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midwifery > pharmacology > Flashcards

pharmacology Flashcards

1
Q

Routes of administration

A

Parenteral – injection such as subcutaneous, intramuscular, intravenous or epidural
Enteral – oral, nasogastric or rectal
Topical - rectal, inhalation, vaginal, sublingual or dermal

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2
Q

Forms of drugs

A

solid form - capsules, tablets and trochees
liquid forms - syrups, solutions, aqueous suspensions, elixirs, tinctures and gases
ointments, pastes, lotions, suppositories

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3
Q

Absorption

A

Absorption refers to the process of how the drug enters the systemic circulation from the point of administration.

It describes how the drug is released from the formulation and how it enters into the circulation. With other words from application to distribution

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4
Q

Factors affecting absorption

A

-Lipid water solubility
Lipid water solubility coefficient is the ratio of dissolution of drug in lipid as compared to water. Greater the lipid water solubility coefficient, more is the lipid solubility of the drug and greater is the absorption. Less the coefficient, less is the lipid solubility and less is the absorption.

  1. Molecular size
    Smaller the molecular size of the drug, rapid is the absorption.
  2. Particle size
    Larger is the particle size, slower will be the diffusion and absorption and vice versa.
  3. Degree of Ionization
    Different drugs are either acidic or basic and are present in ionized or unionized form.
  4. Physical Forms
    Drugs may exist as solids, liquids or gases
  5. Chemical Nature
    Chemical nature is responsible for the selection of the route of administration of drug.
  6. Dosage Forms
    Dosage forms affect the rate and extent of absorption. A drug can be given in the form of tablets, capsules or transdermal packets. Injections may be aqueous or oily. This changes the rate of absorption.
  7. Formulation
    When the drugs are formed, apart from the active form some inert substances are included.
  8. Concentration
    higher the concentration more flux occurs across the membrane. The rate is less affected than the extent of absorption.

Factors Related to Body
1. Area of Absorptive Surface

  1. Vascularity
  2. pH
  3. Presence of other Substances
  4. GI Mobility
  5. Functional Integrity of Absorptive Surface
  6. Diseases
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5
Q

Distribution

A

Distribution is the process whereby the drugs are moved around the body from site of absorption to site of action and finally to the site of excretion.

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6
Q

The factors that affect distribution include

A

amount of drugs available
blood flow, vascularisation
amount of plasma proteins
water in fluid compartments

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7
Q

Drugs are carried in the blood in 2 forms

A

attached to proteins (protein-bound) or in the free form (unbound).

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8
Q

free drug

A

The free (non-protein-bound) drug is dissolved in solution and can enter cells directly.

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9
Q

protein bound

A

The protein-bound is attached to protein. This binding is reversible because the drug needs to be released from the protein before entering cells. This form of drug transport acts like a reservoir

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10
Q

Metabolism

A

Metabolism or biotransformation is the process of how the body breaks down the drugs.

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11
Q

where does most metabolism take place

A

liver

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12
Q

metabolism is necessary to

A 
activate pro-drugs
inactivate drugs (normal process)
change drugs to water-soluble forms for excretion
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13
Q

Factors affecting metabolism include

A 
hepatic function and the hepatic first-pass effect
genetic differences (enzymes) eg PKU, porphyria
interference of other drugs (interaction)
concomitant diseases (renal, liver disease)
metabolic status (age, weight)
drug storage (fat)
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14
Q

The hepatic first-pass effect refers to

A

The hepatic first-pass effect refers to enteral drugs which once they are absorbed, have to go to the liver first before reaching the target organ. This means that some of the drugs will already be metabolized before reaching the systemic circulation.

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15
Q

Bio availability

A

Bioavailability is the fraction (proportion) of the active drug which reaches the target organ and which can thus produces a biological effect.

The bioavailability is affected by amount of drug absorbed and the metabolism in the first-pass phenomenon through the liver.

A low bioavailability means that most of the drug is lost or destroyed before actually reaching the target cells.

