Fakhir Falamgir Flashcards
What does affinity of a drug mean
What is an agonist
How strongly a drug can bind to its receptor
A drug that binds to receptors to initiate a physiological response
What are the mechanisms of entry of drugs into cells
4
Diffusion
Carrier mediated transport
Aquaporins
Pinocytosis
What are noradrenalines receptors
3
What type of receptors are they
Alpha 1 receptors
Alpha 2 receprors
Beta receptors
G coupled protein receptors
What does alpha 1 receptors initiate
What do alpha 2 receptors initiate
What do beta receptors initiate
Smooth muscle contraction
Smooth muscle relaxation, inhibition of neurotransmitter release
Smooth muscle relaxation, Heart muscle contraction, glucogenolysis
What is ED50
What is TD50
What is LD50
What is Emax
Effective median dose- dose required to achieve 50% of desired effect in 50% of population
Median toxic dose- dose that causes specific toxic side effect in 50% of population
Median lethal dose- dose required to cause 50% mortality in population
Maximum response achieved by a drug
What is the difference between tachyphylaxis and tolerance
Tachyphylaxis is the decreased response to agonist caused by desensitisation of receptors, it occurs within mins
Tolerance is decreased response to agonist caused by down regulation of receptors occurring over days and weeks
What is a partial agonist
Drugs that do not elicit the maximum response a full agonist would no matter what dose is given
What is an antagonist
What change does it cause in dose response curve
Drugs that bind to receptors and block them to inhibit or reduce the response of agonist
Shifts dose response curve to right- higher doses of agonist required for same response
What is a competitive agonist
What is its effect on dose response curve
What is a non competitive agonist
What is an irreversible agonist
What are its effect on dose response curve
What are chemical antagonists
What are physiological antagonists
An antagonist that binds to the same receptor site as agonist competitively and reversibly- dose response curve shifts to right as more drug required to out compete antagonist and reach Emax
An antagonist that binds somewhere other than agonist receptor site
An antagonist that once bound to receptor cannot unbind so Emax cannot be reached as response elicited directly proportional to number of free receptor sites available- curve gets flatter and sifts to right
Antagonists that bind directly to agonist usually in bloodstream to inactivate it
An agonist that cancels out the effect of another agonist by different mechanism
What is the therapeutic index
The margin of safety between dose of drug that achieves desired effect and dose that results in toxicity
What does it mean when a drug has a narrow therapeutic index
Only small difference between minimum and maximum effective drug concentrations in blood so small increase in dose can cause toxic or lethal side effects
What do the following drugs with narrow theraputic indices do
Aspirin Carbamazepine Gentamicin Phenytoin Vancomycin Warfarin
Aspirin- blood thinner
Carbamazepine- anticonvulsant used to decrease nerve impulses that cause seizures and pain used to treat trigeminal neuralgia, diabetic neuropathy and bipolar disorder
Gentamicin- antibiotic for bacterial infections such as bone infections,endocarditis, meningitis, sepsis
Phenytoin- anti seizure medication
Vancomycin- bacterial antibiotic used to treat infections of the intestines
Warfarin- an anticoagulant
What are the actions of these dental drugs
Hydrocortisone Lignocaine Anti histamines Nicotine Muscarine Pilocarpine Atropine
Hydrocortisone- DNA linked cytosolic receptor blocker
Lignocaine- sodium channel blocker
Anti histamines- cell surface G protein linked receptor blocker
Nicotine- nicotinic acetycholine ligand gated ion channel receptor agonist
Muscarine- muscarinic acetycholine G protein receptor agonist
Pilocarpine- muscarinic receptor agonist
Atropine0 muscarinic receptor blocker
What is the mode of action of adrenaline
What is its effects on alpha 1 receptors
What is its effect on beta receptors
What is the mode of action of salbutamol
Adrenalin is a non selective adrenergic agonist
Agonises alpha 1 receptors to cause constriction of large blood vessels
Agonises beta receptors to increase cardiac muscle force, smooth muscle relaxation and gluconeogenesis
Salbutamol is a beta 2 adrenergic agonist that causes relaxation of bronchiolar smooth muscle in asthma of COPD
What type of alcohol is found in alcoholic drinks
Ethanol
What is a unit of alcohol
How is it calculated
How is percentage absolute volume by content calculated
10ml or 8g of absolute alcohol
Units of alcohol=
(%ABV x vol ml ) / 1000
%ABV=
(g of alcohol/100ml) / 0.78
What is the drink drive limit of alcohol
At what units is death possible
What is the certain lethal dose of alcohol
5
30
38
What is the maximum units of alcohol advised per week for men and women
Women- 2-3 units per day
Men- 3-4 units per day
What do glutamate and GABA do
What is alcohols pharmacokinetical effect on these
Glutamate- excitary neurotransmitter of CNS that binds to NMDA receptors, it is responsible for thinking and pleasure seeking
GABA- inhibitory neurotransmitter in CNS binding to GABAa and GABAb
Alcohol inhibits post synaptic glutamate release and NDMA receptors, thus glutamate cannot bind to its post synaptic receptor and induce signal
Alcohol also increases effect of GABA , thus slowing down AP and having a sedative effect
What are the long term biological effects of alcohol on CNS
Pathophysiological effects
4
Blood markers
2
Intoxication
Withdrawal symptoms
Progressive dementia
Wernicke korsakoff syndrome - brain disorder cased by lack of thiamine
