The third edition of The Color Atlas of Pharmacology makes it easier than ever for students, nurses, and practicing physicians to keep up with the latest developments in this constantly changing field. Featuring a user-friendly layout, jargon-free language, and more than 160 spectacular color charts and illustrations, the atlas is divided in to four, color-coded sections:

• Part 1 – General pharmacology – includes descriptions of substance formulation, absorption, distribution, elimination, and molecular mechanisms of action

• Part 2 – Systems pharmacology – with special emphasis on the functional and therapeutic aspects of a wide range of medicinal agents

• Part 3 – Therapy of selected diseases – such as osteoporosis, acute myocardial infarction, migraine, asthma, tropical diseases, and many more

• Part 4 – Drug Index – helpfully listed by substance, generic, and brand names

Concise, portable, and packed with information, the third edition of The Color Atlas of Pharmacology is the most practical first-stop reference for today’s busy healthcare professional.

[ssquiz #3]

Dyslipidemia is change in the normal lipid concentrations in the blood.

• In particular, hypercholesterolemia is a major cause of increased atherogenic risk, leading to atherosclerosis and atherosclerosis-associated conditions, such as coronary heart disease, ischemic cerebrovascular disease and peripheral vascular disease.
• Both genetic disorders and diets enriched in saturated fat and cholesterol contribute to the elevated lipid levels in a considerable part of the population of developed countries.
• Hypertriglyceridemia, when severe, may cause pancreatitis. Moderately elevated levels of triglycerides are often associated with a syndrome distinguished by insulin resistance, obesity, hypertension and substantially increased risk of coronary heart disease.
• Hypercholesterolemia, especially, requires treatment either by diet and/or with lipidlowering drugs (e.g. statins, anion exchange resins).

The Dubin–Johnson Syndrome is a rare hereditary disease, which is associated with hyperbilirubinemia (high bilirubin and bilirubin-glucuronide plasma  concentrations).

• The disease is caused by loss of function mutations in the ABCC2 gene, which is coding for the ABC-transporter MRP2 (also termed as multispecific organic anion transporter (MOAT)).

• Normally, this transporter is localized in the canalicular membrane of hepatocytes, where it eliminates bilirubin-glucuronide and other organic anions into the bile.

Dyskinesias are abnormal movements, usually caused by neurological diseases or by drugs used to treat neurological (e.g., levodopa) or psychiatric diseases (e.g., neuroleptics).

Desmoplakin is the most abundant desmosomal component that plays a critical role in linking intermediate filament networks to the desmosomal plaque. Desmoplakin
forms rod-like dimers that bind to intermediate filaments and to the cadherin-associated proteins plakoglobin and plakophilin. Gene knock-out experiments have revealed an essential role of desmoplakin in establishing cell–cell contacts in early mouse embryos.

A condition in which a receptor is unresponsive despite the presence of agonist; also referred to as a ‘refractory state’. Typically this state is the consequence of prolonged exposure to agonist, and occurs after receptor activation; it is a built in mechanism to limit a receptor’s effects.

Mechanistically the desensitised state differs from the resting, closed state of a receptor because in the latter state, a receptor can respond to agonist. This difference predicts that these states are structurally distinct.

• The desensitised state may also be stabilised by very low concentrations of agonist, such that no measurable activation of the receptor precedes it.
• Desensitisation is an intrinsic property of many receptors but can also be influenced by other interactions or modifications, such as phosphorylation.

Desensitization is the rapidly attenuation of receptor activation as a result of stimulation of cells and occurs in seconds to minutes. Receptor phosphorylation by  G-protein-coupled receptor kinases and secondmessenger- regulated kinases as well as receptor/ G-protein uncoupling contribute to this process.

In the continued presence or at high concentrations of agonistic ligands, ligand gated ion channels may undergo desensitization by entering a permanently closed state.While the ligand binding domain is occupied by the agonist, the desensitized channel is unable to re-open. For ligandgated ion channels, the structural basis of desensitization is not understood. For voltage-gated K+ channels, the ‘ball and chain’ model suggests a mechanism of ion channel desensitization.

Dependence is a somatic state which develops after chronic administration of certain drugs.

• This condition is characterized by the necessity to continue administration of the drug to avoid the appearance of withdrawal symptoms.

• Withdrawal symptoms are relieved by the administration of the drug upon which the body was  “dependent”.

• Psychological dependence is due to (e.g., social) reinforcement processes in the maintenance of drug-seeking behavior.