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16
Q

Excretion or elimination is

A

the removal of any part of the drug which is no longer used by the body.

The body can eliminate chemicals by various means. These include bile and faeces, urine, exhalation of air, sweat or saliva, breast milk and vomiting.

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17
Q

Pharmacodynamics is

A

Pharmacodynamics is the pharmacological mode of action or effect of the drug. It is the action of drugs on living tissue.

It can also be defined as the biological effects produced by the interaction of a drug and the target site (cells, fluids, receptors).

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18
Q

therapeutic effect

A

minimum effective concentration

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19
Q

the pharmacological action of drugs can be put into 2 categories

A
  • non-receptor mediated and receptor mediated.
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20
Q

The receptor mediated actions are more specific and can be on

A
  1. receptors on the cell membrane or receptors inside the cell
  2. enzymes
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21
Q

The non-receptor mediated actions include

A
  1. physical
  2. chemical
  3. antibody
  4. placebo
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22
Q

second messenger concept

A

Receptors on the cell membrane (outside) can be activated by a drug which binds to the receptor.

The drug is the 1st messenger and is lipophobic (water-soluble) and cannot diffuse across the cell membrane.

The drug-receptor binding activates the 2nd messenger inside the cell and this alters cell activity.

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23
Q

Steroid hormones or lipid-soluble drugs

A

can directly enter the cells

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24
Q

protein hormones or lipid-insoluble drugs

A

work by second messenger

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25
Q

1st messenger concept

A

Receptor inside the cell will be activated by drugs that are lipophilic (water-insoluble), which have diffused across the cell membrane.

The 1st messenger (drug) enters the cells and directly alters cell activity.

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26
Q

Enzyme action

A

Enzymes also have receptors and drugs binding to these receptors can activate or inhibit the enzyme action.

The following are examples of drugs which inhibit enzymes. Angiotensin-converting enzymes (ACE) play a role in blood pressure control. ACE inhibitors are used to lowers blood pressure.

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27
Q

Specificity is the

A

ability of the drug to bind to a receptor. It depends on the chemical structure of the drug and the specific fit with a receptor (lock and key).

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28
Q

The affinity is the

A

strength of binding of drug and receptor.

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29
Q

Efficacy is the

A

magnitude of effect (maximum effect) the drug can have.

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30
Q

The potency of a drug is the

A

strength of the drug (amount of drug needed to get the effect).

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31
Q

A drug that is an agonist

A

mimics natural neurotransmitters, hormones or chemical by stimulating receptors eg adrenaline and nor-adrenaline. These drugs have affinity and efficacy and specificity.

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32
Q

An antagonist is

A

when a drug combines with a receptor but does not produce a biological response, or prevents other molecules from binding to the receptor, thus not producing a response.

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33
Q

Minimum effective concentration (MEC) or therapeutic level is

A

the lowest drug plasma level at which the drug produces the desired drug effect (therapeutic effect).

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34
Q

The toxic level is

A

when the drug plasma level at which the drug produces serious adverse effects.

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35
Q

The loading dose is

A

an initial larger dose given to reach a steady state quicker.

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36
Q

The maintenance dose

A

is the dose needed to keep the plasma levels in the therapeutic range/steady state.

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37
Q

The duration of action

A

covers the time when there is enough drug to cause a response.

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38
Q

Dose interval is

A

the time between doses of a drug.

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39
Q

The onset of action

A

is the time from administration of the drug to the first clinical response.

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40
Q

Side Effect or type A reaction

A

These are known, undesirable response to a drug at normal drug dosage. They are usually predictable, a secondary effect and unavoidable.

Side effects are related to the mechanism of drug action, the characteristic of the drug.

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41
Q

Adverse reaction or type B reaction

A

These are any unintended, undesirable effect due to drug administration at normal dosages.

The effects are unexpected and unpredictable. They can be dangerous, bizarre, or idiosyncratic and are due to patient characteristics, not related to the mechanism of drug action.

