Hypertension: Elevated arterial BP
- Rise in systolic pressure > in men
- 20-30% if adult population
- Rates are higher in black Africans
High BP 130-139/ 85-89
Hypertension
Grade 1: 140-149/ 90-99
Grade 2: 160-179/100-109
Grade 3: >180/ >10
Isolated systolic Hypertension
Grade 1: 140-149/ <90
Grade 2: >160/ <90
Causes:
Essential: idiopathic 90% of people with hypertension
1. Genetic
2. Fetal factors: Low birthweight associated with high BP. Fetal adaptation to intrauterine undernutrition with long-term changes in vessel structure or function of crucial hormone systems
3. Environment
a. Obesity
b. Alcohol: small amts good though
c. Sodium intake
d. Stress: however, chronic stress is not proven to be a cause
4. Humoral mechanism: ANS, as well as rennin-angiotensin etc has a role in physiological regulation of BP short-term.
5. Insulin resistance: hyperinsulinaemia, glucose intolerance, reduced levels of HDL cholesterol, hypertriglyceridaemia, central obesity (metabolic syndrome)
Secondary: has specific cause
1. Renal diseases: Na, H20 retention, plasma rennin elevation
2. Endrocrine: Conn’s syndrome, adrenal hyperplasia, phaeochromocytoma, Cushing’s syndrome, acromegaly
3. Congenital CV: coarctation of aorta
4. Drugs: monoamine oxidase inhibitors, consuming tyramine-containing foods etc
5. Pregnancy: Usually resolves after delivery. Pre-eclmapsia: pregnancy-induced hypertension with proteinuria.
Pathophysiology
- Causes changes in large arteries. Thickening of media, increase in collagen & secondary deposition of calcium. Loss of arterial compliance. Atheroma develop in large arteries due to interaction of mechanical stress & low-growth factors. Endothelial dysfunctions with alternations in NO & endothelins.
- Chronic hypertension: cardiac output normal, increased peripheral resistance (small arteries and arterioles have structural changes) Increase wall thickness with reduced lumen diameter.
- Left ventricular hypertrophy: increased peripheral vascular resistance, increased LV load
- Renal vasculature affected: reduced renal perfusion, glomerular filtration rate, reduction in sodum, water excretion. Activation of rennin-angiotensin system with further sodium, water retention.
Complications
Cerebrovascular disease, CAD, renal failure, peripheral vascular disease, stroke
Malignant hypertension: BP rises rapidly, severe. (Diastolic >120) Fibrinoid necrosis of vessel wall, if untreated, death by renal failure, heart failure, aortic dissection or stroke. High risk of cerebral oedema and haemorrhage.
Investigations
ECG, Urine stix test for blood & prot, fasting blood for lipids & glucose, serum urea, creatinine, electrolytes
Treatment:
Non-Pharmacological
Weight reduction
Low-fat, saturated fat diet
Low sodium diet
Limited alcohol consumption
Exercise
Increase fruit & vege
Stop smoking & increase oily fish consumption
Pharmacological
1. ACE-inhibitors or angiotensin receptor antagonist: block conversion of angiotensin 1 to 2 (vasoconstrictor), block degradation of bradykinin (vasodilator) OR block receptors for angiotensin 2, no effect on bradykinin (no cough)
2. beta-blockers: change effects of sympathetic nervous and rennin-angiotensin, reduce force of cardiac contraction & HR
3. calcium-channel blockers: arteriolar dilatation, reduce force cardiac contraction
4. diuretic
Note: Cannot reduce blood too rapidly as it may lead to cerebral, renal, retinal or myocardia infarct
Source: K & C
Friday, March 20, 2009
Thursday, March 19, 2009
renal aspect of hypertension
Renal aspect of hypertension
How the kidney helps to maintain blood pressure?
The kidney functions as the long-term control mechanism for arterial pressure. This is largely linked to the ability of the kidney to maintain balance between fluid intake and output in the body. Among the functions of kidney:
1. Maintain normal sodium balance
2. Maintain ECF volume
3. Maintain normal blood volume at normotensive arterial pressures.
Chronic hypertension:
Caused by impaired renal function (unable to excrete fluid efficiently)
1. Volume-loading hypertension:
When a person with impaired kidney consumes a lot of water and salt, this will increase the ECF volume, increase the blood volume, and eventually CO. However, the baroreceptor reflex mechanism will act to decrease TPR of the vascular to maintain the normal MAP. After few days, the barorecepter adapt(reset), and the TPR begin to increase as the “autoregulation” mechanism constricts all the vascular to maintain normal blood flow. This leads to increase in MAP.
2. Hypertension due to primary aldosteronism:
Tumor in one of the adrenal glands causes the glands to secrete excess aldosterone hormones, leading to ‘primary aldosteronism’. Aldosterone act to increase salt and water reabsorption by the tubules of the kidneys. Less urine will be excreted and the ECF volume will increase as well as the blood volume. Eventually, this will lead to hypertension.
Hypertension involving renin-angiotensin system:
1. “One-kidney” Goldblatt hypertension:
One kidney is removed and the renal artery is constricted, the pressure in the renal artery will decreased, causing kidney to release renin enzyme. Renin will then produce angiotensin I and II which have direct effect to constrict blood vessels and longer term effect of retaining salt and water in kidney. This in turn will increase the MAP.
2. “Two-kidney Goldblatt hypertension:
Artery to one of the kidney is constricted while the other is normal. The constricted kidney secrete renin, produce angiotensin which affects both kidney. The same processes occur and hypertension develops.
3. Hypertension by diseased kidney:
Constriction or haemorrhage in one kidney decreases the blood flow in renal artery. Kidney will release renin and the same event as in two-kidney hypertension occurs.
Other types of hypertension:
1. Hypertension in upper part of body caused by coarctation of aorta.
2. Hypertension in preeclampsia (toxaemia of pregnancy).
3. Neurogenic hypertension.
Primary(essential) hypertension:Unknown origin of hypertension. Most of ptx appears to have sedentary lifestyle and overweight. This leads to:
1. Increased CO:
a. Additional blood flow required for extra adipose tissue.
b. Increased blood flow in heart, kidneys, GI tract, skeletal muscle due to increased metabolic rate and organ growth in respond to increased metabolic demands.
c. Consequently, increased TPR.
2. Increased sympathetic nerve activity:
a. Leptin hormone is released from fat cells and stimulate multiple regions on hypothalamus, leads to excitatory influence on vasomotor centers of medulla.
3. Angiotensing II and aldosterone levels increased 2,3 fold in obese ptx:
a. Increased sympathetic nerve activity.
4. Impaired renal-pressure natriuresis mechanism:
a. Kidney excrete less salt and water unless there’s high arterial pressure.
Investigations for hypertension due to kidney failure:
Urine test:
1. Appearance: bloody, dark, smoky, plain.
2. Volume: Lower in ptx with hypertension.
3. Chemical (stix) testing: test the urine for blood, protein and sugar.
a. Blood: haematuria. highly sensitive. Can be positive even there’s only 1 or 2 red cells.
b. Protein: proteinuria. The stix react with albumin and insensitive to globulin. High protein indicates kidney failure.
c. Microalbuminuria: albumin leak into urine since kidney fail to separate from it from wastes.
Calculation of protein-to-creatinine ratio. Creatinine is waste product in blood produced during normal breakdown of muscle cells during activity. Impaired kidney will cause builds up of creatinine in blood.
Glomerular filtration rate (GFR):
1. To calculate how efficient the kidney filter waste from blood. It requires withdrawal of blood and testing for creatinine levels.
Blood urea nitrogen:
1. Blood carries protein to cells throughout the body. After the cells use the protein, the remaining waste product is returned to the blood as urea, a compound containing nitrogen. If a person’s kidneys are not working well, the urea will stay in the blood.
2. A deciliter of normal blood contains 7 to 20 milligrams of urea. If a person’s BUN is more than 20 mg/dL, the kidneys may not be working at full strength. Other possible causes of an elevated BUN include dehydration and heart failure.
other techniques:
1. Radionucleotide studies: can demonstrate decreased renal perfusion on affected side. Disproportionate fall in uptake of substance on affected side following administration ofACE inhibitor or NSAIDs suggest presence of significant renal artery stenosis.
2. Doppler ultrasound: generates data about intrarenal vascular resistance.
3. MRA: magnetic resonance angiography. Visualize renal arteries to see comparison with findings of renal arteriography.
4. Renal arteriography: use a contrast medium to inject into artery via a fine transfemoral arterial catheter (arterial digital subtraction angiography). Used to define extrarenal or intrarenal arterial disease.
How the kidney helps to maintain blood pressure?
The kidney functions as the long-term control mechanism for arterial pressure. This is largely linked to the ability of the kidney to maintain balance between fluid intake and output in the body. Among the functions of kidney:
1. Maintain normal sodium balance
2. Maintain ECF volume
3. Maintain normal blood volume at normotensive arterial pressures.
Chronic hypertension:
Caused by impaired renal function (unable to excrete fluid efficiently)
1. Volume-loading hypertension:
When a person with impaired kidney consumes a lot of water and salt, this will increase the ECF volume, increase the blood volume, and eventually CO. However, the baroreceptor reflex mechanism will act to decrease TPR of the vascular to maintain the normal MAP. After few days, the barorecepter adapt(reset), and the TPR begin to increase as the “autoregulation” mechanism constricts all the vascular to maintain normal blood flow. This leads to increase in MAP.
2. Hypertension due to primary aldosteronism:
Tumor in one of the adrenal glands causes the glands to secrete excess aldosterone hormones, leading to ‘primary aldosteronism’. Aldosterone act to increase salt and water reabsorption by the tubules of the kidneys. Less urine will be excreted and the ECF volume will increase as well as the blood volume. Eventually, this will lead to hypertension.
Hypertension involving renin-angiotensin system:
1. “One-kidney” Goldblatt hypertension:
One kidney is removed and the renal artery is constricted, the pressure in the renal artery will decreased, causing kidney to release renin enzyme. Renin will then produce angiotensin I and II which have direct effect to constrict blood vessels and longer term effect of retaining salt and water in kidney. This in turn will increase the MAP.
