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Pharmacology

Prostaglandines:

Every cell in the body is capable of synthesizing one or more types of PGS. The four major group of PGs are E, F, A, and B.

Pharmacological actions:

stimulation of cyclicAMP production and calcium use by various cells

CVS
PGE2 acts as vasodilator; it is more potent hypotensive than Ach and histamine

Uterous
PGE2 and PGF2α Contract human uterus

Bronchial muscle

PGF2α and thromboxan A2 cause bronchial muscle contraction.

PGE2 & PGI2 cause bronchial muscle dilatation

GIT: PGE2 and PGF2α cause colic and watery diarrhoea

Platelets

Thromboxan A2 is potent induce of platelets aggregation

Kidney

PGE2 and PGI2 increase water, Na ion and K ion excretion (act as diuresis) that cause renal vasodilatation and inhibit
tubular reabsorption

USE
PGI2: Epoprostenol (inhibits platelets aggregation)
PGE1: Alprostadil (used to maintain the potency of arterioles in neonates with congenital heart defects).
PGE2: Dinoproste (used as pessaries to induce labor)
Synthetic analogue of PGE1: Misoprostol (inhibit the secretion of HCl).

Ciclopirox:Ciclopirox is a synthetic antifungal agent for topical dermatologic use.

Agonist, Antagonist, and Partial Agonists

Agonists:  molecules that activate receptors.  A drug that mimics the body's own regulatory processes.
Antagonists:  produce their effects by preventing receptors activation by endogenous regulatory molecules and drugs.  Block activation of receptors by agonists.
Noncompetive Antagonist:  Bind irreversibly to receptors, and reduce the maximal response that an agonist can elicit.
Competitive Antagonist:  Bind reversibly to receptors, competing with agonists for binding sites.
Partial Agonists:  Have moderate intrinsic activity, the maximal effect that a partial agonist can produce is lower than that of a full agonist.  Act as antagonists as well as agonists.
 

Sulfonylureas

1st generation
tolbutamide
chlorpropamide

2nd generation

glyburide
glimepiride
glipizide

Mechanism

glucose normally triggers insulin release from pancreatic β cells by increasing intracellular ATP
→ closes K+ channels → depolarization → ↑ Ca2+ influx → insulin release

sulfonylureas mimic action of glucose by closing K+ channels in pancreatic β cells 
→ depolarization → ↑ Ca2+ influx → insulin release

its use results in

↓ glucagon release
↑ insulin sensitivity in muscle and liver

Clinical use

type II DM

stimulates release of endogenous insulin 
cannot be used in type I DM due to complete lack of islet function

Toxicity

first generation

disulfiram-like effects
especially chlorpropamide

second generation

hypoglycemia
weight gain

Operator position

For the right-handed operator, the 8 and 10 o’clock position and for left-handed operators, the corresponding 2 and 4 o’clock position almost always allows for optimal visualization of the injection field.

Flucloxacillin, important even now for its resistance to beta-lactamases produced by bacteria such as Staphylococcus species. It is still no match for MRSA (Methicillin Resistant Staphylococcus aureus).

The last in the line of true penicillins were the antipseudomonal penicillins, such as ticarcillin, useful for their activity against Gram-negative bacteria

Thiopental 

- A barbiturate that is generally used to induce anesthesia.
- The temporal course of effects from induction to recovery depends almost entirely upon progressive redistribution.
- Metabolic degradation or excretion during anesthesia is negligible, except in the case of methohexital.
- The barbiturates produce minimal analgesia.
- Respiratory depression may be pronounced.
- Cardiac output is reduced while total peripheral resistance is increased.
- It does not sensitize the heart to catecholamines.
- It may cause bronchiospasm, especially in asthmatics.
- It is contraindicated in acute intermittent porphyria.

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