Wednesday [19/4/23] Flashcards
where is adh released from?
posterior pituitary
how does increase adh effect people? [2]
increase aquaporins, then increase absorption water kidneys, increase ECF space, dilution of blood solutes including sodium, then in the intracellular space cells swell
how can hyponatraemia cause severe Cx? [2]
intracellular swelling brain cells can cause neurological abnormalities which can lead to convulsions, coma or death -> cerebral oedema
what may cerebral oedema necessitate Mx?
IV isotonic or hypertonic saline administration
Sx SIADH
anorexia, nausea, vomiting, muscle aches, myoclonus, tremor, asterixis, lethargy, delirium, sexiures, death
CNS causes SIADH
infections like meningitis, mass/bleed, hydrocephalus, GBS, MSA, MS
Cancer causes SIADH
Carcinomas
Lung cancers (small-cell lung cancer, mesothelioma)
Gastrointestinal cancers (stomach, duodenum, pancreas)
Genitourinary cancers (bladder, urethral, prostate, endometrial)
Lymphoma
Sarcomas (Ewing’s sarcoma)
pulmonary causes SIADH
Infection
Pneumonia
Lung abscess
Asthma
Cystic fibrosis
medication causes SIADH
Chlorpropamide
Clofibrate
Phenothiazine
Ifosfamide
Cyclophosphamide
Carbamazepine
Oxcarbazepine
Valproic acid
Selective serotonin reuptake inhibitors (SSRIs, a class of antidepressants)
3,4-Methylenedioxymethamphetamine (MDMA, commonly called Ecstasy. SIADH due to taking ecstasy was cited as a factor in the deaths of Anna Wood and Leah Betts)
Oxytocin
Vincristine
Morphine
Amitriptyline
medication causes SIADH
Chlorpropamide
Clofibrate
Phenothiazine
Ifosfamide
Cyclophosphamide
Carbamazepine
Oxcarbazepine
Valproic acid
Selective serotonin reuptake inhibitors (SSRIs, a class of antidepressants)
3,4-Methylenedioxymethamphetamine (MDMA, commonly called Ecstasy. SIADH due to taking ecstasy was cited as a factor in the deaths of Anna Wood and Leah Betts)
Oxytocin
Vincristine
Morphine
Amitriptyline
what is cytochrome CYP450? [1]
Cytochrome P450 (CYP450) are a group of enzymes encoded by the P450 genes and responsible for the metabolism of most drugs seen in clinical practice.
90% of drugs are metabolised by CYP3A5, CYP3A4, CYP2D6, CYP2C19, CYP2C9 and CYP1A2. CYP3A4 and CYP2D6 are the most significant enzymes.1
what are poor metoblisers in the context of Py450?
Poor metabolisers are characterised by the inability to metabolise drugs via the CYP2D6 metabolic pathway, resulting in an increased risk of adverse effects and toxicity. PM phenotype affects up to 10% of Caucasians and 30% of the Chinese population
what are ultra rapid metabolisers?
At the other extreme, ultrarapid metabolisers metabolise the drug rapidly, resulting in a lack of therapeutic response in these individuals.
what are prodrugs? [2]
However, the reverse applies to prodrugs (drugs that are converted to their active forms in the body). Poor metabolisers fail to convert the prodrug into its active form leading to a lack of therapeutic response. In contrast, ultrarapid metabolisers rapidly convert the prodrug to its active form, causing potential toxicity.
example of ultra-metabolisers of codeine
Example: Propranolol (a drug metabolised by CYP2D6)
Propranolol is a beta-blocker and a substrate of CYP2D6. In poor metabolisers, the metabolism of propranolol is greatly reduced. As a result, the higher plasma concentration of propranolol increases the risk of side effects and in some cases may lead to toxicity.
Signs and symptoms of beta-blocker overdose include light-headedness, dizziness, syncope, bradycardia and hypotension.