2. “Two-kidney Goldblatt hypertension:
Artery to one of the kidney is constricted while the other is normal. The constricted kidney secrete renin, produce angiotensin which affects both kidney. The same processes occur and hypertension develops.
3. Hypertension by diseased kidney:
Constriction or haemorrhage in one kidney decreases the blood flow in renal artery. Kidney will release renin and the same event as in two-kidney hypertension occurs.
Other types of hypertension:
1. Hypertension in upper part of body caused by coarctation of aorta.
2. Hypertension in preeclampsia (toxaemia of pregnancy).
3. Neurogenic hypertension.
Primary(essential) hypertension:Unknown origin of hypertension. Most of ptx appears to have sedentary lifestyle and overweight. This leads to:
1. Increased CO:
a. Additional blood flow required for extra adipose tissue.
b. Increased blood flow in heart, kidneys, GI tract, skeletal muscle due to increased metabolic rate and organ growth in respond to increased metabolic demands.
c. Consequently, increased TPR.
2. Increased sympathetic nerve activity:
a. Leptin hormone is released from fat cells and stimulate multiple regions on hypothalamus, leads to excitatory influence on vasomotor centers of medulla.
3. Angiotensing II and aldosterone levels increased 2,3 fold in obese ptx:
a. Increased sympathetic nerve activity.
4. Impaired renal-pressure natriuresis mechanism:
a. Kidney excrete less salt and water unless there’s high arterial pressure.
Investigations for hypertension due to kidney failure:
Urine test:
1. Appearance: bloody, dark, smoky, plain.
2. Volume: Lower in ptx with hypertension.
3. Chemical (stix) testing: test the urine for blood, protein and sugar.
a. Blood: haematuria. highly sensitive. Can be positive even there’s only 1 or 2 red cells.
b. Protein: proteinuria. The stix react with albumin and insensitive to globulin. High protein indicates kidney failure.
c. Microalbuminuria: albumin leak into urine since kidney fail to separate from it from wastes.
Calculation of protein-to-creatinine ratio. Creatinine is waste product in blood produced during normal breakdown of muscle cells during activity. Impaired kidney will cause builds up of creatinine in blood.
Glomerular filtration rate (GFR):
1. To calculate how efficient the kidney filter waste from blood. It requires withdrawal of blood and testing for creatinine levels.
Blood urea nitrogen:
1. Blood carries protein to cells throughout the body. After the cells use the protein, the remaining waste product is returned to the blood as urea, a compound containing nitrogen. If a person’s kidneys are not working well, the urea will stay in the blood.
2. A deciliter of normal blood contains 7 to 20 milligrams of urea. If a person’s BUN is more than 20 mg/dL, the kidneys may not be working at full strength. Other possible causes of an elevated BUN include dehydration and heart failure.
other techniques:
1. Radionucleotide studies: can demonstrate decreased renal perfusion on affected side. Disproportionate fall in uptake of substance on affected side following administration ofACE inhibitor or NSAIDs suggest presence of significant renal artery stenosis.
2. Doppler ultrasound: generates data about intrarenal vascular resistance.
3. MRA: magnetic resonance angiography. Visualize renal arteries to see comparison with findings of renal arteriography.
4. Renal arteriography: use a contrast medium to inject into artery via a fine transfemoral arterial catheter (arterial digital subtraction angiography). Used to define extrarenal or intrarenal arterial disease.
CV Exam
Cardiovascular Exam
Sources: Epstein, Study Guide Wk 3 Th4 Tute,
CV examination of the periphery
· General Appearance
o Dyspnoea, fatigue, cachexia.
· The Hands
o Temperature – extent of vasodilation in hands – guide to peripheral vasodilation. Pts with CHF have cold and sometimes sweaty hands from adrenaline secretion
o Clubbing – endocarditis or cyanotic congenital heart disease
o Splinter Haemorrhages (small bleeds under nail ) and osler’s nodes (painful raised red lesions on finger pulps) – subacute infective endocarditis
o Xanthomata
o Cyanosis
· The Arterial Pulses
o used to assess heart rate and rhythm and the carotid and femoral used to assess pulse character and cardiac performace due to proximity to heart.
o Sometimes good to feel the same pulse on both sides to assess proximal arterial pathology
o Sometimes good to feel femoral and radial simultaneously - a delayed femoral pulse is a feature of aortic coarctation (stenosis)
§ Radial
· located on the lateral of the wrist (radial artery). It can also be found in the anatomical snuff box.
§ Brachial
· Medial to biceps brachii tendon
§ Carotid
· Carotid artery can be felt against the precervical muscles lateral to larynx (a slow rising carotid pulse, often with a palpable shudder, indicates aortic stenosis.) Also listen for bruits while patient holds their breath with stethoscope.
§ Femoral
· Directly above the pubic ramus, midway between the ASIS and pubic tubercle.
§ Popliteal
· Popliteal fossa, felt against distal femur.
§ Dorsalis pedid + tibialis posterior
· Dorsum of foot lat. To ext. hal. Long. Tendon.
· Post to med. malleolus
· The Blood Pressure
o Covered in another topic
· The face
o Jaundice anaemia, xanthelasma, cyanosis
· The neck (JVP)
o Lie pt. on 45 degrees to view JVP without sternocleidomastoid muscle getting in the way (int. jugular collapsed on standing or sitting and completely filled when lying)
o If internal jugular pulsation is seen more than 4cm above manubriosternal angle, then JVP is raised.
o If raised DDx: CHF, tamponade, PE, Sup. VC obstruction
· The Lower limbs
o Oedema, Capillary Return, Pallor
CV examination of the precordium (external surface of the body overlying the heart)
Inspection
Pt lying supine 45 degrees.
Breathing rate and pattern.
Position of apex beat, defined as lowest and outermost point of cardiac pulsation, usually in 5th IC space, mid clavicular line. If you see other pulsations usually abnormal
Palpation
Locate apex beat (may have to lie pt on left side as this brings apex closer to chest wall.) – characteristics of this beat outlined in textbook to look for.
Presence of thrills (palpable vibration which sometimes accompanies a loud heart murmur)
Parasternal heave or impulse - A parasternal heave is detected by placing the heel of the hand over the left parasternal region. In the presence of a heave the heel of the hand is lifted off the chest wall with each systole.
Percussion
Not relevant in CV exams anymore.
Auscultation
Listening for heart sounds can be aided by, positioning pt differently, eg. Lying pt on their left to bring mitral valve closer to chest wall. Sitting pt forward to hear aortic and pulmonary valve better.
Getting patient to inspire and expire heavily, expiartion squeezes blood into left heart from pulmonary bed, aortic and pulmonary murmurs. Get pt to hold breath, lung thickness reduced, distance b/w heart and steth is decreased, easier to hear.
Heart Sound Areas:
1. Mitral : near apex of heart
2. Tricuspid: right sternal border, 5th IC
3. aortic: right of sternum, 2nd IC
4. pulmonary : left sternum 2nd IC
Sounds to listen for:
First and second heart sounds -
Third heart sound, can be normal in young fit people, pathological otherwise – impairment of LV fn
Fourth heart sound – coincides with atrial contraction – LA hypertrophy
Ejection click – high pitched ringing after S1 – aortic pulmonary valve stenosis
Opening snap – diastolic sound in mitral stenosis
Mid-systolic clicks – mitral valve prolapse – may be associated with late systolic murmur.
Sounds from artificial valves – have soft opening clicks and loud closing clicks
Murmurs (graded 1 – 5)
Sources: Epstein, Study Guide Wk 3 Th4 Tute,
CV examination of the periphery
· General Appearance
o Dyspnoea, fatigue, cachexia.
· The Hands
o Temperature – extent of vasodilation in hands – guide to peripheral vasodilation. Pts with CHF have cold and sometimes sweaty hands from adrenaline secretion
o Clubbing – endocarditis or cyanotic congenital heart disease
o Splinter Haemorrhages (small bleeds under nail ) and osler’s nodes (painful raised red lesions on finger pulps) – subacute infective endocarditis
o Xanthomata
o Cyanosis
· The Arterial Pulses
o used to assess heart rate and rhythm and the carotid and femoral used to assess pulse character and cardiac performace due to proximity to heart.
o Sometimes good to feel the same pulse on both sides to assess proximal arterial pathology
o Sometimes good to feel femoral and radial simultaneously - a delayed femoral pulse is a feature of aortic coarctation (stenosis)
§ Radial
· located on the lateral of the wrist (radial artery). It can also be found in the anatomical snuff box.
§ Brachial
· Medial to biceps brachii tendon
§ Carotid
· Carotid artery can be felt against the precervical muscles lateral to larynx (a slow rising carotid pulse, often with a palpable shudder, indicates aortic stenosis.) Also listen for bruits while patient holds their breath with stethoscope.
§ Femoral
· Directly above the pubic ramus, midway between the ASIS and pubic tubercle.
§ Popliteal
· Popliteal fossa, felt against distal femur.
§ Dorsalis pedid + tibialis posterior
· Dorsum of foot lat. To ext. hal. Long. Tendon.
· Post to med. malleolus
· The Blood Pressure
o Covered in another topic
· The face
o Jaundice anaemia, xanthelasma, cyanosis
· The neck (JVP)
o Lie pt. on 45 degrees to view JVP without sternocleidomastoid muscle getting in the way (int. jugular collapsed on standing or sitting and completely filled when lying)
o If internal jugular pulsation is seen more than 4cm above manubriosternal angle, then JVP is raised.
o If raised DDx: CHF, tamponade, PE, Sup. VC obstruction
· The Lower limbs
o Oedema, Capillary Return, Pallor
CV examination of the precordium (external surface of the body overlying the heart)
Inspection
Pt lying supine 45 degrees.
Breathing rate and pattern.
