BP SSA Flashcards
Targets of drug 14-alpha demethylase
Azole antifungal drugs (except for abafungin) inhibit the enzyme lanosterol 14 α-demethylase; the enzyme necessary to convert lanosterol to ergosterol.
Depletion of ergosterol in fungal membrane disrupts the structure and many functions of fungal membrane leading to inhibition of fungal growth
Routes of administration for antifungal drugs
topical, creams, ointments, soaps, shampoo. Can also be given systemically to treat severe infections or orally for other such infections
Vd -
Clearance -
Half life
Vd - initial dose/T0
Clearance - ke x vd or (0.693/HL)xVd
Half life - 0.693/ke or use the
graph
How do you tell using the data how the drug was administered
bioavailability of 1 indicates intravenously, anything less than that is a different form of administration
Why is clavulanic acid commonly prescribed with beta lactam antibiotics
while not effective by itself as an antibiotic, when administered with beta lactam antibiotics it can overcome antibiotic resistance in bacteria that secrete β-lactamase, which otherwise inactivates most penicillins.
Graded concentration curves and how to quantify the response of a specific drug
which has higher efficacy (up the y axis); which has greatest affinity (Kd/EC50 ) - left and right along the x axis
What drugs increase the likelihood of finding candida in the mouth
immunosuppressants and a steroid inhaler
Codeine and morphine
Opiod analgesics - given for chronic pain (morphine); weak opiod - codeine
3 receptors - µ (analgesics) δ (peripheral analgesia) and κ (euphorics)
Act on descending inhibitory pathways to stop excitation of transmission of the neurone and inhibit release of neuropeptides
Benzodiazepines - why it is fat soluble, side effects, mechanisms of how they inhibit
Act on the GABA-A receptor resulting in sedative, hypnotic (sleep-inducing), anxiolytic (anti-anxiety), anticonvulsant, and muscle relaxant properties.
Benzodiazepines work by increasing the efficiency of a natural brain chemical, GABA, to decrease the excitability of neurons.
High volume of distribution means they are lipid soluble and can be stored in the adipose tissues of the body
Side effects - fewer than barbiturates as they do not effect the excitatory system. drowsiness, light-headedness, confusion; sexual fantasies. Interact with alcohol. Development of dependence
2 other ways to sedate a patient -
increase dose of anxiolytics, gaseous anaesthetics e.g. NO, IV general anaesthetics
Blood and anticoagulants - heparin
family of sulphated mucopolysaccharides found in secretory mast cells. Sulphate group is required for binding to antithrombin III which
inactivates thrombin (direct effect), IX, X, XI and XII (indirect via positive feedback loops).
Inactive orally - administered iv or sc
Short half life <1hr; eliminated by renal excretion. Rapid effect
Blood and anticoagulants - warfarin
Inhibits hepatic synthesis of vitamin K1 dependent clotting factors - II, VII, IX and X - inhibits vitamin K reductase
1-2 day lag period; oral drug (rapid absorption)
Anaesthetics
Prevent pain for a limited period of time for surgical or other procedures
Inhalation Anaesthetics
Depth of anaesthesia determined by conc. in the brain or spinal cord (oil/gas partition coefficient) and vascularisation of the tissue
Absorbed and eliminated by the lungs. Limited hepatic metabolism
Side effects - malignant hyperthermia, hypotension, depressed respiration, depressed glomerular filtration
Intravenous Anaesthetics
Act on GABA-A receptor - subunit interface dependent on the drug or NMDA receptor antagonist
Rapid onset and metabolism
How do antidepressants work- Tricyclic antidepressants
nhibit 5-HT and NA uptake but block M1 receptors (dry mouth), H1 receptors (sedation and weight gain) and alpha1 receptors (postural hypotension
How do antidepressants work- Selective serotonin reuptake inhibitors
selective for 5-HT and NA transporter - fewer side effects
How do antidepressants work- Monoamine oxidase inhibitors
stop the break down of 5-HT, NA and DA by blocking monoamine oxidase. Old forms blocked irreversibly; new are reversible and only inhibit MAO-A.
Can lead to hypertensive crisis (cheese effect)
Antidepressants and dry mouth?
TCAs block M1 receptors which lead to dry mouth
Local anaesthetics
Block electrical signalling in neurones by blocking voltage gated Na+ channels
Interact with alpha subunit in ionised form
General structure - basic side chain ensures that molecules are ionised at physiological pH, aromatic group determines lipid solubility, duration of action is limited by the hydrolysis of the ester/amide bond and by the lipid solubility of the agent.
Esters are metabolised in the plasma by esterases (shorter half life)
Amides are metabolised in the liver by CYP - longer half life
Injected as a hydrochloride salt in acid solution
Use dependent block - anaesthetic gains access to and has higher affinity for channels more readily when open or inactive
Works better on small myelinated fibres e.g. C fibres
Difference in amide and ester with local anaesthetics
Duration of action is limited by the hydrolysis of the ester/amide bond
Ester group - allergic reactions
ovary hormones
GRH - gonadotrophin releasing hormone
FSH - follicle stimulating hormone
LH - lutensing hormone
Oestrogen - sensitises LH releasing cells, proliferation of the endometrium, inhibits FSH so regulates the cycle
Progesterone - renders the endometrium suitable for implanting the fertilised ovum, inhibits further release of GRH, FSH and LH
DIAGRAM FROM LECTURES
What affects volume of distribution
Membrane permeability Blood perfusion Lipid solubility pH-pKa Plasma protein binding Tissue binding
What most affects drug clearance from body:
Physiochemical properties of the compound e.g. volatile gases are eliminated by exhalation; water soluble unchanged in the urine
Elimination mechanisms e.g. enzymes can become saturated at doses outside the therapeutic dose
Exposure to chemicals