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42
Q

Drug interactions

A

Drugs can interact with each other in their passage through the body (pharmacokinetics) or at the site of action (pharmacodynamics).

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43
Q

A pharmacokinetic interaction is

A

where one drug interferes with the absorption or metabolism of another drug

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44
Q

Pharmacodynamic interactions are

A

where one drug interferes with the effects of another at the cellular level (agonist, antagonist, desirable, undesirable).

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45
Q

Monitoring the patient and the effects

A 
Baseline vital signs
Compliance
Therapeutic (clinical) effect
Plasma concentrations
Side effects and adverse reactions
Toxicity
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46
Q

Clinical response to adverse drug reaction should include

A

Discontinue administration or modifying the dose
Prevent further absorption – gastric lavage, haemodialysis
Hospitalise client – monitor signs and symptoms, blood levels
Provide supportive measures
Antidote – atropine or naloxone
Increase elimination - diuretics
Record event

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47
Q

Contraindications refer to

A

situations when a drug is not recommended eg age, pregnancy, allergies

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48
Q

Adrenergic medications work on the

A

sympathetic nervous system, affecting the central nervous system and the peripheral alpha- and beta-receptors.

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49
Q

Beta-blockers are used to

A

reduce the myocardial workload (reduce the force of contraction and reduce the rate of contraction).

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50
Q

Alpha-blockers have a

A

vasodilatory effect on the blood vessels, thus lowering the blood pressure.

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51
Q

The therapeutic effect of beta-blockers is to

A

The therapeutic effect of beta-blockers is to reduce the force of contraction of the myocardium (negative inotropic effect) and to reduce the heart rate (negative chronotropic effect). This reduces the myocardial oxygen demand and prevents or reduces myocardial ischaemia.

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52
Q

The pharmacological effect of alpha-blockers is

A

smooth muscle relaxation in the arteries thus reducing the afterload and decreasing blood pressure.

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53
Q

Labetalol is indicated

A

in pregnancy and mainly has an alpha-blocking effect and is a lesser beta-blocker.

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54
Q

Methydopa is a

A

centrally acting sympatholytic used in hypertensive crises. Methyldopa does not reduce renal or cardiac function like some of the other adrenergic blockers. Because of the effect on the brainstem, the client may experience drowsyness.

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55
Q

Calcium channel blockers are used in

A

the treatment of arhythmias, angina and hypertension.

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56
Q

The pharmacological action of these drugs

A

embedded in the name - these drugs stop calcium entering the cells by blocking the calcium channels (pores). The result is smooth muscle relaxation. Not all calcium channel blockers have the same therapeutic effect.

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57
Q

When the coronary arteries dilate

A

more oxygenated blood can flow to the myocardium and angina is relieved.

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58
Q

When the peripheral arteries dilate

A

the systemic vascular resistance decreases and the blood pressure is reduced.

59
Q

The commonly used calcium channel blockers include

A

felodipine, nifedipine and verapamil.

60
Q

The main effect of nifedipine is

A

coronary and systemic vasodilation.

61
Q

Magnesium sulphate is mainly used as a

A

tocolytic but will also reduce blood pressure. Magnesium competes with calcium for entry into the pre-synaptic membrane resulting in smooth muscle relaxation.

62
Q

Verapamil is a calcium channel blocker

A

used to treat atrial arhythmias. It slows the impulse conduction (negative dromotrope effect) in the heart and thus stabilizes the cardiac rhythm and prevents premature beats.

63
Q

Frusemide (furosemide) is a loop diuretic and works on the ascending loop of Henle in the nephron.

A

The pharmacological action is by blocking the sodium and potassium transport. The sodium and potassium are not reabsorbed but stay in the tubular fluid. This makes the extracellular fluid hypotonic and creates an osmotic pull, increasing the volume of the tubular fluid.

64
Q

Digoxin is a

A

cardiac glycoside with a positive inotropic effect. It also has negative chronotropic properties. Digoxin is used to threat atrial arhyhtmias and cardiac failure.