Position of apex beat, defined as lowest and outermost point of cardiac pulsation, usually in 5th IC space, mid clavicular line. If you see other pulsations usually abnormal
Palpation
Locate apex beat (may have to lie pt on left side as this brings apex closer to chest wall.) – characteristics of this beat outlined in textbook to look for.
Presence of thrills (palpable vibration which sometimes accompanies a loud heart murmur)
Parasternal heave or impulse - A parasternal heave is detected by placing the heel of the hand over the left parasternal region. In the presence of a heave the heel of the hand is lifted off the chest wall with each systole.
Percussion
Not relevant in CV exams anymore.
Auscultation
Listening for heart sounds can be aided by, positioning pt differently, eg. Lying pt on their left to bring mitral valve closer to chest wall. Sitting pt forward to hear aortic and pulmonary valve better.
Getting patient to inspire and expire heavily, expiartion squeezes blood into left heart from pulmonary bed, aortic and pulmonary murmurs. Get pt to hold breath, lung thickness reduced, distance b/w heart and steth is decreased, easier to hear.
Heart Sound Areas:
1. Mitral : near apex of heart
2. Tricuspid: right sternal border, 5th IC
3. aortic: right of sternum, 2nd IC
4. pulmonary : left sternum 2nd IC
Sounds to listen for:
First and second heart sounds -
Third heart sound, can be normal in young fit people, pathological otherwise – impairment of LV fn
Fourth heart sound – coincides with atrial contraction – LA hypertrophy
Ejection click – high pitched ringing after S1 – aortic pulmonary valve stenosis
Opening snap – diastolic sound in mitral stenosis
Mid-systolic clicks – mitral valve prolapse – may be associated with late systolic murmur.
Sounds from artificial valves – have soft opening clicks and loud closing clicks
Murmurs (graded 1 – 5)
Wednesday, March 18, 2009
Effects of Smoking
Effects of Smoking
1. Death
· Life expectancy of smokers is shorter than that of non-smokers – 40% of heavy smokers die between 35 and 65 compared with 15% in non-smokers.
· By a large margin, biggest preventable cause of death.
· Responsible for 1 in 10 adult deaths.
2. Cancer
· Especially lung and upper respiratory but also oesophagus, pancreas and bladder.
· Smoking 20 cigarettes a day increases risk 10-fold.
· 90% of lung cancers caused by smoking.
· Tar is causative.
3. Coronary heart disease and peripheral vascular diseases
· Mortality in men aged 55-64 from coronary thrombosis 60% greater in men who smoke 20 cigarettes a day than non-smokers.
· Stroke, intermittent claudication, diabetic gangrene, etc. also strongly smoking-related.
· Nicotine mainly responsible.
· Another factor may be carbon monoxide.
4. Chronic obstructive pulmonary disease (chronic bronchitis and emphysema)
· Much more common in smokers than in non-smokers.
· Probably due to tar and other irritants.
5. Teratogenicity and harmful effects in pregnancy
· Particularly during latter half of pregnancy, significant decrease in birth weight and perinatal mortality.
· Increased incidence of spontaneous abortion, premature delivery and placenta praevia.
· Nicotine in breast milk may cause tachycardia in infant.
· Nicotine responsible for retarded foetal development.
6. Dependence and withdrawal
7. ?Protective effects
· Parkinson’s disease twice as common in non-smokers as in smokers.
· Reduced symptoms from inflammatory bowel disease.
Agents of harm
1. Tar and irritants
· Carcinogenic hydrocarbons and tumour promoters.
· Various irritants responsible for bronchitis and emphysema.
2. Nicotine
· Complex CNS effects.
o Activation and desensitisation of cortex and hippocampus (cognitive function) as well as ventral tegmental area (dopaminergic neurons).
o Inhibition of spinal reflexes leading to skeletal muscle relaxation.
· Peripheral effects
o Stimulation of autonomic ganglia causing tachycardia, increased cardiac output, increased arterial pressure, reduction of gastrointestinal motility and sweating.
o Secretion of adrenaline and noradrenaline from adrenal medulla contributes to cardiovascular effects.
o Release of antidiuretic hormone from posterior pituitary causing decreased urine flow.
o Increased plasma concentration of free fatty acids.
3. Carbon monoxide
· Higher affinity than oxygen for haemoglobin.
· Contributes to increased incidence of heart and vascular disease.
4. Increased oxidative stress
· May be responsible for atherogenesis and chronic obstructive pulmonary disease.
Resource: Rang and Dale's Pharmacology
Cholesterol - Sarah
What is cholesterol?
• If your cholesterol level is 6.5mmol/L or greater your chances of heart disease are 4 times greater than that of a person with a cholesterol level of 4mmol/L.
• Changing dietary intake can alter your cholesterol by approximately 10%
What type of foods are low in bad cholesterol (LDL) and high in good cholesterol (HDL)?
• Dietary cholesterol
• Saturated fatty acids should provide 10% of dietary energy
• Cis-monosaturated acids (mainly olein acid) should provide approx. 12% of dietary energy.
• Cis-polyunsaturated acids should provide 6% of dietary energy.
• Total fat intake should ne no more than 35% of total dietary energy and restricted to 30% is desirable.
SO what does this mean for Roger, he should
o Decrease red meat
o Increase fruits, vegetables, beans, pasta, bread
o Decrease sugary drinks
o Increase vegetable (including olive oil) and fish oil
o Decrease animal fat
o Cholesterol – decrease meat and eggs (maybe?)
o Eat less salt.
o Limit eggs to 1/day
Some recent research
• Has found that cholesterol in the diet has much less of an effect than saturated fats in the diet. So food like eggs even though they are relatively high in cholesterol may not be bad. They also have unsaturated fat which is good for lowering LDL in the blood stream. However, if you already have high cholesterol, this is different and may actually raise the ‘bad’ (LDL) cholesterol levels.
References
• Eat Fat Get Thin lecture notes, week 3, semester 1, 2008
• Kumar and Clarke
• http://www.csiro.au/resources/CholesterolFacts.html
• http://www.abc.net.au/health/healthyliving/stories/2008/05/27/2235487.htm
• http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Cholesterol_explained?OpenDocument
- A core of insoluble lipid (cholesterol) surrounded by an external polar coat of protein. This transports the cholesterol around the body
- The amount of protein to cholesterol determines the ‘goodness’ of the cholesterol.
- There are 4 types of lipoproteins which carry around cholesterol
- Highest in TAGs (Triacylglycerols) content
- Transports TAGs and cholesteral to adipose tissue after meal.
- Removed by liver
- Synthesized by liver (56%TAG)
- Transport TAG from the liver to the tissues in between meals.
- Either returned to liver or converted to LDL
- Carry cholesterol to the tissues (adrenal glands or liver)
- Chief carrier of cholesterol
- Long lifetime in blood
- Involved in development of atherosclerosis
- Want low levels
- Protein rich particles containing little cholesterol
- Transport cholesterol away from tissues
- Protect arteries from high cholesterol
- Synthesised in the intestines and liver
- Want high levels
• If your cholesterol level is 6.5mmol/L or greater your chances of heart disease are 4 times greater than that of a person with a cholesterol level of 4mmol/L.
• Changing dietary intake can alter your cholesterol by approximately 10%
What type of foods are low in bad cholesterol (LDL) and high in good cholesterol (HDL)?
• Dietary cholesterol
- Brain, liver, eggs, prawns, lean meat• Intake has little effect on lipoprotein levels.
- Soluble fibre
- Oatbran, fruit, vegetables
- Can decrease total cholesterol by aiding cholesterol excretion.
- Saturated fat
- Butter, cream, meat fat, pastry
- And trans fatty acids – hydrogenation of oils to fats eg. Margarines
- Both increase LDL
- Carbohydrates
- Bread, pasta, starchy vegetables, rice
- Decrease LDL
- However if carbohydrate is high in sucrose or fructose and low in dietary fibre
- VLDL may increase, and HDL may decrease
- Monounsaturated fatty acids
- E.g. olive oil, canola oil, avocado, almonds, macadamias
- Decrease LDL
- No rise in VLDL
- No rise in HDL
- Polyunsaturated fatty acids
- Sunflower oil, walnuts
- Decrease LDL
- No rise in VLDL
- LDL susceptible to oxidation high intake may decrease HDL
- Sardine, salmon
- Decrease VLDL
- The Mediterranean diet
- Rich in omega-3 – found in fish – reduces risk of CV mortality
- Low in saturated fats
- Decrease in total serum cholesterol and LDL, little change in HDL
• Saturated fatty acids should provide 10% of dietary energy
• Cis-monosaturated acids (mainly olein acid) should provide approx. 12% of dietary energy.
• Cis-polyunsaturated acids should provide 6% of dietary energy.
• Total fat intake should ne no more than 35% of total dietary energy and restricted to 30% is desirable.
SO what does this mean for Roger, he should
o Decrease red meat
o Increase fruits, vegetables, beans, pasta, bread
o Decrease sugary drinks
o Increase vegetable (including olive oil) and fish oil
o Decrease animal fat
o Cholesterol – decrease meat and eggs (maybe?)
o Eat less salt.
o Limit eggs to 1/day
Some recent research
• Has found that cholesterol in the diet has much less of an effect than saturated fats in the diet. So food like eggs even though they are relatively high in cholesterol may not be bad. They also have unsaturated fat which is good for lowering LDL in the blood stream. However, if you already have high cholesterol, this is different and may actually raise the ‘bad’ (LDL) cholesterol levels.
References
• Eat Fat Get Thin lecture notes, week 3, semester 1, 2008
• Kumar and Clarke
• http://www.csiro.au/resources/CholesterolFacts.html
• http://www.abc.net.au/health/healthyliving/stories/2008/05/27/2235487.htm
• http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Cholesterol_explained?OpenDocument
Lung Function Test
Total Lung Capacity
IC = inspiratory capacity
IRV = inspiratory reserve volume
ERV = expiratory reserve volume
FVC = forced vital capacity
FEV1 = forced expiratory volume in 1 sec.
FER = forced expiratory ratio
= FEV1 / FVC (approx. 80%)
FRC = ERV + RV
A spirometer is used to obtain FEV and FVC. These measurements are subject to height, age and sex.
