Notes and PBL Stuff

Monday, February 25, 2008

Medical management of Obesity

Medical management of Obesity
When managing obesity, the primary aim is, naturally, weight-loss. It is important, however, not to focus on weight-loss alone; mental health support must complement weight-loss at every stage.

Weight loss should ideally occur at a rate of 0.9-1.5kg/week, but this figure should be individualised, and as such, should vary person to person. This initial weight-loss goal should be set with the patient’s norms in mind, taking into account natural variation in culture and family.

Studies have indicated that a 10% loss in weight for those >40 BMI is sufficient to reduce co-morbidities. Weight-loss beyond this point is considered beneficial, but not essential; as such, it is generally spurred by cosmetic needs.

In children, however, reduction beyond 10% of weight loss is recommended. Paediatric cases should aim to return to the normal curve for their age/height. This is achieved primarily through modified diet, increased exercise and decreased sedentary activity. Medication should not be considered in majority of paediatric cases.

Caloric intake remains an efficient and first-line treatment for weight-loss. Approximately 22kcal are required to maintain each kg of body weight. Caloric intake should be restricted as such. This should be adjusted by approximately 100kcal per decade above the age of 30.

Very low caloric diets (<800kcal/day) are useful in losing 1.5-2.5kg/week; they are, however, ineffective at long-term weight loss, and often lead to further complications. Electrolyte levels must be monitored strictly as it can easily lead to cardiac arrhythmia. Hair loss, hypothermia, skin thinning and cholelithiasis are all common side effects. The only indication for a VLCD is pre-operatively.

When choosing which diet to adhere to, or of what the diet should be composed, the National Weight Loss Institute (US) has shown compliance to a diet more important than any other aspect including exercise levels, and overall caloric reduction more important that reduction in any of the main energy groups (fats, proteins, carbohydrates). This said, a reduced fat diet has proved greater success than a reduced carbohydrate diet, owing probably to increased compliance. It is important that no matter what diet is chosen, micro- and macronutrients intake is continued.

As a minimum, sustained aerobic exercise of 30-60 mins, 5-7 times a week is recommended for weight loss. This is higher in children.

Many drugs have been trialled in weight-loss, and whilst majority of them have been quite successful, the side effects have nearly always outweighed the benefits. Addiction, cataracts, neuropathy, arrhythmias, electrolyte imbalance, pulmonary hypertension and sudden deaths have all been the result of drugs. Even those drugs approved for use today have unwanted side-effects.

Surgery is the only available modality that has been shown to reduce weight significantly and sustainable. A wide variety of surgeries are available, all involving a modification of stomach or bowel. Surgery is not, however, indicated in those <40 BMI.

To successfully implement this programme, a multi-disciplinary approach is essential. The physician, counsellor, dietician, physical/exercise therapists and other sub-specialties should be involved in the initial management team. Further specialists such as surgeons may be required later in the treatment plan.

Public health initiatives seem to hold the most hope for obesity, and the implication of advertising and infiltration of the market with high-energy, low-nutritional value foods must be taken seriously. A campaign similar to that undertaken with smoking has been put forth by many. Significant changes are yet to occur.

Thanks to the folk at eMedicine.
http://www.emedicine.com/med/topic1653.htm

Thursday, February 21, 2008

PBL - Obesity

Physiology of Appetite and Hunger and Stuff

Definitions in Physiology
Hunger = a craving for food, rhythmical contractions of the stomach, restlessness. A desire to search for adequate food supply
Appetite = a desire for food, usually of a particular type, and quality of food.
Satiety = success in achieving hunger and appetite.

Each of these is associated with specific centres in the brain, esp. the hypothalamus, which responds to environmental and cultural factors as well as neural, chemical and endocrine messengers.

There are two types of neurons in the arcuate nuclei of the hypothalamus that have really long complicated names and descriptions. POMC decreases food intake, increases energy expenditure. NPY-AGRP does the reverse. These are the major targets for appetite-regulating hormones such as leptin, insulin, CCK and grehlin.

Not Hungry:
Gastrointestinal filling: stretch receptors send inhibitory signals via the vagus nerve
Gastrointestial hormones that suppress hunger:
" CCK is released in response to fat in duodenum to stimulate gall bladder contractions, but also directly affects POMC.
" PYY is released mostly from ileum and colon, 1-2 hours after eating esp in response to fat.
" Insulin is released from beta-cells in the pancreas in the presence of glucose, and to some degree at food intake.
" GLP is released by intestines when filled with food, enhances insulin secretion from pancreas.
Leptin is a peptide hormone released from adipocytes that acts on POMCs and NPY-AgRP receptors as well as the pancreas re: insulin levels.

