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PPE > Pharma > Flashcards

Pharma Flashcards

1
Q

Give 3 reasons why someone may make a prescribing errors

A
  • Loss of attention due to exhaustion
  • Inappropriate training
  • Illiterate hand writing
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2
Q

Define pharmacokinetics

A

-Study of the movement of a drug into and out of the body ie what the body does to the drug

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3
Q

Define pharmacodynamics

A

-Study of the drug effect and mechanism of action oe what the drug does to the body

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4
Q

Define pharmacogenetics. Give an example

A
  • The effect of genetic variability on the pharmacokinetics or pharmacodynamics of a drug on an individual
  • CYP450 enzymes have genetic variation within the population eg 2D6 and thus some people will not react or over react to a drug which is metabolised by this enzyme eg codeine
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5
Q

Give some factors which may effect the pharacokinetics of a drug

A
  • Obesity
  • Alcohol consumption
  • Other medications
  • Liver and renal function
  • Albumin concentration
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6
Q

What is bioavailability of a drug? How do you calclulate it? Give some factors which affect bioavailability

A
  • The fraction of a dose which finds its way into the circulation unchanged
  • [AUC Oral] plasma/[AUC IV]plasma
  • Route of administration, age, lipid solubility of drug, absorption of drug, first pass metabolism
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7
Q

What is first pass metabolism?

A

-The metabolism of a drug which occurs before it reaches the systemic circulation. Includes metabolism in the gut lumen by gastric acid/enzymes, gut wall by absorption and the liver

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8
Q

Broadly describe the 2 phases of drug metabolism in the liver

A
  • Can either enter phase I or go straight into phase II
  • Phase I involves cyp 450 and is a oxidation or reduction reaction which usually inactivaes the drug
  • Phase II is a conjugation reaction with glucaronide, glutathione, sulphate which makes the drug water soluble so it can be eliminated
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9
Q

What are the two key factors which affect drug distribution and how do they do this?

A
  • Protein binding -> Unbound drugs are able to bind to receptors and pass across cell membranes and have a pharmacological affect. Bound drugs remain in the circulation, therefore if a drug is highly bound the distribution will be less
  • Volume of distribution -> a hypothetical measure of instantaneous distribution of drugs into available body compartments. If there is a low volume of distribution it means that the drug will be at high concentration in the body compartments which it can dissolve in
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10
Q

If there was a change in protein binding eg drug interactions, what properties of certain drugs would make you concerned?

A
  • If a drug is highly bound -> displacement would rapidly increase the concentration of active drug
  • If there was a low volume of distribution -> means the drug is in high conc in the places it is. displacing the drug from protein binding would raise the concentration more
  • If the drug had a narrow therapeutic window because displacement could push the drug to toxic levels
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11
Q

Give 3 things which may affect protein binding

A
  • Hypoalbuminaemia
  • Pregnancy
  • renal failure
  • Displacement by other drugs
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12
Q

What factors have an effect on volume of distribution?

A
  • Lipid solubility
  • Regional blood flow
  • Specific receptor sites in tissues
  • Active transport
  • Drug interactions
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13
Q

What is a pro-drug?

A

-A drug which is inactive when administered and becomes activated by the body eg codeine to morphine

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14
Q

Name some CYP inhibitors. What affect do inhibitors have on metabolism?

A
  • Grapefruit juice (simvastatin)
  • Omeprazole
  • Anti-fungals
  • Disulfram
  • Erythromycin
  • Valproate
  • Isoniazid
  • Cimetidine/Ciprofloxin
  • Ethanol (acute)
  • Sulphonamides
  • Decrease metabolism of drugs prolonging the effects
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15
Q

Name some CYP inducers. What affect do inducers have on metabolism?

A
  • Phenytoin
  • Carbamazepine
  • Cranberry Juice (warfarin)
  • Rifampicin
  • Alcohol (chronic)
  • Barbituates
  • St Johns Wort/Sulphonylureas
  • Induce the production of the enzymes to increase metabolism of drugs and thus decrease their effects
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16
Q

What 3 processes determine the renal excretion of drugs? What is the relationship between clearance and half life?

A
  • Glomerular filtration
  • Passive tubular resorption
  • Active secretion
  • The lower the clearance (GFR) the longer the half life
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17
Q

What is first order and zero order kinetics? Why do most drugs exhibit zero order kinetics at high doses?

A
  • 1st order = rate of elimination is proportional to drug level and a constant fraction is eliminated -> half life can be calculated
  • Zero order= rate of elimination is constant regardless of drug level. half life not easily calculated
  • Enzymes and receptors become saturated
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18
Q

Why does digoxin need a loading dose? Why does renal failure affect its toxicity?

A
  • It has a long half life and steady state would take 3-5 half lives and you need rapid affect
  • In renal failure there is less excretion of digoxin meaning that the drug will remain at toxic levels for longer and the same dose may reach toxic levels as that in a normal kidney
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19
Q

Describe the metabolism of paracetamol at therapeutic and toxic doses
What is the treatment for paracetamol overdose?

A
  • Therapeutic -> 90% Paracetamol enters phase II metabolism and excreted, 10% enters phase II and converted to NAPQI but quickly undergoes conjugation with glutathione and inactivated
  • Toxic -> Phase II saturated so much higher conc enters phase I metabolism. Produced large amounts of NAPQI and not enough glutathione to reduce so oxidative damage to the liver
  • Activated charcoal within 1 hour
  • N-acetylcysteine
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20
Q

How do competitive antagonist change the dose response curve? How is this over come?

A
  • Keeps the same shape but shifts it to the right

- Adding more agonist (its surmountable)

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20
Q

How do non-competitive antagonist change the dose response curve? How is this over come?

A
  • You get the same shape but the total response is decreased
  • It cannot as it alters the conformational shape of target
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21
Q

What is the difference between drug selectivity and drug specificity?

A
  • Selectivity refers to how well a drug binds to one group of receptor targets without binding to other targets and producing undesirable effect
  • Specificity refers to how well the drug binds to a receptor subtype allowing it to be organ specific
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22
Q

What is affinity? What pharmacological term is used to measure affinity and how is it interpreted?

A
  • A measure of the tendancy of a ligand to bind to its target
  • Kd -> The lower the Kd the higher the affinity
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23
Q

What is efficacy? What is potency?

A
  • The abolity of a drug to be able to activate the receptor and produce a response once it is bound
  • Potency is how much of the drug is needed to generate a response taking into account affinity and efficacy
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24
Q

What is the therapeutic window? How is it calculated?