Patients with obstructive pulmonary disorder would have in their lung function report a normal (or low) FVC, a low FEV1, and thus a low FER. The obstruction of the bronchus is the cause of a low FEV1 as forced expiratory time is prolonged, which appears in asthma, chronic bronchitis, emphysema etc.
In restrictive pulmonary disorder, the capacity of patients’ lungs is reduced i.e. ‘small’ lungs, by pleural effusion, congestion etc. Thus their lung function test would show a low FVC, a low FEV1, which gives a normal (or high) FER.
A Flow-volume loop can also help differentiate between different pulmonary disorders.
Respiratory Examination
The Respiratory Examination
1. Inspection
Surface anatomy
Cyanosis
Respiratory Rate and Character
Count the respiratory rate at rest
Inspection of the hands
--clubbing
--nicotine staining
--wasting and weakness
--flapping tremor
Inspection of the chest
--abnormal shape (barrel chest, pigeon chest and funnel chest).
--scars - evidence of previous chest operations or injury.
--asymmetry in the movement of the chest wall
--use of accessory muscles
3. Palpation
Feel the trachea
Palpate the cervical and supraclavicular nodes.
Measure chest expansion
Assess vocal fremitus
Percussion
To examine the lung apices, percuss the clavicles directly. Percuss the front of the chest,
moving the percussed finger down about 6-8 cm at a time. Identify the upper border of the liver,
which is usually at the level of the 5th intercostal space on the right.
When examining a patient, solid tissue sounds less resonant than air filled tissue. Fluid filled
tissue is said to sound “stony dull”.
4. Auscultation
Four aspects of auscultation of lung fields should be considered:
• Quality of Breath Sounds
• Intensity of Breath Sounds
• Added or Abnormal Breath Sounds
• Vocal Resonance
Very succint overview - expansion on given points to be found on week five study guide/workbook.
A reasonably good video tutorial for chest examination (includes respiratory and cardiac) can be found here (http://www.med-ed.virginia.edu/courses/pom1/videos/index.cfm) under 'vital signs and chest', and the 'chest examination'.
There are lots of audio/video files available for chest sounds. I listened to the one on oscetube.com.
Sam
1. Inspection
Surface anatomy
Cyanosis
Respiratory Rate and Character
Count the respiratory rate at rest
Inspection of the hands
--clubbing
--nicotine staining
--wasting and weakness
--flapping tremor
Inspection of the chest
--abnormal shape (barrel chest, pigeon chest and funnel chest).
--scars - evidence of previous chest operations or injury.
--asymmetry in the movement of the chest wall
--use of accessory muscles
3. Palpation
Feel the trachea
Palpate the cervical and supraclavicular nodes.
Measure chest expansion
Assess vocal fremitus
Percussion
To examine the lung apices, percuss the clavicles directly. Percuss the front of the chest,
moving the percussed finger down about 6-8 cm at a time. Identify the upper border of the liver,
which is usually at the level of the 5th intercostal space on the right.
When examining a patient, solid tissue sounds less resonant than air filled tissue. Fluid filled
tissue is said to sound “stony dull”.
4. Auscultation
Four aspects of auscultation of lung fields should be considered:
• Quality of Breath Sounds
• Intensity of Breath Sounds
• Added or Abnormal Breath Sounds
• Vocal Resonance
Very succint overview - expansion on given points to be found on week five study guide/workbook.
A reasonably good video tutorial for chest examination (includes respiratory and cardiac) can be found here (http://www.med-ed.virginia.edu/courses/pom1/videos/index.cfm) under 'vital signs and chest', and the 'chest examination'.
There are lots of audio/video files available for chest sounds. I listened to the one on oscetube.com.
Sam
Tuesday, March 17, 2009
Alcohol Guidelines
ALCOHOL GUIDELINES
Australian guidelines refer to ‘Standard Drinks’ which vary from country to country. In Australia, this is defined as containing 10g of alcohol (equivalent to 12.5mL of pure alcohol).
RANK COUNTRY GRAMS OF ALCOHOL
1 Japan 19.75g
2 Hungary 17g
3 United States 14g
4 Portugal 14g
5 Canada 13.5g
6 Denmark 12g
7 France 12g
8 Finland 11g
9 New Zealand 10g
10 Spain 10g
11 Italy 10g
12 Ireland 10g
13 Poland 10g
14 Australia 10g
15 Netherlands 9.9g
16 Iceland 9.5g
17 United Kingdom 7.9g
So what is a Standard Drink?
· 100ml of wine (13.5%) – 1 standard drink
· 30ml spirits – 1 standard drink
· Can of spirits
o 5% - 1.2-1.7 standard drinks
o 7% - 1.6-2.4 standard drinks
· Beer – Can or Stubby
o Low strength – 0.8 standard drinks
o Mid strength – 1 standard drinks
o Full strength – 1.4 standard drinks
What is the recommended intake of alcohol?
March 2009 –
Reducing risk of alcohol-related harm over a lifetime
- Men – no more than 2 standard drinks per day
- Women – no more than 2 standard drinks per day
Reducing the risk of injury on a single occasion
- Men – no more than 4 standard drinks
- Women – no more than 4 standard drinks
Updated guidelines are due for release in April as it has been determined that the current guidelines are not achievable for the majority of the population.
Georgia
http://www.nhmrc.gov.au/publications/synopses/_files/ds10-alcohol.pdf
http://www.nhmrc.gov.au/your_health/healthy/alcohol/alcoholqa.htm
Australian guidelines refer to ‘Standard Drinks’ which vary from country to country. In Australia, this is defined as containing 10g of alcohol (equivalent to 12.5mL of pure alcohol).
RANK COUNTRY GRAMS OF ALCOHOL
1 Japan 19.75g
2 Hungary 17g
3 United States 14g
4 Portugal 14g
5 Canada 13.5g
6 Denmark 12g
7 France 12g
8 Finland 11g
9 New Zealand 10g
10 Spain 10g
11 Italy 10g
12 Ireland 10g
13 Poland 10g
14 Australia 10g
15 Netherlands 9.9g
16 Iceland 9.5g
17 United Kingdom 7.9g
So what is a Standard Drink?
· 100ml of wine (13.5%) – 1 standard drink
· 30ml spirits – 1 standard drink
· Can of spirits
o 5% - 1.2-1.7 standard drinks
o 7% - 1.6-2.4 standard drinks
· Beer – Can or Stubby
o Low strength – 0.8 standard drinks
o Mid strength – 1 standard drinks
o Full strength – 1.4 standard drinks
What is the recommended intake of alcohol?
March 2009 –
Reducing risk of alcohol-related harm over a lifetime
- Men – no more than 2 standard drinks per day
- Women – no more than 2 standard drinks per day
Reducing the risk of injury on a single occasion
- Men – no more than 4 standard drinks
- Women – no more than 4 standard drinks
Updated guidelines are due for release in April as it has been determined that the current guidelines are not achievable for the majority of the population.
Georgia
http://www.nhmrc.gov.au/publications/synopses/_files/ds10-alcohol.pdf
http://www.nhmrc.gov.au/your_health/healthy/alcohol/alcoholqa.htm
Blood Tests relevant to Hypertension
A blood test is a laboratory analysis performed on a blood sample that is usually extracted from a vein in the arm using a needle, or via finger prick.
Blood tests are used to determine physiological and biochemical states such as disease, mineral content, drug effectiveness, and organ function. Although the term blood test is used, most routine tests (except for most haematology) are done on plasma or serum instead of blood cells.
In Roger’s case, there are two main areas that need to be addressed when deciding what his blood should be tested for, both for possible secondary causes of his hypertension, such as renal failure, and for risk factors associated with hypertension like diabetes.
Secondary Causes
o Renal Failure
§ Serum urea, creatinine and electrolytes
Risk Factors
o Diabetes
§ Fasting Blood glucose and insulin levels
o Hypercholesterolaemia
§ Total and HDL cholesterol levels
o General snapshot of health
§ Full blood count
o Liver Function Test
References
Kumar & Clarke, Underwood's pathology and (inevitably) Wikipedia
by Steph
A blood test is a laboratory analysis performed on a blood sample that is usually extracted from a vein in the arm using a needle, or via finger prick.
Blood tests are used to determine physiological and biochemical states such as disease, mineral content, drug effectiveness, and organ function. Although the term blood test is used, most routine tests (except for most haematology) are done on plasma or serum instead of blood cells.
In Roger’s case, there are two main areas that need to be addressed when deciding what his blood should be tested for, both for possible secondary causes of his hypertension, such as renal failure, and for risk factors associated with hypertension like diabetes.
Secondary Causes
o Renal Failure
§ Serum urea, creatinine and electrolytes
Risk Factors
o Diabetes
§ Fasting Blood glucose and insulin levels
o Hypercholesterolaemia
§ Total and HDL cholesterol levels
o General snapshot of health
§ Full blood count
o Liver Function Test
References
Kumar & Clarke, Underwood's pathology and (inevitably) Wikipedia
by Steph
Bronchitis
Definition-
acute or chronic inflammation of the mucous membranes of the tracheobronchial tree.
Acute bronchitis- is characterised by a productive cough, fever, hypertrophy of mucus secreting structures, and back pain. caused by the spread of upper respiratory infections to the bronchi, it is often observed with or after childhood infections, such as measles, whooping cough, diphtheria, and typhoid fever.
or
Acute bronchitis is often caused by the same viruses that cause colds. It usually starts as a sore throat, runny nose or sinus infection, then spreads to your airways. It can cause a lingering dry cough, but it usually goes away on its own.
Bronchitis occurs most often during the cold and flu season, usually coupled with an upper respiratory infection.
Several viruses cause bronchitis, including influenza A and B, commonly referred to as "the flu."
A number of bacteria are also known to cause bronchitis, such as Mycoplasma pneumoniae, which causes so-called walking pneumonia.
Bronchitis also can occur when you inhale irritating fumes or dusts. Chemical solvents and smoke, including tobacco smoke, have been linked to acute bronchitis.