Hungry:
Grehlin is released from the fundus of the stomach in increasing amounts leading up to a meal. It stimulates NPY/AgRP receptors in the hypothalamus,
Appetite is also increased when blood levels of glucose, amino acids and fatty acids decrease.
Temperature also plays a role in hunger - when it's cold, we need more energy/food to keep warm. Temperature regulation occurs in the hypothalamus, so it's not too far for the to travel

Table 71-2 from guyton and hall summarises the neurotransmitters and hormones that influence feeding centres in the hypothalamus.
Anorexogenic:
-MSH, Leptin, Serotonin, Norepinephrine, CRH, Insulin, CCK, GLP, CART, PYY
Orexogenic:
NPY, AGRP, MCH, Orexin A + B, Endorphins, Galanin, Amino acids, Cortisol, Grehlin

refs:
Chapter 71 of Guyton and Hall - Dietary Balances; regulation of feeding obesity and starvation.
Wilcox, G "Food composition and its effect on human biology" - 21/9/2007 Monash MBBS 2042 Lecture
Saladin

Wednesday, February 20, 2008

DVT/PE

hey, to keep things in order, pls "comment" on this post rather than "new post"


CBL – Deep Venous Thrombosis/Pulmonary Embolus

Differential Diagnoses for presentation with symptoms discussed in case:
- AMI: Tightness, central crushing squeeziness. Radiating pain, dyspnoea, sweating, quick onset.

- Pulmonary oedema: Usually due to left ventricular failure or ischemic heart disease. May present with Dyspnoea, orthopnoea, pink frothy sputum, pale & sweaty, ­pulse and ­JVP, Tachypnoea, lung crackles.

- Pneumonia: This is an acute lower respiratory tract illness involving infection of the lung parenchyma. Main clinical symptoms include dyspnoea, pleuritic chest pain, haemoptysis, cough, purulent sputum, malaise, fever.

- Cellulitis: (Differential for DVT): Cellulitis is an acute inflammation of the connective tissue of the skin, caused by infection with staphylococcus, streptococcus or other bacteria Localized skin inflammation with pain or tenderness in the area, warmth over area of redness. May present with fever, chills, sweating, fatigue, and ache.

- Hyperventilation: Main symptom is dyspnoea, dizziness with tingling of and numbness of limbs, ¯PaCO2 and normal or ­ PaO2.

- Oesophageal spasm: Heartburn and worse with straining. Most common cause of chest pain

- Pulmonary embolism: Dyspnoea, Tachypnoea, Hypoxemia, Hypocarbia with clinical presentation resembling hyperventilation. ¯PaO2 and decrease in partial pressure of PaCO2. Results in a positive D-dimer assay

- Pericarditis: Sudden onset pleuritic pain. Change of posture can influence pain and a friction sound can be heard.

- Costochondral pain: Palpation tenderness and movements of chest influence pain.


References:- http://www.guideline.gov/summary/summary.aspx?doc_id=6534
- Oxford Handbook







Sunday, February 17, 2008

T2DM + CAD

Diabetes and Heart Troubles
Type 2 Diabetes Mellitus has been shown increase the risk of coronary artery disease in both men and women. Men are at two to four-fold increased risk of CAD, and women three to five-fold. This risk is primarily due to diabetes assisting in plaque formation.

The effects of diabetes are also thought to magnify other underlying risk factors such as obesity, hypercholesterolaemia, hypertension and smoking. As such, it is vital that a multidisciplinary team is involved to treat those with CAD.

The primary care physician may be able to be involved in most areas of treatment and prevention, however, it may be best to refer on for additional support.

A dietitian can assist with improved eating habits and understanding of food and its effects on the body. Through this, it is possible to reduce hyperlipidaemia and hypertension, respectively responsible for an estimated 45% and 12% of deaths due to CAD. A Mediterranean diet has, in some cases, been responsible for a 75% reduction in CAD events in post MI patients.

Exercise physiologists can be employed to assist in modifying diet, responsible for up to 30% of deaths due to CAD, and also in eliminating obesity, responsible for 5% of deaths due to CAD.

Finally, a psychologist or support groups may assist in the cessation of smoking, responsible for approximately 20% of deaths due to CAD.