Give 3 drugs with a narrow therapeutic window

A
  • The range of doses which can effectively treat a condition whilst still remaining safe. It is between the lowest concentrations which cause the desired affect and lowest concentrations causing adverse effects
  • EC50-> TD50
  • Warfarin, digoxin and gentamicin
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25
Q

How can drug interactions be caused during the absorption of a drug?

A

-Something may prevent the drug being absorbed due to inducible/inhibitable active transporters in the gut

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26
Q

Name some drugs which prolong the QT interval

A
  • Cocaine
  • Haloperidol
  • Erythromycin
  • Amiodarone
  • Tricyclic antidepressants
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27
Q

How can renal disease affect the pharmacodynamics/kinetics of drugs?

A
  • Decreased clearance
  • Disturbances in electrolytes may predispose to toxicity eg digoxin and hypokalaemia
  • Nephrotoxins will further damage the kidney
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28
Q

How can hepatic disease affect the pharmacodynamics/kinetics of drugs?

A
  • Decreased albumin production affects protein binding
  • Decreased CYP450 production will change metabolism of drugs
  • Reduced hepatic clearance of drugs
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29
Q

How can cardiac disease affect the pharmacodynamics/kinetics of drugs?

A
  • Excessive response to hypotensive agents

- Reduced organ perfusion may lead to reduced hepatic flow and clearance and reduced renal flow and clearance

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30
Q

What is an adverse drug reaction? Give some risk factors for ADRs

A
  • An unwanted or harmful reaction which occurs after administration of drugs and is suspected or known to be from the drugs
  • Reckless prescribing, extremes of age, unknown allergies,co-morbidities, narrow therapeutic index
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31
Q

Give some causes of variability of individuals to a drug

A
  • Pharmacogenetics
  • Weight
  • Age and sex
  • Health condition
  • Placebo effect
  • Route of admission
  • Drug interactions
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32
Q

Describe the first step in treating type 2 diabetes

A

-Diet and lifestyle eg reduce calorie intake in overweight, decreased saturated fat intake, limit salt intake, limit alcohol intake, stop smoking, exercise

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33
Q

What type of drug is metformin? What is its MOA? How is it eliminated? List some side effects

A
  • Biguanide
  • Increases insulin receptor sensitivity in muscle and adipose and inhibits hepatic gluconeogenesis
  • Completely renally excreted (toxicity risk in renal failure)
  • Diarrhoea, cough, muscle cramping
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34
Q

Name a sulphonylurea. What is its MOA? Give some adverse affects

A
  • Gliclazide
  • Stimulates pancreatic B cells to produce insulin by causing closure of ATP-sensitive K-channel leading to depolarisation and influx of Ca causing insulin release
  • Hypoglycaemia and weight gain
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35
Q

Name some metglitinides. What is its MOA? Give some adverse effects. What is the difference between metglinides and sulphonylureas?

A
  • Repaglinide/Nateglinide
  • Rapid acting insulin secretagogues which work on ATP-sensitive K channel at distinct site from sulphonylureas
  • Metglinides are rapid acting and have shorter halflives than SU
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36
Q

Name a thiazolidinedione. What is the MOA? Give some adverse effects

A
  • Pioglitazone
  • Insulin sensitiser by stimulating PPAR-g (peroxisome proliferator-activated receptor gamma) which regulates adipose, muscle and liver gene expression of insulin receptors. Causes increased glucose utilisation and decreased gluconeogenesis
  • Weight gain, oedema, bladder cancer
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37
Q

Name a GLP-1 agonist. What is its MOA?

A
  • Exanatide
  • Agonist of glucose-like-peptide 1 which self-regulates blood glucose levels by promoting satiety, enhances insulin secretion, reducing hepatic gluconeogenesis
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38
Q

Name a DPP4 inhibitor. What is the MOA?

A
  • Sitagliptin
  • Inhibits DPP4. DPP4 usually breaks down incretins. Incretins are gut hormones which increase b-cell secretion of insulin promoting glucose utilisation and decrease hepatic gluconeogenesis
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39
Q

Name an a glucosidase inhibitor. What is its MOA. Gove some adverse effects

A
  • acarbose
  • Inhibits a glucosidase activity in the gut which delays glucose absorbtion into the blood
  • Flatulence and diarrhoea
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40
Q

How do SGLT2 inibitors work? Give some adverse effects

A
  • Prevent glucose reabsorption in the PCT causing increased glucose excretion
  • Polyuria, dehydration, thrush, UTI
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41
Q

What is orlistat? Give some adverse effects

A
  • Pancreatic and gastric lipase inhitior preventing breakdown and absorption of fats
  • Foul smelling fatty diarrhoea
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42
Q

Give some adverse effects of exogenous insulin

A
  • Hypoglycaemia
  • Weight gain
  • Lipid dystrophy
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43
Q

Briefly describe the main roles of insulin

A
  • Stimulates uptake of glucose into liver, muscle and adipose tissue
  • Decreases hepatic gluconeogenesis and inhibits glycogenolysis
  • Promotes uptake of fats and inhibits lipolysis
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44
Q

Describe a typical insulin regime

A
  • Long acting basal insulin

- Short acting insulin at meal times

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45
Q

How is insulin genetically engineered?

A
  • Human insulin gene inserted into plasmid
  • Transfected into bacterium
  • Bacterium produces insulin
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46
Q

How are sex steroids transported? Where are they stored?

A
  • Bound to Steroid Hormone Binding Globulin in the blood and albumin
  • 1-2% is free and active
  • Adipose tissue
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47
Q

How do steroid hormones exhibit their action?

A
  • Lipophillic meaning they can diffuse across a PM
  • Bind to corresponding cytoplasmic receptors which are translocated to nucleus or straight to nuclear receptors
  • Cause an alteration in gene transcription to produce desired response
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48
Q

What is the common precursor to all sex steroids? What enzyme is involved in producing oestrogen from androgens?

A
  • Cholesterol

- Aromatase

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49
Q

List some side effects of oestrogen, progesterone and testosterone

A
  • Oestrogen = breast tenderness, water retention and thromboembolism
  • Progesterone = Weight gain, acne, lack of concentration
  • Testosterone = aggression, altered HDL:LDL ratio
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50
Q

Name a synthetic oestrogen and a synthetic progesterone

A
  • Oestrogen = ethinyloestradiol

- Progesterone = Dydrogesterone, Desogestrel or medroxyprodgesterone

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51
Q

Why are OCPs of particular interest regarding drug interactions?

A

-Metabolised by CYP system meaning anything which induces or inhibits CYP enzymes can effect OCP

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52
Q

When is HRT prescribed? Which drugs are used in HRT?