People at increased risk both of getting bronchitis and of having more severe symptoms include the elderly, those with weakened immune systems, smokers, and anyone with repeated exposure to lung irritants.
Treatment includes bed rest, antipyretics, expectorants, and appropriate antibiotic therapy.
Drinking fluids is very important because fever causes the body to lose fluid faster. Lung secretions will be thinner and easier to clear when the patient is well hydrated.
A cool mist vaporizer or humidifier can help decrease bronchial irritation
Bronchodilator inhalers will help open airways and decrease wheezing
references-
MedlinePlus
Mosby's dictionary of medicine, nursing and health professions
http://medical-dictionary.thefreedictionary.com
http://www.emedicinehealth.com/bronchitis
cheers,
jacqui.
acute or chronic inflammation of the mucous membranes of the tracheobronchial tree.
Acute bronchitis- is characterised by a productive cough, fever, hypertrophy of mucus secreting structures, and back pain. caused by the spread of upper respiratory infections to the bronchi, it is often observed with or after childhood infections, such as measles, whooping cough, diphtheria, and typhoid fever.
or
Acute bronchitis is often caused by the same viruses that cause colds. It usually starts as a sore throat, runny nose or sinus infection, then spreads to your airways. It can cause a lingering dry cough, but it usually goes away on its own.
Bronchitis occurs most often during the cold and flu season, usually coupled with an upper respiratory infection.
Several viruses cause bronchitis, including influenza A and B, commonly referred to as "the flu."
A number of bacteria are also known to cause bronchitis, such as Mycoplasma pneumoniae, which causes so-called walking pneumonia.
Bronchitis also can occur when you inhale irritating fumes or dusts. Chemical solvents and smoke, including tobacco smoke, have been linked to acute bronchitis.
People at increased risk both of getting bronchitis and of having more severe symptoms include the elderly, those with weakened immune systems, smokers, and anyone with repeated exposure to lung irritants.
Treatment includes bed rest, antipyretics, expectorants, and appropriate antibiotic therapy.
Drinking fluids is very important because fever causes the body to lose fluid faster. Lung secretions will be thinner and easier to clear when the patient is well hydrated.
A cool mist vaporizer or humidifier can help decrease bronchial irritation
Bronchodilator inhalers will help open airways and decrease wheezing
antipyretic- reducing or relieving fever
expextorants- drugs that loosen and clear mucus and phlegm from the respiratory tract
references-
MedlinePlus
Mosby's dictionary of medicine, nursing and health professions
http://medical-dictionary.thefreedictionary.com
http://www.emedicinehealth.com/bronchitis
cheers,
jacqui.
TYPE 2 DIABETES MELLITUS
What is it?
Insulin resistance (insulin usually facilitates glucose uptake in muscles and fat, and suppresses glucose production in the liver)
There is no immune disturbance, unlike in Type I
NOTE: The normal blood glucose level is 3.5-8.0 mmol/L
Macrovascular disease – can cause coronary artery disease, peripheral vascular disease and stroke Microvascular damage – diabetic retinopathy (diagnostic) and nephopathy Staphylococcal skin infection Polyneuropathy (tingling and numbness in feet) Erectile dysfunction
Insulin resistance (insulin usually facilitates glucose uptake in muscles and fat, and suppresses glucose production in the liver)
There is no immune disturbance, unlike in Type I
NOTE: The normal blood glucose level is 3.5-8.0 mmol/L
It can also cluster with other conditions that increase cardiovascular risk (Insulin resistance syndrome):
- Hypertension
- Obesity
- Hypertriglyceridaemia
- Decreased HDL-cholesterol
- Acanthosis Nigricans (skin condition – dark, hyperpigmented patches of skin, which can appear velvety or warty when advanced)
Four major determinants
- Increasing age
- Obesity (due to reduced exercise rather than increased food intake)
- Ethnicity (Asian, African, Polynesian, and American-Indian)
- Family History
Onset can be accelerated by:
- Pregnancy
- Drug treatment
- Intercurrent illness
Causes
Abnormalities of insulin secretion and action
Insulin can still bind normally to the insulin receptors. However, there is a problem with the insulin signalling within the cell. It is this that produces the insulin resistance (it is thought that intracellular triglyceride in muscle and liver cells contributes to this). When the individual is unable to secrete enough insulin to overcome this resistance is when Type II diabetes develops.
Beta-cells are in a state of high output failure; thus, there is an increased glucose production by the liver and inadequate uptake of glucose peripherally. The gradual loss of beta cells (not to the extent of Type I) means that there is reduced insulin secretion, which is unable to control the glucose concentration in the individual.
Genetics
Type II is a polygenetic disorder, but many of the genes have yet to be identified.
NOTE: Whether an individual develops Type II diabetes is due to genetics. When an individual develops it is due to lifestyle (diet, exercise, drugs which control glucose levels)
Environmental factors
There is an association between low birth weight/weight at 12 months, and glucose intolerance later in life (especially if there is excess weight gain when in adulthood). Poor nutrition when young leads to impaired beta cell development and function, which can then predispose the individual to diabetes.
Immunology and inflammation
There is no evidence of immune involvement in Type II diabetes. Where patients have antibodies against GAD (glutamic acid decarboxylase, an enzyme found in the pancreas which secretes GABA), it can be possible that the Type I diabetes is masquerading as Type II.
The clinical inflammatory changes that occur in Type II also occur in obesity. These include high levels of C-reactive proteins (inflammatory globulins which can reflect the presence and intensity of inflammation), raised fibrinogen, increased plasminogen-activatior-inhibitor-1 (PAL-1) and elevated levels of the proinflammatory cytokines TNF-α and IL-6. These all contribute to cardiovascular risk (the risk can be reduced by the use of anti-inflammatory agents).
Presentation
In older patients:
- Thirst (osmotic diuresis due to increased glucose levels)
- Polyuria (loss of fluid and electrolytes - osmotic diuresis)
- Weight loss (fluid depletion and the breakdown of fat and muscle due to insulin deficiency)
- Fatigue
- Visual blurring (glucose interferes with refraction)
- Candida infection
Other complications:
Diagnosis
- Impaired fasting glucose (fasting plasma glucose between 6.1 and 6.7 mmol/L)
- Glucose tolerance test (test body’s ability to metabolise carbohydrates)
Treatment
Diet
- Low in sugar (not sugar-free)
- High in starchy carbohydrate (Low glycaemic index – thus, they are absorbed at a slower rate, and do not have a sudden impact on blood glucose levels)
- High in fibre
- Low in fat (especially saturated fat)
If diet and life style changes don’t work - use drugs
- Sulphonylureas – promote insulin secretion in response to glucose
- Meglitinides – promote insulin secretion in response to meals
- Biguanides – reduces gluconeogenesis (suppresses glucose release by liver) and increases insulin sensitivity
- Thiazolidinediones – reduce insulin resistance and reduce glucose production by the liver
Intestinal enzyme inhibitors – inhibit enzymes involves in carbohydrate digestion, and thus reduce post-prandial (post-meal) blood glucose increases - Insulin treatment
Sources: Kumar and Clarke
~ Rushmi
Monday, March 16, 2009
Lung Anatomy and Pathology
Lung Anatomy
The pulmonary arteries deliver _____________ blood to the lungs from the right ventricle of the heart. Oxygenated blood returns to the _____________ via the pulmonary veins.
Each lung has a half-cone shape, with a base, apex, two surfaces and 3 borders:
§ The base sits on the _____________
§ The apex projects above _________ and into the neck
The root of each lung is a short tubular collection of structures, covered by mediastinal pleura. This region is called the __________. A thin like fold of pleura that accommodates the down-and-up translocation of structures during breathing is called the ____________.
Within each hilum is:
§ _______________
§ _______________
§ _______________
The artery is __________, the veins __________ and the bronchus are somewhat ___________.
The right lung has 3 lobes (____,_______,________) and 2 fissures (________,_________). The oblique fissure follows the level of the __________, crosses the__________, then follows the contour of the ________)
The left lung has just the oblique fissure, which separates the 2 lobes.
The lungs pass next to a number of important structures in the mediastinum which include:
§ _____________
§ __________________
§ _______________________________
§ ______________________________
Lung Diseases
There are many types of lung diseases. These diseases can be grouped according to how they affect the lungs.
Asthma, chronic bronchitis (the airways become inflamed by infection…excessive amount of mucus produced), emphysema (damage of alveoli and lungs lose elasticity) COPD ( bronchitis and emphysema are together chronic obstructive pulmonary disease ), and cystic fibrosis (hereditary disease where excess mucus production causes frequent infection) - These all affect a person's airways and limit or block the flow of air in or out of the lungs.
Respiratory failure, pulmonary edema, pulmonary embolism, and pulmonary hypertension (high blood pressure) - These are caused by problems with the normal gas exchange and blood flow in the lungs.
Pneumonia and tuberculosis (TB) - Bacteria or viruses can cause these diseases that affect the membrane (or pleura) that surrounds the lungs. Other conditions can also affect the pleura.
Lung cancer - The number one cause of lung cancer is smoking.
Stiffening and scarring of lungs - The spaces between the tissues of the lungs (called the interstitium) can become stiff and scarred. This can be caused by drugs, poisons, infections, or radiation.
Lung disorders from unusual atmospheric pressure - Atmospheric pressures that are not typical can cause lung problems. This includes high altitudes (as in the mountains) where the air has less oxygen, or deep water where there is more atmospheric pressure and higher nitrogen levels in the blood
Friday, March 13, 2009
Hiatus Hernia & GORD
Hiatus hernia - herniation of part of the stomach into the chest region, usually asymptomatic
Sliding hiatus hernia - gastro-0esophageal junction slides through hiatus and lies above diaphragm. no symptoms unless reflux
Para-oesophageal/rolling hernia - small part of fundus of stomach rolls up through the hernia along the oesophagus.. sphincter reamins below the diaphragm & remains competent. sometimes, however, this will produce severe pain & need surgial treatment.
