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NEET MDS Synopsis - Lecture Notes

📖 Pharmacology

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Needle selection

Pharmacology

Needle selection

Nerve blocks:

Inferior alveolar- 25 G short (LLU technique)

PSA- 25 G short

Mental/Incisive- 25 G short

Palatal- 27/30 G short/ultrashort

Gow-Gates/Akinosi- 25 G long

Infraorbital- 25 G long

Field Block:

ASA 25/27 short

Infiltration:

Infiltration/SP 25/27 short

PDL/Intraosseous

PDL 27/30 short

Intraosseous 30 short/ultrashort

Specific Agents

Pharmacology

Specific Agents

Hydralazine [orally effective]

MOA: Not completely understood. Seems to be partially dependent on the release of EDRF and perhaps partially due to K+-channel activation
- in clinical doses action is manifest primarily on vascular smooth muscle (non-vascular muscle is not much affected).
- Re: Metabolism & Excretion. In cases of renal failure the plasma half life may be substantially increased (4-5 fold). One mode of metabolism is
via N-Acetylation (problem of slow acetylators)

Side Effects

- those typical of vasodilation = headache, nasal congestion, tachycardia etc.
- chronic treatment with high doses > 200 mg/day may induce a rheumatoid-like state which may resemble lupus erythematosus.

Minoxidil (Loniten) [orally effective]

MOA: K+-channel agonist

-    very effective antihypertensive. Used primarily to treat life-threatening hypertension or hypertension resistant to other agents.

Side effects - growth of hair

Diazoxide (Hyperstat) [used only IV]

MOA: K+-channel agonist

- Administered by rapid IV injection; action appearing after 3-5 min; action may last from 4 to 12 hours.

Nitroprusside (Nipride) [used only IV]

MOA: increase in cGMP

- unlike the other vasodilators, venous tone is substantially reduced by nitroprusside.
- rapid onset of action (.30 sec); administered as an IV-infusion.
- particularly useful for hypertension associated with left ventricular failure.
 

Catecholamines Agonists

Pharmacology

 Catecholamines Agonists :

Epinephrine
A and B receptors -  B1, A1, B2

- Good for emergency bronchospasm treatment (acute asthma or anaphylactic shock) and open-angle glaucoma
-  Also gives longer duration of anesthetic action via vasocontriction and reducing systemic absorption
- Increases sBP lowers dBP

Norepinephrine
- A and B in therapeutic doses, most A receptor influence
- Good to increase peripheral resistance (A1)
- Good for shock treatment (increase TPR and BP); increases sBP and dBP

Isoproterenol
- Synthetic: B1 and B2, little A stimulation
- Strong cardiac stimulation (b1), dilation of skeletal vessels (b2), and bronchodilation (b2)
- Increases sBP lowers dBP


Dopamine
 - Precursor to NE; A and B activity and dopamine receptors in renal and mesenteric vasculature causing vasodilation
- B1 stimulation of the heart
- Therapeutic: choice drug for shock as it increases BP via cardiac stimulation and also increases kidney blood flow (increased GFR and Na  diuresis)

Dobutamine
- Synthetic B1 agonist
- To increase CO in CHF
- Watch out in Afib as it may increase AV conduction

Phenylephrine - Synthetic A1 agonist – for nasal decongestion

Methoxamine - Synthetic A1 agonist – for hTN in surgery

Clonidine - A2 agonist- - Used to lower pressure in essential HTN (via CNS effect, diminishing sympathetic outflow)

Dental implications of antiepileptic drugs: 

Pharmacology

Dental implications of these drugs: 


1.    Adverse effects: gingival hyperplasia (phenytoin), osteomalacia (phenytoin, Phenobarbital), blood dyscrasias (all but rare)
2.    Drug interactions: additive CNS depression (anesthetics, anxiolytics, opioid analgesics), induction of hepatic microsomal enzymes (phenytoin, Phenobarbital, carbamazepine), plasma protein binding (phenytoin and valproic acid)
3.    Seizure susceptibility: stress can → seizures