A
  • Hot fluses/sweats
  • Vaginal dryness or dyspareunia
  • Osteoporosis
  • Oestradiol and Medroxyprogesterone
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53
Q

What are the main risks of HRT?

A
  • Unopposed oestrogen increases the risk of endometrial and ovarian cancers
  • Opposed oestrogen increases the risk of breast cancer
  • Increased stroke risk
  • Increased venous thromboembolism risk
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54
Q

What is clomiphene (clomid)? When is it used?

A
  • A weak oestrogen (SERM)which blocks oestrogen receptors in ant pit, therefore inhibiting negative feedback and causing induction of ovulation via increased LH
  • IVF
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55
Q

What is tamoxifen (novladex)?

A
  • SERM which binds to ER in breast tissue and thus blocks stimulation of growth
  • ER+ Br Ca
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56
Q

What is finasteride and when is it used?

A

-5a-reductase which is used in BPH

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57
Q

Why would an oral dose of POP need to be higher than a different route of administration?

A

-Subject to first pass metabolism and almost all progesterone metabolised in one pass

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58
Q

Why does oxidised LDL in the intima pro-atherogenic?

A
  • Inhibits macrophage motility
  • Induces T-cell activation and VSMC division/differentiation
  • Toxic to endothelial cells
  • Enhances platelet aggregation
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59
Q

Describe the pathway of cholesterol synthesis. Describe the MOA of statins. State some adverse drug reactions to statins

A
  • HMG-coA -> mevaloate (hmg-coA reductase) -> cholesterol (synthase)
  • Inhibit HMG-CoA reductase to prevent cholesterol synthesis in hepatocytes which increases clearance of LDL by receptor upregulation
  • Increased transaminase levels, myopathy, GI complains, headaches and arthralgia
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60
Q

When are statins used?

A
  • High cholesterol levels

- Decrease cardiovascular event risk

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61
Q

Name a fibric acid derivative. How do they work?When are they used? Give some side effects

A
  • Bezafibrate
  • PPAR-a agonist which increases the production of lipoprotein lipase. Increases the uptake and oxidation of fatty acids -> reduces triglyceride levels
  • Hypertryglyceridemia
  • GI upset, cholelithiasis, myositis
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62
Q

How does ezetimibe work? Give some ADRs

A
  • Inhibits intestinal absorption of cholesterol causing decreased cholesterol delivery to liver so LDL receptor upregulation.
  • Enterohepatically circulates so systemic exposure is little
  • Headaches, abdo pain and diarrhoea
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63
Q

Why is it uncommon to use dual therapy with the lipid lowering drugs statins and fibrates?

A

-Increases risk for myopathy and rhabdomyolysis

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64
Q

Give some non-pharmacological advice to lower cholesterol

A
  • Avoid too much red meat and eggs
  • Eat foods with plant sterols such as flora proactive
  • Take fish oil
  • Get plenty of vitamin C
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65
Q

What is Rheumatoid Arthritis?

A
  • Chronic systemic autoimmune related inflammatory condition characterised by symmetrical deforming peripheral polyarthritis via destruction of the synovium which eventually causes dissolution of the cartilage and bone. There is an imbalance between pro and anti-inflammatory mediators
  • Onset often in young adult females
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66
Q

How is diagnosis of RA made?

A

-History + nodules in >1 joint+ serology for Rheumatoid Factor or Anti-CCP and CRP with a long duration of symptoms

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67
Q

What is the main difference in presentation between RA and OA?

A

-RA if worse on a moring and gets better with exercise whereas OA gets worse with use throughout the day

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68
Q

What is SLE? What serology in SLE?

A
  • Autoimmine condition in shich autoantibodies are made against a variety of antigens. It is multisystemic, remitting and relapsing in nature with a variable presentation which is normally non-specific such as malaise, fatigue and myalgia but can include butterfly rash, renal disease and oral ulcers
  • 95% ANA positive, also Anti-dsDNA +ve
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69
Q

Give 2 drugs which can cause lupus

A
  • Isoniazid

- Phenytoin

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70
Q

What is vasculitis? Give some diseases in which it can be secondary to. Name vasculitis affecting large, medium and small vessels

A
  • Systemic inflammation of the walls of BVs causing destruction or stenosis
  • SLE, RA, HIV
  • Large = Giant cell arteritis, Med = Polyarteritis Nodosa, Sml = Granulomatosis with polyangitis
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71
Q

Which antibody is often found in vasculitis?

A

-ANCA

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72
Q

Name 5 DMARDs

A
  • Methotraxate
  • Sulphasalazine
  • Anti-TNF
  • Rituximab
  • Cyclophosphamide
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73
Q

Describe the MOA of corticosteroids. Give some ADRs of corticosteroids. What is the consequence of immediately stopping corticosteroid use. Give 3 diseases in which corticosteroids are used

A
  • Anti-inflammatory by preventing IL1 and IL6 production by macrophages by inhibiting gene expression and Tcell activation
  • Weight Gain, Striae, glucose intolerance, infection, osteoporosis (cushingoid)
  • Adrenocortical insufficiency
  • IBD, Ashtma, Arthritis
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74
Q

Describe the MOA of Azothioprine. When is azothioprine indicated? Give some ADRs.

A
  • Incorporated into DNA synthesis which halts replication therefore can prevent proliferation of T and B cells.
  • Organ Transplant, SLE/RA/IBD, leukaemia
  • BM suppression, increased infection risk, hepatitis
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75
Q

What test must be performed before initiating azothioprine Tx and why?

A
  • TPMT levels.
  • It is the enzyme responsible for metabolism of Azothioprine into its active 6-mecerptopurine. The TPMT gene is polymorphic and decreased TPMT levels increases the risk of toxicity
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76
Q

Name 2 Calcineurin Inhibitors. What is their MOA. Give some ADRs

A
  • Ciclosporin, tacrolimus
  • Acts as an immunosuppressant by binding to calcineurin and preventing IL2 transcription
  • Nephrotoxic, hypertension, gingival hyperplasia
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77
Q

When is cyclophoshamide indicated? What is its MOA? What is sigificant about its pharmacokinetics? Give some ADRs

A
  • Lymphoma, leukaemia, wegeners
  • An alkylating agent which cross links DNA inhibiting replication of fast proliferating cells so stops T/B cell replication
  • Activated by CYP enzymes
  • BM suppression + infection, hair loss, anaemia and infertility
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78
Q