All stats kindly donated by Kumar and Clark.

Saturday, February 16, 2008

What is the significance of LVH and the old posterolateral MI?


A posterolateral MI is caused by the occlusion of the circumflex artery, a branch of the left coronary artery. This artery supplies the posterolateral left ventricle and anterolateral papillary muscles. Thus, depending on the severity of occlusion, an old posterolateral MI could cause a loss of function of part of the left ventricle and its associated papillary muscles. Such damage would cause weakening of the left ventricle’s ability to sustain systemic blood pressure, both through damage to the ventricle and the mitral valve (through the damage to the papillary muscles). This weakening would result in hypertrophy of the remaining anteromedial muscle of the left ventricle, independent of any other causative factors.

What is an echocardiogram?
An echocardiogram is a type of ultrasound that uses sound waves to produce images of the heart. High-pitched sound waves are sent through a transducer and then bounce off the heart. The transducer receives the echoes of these sound waves and converts them to moving pictures of the heart that are seen on a video screen.

Echocardiograms provide a variety of information, including:
– Size of the heart
– Pumping strength of the heart
– The presence and extent of damage to myocardium
– Valvular disease
– Structural abnormalities

What are the different types of echocardiograms?
Transthoracic echocardiogram (TTE)
– Most common type
– Pictures are obtained by moving the transducer as required over the chest/abdominal wall
– This test is chosen to:
o look for causes of abnormal heart sounds, hypertrophy of the heart, unexplained chest pains, shortness of breath, or irregular heartbeats
o examine the thickness and movement of the walls of the heart
o examine the valves and their functionality
o measure the shape and size of the heart’s chambers
o examine the ability of the heart’s chambers to perform fully à ejection fraction may be measured
o detect disease that affects the myocardium and the heart’s function (eg cardiomyopathy)
o detect clots and tumours in the heart
o detect congenital heart defects
o examine the heart’s function following an infarction
o identify a specific cause of heart failure
o detect a pericardial effusion or a thickening of the pericardium

Transoesophageal echocardiogram (TOE or TEE)
– Pictures are obtained by passing a probe down the (sedated and anaesthetised) oesophageus
– Shows clearer pictures of the heart because the probe is physically located closer to the heart, and there is not interference from the lungs and sternum/ribs
– This test is chosen to:
o monitor heart function during surgery
o examine the function of an artificial heart valve
o detect masses and clots in the left atrium
o identify a cardiac shunt (abnormal blood flow through chambers)
o detect endocarditis
o guide procedures performed during cardiac catheterisation
o detect an aortic dissection

Stress echocardiogram
– Pictures are taken immediately before and immediately following exercise (walking on a treadmill/cycling on stationary bike) à if unable to physically exercise, a chemical (dobutamine) is injected into the bloodstream to stimulate the heart to beat faster and harder, as in exercise
– This test is chosen to:
o identify and monitor ischaemia/coronary heart disease

Doppler echocardiogram
– When sound waves bounce off blood cells moving through the heart and its vessels, they change pitch
– These characteristic changes (Doppler signals) can help measure the speed and direction of blood flow in the heart
– Doppler techniques are incorporated into most TTEs and TOEs and may be used in stress echocardiograms
– This test is chosen to:
o measure the speed at which blood travels through the heart
o measure the blood pressure and speed of blood flow through the heart valves

Sources
http://www.webmd.com/heart-disease/echocardiogram, accessed 16/2/08
http://www.webmd.com/heart-disease/echocardiogram, accessed 16/2/08

Friday, February 15, 2008

My first blog!


Heart + Coronary Artery Anatomy

The heart is slightly larger than a clenched fist and located in the chest (duhhh!). It consists of endocardium (endothelium), myocardium (muscle) and epicardium (mesothelium). There are two atria, two ventricles, separated by a fibrous skeleton, which keeps the valves patent, provides attachments for parts of the valves and the myocardium and electrically isolates the ventricles from the atria to facilitate proper contraction. It has four surfaces, sternocostal, diaphragmatic and right and left pulmonary surfaces. There are four valves (aortic, pulmonary, tricuspid and mitral) of which, the mitral and tricuspid are anchored by papillary muscles and chordae tendineae to prevent backflow into the atria. The upper border of the heart corresponds to a line connecting the inferior border of the second left costal cartilage to the superior border of the right third costal cartilage. The right border is a line connecting the third right costal cartilage to the sixth right costal cartilage. The inferior border is a line connecting the inferior of the right border to a point in the fifth intercostal space close the left MCL. The left border connects the inferior and superior. The apex should be in the fifth intercostal space MCL.