Gastro-oesophageal reflux - reflux of gastric contents which can occur normally
Gastro-oesophageal reflux disease (GORD) - reflux with persistent symptoms
GORD occurs only when anit-reflux mechanism fail to allow gastric contents to make prolonged contact with lower oesophageal mucosa. (can occur without an hiatus hernia)
Lower oesophageal sphincter (LOS) is formed by distal 4cm of oesophageal smooth muscle. After relaxation to allow bolus to enter stomach, it rapidly regains its normal tone & prevents reflux. It is able to increase tone in response to increased pressures.
Pathogenosis:
- Transient LOS relaxations
- Low resting LOS tone which fails to increase when lying flat
- LOS tone fails to increase when pressure increased eg. pregnancy
- Increase oesophageal mucosal
- Large hiatus hernia impairs the mechanism of crural diaphragm.
- Reduced oesophageal clearance of acid due to poor peristalsis and made worse by trapping of acid in hernial sac due to hiatus hernia.
Clinical Features:
1) Heartburn
2) Regurgitation of food & 'acid'
Why I think I was made to research this.. haha..
The difference between GOR & myocardia ischaemia
Gastro-oesophagal reflux
1) Burning pain produced by bending, stooping or lying down
2) Pain seldom radiates to arms
3) Pain precipitated by drinking hot liquids or alcohol
4) Relieved by antacids
Myocardia ischaemia
1) Gripping/crushing pain
2) Pain radiating into neck, shoulders, both arms
3) Pain by exercise
4) Accompanied by dyspnoea
Source: kumar & clarke
Note: words like oesophageal, diaphragm are really hard to spell..
Sliding hiatus hernia - gastro-0esophageal junction slides through hiatus and lies above diaphragm. no symptoms unless reflux
Para-oesophageal/rolling hernia - small part of fundus of stomach rolls up through the hernia along the oesophagus.. sphincter reamins below the diaphragm & remains competent. sometimes, however, this will produce severe pain & need surgial treatment.
Gastro-oesophageal reflux - reflux of gastric contents which can occur normally
Gastro-oesophageal reflux disease (GORD) - reflux with persistent symptoms
GORD occurs only when anit-reflux mechanism fail to allow gastric contents to make prolonged contact with lower oesophageal mucosa. (can occur without an hiatus hernia)
Lower oesophageal sphincter (LOS) is formed by distal 4cm of oesophageal smooth muscle. After relaxation to allow bolus to enter stomach, it rapidly regains its normal tone & prevents reflux. It is able to increase tone in response to increased pressures.
Pathogenosis:
- Transient LOS relaxations
- Low resting LOS tone which fails to increase when lying flat
- LOS tone fails to increase when pressure increased eg. pregnancy
- Increase oesophageal mucosal
- Large hiatus hernia impairs the mechanism of crural diaphragm.
- Reduced oesophageal clearance of acid due to poor peristalsis and made worse by trapping of acid in hernial sac due to hiatus hernia.
Clinical Features:
1) Heartburn
2) Regurgitation of food & 'acid'
Why I think I was made to research this.. haha..
The difference between GOR & myocardia ischaemia
Gastro-oesophagal reflux
1) Burning pain produced by bending, stooping or lying down
2) Pain seldom radiates to arms
3) Pain precipitated by drinking hot liquids or alcohol
4) Relieved by antacids
Myocardia ischaemia
1) Gripping/crushing pain
2) Pain radiating into neck, shoulders, both arms
3) Pain by exercise
4) Accompanied by dyspnoea
Source: kumar & clarke
Note: words like oesophageal, diaphragm are really hard to spell..
Thursday, March 12, 2009
ECG- electrocardiogram
ECG- electrocardiogram or electrocardiograph
Introduction
The contraction of any muscle is associated with electrical changes called ‘depolarisation’, and these changes can be detected by electrodes attached to the surface of the body. Since all muscular contractions will be detected, the electrical changes associated with the heart muscle will only be clear if the patient is fully relaxed and no skeletal muscles are contracting.
The ECG can be used to help determine;
- the anatomical orientation of the heart and the relative sizes of its chambers eg- left ventricular hypertrophy
- disturbances of rhythm and conduction eg- arrhythmias
- the extent and location of ischemic damage to the heart muscle
- the effects of abnormal concentrations of various plasma electrolytes
- digital imbalance of medications eg- Digoxin
Path of electrical impulse through the heart
the electrical discharge fro each cardiac cycle normally starts at the sinoatrial node in the right atrium. Depolarization then spreads through the atrial muscle fibres. There is a delay whilst the depolarization spreads through the atrioventricular node, after which it travels through the bundle of his, through the right and left bundle branches and through specialized fibres known as purkinje fibres.
diagram 1 + 2
How to interpret and ECG
The muscle mass of the atria, when in comparison with that of the ventricles is small, and thus the electrical change accompanying the contraction of the atria is small.
Contractions of the atria are associated with the ‘p’ wave.
The ventricular mass is large and the large deflection of the ECG when the ventricles are depolarized is seen by the ‘QRS’ complex.
The ‘T’ wave of the ECG is associated with the return of the ventricular mass to its resting state- repolarisation.
*in some ECGs and extra wave ‘U’ can be seen, the origin of which is uncertain. However if a ‘U’ wave follows a normally shaped ‘T’ wave, it can be assumed normal.
PR interval- the period between the beginning of the p wave and the QRS complex. I.e.- time taken for excitation to spread from sa node, through the atrial muscles to the AV node. Normally takes ~ 0.12-0.20 sec.
QT interval- beginning of Q wave till the end of T wave. varies with heart rate. Its prolonged in patients with some electrolyte abnormalities, and more importantly it is prolonged by some drugs. [ a prolonged QT interval ,greater then 450ms may lead to ventricular tachycardia.]
ST segment- reflects a time when the entire ventricular myocardium is depolarized, and should therefore have the same potential ad that present when the muscle is relaxed. –isoelectric line.
Few Problems that you might encounter-
-abnormalities of the p wave ~ enlargement of one or other atria
-prolonged pr interval ~ disorder of the AV node
-abnormalities of the QRS complex ~ disorders of cardiac conduction, ischeamic damage to heart muscle
-ST segment deviate from resting potential ~ hypoxia [may indicate myocardial ischaemia]
-abnormalities of T wave~ may indicate myocardial damage, electrolyte disturbances or cardiac hypertrophy.
- a higher than normal T wave~ excess ca++
- missed p wave~ sa node malfunction [av node taken over]
How to attach the leads
diagram 3
arms- attach onto medial anterior side towards the ulna, at the feet- on the medial anterior aspect over the tibia.
The unipolar electrodes on the chest;
V1- 4th right intercostal space to the right of the sternum
V2- 4th left intercostal space adjacent to the sternum
V3- between V2 and V4
V4- 5th intercostal space in the mid clavicular line
V5- in the same horizontal plane as V4 in the anterior axillary line
V6- in the same horizontal plane as V5 in the mid axillary line
~ they all look at the heart in a horizontal plane
V1 and v2- right ventricle
V3 and v4- septum between the ventricles and the anterior wall of the left ventricle
V5 and v6- anterior and lateral walls of the left ventricle
Measurements
A typical electrocardiograph runs at a paper speed of 25 mm/s, although faster paper speeds are occasionally used. Each small block of ECG paper is 1 mm². At a paper speed of 25 mm/s, one small block of ECG paper translates into 0.04 s (or 40 ms). Five small blocks make up 1 large block, which translates into 0.20 s (or 200 ms). Hence, there are 5 large blocks per second. A diagnostic quality 12 lead ECG is calibrated at 10 mm/mV, so 1 mm translates into 0.1 mV. A calibration signal should be included with every record. A standard signal of 1 mV must move the stylus vertically 1 cm, that is two large squares on ECG paper.
To calculate heart rate- 300 divided by the number of large squares between each QRS complex.
Introduction
The contraction of any muscle is associated with electrical changes called ‘depolarisation’, and these changes can be detected by electrodes attached to the surface of the body. Since all muscular contractions will be detected, the electrical changes associated with the heart muscle will only be clear if the patient is fully relaxed and no skeletal muscles are contracting.
The ECG can be used to help determine;
- the anatomical orientation of the heart and the relative sizes of its chambers eg- left ventricular hypertrophy
- disturbances of rhythm and conduction eg- arrhythmias
- the extent and location of ischemic damage to the heart muscle
- the effects of abnormal concentrations of various plasma electrolytes
- digital imbalance of medications eg- Digoxin
Path of electrical impulse through the heart
the electrical discharge fro each cardiac cycle normally starts at the sinoatrial node in the right atrium. Depolarization then spreads through the atrial muscle fibres. There is a delay whilst the depolarization spreads through the atrioventricular node, after which it travels through the bundle of his, through the right and left bundle branches and through specialized fibres known as purkinje fibres.
diagram 1 + 2
How to interpret and ECG
The muscle mass of the atria, when in comparison with that of the ventricles is small, and thus the electrical change accompanying the contraction of the atria is small.
Contractions of the atria are associated with the ‘p’ wave.
The ventricular mass is large and the large deflection of the ECG when the ventricles are depolarized is seen by the ‘QRS’ complex.
The ‘T’ wave of the ECG is associated with the return of the ventricular mass to its resting state- repolarisation.
*in some ECGs and extra wave ‘U’ can be seen, the origin of which is uncertain. However if a ‘U’ wave follows a normally shaped ‘T’ wave, it can be assumed normal.
PR interval- the period between the beginning of the p wave and the QRS complex. I.e.- time taken for excitation to spread from sa node, through the atrial muscles to the AV node. Normally takes ~ 0.12-0.20 sec.
QT interval- beginning of Q wave till the end of T wave. varies with heart rate. Its prolonged in patients with some electrolyte abnormalities, and more importantly it is prolonged by some drugs. [ a prolonged QT interval ,greater then 450ms may lead to ventricular tachycardia.]
ST segment- reflects a time when the entire ventricular myocardium is depolarized, and should therefore have the same potential ad that present when the muscle is relaxed. –isoelectric line.