Name an Anti-TNF. When is it indicated. Describe its MOA. Give some ADRs

A
  • Infliximab
  • IBD, RA, Psoariasis
  • Decreases inflammation by decreasing cytokine production, particularly TNF-a, which decreases leukocyte chemotaxis, angiogenesis and decreases MMPs (joint destructin decreased in RA)
  • TB reactivation, infection
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79
Q

When is Methotrexate indicated? What is its MOA? What is of interest about its pharmacokinetics?Give some ADRs

A
  • RA, malignancy, IBD
  • DHFR inhibitor to prevent the synthesis of purine and thymidine synthesis preventing replication of rapidly dividing cells. In RA MOA is unknown
  • Very long halflife means weekly dosing. Requires toxicity monitoring
  • Mucositis, BM suppression, hepatitis, cirrhosis, teratogenic
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80
Q

What compounds make up sulphasalazine? When is sulphasalazine indicated? What is the MOA? Why is it particularly effective in IBD? Give some ADRs

A
  • Conjugate of 5-ASA and sulphapyridine
  • RA, IBD
  • Inhibit T cell proliferation and IL2 production. Inhibits neutrophil chemotaxis
  • Poorly absorbed so main activity in intestine
  • Myelosuppresion, hepatitis, GI distrubance Rash
81
Q

Describe the stepwise ladder of pharmacology asthma pathway

A
  • Step 1 = short acting b2 agonist eg salbutamol
  • Step 2 = inhaled corticosterpoids eg beclamethasone
  • Step 3 = Add on therapy such as long acting b agonist eg salmetarol
  • Step 4 = leukotrieneR antagonist eg montelukast or methyxanthine eg theophylline or long acting muscurinic antagonist eg tiotropium bromide
  • Step 5 = oral corticosteroids eg prednisolone
82
Q

How does salbutamol work in asthma? Describe the molecular detail. Give some ADRs

A
  • Symptomatic relief by reversing bronchoconstriction
  • B2 adrenoreceptor-> Gas -> AC-> cAMP -> PKA -> decreased intacellular Ca and inhibition of MLCK = bronchodilation
  • Tremor, palpitations, anxiety
83
Q

How do ICS work in asthma? When do you begin ICS? Give some ADRs of ICS

A
  • Regular preventer -> immunosuppressant to dampen bronchial hyperresponsiveness and cytokine production and increase transcription of b adrenoreceptors
  • Using blue more than 3xweek or nighttime waking
  • Headache, adrenal suppression, cushingoid
84
Q

In regards to asthma therapy, what is impotant between each treatment add on?

A

-Check inhaler technique, triggers and compliance

85
Q

What is the function of salmeterol in asthma? When is it used?

A
  • Reduce exacerbations and improve lung function

- Daily

86
Q

How does montelukast work in asthma? Give some ADRs

A
  • Prevents leukotrienes from binding to receptors in airway decreasing bronchoconstiction, mucus secretion and oedema and inflammation
  • Angiooedema, dry mouth, arthralgia
87
Q

How does theophylline work? Give some ADRs

A
  • Adenosine receptor antagonist

- Nausea, headaches, reflux, arrhthmias

88
Q

How does tiotropium bromide work in asthma? Give some ADRs

A
  • Long acting muscurinic antagonist which prevents bronchoconstriction
  • Constipation, dry mouth
89
Q

What are the three properties of NSAIDs?

A
  • Analgesic
  • Anti-inflammatory
  • Anti-pyretic
90
Q

How do NSAIDs exhibit their anti-inflammatory action

A

-Inhibit CycloOXygenase enzymes, to prevent the synthesis of PGs. This decreases local vasodilation to decrease autocoid delivery as well as decreasing the synergystic effect of permeating other autocoids -> decreases inflammation

91
Q

Describe the pathway of PG synthesis. What roles do PG have?

A
  • PM -> arachodonic acid (Phospholipase A2) -> PG ‘G’ (COX)-> PG ‘H’ (COX) to other PGs
  • Vasodilatory to increase bloodflow to areas such as the mucosa, renal parenchyma and myocardium. Also to areas of inflammation
92
Q

Inhibition of which COX enzyme is responsible for ADRs of NSAIDs and which for the Therapeutic. How does COX1 differ from COX2?

A
  • COX1 inhibition produces ADRs
  • COX2 produces therapeutic
  • COX 1 is constitutively expressed in many tissues vs COX2 which is induced by injurious agents in some tissues
93
Q

How do NSAIDs exhibit an analgesic effect

A
  • PGs cause peripheral sensitisation by activating GPCR on C pain fibres -> increased neuronal sensitivity to bradykinin, inhibits K channels/stimulates Na channels to increase neuronal excitability. This results in hyperalgesia and allodynia
  • PGs cause central sensitisation via increasing sensitivity of interneurones which decreases descending inhibition and thus increase pain fibre firing
  • NSAIDs inhibit PGs to prevent sensitisation and therefore is analgesic
94
Q

Describe the pharmacokinetics of NSAIDs

A
  • Highly bound to albumin

- 1st order elimination in therapeutic doses

95
Q

Give some ADRs of NSAIDs

A
  • GI symptoms including pain, N+V, reflux, peptic ulcer
  • In HRH compromised patients can cause renal ADRs due to decreased renal perfusion
  • Increased bruising and haemorrhage risk
  • Hypersensitve skin rash or steven Johnsons syndrome
96
Q

What is Steven Johnson syndrome? Give 3 drugs which can cause it. Who is more susceptible?

A
  • Immune complex mediated hypersensitivity which compromises hepatic function and causes ulceration of the skin and mucous membranes.
  • NSAIDs, lamotrigine/valproate/phenytoin/carbamazepine, sitagliptin, sulphonylureas
  • SLE and HIV infected
97
Q

How does aspirin differ from other NSAIDs?

A

-Irreversibly inhibits COX enzymes by acetylation and also inhibits thromboxane A2 release from platelets which reduces aggregation

98
Q

How does paracetamol work?Give ADRs

A
  • Unknown -> NonNSAID NonOpiate Analgesic Drug (NOAD)
  • no anti-inflammatory action but has antipyretic and mild analgesic
  • V good ADR profile
99
Q

How do opiates have a central psychoactive effect on pain?

A

-Alters the subjective experience of pain by effecting perception, mood and consciousness

100
Q

How do opiates have a peripheral effect on pain?

