the amount of LDLs in the bloodstream, promoting arteriosclerosis

Smoking
Several ingredients of
tobacco lead to the narrowing of blood vessels, increasing the likelihood of a
blockage. Smoking cigarettes causes IHD to occur earlier - approx. 7 years on
average.


Blood pressure
Excess salt intake is
blamed for hypertension in Western countries. As with cholesterol there is no
safe level and a small reduction in BP can have important benefits:
5.0/2.5mmHg
lowering - 11% reduction in IHD
10.0/5.0mmHg lowering - 21% reduction in IHD


Obesity
Known to be associated with
high blood pressure and cholesterol and low HDL as well as with insulin
resistance. Those with a higher waist-hip ratio are at increased risk above that
just for weight.

Alcohol
Consumption of 1-2 units
alcohol reduces risk by 20% compared with tee-totallers. Alcohol increases HDL
cholesterol and reduces thrombotic risk. Higher levels of consumption increases
risks from other causes. Apparently any form of alcohol is as good as another.


Insulin resistance and diabetes
Only
top 5-10% of population levels of fasting glucose are clearly associated with an
increased risk of IHD. But with frank NIDDM there is a much greater risk than
those associated with other risk factors and such patients would benefit greatly
from reduction in other risk factors.


Physical inactivity
A level of
physical activity sufficient to produce cardiorespiratory training (promoting
endurance and muscle strength) clearly reduces the risk of IHD, but lower
intensity activity (likely to concentrate on flexibility) may not.


Serum homocysteine
Homocysteine is
an independent risk factor for IHD, likely to due oxidative damage to
endothelium, platelet activation and thrombus formation. 10% of CHD risk in the
population is attributable to homocysteine, 5-7% of the population having
elevated levels. Supplementation of diet with folic acid (and possibly vitamin
B-6) reduces incidence.




References Used

1. BHF Coronary Heart Disease Statistics 2004.
2. Epidemiology of physical activity, physical fitness and coronary heart disease. J Cardiovascular Risk. 1995; 2(4): 289-95.
3. National Burden of Disease Study. Institute fro Public Health, MOH Feb 2005.
4. Ness AR and Davey Smith G. in Oxford Textbook of Medicine, 4th Edition. Eds; Warrell DA et al. OUP 2003.

5. Otreba P et al An atlas of coronary heart disease mortality, hospital admissions and coronary revascularisatins in South East England; Published by the South East Public Health Observatory Press and the NHS Executive Nov 2003

6.Whaley MH, Blair SN; Epidemiology of physical activity, physical fitness and coronary heart disease.;J Cardiovasc Risk 1995 Aug;2(4):289-95.[abstract]Whaley MH, Blair SN.

By Chris

 

Ischaemic Heart Disease

Clinical Presentation and Differential Diagnosis

-Coronary Artery Disease (CAD)à Manifests as chronic stable angina, acute coronary syndrome (which includes unstable angina, ST elevation MI, and non-ST elevation MI), unrecognized MI or sudden cardiac death.

CAD- explained in Patho



1. Chronic Stable Angina (most likely) - when cardiac metabolic demand exceeds supply.
- usually present with chest pain, described as heavy, tight or gripping.
- pain is central/ retrosternal and may raditate to the jaw or left arm.
- other associated symptomsà sweating, breathlessness and fear.
- can be precipitated by exertion, emotional excitement, mental stress or exposure to cold.
-Symptoms resolve when precipitating events has ceased; resting

2. Acute Coronary Syndromes- when fibrous cap of a coronary artery plaque ruptured/ eroded.
- sudden onset of chest pain, also at rest or deterioration of a pre-existing angina unrelated to any precipitating event.
-ST elevation MI (STEMI)-severe chest pain lasting more than 20 minutes- not alleviated by rest nor sublingual GTN.-Pain often radiates to left arm, neck or jaw.
-Associated symptoms- dyspnoea, diaphoresis, nausea or vomiting and palpitations. -Autonomic symptoms- pale and clammy, with marked sweating.-Atypical presentation in particularly in elderly or diabetic – dyspnoea, fatigue, presyncope or syncope.”

Symptoms Explanations

Dyspnoea- Its COMPLICATED. Impairment of Left ventricular function due to ischaemia leads to an acute rise in left ventricular end-diastolic pressure raised pulmonary venous, interstitial fluid leakage and thus reduced lung compliance. A symptom of anxiety? In ichaemic condition, metabolites are released, stimulating cardiac sympathetic nerves (explains sweating, clamminess and palpitations)

Chest pain- Ischaemia causes visceral pain which stimulates the pain fibres and sympathetic sensory nerves which run closely to cervical and thoracic spinal nerves. Referred pain to chest, neck and arm area.


Provisional Diagnosis
-Ichaemic Heart Disease – Chronic Stable Angina

Differential Diagnosis
Aortic Dissection
Pulmonary Embolism
Acute Coronary Syndrome – Unstable Angina?
Ashma
Congestive Heart Failure.
Cheers,
Alvin

 

Leader: Christopher
Scribe: Maz

Task to complete:
1. Aetiology of IHD, epidemiology-- Christ Sim
2.Clinical Presentation of IHD + Differential Dx.--Alvin
3.Pathophysiology of IHD. --Yazid
4. Risk factors-- Christ Sim
5. Interpretation of Investigation-- Sareeta?
6. Management of IHD (Primary and Secondary prevention)-- Christine
7.Role of Diabetes in IHD. How diabetes affect BP? -- Maz

Have fun!!! :)
Please be aware that there will be radiology tut on Monday morning 8 AM!!

Alvin