Few Problems that you might encounter-
-abnormalities of the p wave ~ enlargement of one or other atria
-prolonged pr interval ~ disorder of the AV node
-abnormalities of the QRS complex ~ disorders of cardiac conduction, ischeamic damage to heart muscle
-ST segment deviate from resting potential ~ hypoxia [may indicate myocardial ischaemia]
-abnormalities of T wave~ may indicate myocardial damage, electrolyte disturbances or cardiac hypertrophy.
- a higher than normal T wave~ excess ca++
- missed p wave~ sa node malfunction [av node taken over]
How to attach the leads
diagram 3
arms- attach onto medial anterior side towards the ulna, at the feet- on the medial anterior aspect over the tibia.
The unipolar electrodes on the chest;
V1- 4th right intercostal space to the right of the sternum
V2- 4th left intercostal space adjacent to the sternum
V3- between V2 and V4
V4- 5th intercostal space in the mid clavicular line
V5- in the same horizontal plane as V4 in the anterior axillary line
V6- in the same horizontal plane as V5 in the mid axillary line
~ they all look at the heart in a horizontal plane
V1 and v2- right ventricle
V3 and v4- septum between the ventricles and the anterior wall of the left ventricle
V5 and v6- anterior and lateral walls of the left ventricle
Measurements
A typical electrocardiograph runs at a paper speed of 25 mm/s, although faster paper speeds are occasionally used. Each small block of ECG paper is 1 mm². At a paper speed of 25 mm/s, one small block of ECG paper translates into 0.04 s (or 40 ms). Five small blocks make up 1 large block, which translates into 0.20 s (or 200 ms). Hence, there are 5 large blocks per second. A diagnostic quality 12 lead ECG is calibrated at 10 mm/mV, so 1 mm translates into 0.1 mV. A calibration signal should be included with every record. A standard signal of 1 mV must move the stylus vertically 1 cm, that is two large squares on ECG paper.
To calculate heart rate- 300 divided by the number of large squares between each QRS complex.
References-
1)Tutorial notes
2)The ECG made easy by John R. Hampton - 7th ed
Pneuomonia
PNEUOMONIA
Pneumonia is defined as an inflammation of the substance of the lungs where it can be caused by both bacteria and virus. Clinically it usually presents as an acute illness with most cases illustrating patients with a cough, purulent sputum and fever.
The various pneuomonias are either localized with the whole of one or more lobes of the lungs or they can often diffuse to the bronchi and bronchioles.
There are many types of pneumonia but the only one which is remotely close to the symptoms illustrated is cryptogenic organizing pneumonia, which is associated with some pleuritic chest pain. However this is still very unlikely.
_ kumar and clarke
Pneumonia is defined as an inflammation of the substance of the lungs where it can be caused by both bacteria and virus. Clinically it usually presents as an acute illness with most cases illustrating patients with a cough, purulent sputum and fever.
The various pneuomonias are either localized with the whole of one or more lobes of the lungs or they can often diffuse to the bronchi and bronchioles.
There are many types of pneumonia but the only one which is remotely close to the symptoms illustrated is cryptogenic organizing pneumonia, which is associated with some pleuritic chest pain. However this is still very unlikely.
_ kumar and clarke
Blood Testing
PCL 2 TASK – Blood Tests & Relevant components
"Nondetectable TN levels in asymptomatic patients at admission and within the first 6 hours after admission can rule out relevant myocardial injury.”
When a patient presents to Emergency with chest pain, generally the first test ordered is a blood test. This is because it is
- Relatively affordable
- Easy to administer
- Convenient
- Results are readily available
Importantly, treatment should commence before results are available.
Components obtained should include –
- Full blood count
- Serum electrolytes
- Glucose
- Lipid profile
Certain components identified in a blood test can indicate the source of a patients chest pain –
- Cardiac Troponin
o Serum troponin level testing is routine in those presenting with cardiopulmonary complaints
o Results within 24 hours
o A marker of cardiac damage from any cause
o Elevated Troponin levels are typically related to cardiac damge –
defining in the diagnosis of acute myocardial infarction
However, it is not pathognomonic for acute coronary syndrome
o Cardiac Troponin is a regulatory protein and is found in striated (skeletal and cardiac) muscle
o It has 3 subunits
TN-T
TN-I
TN-C
TN-C is found in smooth muscle and as such is the least cardiac-specific. Because of this, it is TN-T and TN-I that are tested for in suspected cardiac episodes.
TN-I is the most cardiac-specific as it has not been found in skeletal muscle
TN-T may be indicative of renal damage
DISEASE TROPONIN LEVELS
ACS TN increase
- Indicative of adverse cardiac events
- Should prompt more aggressive treatment
Congestive Heart Failure TN elevations
- High risk patients with poor short term prognosis
- Also associated with increased risk of ventricular dysrhythmias
Myocarditis and Pericarditis TN elevations
- Useful in identifying myocyte necrosis (myocytisis)
- May also be present in pericarditis
While TN levels do not correlate with patient prognosis, there is some correlation between elevated TN and 1-month duration of heart failure symptoms
Cardiac Trauma - Patients with TN elevations have a higher risk of cardiac dysrhythmias and LV dysfunction
- Interestingly, TN level is not related to a patients prognosis
Cardiotoxins - Snakebite can cause acute MI or vasospasm elevated TN levels
- This is as the venom has a direct myocardial effect
Tachycardia - Severe tachycardia can induce TN elevations
- This is due to increased myocardial oxygen demand and decreased supply
Chronic Obstructive Pulmonary Disease - Severe exacerbations are associated with right ventricular strain thus produce TN (as below)
- Another option is that patients may have concurrent acute MI or PE, and thus have elevated TN
- TN elevations correlate with severity of COPD
Pulmonary embolism - TN elevations predict complications and mortality
- The proposed reason for TN release is large PEs induce acute right ventricular pressure overload causes increased wall tension regional wall ischemia
- CKMB
o Results in 2 hours
o
- Haemoglobin
o Results in 2 hours
http://www.medscape.com/viewarticle/582721
Kumar & Clarke
http://www.sydpath.stvincents.com.au/spec_db/
Gah it looked much prettier in word!
Will try and improve this this afternoon
thanks everyone, and apologies for the lateness!
georgia
"Nondetectable TN levels in asymptomatic patients at admission and within the first 6 hours after admission can rule out relevant myocardial injury.”
When a patient presents to Emergency with chest pain, generally the first test ordered is a blood test. This is because it is
- Relatively affordable
- Easy to administer
- Convenient
- Results are readily available
Importantly, treatment should commence before results are available.
Components obtained should include –
- Full blood count
- Serum electrolytes
- Glucose
- Lipid profile
Certain components identified in a blood test can indicate the source of a patients chest pain –
- Cardiac Troponin
o Serum troponin level testing is routine in those presenting with cardiopulmonary complaints
o Results within 24 hours
o A marker of cardiac damage from any cause
o Elevated Troponin levels are typically related to cardiac damge –
defining in the diagnosis of acute myocardial infarction
However, it is not pathognomonic for acute coronary syndrome
o Cardiac Troponin is a regulatory protein and is found in striated (skeletal and cardiac) muscle
o It has 3 subunits
TN-T
TN-I
TN-C
TN-C is found in smooth muscle and as such is the least cardiac-specific. Because of this, it is TN-T and TN-I that are tested for in suspected cardiac episodes.
TN-I is the most cardiac-specific as it has not been found in skeletal muscle
TN-T may be indicative of renal damage
DISEASE TROPONIN LEVELS
ACS TN increase
- Indicative of adverse cardiac events
- Should prompt more aggressive treatment
Congestive Heart Failure TN elevations
- High risk patients with poor short term prognosis
- Also associated with increased risk of ventricular dysrhythmias
Myocarditis and Pericarditis TN elevations
- Useful in identifying myocyte necrosis (myocytisis)
- May also be present in pericarditis
While TN levels do not correlate with patient prognosis, there is some correlation between elevated TN and 1-month duration of heart failure symptoms
Cardiac Trauma - Patients with TN elevations have a higher risk of cardiac dysrhythmias and LV dysfunction
- Interestingly, TN level is not related to a patients prognosis
Cardiotoxins - Snakebite can cause acute MI or vasospasm elevated TN levels
- This is as the venom has a direct myocardial effect
Tachycardia - Severe tachycardia can induce TN elevations
- This is due to increased myocardial oxygen demand and decreased supply
Chronic Obstructive Pulmonary Disease - Severe exacerbations are associated with right ventricular strain thus produce TN (as below)
- Another option is that patients may have concurrent acute MI or PE, and thus have elevated TN
- TN elevations correlate with severity of COPD
Pulmonary embolism - TN elevations predict complications and mortality
- The proposed reason for TN release is large PEs induce acute right ventricular pressure overload causes increased wall tension regional wall ischemia
- CKMB
o Results in 2 hours
o
- Haemoglobin
o Results in 2 hours
http://www.medscape.com/viewarticle/582721
Kumar & Clarke
http://www.sydpath.stvincents.com.au/spec_db/
Gah it looked much prettier in word!
Will try and improve this this afternoon
thanks everyone, and apologies for the lateness!
georgia
Driving after a faint
Information obtained from "Assessing fitness to Drive" handbook published by Austroads, which is an organistional body in charge of relaying current information on Australian road rules from the state authorities.
Following an episode of idiopathic syncope one does not qualify to drive for 2 months privately or 6 months commercially. Except if the patient suffers from unheralded recurrent episodes of blackout/syncope which don't respond to treatment. If the underlying cause of the faint was cardiovascular the minimum non-driving period moves up to three months,
CVD - minimum non-driving periods for non-commercial driving
Acute Myocardial Infarction 2 weeks
Aneurysm repair 4 weeks
Angioplasty 2 days
Cardiac arrest 6 months
Cardiac defibrillator 6 months after cardiac arrest
Cardiac pacemaker insertion 2 weeks
Coronary Artery By-pass Grafts 4 weeks
Deep Vein Thrombosis 2 weeks
Heart/Lung transplant 6 weeks
Pulmonary embolism 6 weeks
Syncope 3 months
Point of interest - according to Vicroads website.