A
  • by binding to opioid receptors in PAG, RF and dorsal horn
  • Dorsal horn -> Inhibit substance P release nociceptors and pain fibres by activating Gai -> decreased AC -> decreased cAMP -> decreased PKA -> decreased Ca -> decreased NT release. Also increase outward K -> hyperpolarisation -> decreased neuronal activity
  • PAG and RF -> Increase descending inhibition
101
Q

Name the endogenous opiods

A
  • Enkephalins (reticular formation)
  • Endorphins (POMC is precursor)
  • Dynorphins
102
Q

Give some ADRs of opioids

A
  • N+V, constipation(increased tone decreased motility), drowsiness, miosis (stimulates CNIII), resp depression (decreases sensitivity of brainstem to PaCO2) and hypotension
  • Repeated use leads to tolerance (gradual decrease in effect) and dependance (physiological and psychological)
103
Q

Why is diamorphine (heroin) more potent than morphine?

A

-Higher lipid solubility meaning can cross bbb quicker

104
Q

Name the opioid receptors and the type of receptors they are

A
  • M, k, d

- GPCR to Gai

105
Q

Describe the clinical uses of opioids

A
  • Analgesic for moderate to severe visceral pain
  • Anaethetics eg remifentanil
  • Analgesic in labour (pethidine)
106
Q

What are the treatments for opioid overdose?

A
  • Partial agonist buprenorphine

- Antagonist naloxone

107
Q

How do local anaethetics work?

A
  • Block conduction of APs by blocking Na channels

- Use dependant are often hydrophilic eg lidocaine

108
Q

Give the difference in appearance of an arterial and venous clot, when they are found and what general categories of drugs are used to treat them

A
  • Arterial = white hard clot in CVA or MI -> antiplatelet and thrombolysis
  • Venous = red soft clot in DVT or PE -> anti coagulants
109
Q

What type of drug is warfarin? What is its MOA? Why does it take a few days to work?

A
  • Anti coagulant
  • Competitively inhibits reduction of vit K needed for synthesising Prothrombinm VII, IX and X so inhibits the clotting cascade
  • Remaining clotting factors have long half lives so got to wait till existing clotting factors are used up
110
Q

Describe the relevant pharmacokinetics of warfarin. What tests are performed to monitor drug effect whilst on warfarin?

A
  • Highly protein bound
  • Slow offset as have to wait for resynthesis of clotting factors
  • Hepatic metabolisn
  • Crosses placenta and is teratogen
  • INR and Prothrombin Time
111
Q

Give some possible situations where the effects of warfarin may be potentiated

A
  • Administering another drug which may inhibit CYP metabolism eg GOADEVICES
  • Adminitstering a drug which is highly protein bound eg NSAIDs
  • Additionally inhibiting platelet function eg aspirin
  • Reducing Vitamin K production from gut bacteria eg cephalosporins
112
Q

Give some examples of when warfarin is used in clinical practice

A
  • DVT
  • PE
  • Post MI
  • AF
  • Mechanical heart valves
113
Q

Give some ADRs of warfarin. How can warfarin Rx be reversed?

A
  • Increased bruising risk
  • Increased bleeding/haemorrhage risk
  • Teratogen
  • Administration of Vit K or Fresh frozen plasma (NB cannot re-warfarinise for upto 6 weeks after high Vit K administration due to long half life of vit K)
114
Q

What type of drug is heparin? What is its MOA? What is the difference between unfractionated and LMWH?

A
  • Anticoagulant
  • Binds to antithrombin III and causes activation through conformational change -> Increased inactivation of thrombin and factor Xa decreasing coagulation
  • Unfractionated inactivates both thrombin and Xa but has unpredictable pharmacokinetics. LMWH only inactivates Xa but is easily predictable in action and bioavailability. unfractionated is IV LMWH is subcut
115
Q

When is heparin used clinically?

A
  • DVT
  • PE
  • MI/unstable angina
  • Perioperatively/immobility
  • AF
  • Pregnancy
116
Q

Give some ADRs of heparin. What is HIT?

A
  • Increased bleeding/haemorrhage risk
  • Increased bruising
  • Heparin-induced thrombocytopenia -> Autoimmune phenomenon where Abs are produced to heparin and systemic cause activation of platelets by forming complexes with anti-heparinAbs and platelets. This results in systemic formation of thrombi but also a decreased platelet count which predisposes to haemorrhage
117
Q

How is heparin Rx reversed?-

A

-Protamine sulphate administration which dissociates heparin from antithrombin-III by irreversible inhibition

118
Q

How does dipyridamole work as an antiplatelet?

A

-Phosphodiesterase inhibitor which increases cAMP. cAMP inhibits platelet aggregation

119
Q

How does clopidogrel work as an antiplatelet?

A

-ADP antagonist to decrease activation of platelets

120
Q

Give the general functions of anaesthesia in surgery and give examples of drugs used in each

A
  • Premedication to relax patient eg benzos
  • Induce anaesthesia by inhibiting sensory, motor and sympathetic nerve transmission eg ketamine
  • Intraoperative analgesia eg opioid+NSAID
  • Intubation -> suxamethosone
  • Maintenance -> propofol
121
Q

Describe the general MOA of anaethetics in the different ion channels

A
  • Act on ligand gated ion channels -> primarily GABA -> increase in Cl’ conductance = hyperpolarisation of neurone causing decreased excitability
  • Inhibition of nicotinic AchR to reduce excitatory currents of Na
  • Inhibition of NMDAR by decreasing Ca influx into pre-synpatic terminals
122
Q

What is the minimal alveolar concentration? How is this a measure of potency?

A
  • the % of inhaled anaesthetic which abolishes all response to incision in 50% of population
  • The lower the MAC the higher the potency of drug as less is needed to get the effect
123
Q

Describe some ADRs of anaesthetic

A
  • Death due to CNS depression
  • Hypotension
  • Raised ICP
  • Malignant hyperthermia
124
Q

Describe the general depths of anaesthesia

A

1) Inhibition of ST pathway
2) Excitement of GABA pathways
3) Profound CNS depression leading to relaxation of skeletal muscle, breathing may need to be assisted -> sufficient for surgery
4) Severe medullary depression

125
Q

Give an example of a carbonic anhydrase inhibtor. What is its MOA? When is it used? Give some ADRs

A
  • Atezolamide
  • Idiopathic intracranial hypertension/ glaucoma
  • NaHCO3- diuresis by inhibiting carbonic anydrase in PCT
  • Metabolic acidosis
126
Q

Give an example of an osmotic diuretic. What is its MOA? When is it used? Give some ADRs

A
  • Mannitol
  • Filtered at the glomerulus raising the osmotic potential of PCT -> water remains in nephron and is excreted
  • Cerebral oedema
  • Hypernatraemia
127
Q

Give an example of a Thiazide diuretci. What is its MOA? When is it used? Give some ADRs

