Fakhir Falamgir Flashcards

1
Q

What does affinity of a drug mean

What is an agonist

A

How strongly a drug can bind to its receptor

A drug that binds to receptors to initiate a physiological response

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2
Q

What are the mechanisms of entry of drugs into cells

4

A

Diffusion
Carrier mediated transport
Aquaporins
Pinocytosis

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3
Q

What are noradrenalines receptors
3

What type of receptors are they

A

Alpha 1 receptors
Alpha 2 receprors
Beta receptors

G coupled protein receptors

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4
Q

What does alpha 1 receptors initiate

What do alpha 2 receptors initiate

What do beta receptors initiate

A

Smooth muscle contraction

Smooth muscle relaxation, inhibition of neurotransmitter release

Smooth muscle relaxation, Heart muscle contraction, glucogenolysis

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5
Q

What is ED50
What is TD50
What is LD50
What is Emax

A

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

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6
Q

What is the difference between tachyphylaxis and tolerance

A

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

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7
Q

What is a partial agonist

A

Drugs that do not elicit the maximum response a full agonist would no matter what dose is given

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8
Q

What is an antagonist

What change does it cause in dose response curve

A

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

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9
Q

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

A

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

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10
Q

What is the therapeutic index

A

The margin of safety between dose of drug that achieves desired effect and dose that results in toxicity

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11
Q

What does it mean when a drug has a narrow therapeutic index

A

Only small difference between minimum and maximum effective drug concentrations in blood so small increase in dose can cause toxic or lethal side effects

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12
Q

What do the following drugs with narrow theraputic indices do

Aspirin
Carbamazepine
Gentamicin
Phenytoin
Vancomycin
Warfarin
A

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

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13
Q

What are the actions of these dental drugs

Hydrocortisone
Lignocaine
Anti histamines
Nicotine
Muscarine
Pilocarpine
Atropine
A

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

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14
Q

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

A

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

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15
Q

What type of alcohol is found in alcoholic drinks

A

Ethanol

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16
Q

What is a unit of alcohol

How is it calculated
How is percentage absolute volume by content calculated

A

10ml or 8g of absolute alcohol

Units of alcohol=
(%ABV x vol ml ) / 1000

%ABV=
(g of alcohol/100ml) / 0.78

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17
Q

What is the drink drive limit of alcohol

At what units is death possible

What is the certain lethal dose of alcohol

A

5

30

38

18
Q

What is the maximum units of alcohol advised per week for men and women

A

Women- 2-3 units per day

Men- 3-4 units per day

19
Q

What do glutamate and GABA do

What is alcohols pharmacokinetical effect on these

A

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

20
Q

What are the long term biological effects of alcohol on CNS

Pathophysiological effects
4

Blood markers
2

A

Intoxication
Withdrawal symptoms
Progressive dementia
Wernicke korsakoff syndrome - brain disorder cased by lack of thiamine

Increased blood alcohol
Decreased thiamine (vit B1)
21
Q

What are the long term biological effects of alcohol on Hepatic region

Pathophysiological effects
3

Blood markers
3

A

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

22
Q

What are the long term biological effects of alcohol on heamatologic region

Pathophysiological effects
4

Blood markers
2

A

Anaemia
Leukopenia
Thrombocytopenia
Decreased clotting

Increased PTT
Decreased haematocrit, RBC, WBC, platelets, clotting factors

23
Q

What are the long term biological effects of alcohol on CVS

Pathophysiological effects
3

Blood markers
1

A

Cardiomyopathy
Cardiac dysrhythmias
Hypertension

Abnormal ECG

24
Q

What are the long term biological effects of alcohol on immunologic system

Pathophysiological effects
3

Blood markers
1

A

Increased susceptibility to infection
Decreased humoral response
Delayed wound healing

Decreased WBC- alcohol damages bone marrow where many white blood cells mate

25
Q

What are the long term biological effects of alcohol on GIT

Pathophysiological effects
4

Blood markers
1

A

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

26
Q

What are the symptoms of foetal alcohol syndrome

3

A

Reduced IQ
Speech abnormalities
Hearing impairments

27
Q

What is the significance of acetyl aldehyde and alcohols link with oral cancer

A

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

28
Q

What is the proportion of absorbtion of alcohol in
Oral mucosa
Stomach
Small intestine

A

Small amount
20% (alcohol acidic)
80%

29
Q

What is the metabolism rate of alcohol

How long does it take to eliminate alcohol from body

How is alcohol excreted

A

1 unit per hour

12 hours

10%- perspiration, kidneys, lungs
90%- liver, gut

30
Q

What is the process of alcohol metabolism in the liver

A

Alcohol converted to acetaldehyde by cytochrome p450, alcohol dehydroginase and catalase enzymes
Acetaldehyde converted to water and carbon dioxide by acetaldehyde dehydrogenase

31
Q

What is antabuse and what does it do

A

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

32
Q

What is phase 1 of the p450 cytochrome system

What is phase 2 of the p450 cytochrome system

A

Addition of a molecule- oxidation, reduction, hydrolysis

Conjugation- glucuronidation, glycosidation, sulphation, methylation, acetylation, amino acid conjugation, glutathione conjugation

33
Q

How does alcohol interact with warfarin

How does alcohol interact with aspirin

A

Alcohol prevents warfarin and aspirin metabolism, so more of it is in blood, increasing risk of major bleeding

34
Q

How does alcohol interact with paracetamol

How does alcohol interact withmetronidazole

A

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

35
Q

What is the mechanism of alcohol dependence

3 stages

A

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

36
Q

What is primary fracture healing
What is the main type of repair

What is the process
3

A

The direct healing of fractured cortical bone ends with bone ends held in close apposition
- osteonal remodelling

  1. Fracture occurs eliciting response in adjacent tissues
  2. Localised inflammation recruits osteoclasts
  3. Osteoclasts trigger local remodelling with osteoclasts eliciting bone resorption followed by osteod deposition and new bone formation to bridge fracture and restore mechanical continuity
37
Q

What is secondary fracture healing

A

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

38
Q

What are the stages of fracture repair and when do they occur
7

A
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
39
Q

What are the structural properties of immature callus
1

What are structural properties of mature callus
2

A

Disorganised collagen fibres

Lamellar structure peripherally
Haversian canals

40
Q

What is a simple fracture
What is a compound fracture
What is a comminuted fracture

A

Linear undisplaced closed fracture

Open fracture with wound near site of break

Brake of bone into more than two fragments

41
Q

What is a complex fracture
What is a green stick fracture
What is a pathological fracture

A

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