Doctors do have a power to grant exemptions for patients to not wear helmets on pushbikes or seatbelts in cars. No exemption can be granted for a motorcycle helmet.
http://www.austroads.com.au/aftd/downloads/AFTD_2003_FA_WEBREV1.pdf
http://www.vicroads.vic.gov.au/Home/Licensing/MedicalConditions/MedicalExemptionsSeatBeltHelmet.htm
Following an episode of idiopathic syncope one does not qualify to drive for 2 months privately or 6 months commercially. Except if the patient suffers from unheralded recurrent episodes of blackout/syncope which don't respond to treatment. If the underlying cause of the faint was cardiovascular the minimum non-driving period moves up to three months,
CVD - minimum non-driving periods for non-commercial driving
Acute Myocardial Infarction 2 weeks
Aneurysm repair 4 weeks
Angioplasty 2 days
Cardiac arrest 6 months
Cardiac defibrillator 6 months after cardiac arrest
Cardiac pacemaker insertion 2 weeks
Coronary Artery By-pass Grafts 4 weeks
Deep Vein Thrombosis 2 weeks
Heart/Lung transplant 6 weeks
Pulmonary embolism 6 weeks
Syncope 3 months
Point of interest - according to Vicroads website.
Doctors do have a power to grant exemptions for patients to not wear helmets on pushbikes or seatbelts in cars. No exemption can be granted for a motorcycle helmet.
http://www.austroads.com.au/aftd/downloads/AFTD_2003_FA_WEBREV1.pdf
http://www.vicroads.vic.gov.au/Home/Licensing/MedicalConditions/MedicalExemptionsSeatBeltHelmet.htm
Wednesday, March 11, 2009
Aneurysmal Disease
Aneurysm
Definition: Localised abnormal dilatation of a blood vessel or the heart.
True Aneurysm
Definition: An aneurysm which involves all 3 layers of blood vessel wall or heart
Abdominal Aortic Aneurysm (AAA)
Definition: Aneurysm occurring in abdominal portion of aorta (usually infra-renal).
Demographics: More common with increasing age, present in 5% of population above 60 years of age. 5 times more frequent in males. 1 in 4 male children of affected individual will develop it.
Causes: Secondary to atherosclerosis, infection, trauma, genetic diseases (eg. Marfan’s / Ehlers-Danlos syndromes).
Symptoms: Most asymptomatic. Obstruction of proximal organs (eg. ureter, duodenum, vena cava). Rupture: Severe pain (epigastric with radiation to back), hypotension, tachycardia, anaemia, sudden death (90% mortality).
Signs: Pulsatile, expansile abdominal mass. “Trash feet” (ie. forefoot / toe ischaemia) due to emboli.
Investigations: Ultrasound, CT scan.
Management: Lifestyle changes (smoking, diet, hypertension control etc.), medical (lipid-lowering, anti-hypertensive drugs), surgery (necessary in emergency case of rupture, otherwise elective).
Prognosis: Return to normal activities within few months of repair.
Thoraco-Abdominal Aneurysm (TAA)
Definition: Aneurysm occurring in ascending, arch or descending thoracic aorta.
Demographics: Most common in individuals with Marfan’s syndrome and hypertension.
Causes: Secondary to atherosclerosis.
Symptoms: Most asymptomatic. Stridor (high-pitched, turbulent air flow in upper airway) due to compression, haemoptysis (coughing blood) due to aortobronchial fistula, hoarseness due to compression of recurrent laryngeal nerve. Rapid expansion: Chest pain radiating to back. Rupture: Hypotension, tachycardia, death.
Investigations: CT scan, aortography, transoesophageal echocardiography.
Management: Operative repair, stenting.
Syphilitic Aneurysm
Syphilis causes inflammation and narrowing of vasa vasorum in ascending and arch of aorta. This leads to ischaemic damage to media, causing fibrosis and loss of elasticity. Aneurysm results.
Mycotic Aneurysm
Infection of media via vasa vasorum (can occur in root of aorta) weakens arterial wall causing aneurysm. Often underlying bacterial endocarditis.
False Aneurysm (Pseudoaneurysm)
Definition: An aneurysm which breaches the vascular wall but is contained by extra-vascular tissues, forming a haematoma.
Ventricular Rupture
Following myocardial infarction, fibrosis of ventricular walls may cause a rupture, resulting in a haematoma that is contained within the pericardium.
Traumatic Rupture
Often the result of traumatic rupture or perforating injury (eg. during arteriography or angioplasty).
Dissection
Definition: Blood enters the wall of an artery as a haematoma, dissecting its layers.
Aortic Dissection
Definition: Blood enters lamina planes of the media to form blood filled channels within the aortic wall. Type A: aortic arch and valve proximal to origin of left subclavian artery. Type B: descending thoracic aorta distal to origin of left subclavian artery.
Demographics: Either hypertensive men aged 40-60 (90% of cases) or younger individuals with systemic or localised connective tissue abnormalities (eg. Marfan’s syndrome).
Causes: Hypertension, connective tissue disorder (eg. Marfan’s syndrome, Ehlers-Danlos syndrome, vitamin C deficiency, etc.) iatrogenic (eg. diagnostic catheterisation, pulmonary bypass), during or after pregnancy.
Symptoms: Severe central chest pain radiating to back and down arms.
Signs: Shock, neurological symptoms secondary to spinal cord ischaemia, renal failure, acute lower limb ischaemia, visceral ischaemia, absent peripheral pulses.
Investigations: Chest X-ray, CT scan, transoesophageal echocardiography.
Management: Medical (urgent anti-hypertensive drugs). Type A: arch replacement surgery. Type B: medical treatment.
References:
1. Kumar and Clark: Clinical Medicine, 6th ed.
2. Robbins Basic Pathology, 8th ed.
3. Underwood: General and Systemic Pathology, 4th ed.
Definition: Localised abnormal dilatation of a blood vessel or the heart.
True Aneurysm
Definition: An aneurysm which involves all 3 layers of blood vessel wall or heart
Abdominal Aortic Aneurysm (AAA)
Definition: Aneurysm occurring in abdominal portion of aorta (usually infra-renal).
Demographics: More common with increasing age, present in 5% of population above 60 years of age. 5 times more frequent in males. 1 in 4 male children of affected individual will develop it.
Causes: Secondary to atherosclerosis, infection, trauma, genetic diseases (eg. Marfan’s / Ehlers-Danlos syndromes).
Symptoms: Most asymptomatic. Obstruction of proximal organs (eg. ureter, duodenum, vena cava). Rupture: Severe pain (epigastric with radiation to back), hypotension, tachycardia, anaemia, sudden death (90% mortality).
Signs: Pulsatile, expansile abdominal mass. “Trash feet” (ie. forefoot / toe ischaemia) due to emboli.
Investigations: Ultrasound, CT scan.
Management: Lifestyle changes (smoking, diet, hypertension control etc.), medical (lipid-lowering, anti-hypertensive drugs), surgery (necessary in emergency case of rupture, otherwise elective).
Prognosis: Return to normal activities within few months of repair.
Thoraco-Abdominal Aneurysm (TAA)
Definition: Aneurysm occurring in ascending, arch or descending thoracic aorta.
Demographics: Most common in individuals with Marfan’s syndrome and hypertension.
Causes: Secondary to atherosclerosis.
Symptoms: Most asymptomatic. Stridor (high-pitched, turbulent air flow in upper airway) due to compression, haemoptysis (coughing blood) due to aortobronchial fistula, hoarseness due to compression of recurrent laryngeal nerve. Rapid expansion: Chest pain radiating to back. Rupture: Hypotension, tachycardia, death.
Investigations: CT scan, aortography, transoesophageal echocardiography.
Management: Operative repair, stenting.
Syphilitic Aneurysm
Syphilis causes inflammation and narrowing of vasa vasorum in ascending and arch of aorta. This leads to ischaemic damage to media, causing fibrosis and loss of elasticity. Aneurysm results.
Mycotic Aneurysm
Infection of media via vasa vasorum (can occur in root of aorta) weakens arterial wall causing aneurysm. Often underlying bacterial endocarditis.
False Aneurysm (Pseudoaneurysm)
Definition: An aneurysm which breaches the vascular wall but is contained by extra-vascular tissues, forming a haematoma.
Ventricular Rupture
Following myocardial infarction, fibrosis of ventricular walls may cause a rupture, resulting in a haematoma that is contained within the pericardium.
Traumatic Rupture
Often the result of traumatic rupture or perforating injury (eg. during arteriography or angioplasty).
Dissection
Definition: Blood enters the wall of an artery as a haematoma, dissecting its layers.
Aortic Dissection
Definition: Blood enters lamina planes of the media to form blood filled channels within the aortic wall. Type A: aortic arch and valve proximal to origin of left subclavian artery. Type B: descending thoracic aorta distal to origin of left subclavian artery.
Demographics: Either hypertensive men aged 40-60 (90% of cases) or younger individuals with systemic or localised connective tissue abnormalities (eg. Marfan’s syndrome).
Causes: Hypertension, connective tissue disorder (eg. Marfan’s syndrome, Ehlers-Danlos syndrome, vitamin C deficiency, etc.) iatrogenic (eg. diagnostic catheterisation, pulmonary bypass), during or after pregnancy.
Symptoms: Severe central chest pain radiating to back and down arms.
Signs: Shock, neurological symptoms secondary to spinal cord ischaemia, renal failure, acute lower limb ischaemia, visceral ischaemia, absent peripheral pulses.
Investigations: Chest X-ray, CT scan, transoesophageal echocardiography.
Management: Medical (urgent anti-hypertensive drugs). Type A: arch replacement surgery. Type B: medical treatment.
References:
1. Kumar and Clark: Clinical Medicine, 6th ed.
2. Robbins Basic Pathology, 8th ed.
3. Underwood: General and Systemic Pathology, 4th ed.
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