A
  • Bendrofluathiazide
  • Inhibits NCCT channel in DCT preventing Na and water resorption
  • Hypertension
  • ADRs = hypecalcaemia, hypokalaemia and hyperuricaemia, erectile dysfunction
128
Q

Give an example of a loop diuretic. What is its MOA? When is it used? Give some ADRs

A
  • Furosemide
  • Blocks NKCC2 channels in the thick ascending limb of the LoH preventing Na and Cl resporption with concomitant loss of Ca and Mg
  • Oedematous states eg HF
  • Hypokalaemia (increased Na in DCT promoted K secretion), hypocalceamia and hypomagnesia
129
Q

Name an aldosterone antagonist. What is its MOA. When are they used? Give some ADRs

A
  • Spironolactone
  • Antagonising the actions of aldosterone in the collecting duct ie prevents Na and H2O resorption by decreasing ENaC expression, Decreasing ROMK channels, Decreasing NaKAPase
  • HF and non-responsive hypertension
  • Hyperkalaemia, androgenic cross reactivity eg gynaecomastia
130
Q

Give an example of an ADH antagonist. When is it used? Give some ADRs

A
  • Lithium
  • SIADH
  • Confusion and frequent urination
131
Q

What the MOA of Amiloride? When is it used? Give some ADRs

A
  • Blocks ENaC in late DCT/CT
  • Added in conjunction with furosemide in HF
  • Hyperkalaemia
132
Q

Give 3 reasons for diuretic resistance

A
  • Non-compliance
  • Poor absorption ->gut oedema
  • Volume depletion -> increased aldosterone or decreased GFR
  • NSAIDs -> decreased renal bloodflow
133
Q

Name some potentially nephrotoxic drugs

A
  • Gentamicin
  • ACE Inhibitors (vasodilation of efferent arteriole causes decreased pressure across glomerlus -> decreased renal BF
  • NSAIDs
  • Metformin
  • Penecillins
134
Q

Describe the ECG changes in hyperkalaemia

A

1) Peaked T waves
2) Absent P wave
3) Prolonged QRS
4) VF

135
Q

Describe the non-pharmalogical approach to treating hypertension

A
  • Educate the patient about the disease
  • Maintain normal BMI
  • Decrease salt intake <6g
  • Decreased alcohol intake
  • Aerobic exercise
  • 5+ fruit and veg
  • Smoking cessation
  • Decreased sat fats
136
Q

Describe the pharmacological steps to treating hypertension

A
  • Under 55 -> Ace inhibitor/ARB then CCB then Thiazide/Thiazide like
  • Over 55 or black -> CCB then ARB/Ace inhibitor then thiazide/thiazide like
  • After thiazide seek expert help who my consider spironolactone
137
Q

How do ACE inhibitors work? Name one. Give some ADRs

A
  • Competitively inhibits angiotensin converting enzyme to prevent AngI being converted to AngII to prevent vasoconstriction, aldosterone production and SNS activity
  • Ramipril/lisinopril
  • Dry coughm angiooedema, renal failure, hyperkalcaemia
138
Q

Give an example of an ARB. What is MOA? Give some ADRs

A
  • Losartan/candesartan
  • Binds to AtRI and inhibits AgII binding
  • Hyperkalaemia
  • Renal failure
139
Q

Give examples of the different classes of CCB and when they are used. What is MOA? Give some ADRs

A
  • Dihydropyridines = Amlodipine/nifedipine -> hypertension -> ADRs= tachycardia (baroreflex), flushing, headache, gingival hyperplasia
  • Phenylalkamines= verapamil -> Anti-arrhythmic by prolonging AP to slow HR -> ADRs= constipation, bradycardia
  • Benzothiazepines = Diltiazem -> anti-angina by vasodilating coronary vessels -> ADR = bradycardia
140
Q

Give an example of an alpha channel blocker. What is MOA? Give some ADRs

A
  • Doxazosin
  • Selective antagonism of a1 adrenoreceptors in vascular smooth muscle
  • Causes vasodilation and a decrease in TPR
  • ADRs = postural hypotension, headaches and oedema aha
141
Q

Give an example of a b-blocker. What is MOA? Give some ADRs

A
  • Atenolol, bisoprolol
  • Antagonises b-adrenoreceptors in the heart to decrease HR and SV
  • Lethargy, impaired concentrarion, bradycardia
142
Q

Describe the classes of drugs which are used in heart failure and why they are used

A
  • Loop Diuretics eg furosemide -> relieve symptoms by decreasing fluid volume
  • ACEi/ARB ->decrease effects of activated RAS system by preventing angiotensin II -> decreases vasoconstriction and aldosterone activation
  • B-blocker -> decreases heart rate to increase filling time -> starlings curve
  • Spironolactone -> antagonise effects of aldosterone in DCT preventing water resorption
  • Digoxin -> improve symptoms by increasing CO
  • Vasodilators
143
Q

When would you not give verapamil or diltiazem and why?

A
  • HF or AV block

- Negative inotrope would further decrease CO

144
Q

What is the MOA of digoxin?

A

-Competes with K+ for NaKATPase -> decreases Na outflow -> Na accumulates in cell -> NCX reverses -> brings Ca in -> increased force of contraction of heart

145
Q

What is dobutamine and when is it used?

A
  • B1 agonist

- Cardiogenic shock

146
Q

What is the fractional cell kill hypothesis in chemotherapy?

A
  • Finding a balance between killing the cancer cells and destroying bone marrow cells
  • Need to give adequate dosing and time between doses to allow bone marrow recovery but not long enough for Ca to grow back
147
Q

Name a spindle poison. What is its MOA?

A
  • Vinca Alkaloids (vincristine) or Taxanes (Paclitaxel)
  • Vinca alkaloids prevent microtubule formation whereas taxanes prevent microtubule disassembly. Both resulting in the inability to complete mitosis leading to cell cycle arrest and apoptosis
148
Q

Name an alkylating agent and describe its MOA

A
  • Cisplatin
  • Directly affect DNA by covalently binding to strands causing cross linking which prevents DNA uncoiling and triggers apoptosis
149
Q

Name an antimetabolite and describe how it works

A
  • Fluorouracil/methotrexate
  • FU ->Impedes DNA synthesis by mimicing nucleotides and preventing synthesis or blocking the use of enzymes needed for DNA synthesis
150
Q

How do cancer cells exhibit mechanisms of resistance to drugs?

A
  • Efflux of drugs
  • Inactivation of drugs
  • Enhanced DNA repair mechanisms
151
Q

What are PICC and hickman lines?