65
Q

Loop diuretics eg frusemide

A

Furosemide is short-acting and produces a rapid, powerful diuresis. Due to their high efficacy, loop diuretics are sometimes called ‘high-ceiling diuretics’.

This diuretic works even if the renal blood flow is decreased eg in acute or chronic renal failure.

Furosemide works mainly on the ascending loop of Henle, inhibiting sodium-potassium-chloride transporters. These electrolytes are thus all excreted, resulting in potential electrolyte imbalances.

66
Q

Thiazide diuretics eg hydrochlorothiazide or chlorthalidone

A

Thiazide diuretics work on the cortical aspect of the ascending loop of Henle and distal convoluted tubule and there they block chloride and sodium reabsorption.

The diuretic effect is milder than with furosemide but there is still a potential for hypokalaemia to occur. Other serious adverse reactions are intrahepatic cholestatic jaundice and haemmatological effects. It is a pregnancy safety category C and have been shown to cross the placenta.

67
Q

Potassium-sparing diuretics are

A

aldosterone-antagonsits with an effect on the distal convoluted tubules and collecting ducts.

They are not powerful diuretics but have the advantage of not causing hypokalaemia.

The potassium-sparing diuetics are often used in combination therapy. They are contraindicated in pregnancy.

68
Q

Osmotic diuretics

A

create an osmotic pull and water enters the proximal convoluted tubule of the nephron. These diuretics also pull water from the interstitial fluid into the systemic capillaries.

These medications are very water-soluble and are not reabsorbed from the tubular fluid.

There is a potential for dehydration or hypervolaemia and electrolyte imbalance.

69
Q

Bronchodilators are a

A

group of drugs with different modes of action but they all cause the bronchial muscles to relax and the bronchioles to open wider or dilate.

70
Q

the 3 types of bronchodilators

A

beta-2 agonists,
anticholinergics
methylxanthines

71
Q

Beta-2 agonists

A

These drugs work by stimulating the beta-2 receptors in the bronchial smooth muscles causing the muscles to relax and the bronchi to dilate.

This group of drugs can also be called a sympathomimetic or an adrenergic drug.

72
Q

Anticholinergic or antimuscarinic drugs

A

These drugs block the parasympathetic nervous system (parasympatholytic) and thus cause bronchodilation.

73
Q

Corticosteroids

A

Corticosteroids are drugs with similar structures and effects as endogenous cortisone.

The drugs decrease inflammation and are used in several forms in the treatment of many different conditions.

Corticosteroids are used by patients of all ages to treat different levels of persistent asthma. They work by reducing the inflammation in the airways which results in few asthma symptoms and fewer exacerbations.

Inhaled corticosteroids are maintenance medicines and they need to be taken regularly to prevent severe asthma symptoms. They are also called ‘preventers’ or ‘long-term control medications’.

74
Q

Antitussive medications are used to

A

suppress coughing.

These medications suppress the cough center in the medulla of the brain.

75
Q

Expectorants are used to

A

increase mucus production, decrease viscosity (mucolytic) and facilitate expectoration (coughing up) of secretions.

76
Q

Protussives will

A

stimulate a cough. This is used where there is a productive cough and airway clearance is important. This approach is beneficial in cystic fibrosis but not in most other causes of chronic cough.

77
Q

Mucolytics

A

loosen the secretions (mucus, sputum), making them less viscous

78
Q

Antihistamine drugs

A

block the effect of histamine in the body and thus prevent inflammation or ease the allergic reactions. This means the drug must be taken before exposure to an allergen or at the first signs of inflammation.

79
Q

Anti-leukotrienes and cromoglycolates

A

These drugs block the leukotriene receptors and stop the inflammatory response.

80
Q

Antacid drugs

A

have a non-specific chemical action by neutralising gastric acid, stimulating mucus and bicarbonate production to increase the protective layer in the stomach.

Antacids DO NOT prevent the over-production of acid but NEUTRALISE the acid once it is in the stomach.

The OTC antacids contain any or all of the following - sodium bicarbonate, alginic acid, aluminum, magnesium, and calcium.