Increased blood alcohol Decreased thiamine (vit B1)
What are the long term biological effects of alcohol on Hepatic region
Pathophysiological effects
3
Blood markers
3
Steatosis- abnormal fat retention
Hepatitis- inflammation of liver
Cirrhosis- scaring of liver
Increased AST, ALT, GGT - enzymes released by liver into bloodstream when damaged
Increased bilirubin- indicates liver not breaking down waste properly
Decreased albumin- liver failing to synthesise albumin
What are the long term biological effects of alcohol on heamatologic region
Pathophysiological effects
4
Blood markers
2
Anaemia
Leukopenia
Thrombocytopenia
Decreased clotting
Increased PTT
Decreased haematocrit, RBC, WBC, platelets, clotting factors
What are the long term biological effects of alcohol on CVS
Pathophysiological effects
3
Blood markers
1
Cardiomyopathy
Cardiac dysrhythmias
Hypertension
Abnormal ECG
What are the long term biological effects of alcohol on immunologic system
Pathophysiological effects
3
Blood markers
1
Increased susceptibility to infection
Decreased humoral response
Delayed wound healing
Decreased WBC- alcohol damages bone marrow where many white blood cells mate
What are the long term biological effects of alcohol on GIT
Pathophysiological effects
4
Blood markers
1
Pancreatitis- alcohol may trigger enzymes ion pancrease to digest itself
Increased gastric acid secretion
Oesophageal bleeds
Mallory weiss syndrome- tear in mucous membrane leading to heamatemesis and malaena
Abnormal amylase levels
What are the symptoms of foetal alcohol syndrome
3
Reduced IQ
Speech abnormalities
Hearing impairments
What is the significance of acetyl aldehyde and alcohols link with oral cancer
Acetyl aldehyde is a carcinogen that may be associated with alcohol consumption by disrupting DNA synthesis and repair, causing oxygen free radical production and reducing saliva flow which reduces removal of carcinogens
Alcohol may also act as a co carcinogen
What is the proportion of absorbtion of alcohol in
Oral mucosa
Stomach
Small intestine
Small amount
20% (alcohol acidic)
80%
What is the metabolism rate of alcohol
How long does it take to eliminate alcohol from body
How is alcohol excreted
1 unit per hour
12 hours
10%- perspiration, kidneys, lungs
90%- liver, gut
What is the process of alcohol metabolism in the liver
Alcohol converted to acetaldehyde by cytochrome p450, alcohol dehydroginase and catalase enzymes
Acetaldehyde converted to water and carbon dioxide by acetaldehyde dehydrogenase
What is antabuse and what does it do
A drug licensed for use by alcoholics
It inhibits acetaldehyde dehydrogenase so acetaldehyde builds up and makes person feel unwell (hangover symptoms) when they drink, thus acting asa deterrent
What is phase 1 of the p450 cytochrome system
What is phase 2 of the p450 cytochrome system
Addition of a molecule- oxidation, reduction, hydrolysis
Conjugation- glucuronidation, glycosidation, sulphation, methylation, acetylation, amino acid conjugation, glutathione conjugation
How does alcohol interact with warfarin
How does alcohol interact with aspirin
Alcohol prevents warfarin and aspirin metabolism, so more of it is in blood, increasing risk of major bleeding
How does alcohol interact with paracetamol
How does alcohol interact withmetronidazole
Alcohol prevents full breakdown of paracetamol so toxic middle pathway metabolites may build up and cause liver damage
Alcohol prevents metabolism of metronidazole so metabolites build up causing nausea, sweating, headache, palpitations
What is the mechanism of alcohol dependence
3 stages
Alcohol results in release of pleasure neurotransmitters dopamine and serotonin
Over time dopamine and serotonin receptors become desensitised leading to down regulation and tolerance so more alcohol is required to create same effect
Withdrawal symptoms (anxiety, depression, weakness, inability to sleep, shaking, hallucinations) will occur if alcohol not taken as brain has become accustomed to high levels of dopamine and serotonin
What is primary fracture healing
What is the main type of repair
What is the process
3
The direct healing of fractured cortical bone ends with bone ends held in close apposition
- osteonal remodelling
- Fracture occurs eliciting response in adjacent tissues
- Localised inflammation recruits osteoclasts
- Osteoclasts trigger local remodelling with osteoclasts eliciting bone resorption followed by osteod deposition and new bone formation to bridge fracture and restore mechanical continuity
What is secondary fracture healing
Fracture healing in which bone ends are not in apposition or rigidly fixed with fibrous callus formation eventually maturing into strong mass of scar tissue
What are the stages of fracture repair and when do they occur
7
12 hrs- heamatoma formation 24hrs- debridement and angiogenesis 48hrs- granulation tissue formation 5 days- earliest bone formation 3 weeks- fibrous union 6 weeks- woven bone formation 6 weeks to 6 months- bone remodelling
What are the structural properties of immature callus
1
What are structural properties of mature callus
2
Disorganised collagen fibres
Lamellar structure peripherally
Haversian canals
What is a simple fracture
What is a compound fracture
What is a comminuted fracture
Linear undisplaced closed fracture
Open fracture with wound near site of break
Brake of bone into more than two fragments
What is a complex fracture
What is a green stick fracture
What is a pathological fracture
Brake of bone into many peices alongside damage to surrounding tissue and cartilage
Bone bends and cracks occurring in young bone usually seen in patients under 10
Fracture caused by disease causing bone weakening