A
  • Peripherally inserted central catheter -> IV access which can be used for a prolonged time (2 weeks) by entering a catheter periperally which extends into SVC
  • Hickman is central venous catheter inserted internal jugular and entended into SVC
152
Q

Describe some common ADRs of chemo drugs

A
  • Alopecia
  • NV
  • Mucositis
  • Dairrhoea
  • Myalgia
  • Candida
  • BM suppression
153
Q

Name 3 drugs which can cause pulmonary fibrosis

A
  • Bleomycin
  • Methotrexate
  • Isoniazid
154
Q

Name a type 1A antiarrythmic. What is its MOA? What change does it produce on ECG, when is it used? Give some ADRs

A
  • Procainamide
  • Blocks Na channels in ventricular myocytes in order to decease electrical conduction and increase the refractory period
  • ECG has wider QRS and longer QT
  • AF/Atrial flutter
  • Hypotension and CNS effects (dizziness, confusion, insomnia)
155
Q

Name a type 1B antiarrythmic. What is its MOA? What change does it produce on ECG, when is it used? Give some ADRs

A
  • Lidocaine
  • Blocks Na channels in cardiac myocytes to decrease conduction in fast ischaemic tissue
  • Widens QRS complex
  • VT/VF
  • CNS ADRs
156
Q

Name a type 1C antiarrythmic. What is its MOA? What change does it produce on ECG, when is it used? Give some ADRs

A
  • Flecainide
  • Blocks Na channels in cardiac myocytes to decrease automaticity and increase AP duration
  • Increases PR interval, widens QRS complex and increases QT
  • Cardioversion of AF, atrial flutter, SVT, WPW
  • ADRs = pro-arrhthmic, headache and CNS
157
Q

Name a type 2 antiarrhythmic. What is its MOA? ? What change does it produce on ECG, when is it used? Give some ADRs

A
  • Atenolol, bisoprolol
  • prolongs plateau phase by decreasing conduction in the AVN which decreases the automaticity of the heart (slows HR) and increases the duration of the AP
  • Increases PR and decreases HR
  • Sinus tachycardia, Re-enterant AV arrhythmias
  • ADRs = bronchospasm and decreased BP
158
Q

Name a type 3 antiarrhythmic. What is its MOA? ? What change does it produce on ECG, when is it used? Give some ADRs

A
  • Amiodarone
  • Blocks K channels which increases duration of depolarisation by preventing K leaving. Also extends refractory period and decreases speed of AVN conduction
  • Increased PR, widened QRS, increased QT decreased HR
  • Can be used in most arrhythmias esp WPW, VT/VF
  • Pulmomnary fibrosis, hepatotoxic, hyperthyroidism, pro-arrhythmic
159
Q

Name a type 4 antiarrhythmic. What is its MOA? What change does it produce on ECG, when is it used? Give some ADRs

A
  • Calcium channel blockers eg verapamil
  • Decreases inward flux of Ca2+ which decreases force of contraction and prolongs the plateau phase increasing duration of AP
  • Also slow conduction of AVN
  • Increase PR interval and decrease HR
  • Rate control in SVT
  • ADRs = GI and hypotension
160
Q

What is adenosine and when is it used?

A
  • A drug which binds to A1 receptors in the heart to activate K currents in SAN/AVN in order to hyperpolarise cells and reset the electrical current. (Has half life of seconds)
  • Used to convert re-entrant SVT
  • ADRs = Hypotension if used in surgery
161
Q

When is digoxin used in AF?

A

-Permanent or persistant AF

162
Q

What is atropine and when is it used?

A
  • Selective muscarinic antagonist

- Vagal bradycardia and glaucoma

163
Q

Why are dopamine receptor agonist used in parkinsons? Give an example. Describe some ADRs

A
  • Stimulates striatum of basal ganglia without needed dopaminergic neurones
  • Ropinrole
  • Hypersexuality, impulse control disorders eg punding, hallucinations
164
Q

What is entacapone?

A

-COMT inhibitor used in parkinsons to inhibit dopamine breakdown and prolong the response to LDOPA

165
Q

Give some side effects of AchE Inhibitors

A
  • Sweating
  • Lacrimation
  • Salivation
  • Urinary incontinence
  • Diarrhoea
166
Q

What is the MOA of Na channel blockers in epilepsy? Which antiepileptic drugs are Na channel blockers

A
  • Use-dependant drugs which block Na channels to prevent hyperexcitability of neurones by prolonging the inactivation state and detaching when RMP returns to normal
  • Carbamazepine, Phenytoin and Lamotrigine
167
Q

Describe the relevant PK of carbamazepine. State when it is used and ADRs

A
  • Highly protein bound, CYP inducer including its own metabolism -> need to lower dose with repeated use
  • All seizures apart from absence
  • CNS, ataxia, numbness, hyponatraemia, rash, teratogen
168
Q

Describe the relevant PK of Phenytoin. State when it is used and ADRs

A
  • Highly protein bound, CYP inducer, Non-linear,
  • Status epilepticus
  • CNS, ataxia, gingival hyperplasia, steven johnson, teratogen
169
Q

Describe the relevant PK of lamotrigine. State when it is used and ADRs

A
  • Linear and no CYP induction so best antiepileptic

- Less marked CNS effects, rash, safe in pregnacy

170
Q

How are GABA mediators used in epilepsy? Which antiepileptic drugs are GABA mediators?

A
  • GABA receptor agonists which increase Cl conduction through GABA channels to make neurones less excitable to decrease hyperactivity
  • Sodium valporate
  • Benzodiazeopines
171
Q

Describe the relevant PK of Sodium Valporate. State its MOA. State when it is used and ADRs

A
  • Mixed action but mostly GABA agonist
  • Highly Protein bound
  • All seizures
  • Weight gain, CNS, ataxia, sedation
172
Q

Describe the relevant PK of Benzodiazepines. State when it is used and ADRs

A
  • Enhances GABA binding by acting at a disting receptor site, highly protein bound, variable kinetics
  • Status Epilepticus
  • Sedation, tolerance and depenance , aggression
173
Q

How are AEDs controlled in birth control/pregnancy?

A
  • Its finding a balance between epilepsy risk vs teratogen
  • AEDs increase the failure rate of OCPs by 4x and increases the risk of birth defects from 2% to 8%
  • Lamotrigine is safest
174
Q

What DDI do antidepressants have with AEDs?

A

-Lower the convulsant threshold

175
Q

What are the symptoms of depression? Which NT are involved?

