A group of brain cells called orexin neurons are found in the hypothalmus and are very sensitive to glucose levels, which spike after a CHO meal. These neurons produce orexin, which moderates wakefulness in the brain.
But orexin isn't the only sleep-‐related neurohormone affected by food. As the quantity of food increases, so too is the amount of insulin released. The insulin increases the amount of seratonin and melatonin that flood the brain, two
chemicals associated with drowsiness (and, for that matter, happiness). Remember the Melatonin tablet sold at airports to help travellers sleep? Now you know also why when some people are stressed they EAT! Natural SSRI !
Hence we feel Happy after our CNY reunion dinner. Drinking tea helps to keep us awake. And we just want to slouch on the sofa and sing or chit chat or 'chill'
So what can the med student or post grad do to solve this dilemma? Easy. Give me the food. I can afford to sleep!
71) on Beta blockers and Hypoglycaemia
Dear Yin Ling,
What hypoglycemic symptom is not masked by beta blockers?
Symptoms and Signs of Hypoglycemia Autonomic: Loss of concentration Drowsiness
Dizziness Hemiplegia
Arrhythmias, Seizures, Coma, Death
Nonspecific:
Nausea Hunger Weakness
Chor Kuan:
1)Because of its ability to mask autonomic symptoms and suppress glycogenolysis, beta blockers must be used with caution by diabetic patients
2)First, by blocking beta-‐1 receptors, autonomic symptoms are inhibited. Among them is tachycardia, which normally serves as an early warning signal that blood glucose levels are falling too low. (When glucose drops, the sympathetic nervous system is activated, causing autonomic symptoms)
3) Second, by blocking beta-‐2 receptors in muscle and liver, beta-‐blockers suppress glycogenolysis, thereby eliminating an important mechanism for correcting
hypoglycemia (which can occur when insulin dosage is excessive).
4) By “masking” these autonomic symptoms, beta-‐blockers can delay awareness of hypoglycemia, thereby compromising the patient's ability to correct the problem in a timely fashion.
5) Therefore, patients should be taught to recognise alternative signs which are NOT masked namely the cognitive and non-‐specific signs (eg: hunger, fatigue, poor concentration, confusion) that blood glucose is falling dangerously low.
6) SWEATING is an exception to this. Since sweating during activation of the ANS is mediated by release of Acetylcholine via activation of a nicotinic receptor and NOT BY NORADRENALINE via an adrenergic receptor, sweating may be one of the only signs recognised by diabetic patients on a beta-‐blocker.
Hypoglycemia related symptoms is seen in patients who are either “aware”,
or have attenuated sympathetic neural response (hypoglycemia unawareness) that can develop in older patients, patients suffering from recurrent hypoglycemia, given beta blockers or those with diabetic autonomic neuropathy.
In patients who are hypoglycemic aware, a fall in blood glucose below ~3.8 mM results in an acute release of counter-‐regulatory hormones including glucagon &
norepinephrine. The release of norepinephrine results from a CNS-‐mediated sympathetic discharge triggered by hypoglycemia. The sympathetic discharge produces adrenergic symptoms produced by the release of norepinephrine (and possibly by epinephrine release from the adrenals) such as palpitations, tremor &
anxiety.
Cholinergic symptoms such as sweating & hunger occur from the release of acetylcholine from sympathetic postganglionic (cholinergic) neurons.
Cognitive dysfunction begins to deteriorate when blood glucose falls to ~ 3 mM. The onset of autonomic symptoms is important because it makes the patient aware of their condition & enables them to take appropriate corrective action before
cognitive impairment occurs.
However in patients who are “hypoglycemic unaware” this early phase of
sympathetic discharge (with associated warning signs) does not occur until after cognitive impairment begins, which increases the likelihood that they can become severely hypoglycemic.
The threshold for cognitive impairment does not change when patients develop hypoglycemia unawareness.
Beta-‐blockers should be used with caution (have a “relative contraindication”) in diabetics because of their ability to block these sympathetic increases and thus make proper awareness more difficult. However, if a diabetic patient had suffered a previous MI, has CHF, or has a combination of hypertension and coronary artery disease, the concern about the potential benefits of beta blocker therapy would generally outweigh the concern about its affects to blunt reactions to hyperglycemia in most diabetic patients.
Note that some responses to hypoglycemia (such as sweating) would not be blocked by beta blockers. Because Cholinergic symptoms such as sweating & hunger occur from the release of acetylcholine from sympathetic postganglionic (cholinergic) neurons, beta blockers do not mask these symptoms!
Kudos to basic physiology!! ALL HAIL the late Prof Raman!!
In CCF, Beta blockers block beta receptors in the kidneys which leads to reduction of Renin Angiotensin Aldosterone output.
Choose beta blockers with no ISA activity because the partial agonist properties negates its beneficial effects.
Bisoprolol being a highly selective beta1 blocker has minimal effects on lung function in asthmatics.
It appears also to have no effect on Hba1c in diabetics.
In patients with LVef of less than 40% beta1 selective beta blockers should be used.
Bisoprolol or Cardivelol are the drugs of choice after optimization of volume status and successful discontinuation of iv diuretics.
Start LOW and GO SLOW in uptitration.
Patients with CCF in early stages die from arrthymias at home, beta1 selective blockers reduce that risk.
In advanced CCF PATIENTS die from pump failure
72) on Triglycerides and DM