The heart is supplied by the coronary arteries, which can be varied in position and supply, thay are the first branch of the aorta and consist of left and right coronary arteries, which take separate routes around the pulmonary trunk. The right coronary artery originates at the right aortic sinus and passes right of the pulmonary trunk, giving a branch to the sino-atrial node (60% of the time). It than travles in the coronary groove, giving the right marginal branch to supply the right border of the heart. It then continues to the posterior aspect of the heart giving a branch to the AV node. In the majority (67%) the right will give the posterior interventricular branch making it the dominant artery. In conclusion, the RCA supplies the right atrium, most of right ventricle, part of the left ventricle, part of the IV septum, and the SA and AV nodes. The left coronary artery arises from the left aortic sinus, passing left of the pulmonary trunk and into the coronary groove. In 40% of people it will supply the SA node, while it also divides into the left descending and circumflex branches, with the former dividing again into the anterior Iv and lateral diagonal branches, while the circumflex gives a left marginal branch, and in one third of people will continue to form the posterior IV, making it the dominant artery. The LCE therefore, supplies the left atrium, most of the left ventricle, part of the right ventricle most of the IVS and occasionally the SA node. Hearts are 67% right dominant, 15% left dominant and 18% co-dominant.






Hope you are confused, because I most certainly am. Pictures help, this all came from Moore and Dalley which did a great job.

Angiography


This is done by inserting dye into the coronary arteries via a catheter inserted in femoral or brachial arteries. Radio-opaque dye is injected and radiographs are taken to determine the paths and any blockage or stenotic areas of the vessels. Pretty simple?

For video: http://ccal.stanford.edu/case/case16/movie16_3.html

IHD - Symptoms/Investigations/Complications/Prognosis

Symptoms of IHD:
Angina
Radiating pain
Nausea
Breathlessness
Weakness
Feeling faint

Signs of IHD:
Diskinetic cardiac apex (no apex beat)
Mitral regurgitation
Pulmonary Oedema
Cardiac enlargement
Arterial bruits
3rd and or 4th heart sounds – sometimes only if examined during an anginal attack due to transient left ventricular failure.
Apical systolic murmur (papillary muscle death)


There may be evidence of other atherosclerotic disease at other sights i.e.
o Abdominal aortic aneurism
o Carotid bruit
o Diminished peripheral pulses
o Increased light reflexes because of hypertension
o Anemia
o Thyroid disease

If the chest wall is tender or if pain can be reproduced by chest palpation then it is unlikely to be

Investigations

Cardiac Markers












Troponin and CK/CKMB are the cardiac markers that are currently investigated.
CK is released as in skeletal muscle breakdown (trauma, prolonged exercise, hypothermia) but CKMB is specific to cardiac muscle.

CK-CKMB ratio is usually less than 5% anything higher = bad

Troponin is great but it stays elevated (as one can see from the beautiful graph) for many days after an event making it less useful for repeat infarctions or after any cardiac surgery. Also it peaks after 12 to 24 hours so it can show the size of the infarct but not immediately. Last interesting thing is that Troponin levels are thought to rise before injury actually occurs thus it can be used for early detection.


Complications of MI

Heart failure

Myocardial rupture and aneurismal dilation – Rupture of the free wall of the ventricle is normally early and fatal. A sub acute rupture may allow for pericardiocentesis followed by the surgical repair of the rupture. Aneurysmal dilation of the infracted myocardium is a late complication that may require surgical repair.

Ventricular septal Defect VSD – Mortality is very high with a 12-month inoperative mortality of 92%.

Mitral Regurgitation

Cardiac Arrhythmias - including ventricular tachycardia, atrial fibrillation and bradyarrhythmias

Conduction Disturbances – Are very common following an MI. Heart Block can last for only a few minutes, but frequently continues for several days. Permanent pacing may need to be considered if heart block persists for over two weeks.


Prognosis of IHD:

Principal prognostic indicators:
o Age
o Functional state of the left ventricle
o Locations and severity of arterial narrowing
o And activity and severity of myocardial infarction
o Blood pressure
o Diabetes
o ST segment deviation
Using these factors, 90-day mortality ranged from as low as 0.4% in patients with no risk factors to 21.1% for those with more than 4 risk factors.