A
  • 3 core -> Persistant low mood, low energy and anhedonia
  • Secondary include -> decreased appetite, altered sleeping patterns, hopelessness, poor concentration
  • NA and Serotonin
176
Q

Name an SSRI. What is their MOA? When are they used? Is there any PK of interest? Give some ADRs

A
  • Fluoxatine/Citalopram
  • Inhibit the reuptake of serotonin into the presynaptic terminal which increases the presence of the NT in the synaptic cleft for longer, increasing the signal across the synapse
  • Moderate to severe depression
  • Anorexia, nauseam diarrhoea, possible precipitation of ideation and prolonging of QT
177
Q

Name a TCA. What is their MOA? When are they used? Is there any PK of interest? Give some ADRs

A
  • Amitryptilline
  • Block the noradrenaline and serotoning reuptake transporter on presynaptic terminal. Also a1-adrenergic antagonist. Work together to produce an elevated mood and also a little sedation
  • Not really used any more for depression
  • CNS effects, sedation, tachycardia, hypotension
178
Q

Name an SNRI. What is their MOA? When are they used? Is there any PK of interest? Give some ADRs

A
  • Duloxetine
  • Serotonin and Noradrenaline Reuptake inhibitor which prolongs NT presence in synaptic cleft
  • 2/3 line use in non-responsive depression
  • Low doses have a serotonin effect, high doses have a NA effect
  • ADRs include anorexiam nausea, diarrhoea,
179
Q

What are the symptoms in paranoid schizophrenia and give some possible mechanisms behind the cause?

A
  • Thinking disturbances, hallucinations, delusions, lack of insight
  • Possible increased dopamine function and altered Serotonin function
180
Q

Name a typical and atypical antipsychotics. Which are given first line? Give some ADRs

A
  • Typical = Haloperidol
  • Atypical = Clozapine
  • Atypical are first line
  • ADRs = extrapyramidal side effects including parkinsonism and acute dystonia, CNS depression, weight gain, postural hypotension
181
Q

What is anxiety and what symptoms does it produce?

A
  • Fear out of proportion to the situation which often leads to avoidance of situations and the fear of dying/going crazy
  • Physical symptoms include light headedness, SOB, palpitations, hot flushes
182
Q

What classes of drugs can be used to treat anxiety?

A

-Antidepressants, antipsychotics, anxiolytics,

183
Q

Give an example of an anxiolytic which can be used to treat anxiety. Give some ADRs

A
  • Benzodiazepines eg diazepam/lorazepam

- ADRs= tolerance and dependance, sedation, CNS effects, teratogen

184
Q

Which 3 factors contribute to the physiological control of gastric motility?

A
  • Myogenic control -> Rhythmic contraction by waves of slow depolarisation which spreads through gap junctions
  • Neural control -> Stimulation of cholinergic nerves increase force of contraction. Stimulation of noradrenergic nerves inhibits contraction
  • Hormonal control -> Hormones produced by enteroendocrine cells
185
Q

What is intestino-intestinal inhibition and anointestinal inhibition?

A

-Distention of the intestines or anus produces an inhibitory effect on contraction

186
Q

What are the gastrocolic or duodenocolic reflexes?

A

-Food entering the stomach or duodenum stimulates gastric motility

187
Q

Describe the physiology of emesis and give some causes and preliminary signs

A
  • Pyloric sphincter closes, cardia and oesphagus relax, gastric contents propelled by contraction of diaphragm and abdo wall, glottic gloses and soft palate elevates to protect trachea and nasopharyx respectively
  • Pregnancy, medsm toxins, smell, ICP, infection, rotational
  • Dilated pupils, hypersalivation, sweating, pale
188
Q

What controls emesis? What NT are involved?

A
  • Vomiting centres in medulla
  • Vestibular apparatus
  • Serotonin, dopamine, Ach, histamine
189
Q

How are D2 antogonists used in emesis. Name one. When is it indicated? Give some ADRs

A
  • Domperidone/metacopamide
  • Acts on prostrema of 4th ventricle to stop D2 release and increase the rate of gastric emptying
  • Acute NV
  • ADRs= Diarrhoea, drowsiness, stimulates prolactin release, possible dystonia
190
Q

How are 5-HT antogonists used in emesis. Name one. When is it indicated? Give some ADRs

A
  • Ondansteron
  • Inhibits vagal stimulation by 5-HT
  • Radiation and chemo sickness
  • ADRs= headaches and flushing
191
Q

How are Ach antogonists used in emesis. Name one. When is it indicated? Give some ADRs

A
  • Scopolamine
  • Inhibits vagal activity
  • Motion sickness
  • ADRs = Bradycardia
192
Q

How are H1 antogonists used in emesis. Name one. When is it indicated? Give some ADRs

A
  • Cyclizine
  • Inhibits H release from vomiting centre
  • Acute NV
  • ADRs = QT prolongation and sedation
193
Q

What are the non-pharmacological treatments for constipation?

A

-Increase fluids, high fibre diet and exercise

194
Q

How do bulk laxatives work for constipation? When are they indicated? Give some ADRs

A
  • Insoluble and non-absorbable substances which distend the gut and activate the stretch receptors causing contraction behind and relaxation in front. Takes a few days to work
  • Pregnancy, IBS
  • Flatulence
195
Q

How do faecal softeners work for constipation? When are they indicated? Give some ADRs

A
  • Glycerol supplements can lubricate and soften stools allowing it to pass easier
  • Pregancy, IBS, Adhesions, Haemorrhoids
  • Dehydration and Diarrhoea
196
Q

How do osmotically active laxatives work for constipation? Give an example. Give some ADRs

A
  • Cause water retention to increase peristalsis. These are the quickest acting laxative
  • Lactulose
  • Dehydration and diarrhoea
197
Q

How do irritants and stimulants work for constipation? When are they indicated? Give some ADRs

A
  • Excite sensory nerve endings causing H2O and electrolyte retention causing peristalsis
  • Faecal impaction and surgical prep
  • ADRs = repeated use causes colonic atony, hypokalaemia and melanosis coli
198
Q

How do anti-motility drugs work for diarrhoea? Give an example When are they indicated? Give some ADRs

A
  • Decrease bowel movement to increase transit time and increase reabsorption. Also increase anal tone and decrease sensory defecation reflex
  • Codiene and imodium
  • Constipation, drowsiness
199
Q

How do Bulk formers drugs work for diarrhoea?

A

-Increase bulk to water ratio to slow transit time

200
Q

How do Fluid adsorbents work for diarrhoea?

A

-Absorb fluid creating a more formed stool

201
Q

Give an example of a pharmacological anti-spasmodic and an OTC anti-spasmodic

A
  • Mebeverine

- Peppermint oil

PPE (15 decks)

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