The Lay Medical Man

Category: Drugs and Pharmacology

  • JNC 8 GUIDELINES FOR MANAGEMENT OF SYSTEMIC HYPERTENSION 

    (1)📌In the general population aged 60 years or more , initiate pharmacologic treatment to lower blood pressure (BP) at systolic blood pressure (SBP) ≥150 mm Hg or diastolic blood pressure (DBP) ≥90 mm Hg and treat to a goal SBP <150 mm Hg and goal DBP <90 mm Hg

    (2)📌In the general population aged ≥60 years, if pharmacologic treatment for high BP results in lower achieved SBP (eg, <140 mm Hg) and treatment is well tolerated and without adverse effects on health or quality of life, treatment does not need to be adjusted.
    (3)📌In the general population <60 years, initiate pharmacologic treatment
    (a) to lower BP at DBP ≥90mmHg and treat to a goal DBP <90mmHg.
    (b) to lower BP at SBP ≥140 mm Hg and treat to a goal SBP <140 mm Hg.
    (4)📌In the population aged ≥18 years with (i) diabetes & (ii) chronic kidney disease (CKD), initiate pharmacologic treatment to lower BP at SBP ≥140 mmHg or DBP ≥90 mmHg and treat to goal SBP <140mmHg and goal DBP <90mmHg.
    (5)📌In the general nonblack population, including those with diabetes, initial antihypertensive treatment should include a thiazide-type diuretic, calcium channel blocker (CCB), angiotensin-converting enzyme inhibitor

    (ACEI), or angiotensin receptor blocker (ARB).
    (6)📌In the general black population, including those with diabetes, initial antihypertensive treatment should include a thiazide-type diuretic or CCB.
    (7)📌In the population aged 18 years with CKD, initial (or add-on) antihypertensive treatment should include an ACEI or ARB to improve kidney outcomes. This applies to all CKD patients with hypertension regardless of race

    or diabetes status.
    (8)📌If goal BP is not reached within a month of treatment, increase the dose of the initial drug or add a second drug from one of the classes : thiazide-type diuretic, CCB,ACEI, or ARB. The clinician should continue to assess BP and adjust the treatment regimen until goal BP is reached.
    (9)📌If goal BP cannot be reached with 2 drugs, add and titrate a third drug from the list mentioned above (). Do not use an ACEI and an ARB together in the same patient.
    (10)📌If goal BP cannot be reached using only the drugs mentioned above, because of a contraindication or the need to use more than 3 drugs to reach goal BP, antihypertensive drugs from other classes can be used.
    #hypertension , #medicine , #TheLayMedicalMan , #jnc8 , #HTN , #anesthesia , #pharmacology , #BloodPressure ,#BP

  • NORADRENALINE: PHARMACOLOGICAL HIGHLIGHTS & COMPARISON WITH ADRENALINE 

    Noradrenaline (Norepinephrine) is a directly and indirectly acting sympathomimetic amine which stimulates alpha 1 and β1 adrenoceptors, but, in contrast to Adrenaline (epinephrine), has little effect on β2 adrenoceptors.

    🖍These actions produce positive inotropic effects, intense vasoconstriction, increases in arterial pressure, and relative maintenance of cardiac output.

    🖍Noradrenaline increases arterial pressure while simultaneously enhancing contractile state and venous return by reductions in venous capacitance, thereby augmenting stroke volume and ejection fraction. In contrast, pure alpha 1 adrenoceptor agonists such as phenylephrine and methoxamine further compromise cardiac output in failing myocardium and contribute to peripheral hypoperfusion despite an increase in arterial pressure.

    🖍In contrast to adrenaline, noradrenaline does not substantially affect heart rate because activation of baroreceptor reflexes resulting from arterial vasoconstriction usually counteracts β1 mediated, direct, positive, chronotropic effects.

    🖍Its arrhythmogenic potential is considerably less than that of adrenaline. Thus, substitution of noradrenaline for adrenaline may be appropriate in the therapeutic management of cardiogenic shock when atrial or ventricular arrhythmias are present.

    🖍Intravenous infusions of noradrenaline (0.03–0.90 mg kg –1 per minute) have been shown to increase arterial pressure, LV stroke work index, cardiac index, and urine output in septic patients with hypotension that was unresponsive to volume administration, dopamine or dobutamine

    🖍Causes relatively greater increases in systemic vascular resistance and diastolic arterial pressure than adrenaline.

    🖍The drug has a duration of action of 30–40 minutes; tachyphylaxis occurs with prolonged administration.

    🖍The drug produces coronary vasodilatation, leading to a marked increase in coronary blood flow. However, as myocardial work may increase, the balance of myocardial oxygen consumption and delivery may lead to ischaemia on noradrenaline.

    🖍Reflex vagal stimulation leads to a compensatory bradycardia

    🖍The cerebral blood flow and oxygen consumption are decreased by the administration of noradrenaline; mydriasis also occurs

    🖍The glomerular filtration rate is usually well maintained with noradrenaline; but it decreases the renal blood flow and this represents a major limitation on the prolonged use of high doses of norepinephrine.

    🖍Noradrenaline increases the contractility of the pregnant uterus; this may lead to fetal bradycardia and asphyxia

    🖍Noradrenaline may decrease insulin secretion, leading to hyperglycaemia

    🖍The drug is pharmaceutically incompatible with barbiturates and sodium bicarbonate

    (Reference: Paul S. Pagel and David C. Warltier, Essential drugs in anesthesia practice Positive inotropic drugs, Anesthetic Pharmacology, 2nd edition)

  • #Tapentadol

    🚩Is a new centrally acting analgesic that relies on a dual mechanism of action. These are mu opioid receptor agonism and norepinephrine (noradrenaline) reuptake inhibition
    🚩It is therefore not a classical opioid, but represents a unique class of analgesic drug (MOR-NRI).
    🚩It is now registered for use in the treatment of moderate to severe chronic pain that proves unresponsive to conventional non-narcotic medications in many countries.
    🚩Tapentadol has a much lower affinity (20 times less) to the mu receptor than morphine, but its analgesic effect is only around three times less than morphine.
    🚩This discrepancy is explained by its inhibitory effect on norepinephrine reuptake, strengthening descending inhibitory pathways of pain control
    🚩Tapentadol is seen by some as similar to tramadol, but differs in a number of important points:
    ▶️It is not a racemic mixture of two enantiomers with different pharmacological effects
    ▶️Has no active metabolites (which are relevant for tramadol’s mu opioid receptor agonism)
    ▶️Has only minimal serotonin effects
    🚩This means that interactions with other serotonergic drugs (such as anti-depressants) are unlikely, reliance on metabolism by the cytochrome P450 system for increased efficacy is not required and retention of active metabolites causing potential adverse effects is not a concern.

    NB

    🔻Tramadol is a 4 phenyl piperidine analogue of codeine
    🔻It has a weak central action at opioid receptors
    🔻And also on descending monaminergic pathways (also responsible for the side effects)
    🔻Hence known as an atypical centrally acting opioid
    🔻It’s M1 metabolite has more affinity to opioid receptors than parent compound
    🔻So metabolites are important in maintaining efficacy
    #Opioids , #Pharmacology , #analgesia , #PalliativeCare , #Pain , #SideEffects , #NewDrugs , #medicine , #anaesthesia
    Reference: Recent advances in the pharmacological management of acute and chronic pain Stephan A. Schug, Catherine Goddard, Annals of Palliative Medicine, Vol 3, No 4 October 2014