Antacids are used to treat various types of reflux disease and peptic ulcers.

81
Q

H2 blockers/antagonists

A

These medications are called acid-reducers and their mode of action is to bind to the histamine receptors located on parietal cells in the gastric glands.

This makes the parietal cells less responsive to stimuli and thus acid secretion is reduced by about 70%.

H2 blockers are used to treat peptic ulcers and gastro-oesophageal reflux disease.

Commonly used H2 blockers are ranitidine and cimetidine.

Adverse effects of H2 blockers include headaches and lethargy, increased prolactin, jaundice and agranulocytosis, to mention but a few.

82
Q

Proton pump inhibitors are

A

acid reduces and are more effective than H2 blockers.

Their mode of action is to block the final step in the acid production pathway and thus all acid secretion is inhibited.

The most commonly used proton pump inhibitor is omeprazole.

83
Q

Anti-diarrhoeals

A

Both acute and chronic diarrhea can lead to fluid and electrolyte imbalances.

Although the lost fluids and electrolytes can easily be replaced, the cause (and there are many) of the diarrhoea needs to be treated.

84
Q

Adsorbents

A

These medications have the property of attracting and holding onto substances, thus they are bulking agents. This is a surface phenomenon where the adsorbate creates adhesions with the adsorbent.

Examples include kaolin, pectin, aluminum silicate and bismuth subsalicylate.

85
Q

Anticholinergics

A

Anticholinergic drugs inhibit parasympathetic nerve impulses and thus reduce spasms of smooth muscles.

Anticholinergic drugs, atropine and hyoscyamine will slow intestinal motility and relieve abdominal cramping.

86
Q

Opiates

A

Loperamide acts on the opioid receptors along the small intestine to decreasing muscle activity. This has an antidiarrheal action by slowing intestinal transit time. This may stimulate salt and water absorption.

87
Q

Intestinal flora modifiers

A

Probiotics consist of harmless organisms that interfere with the colonization of the gastrointestinal tract by pathogenic organisms.

Probiotics commonly used in the treatment of diarrhea include preparations of the bacterium Lactobacillus acidophilus.

88
Q

Drugs for constipation are laxatives and include

A

bulk-forming laxatives
osmotic laxatives
stimulant/irritant laxatives
stool softeners (emollients)

89
Q

Bulk-forming laxatives

A

These laxatives increase the bulk of the stools in a similar way to fiber. The fiber absorbs water, which will soften the stool and the increased bulk will stimulate peristalsis. Thus for these laxatives to be effective, the client needs to drink extra fluids.

Bulk-forming laxatives include unprocessed bran and fiber supplements such as psyllium, linseeds and methylcellulose.

90
Q

Osmotic laxatives

A

These laxatives work by increasing the amount of fluid secreted within the intestines, thus retaining fluid in the large bowel and less fluid is absorbed into the bloodstream. This stimulates peristalsis.

The most commonly used osmotic laxative is lactulose.

91
Q

Stimulant laxatives

A

These laxatives stimulate the nerves in the large bowel, thus speeding up the movement of intestinal muscles inducing a bowel movement.

Stimulant laxatives are generally used in the short-term treatment of constipation.

Stimulant laxatives include docusate sodium, bisacodyl and senna.

92
Q

Faecal or stool softeners

A

These work by making the faeces wetter and softer.

Bulk-forming and osmotic laxatives also have some faecal-softening properties.

The most commonly used faecal softners are docusate sodium and liquid paraffin.

93
Q

Vomiting occurs following signals from the

A

gastrointestinal tract or the labyrinth in the ear which go to the chemoreceptor trigger zone (CTZ) which then sends the message to the vomiting center in the medulla.

94
Q

The neurotransmitters involved in this process are

A

dopamine (GI tract and CTZ), histamine-1 and acetylcholine (vestibular, vomiting center, and labyrinth pathways), prostaglandins (GI tract) and serotonin (GI tract, CTZ, and vomiting center)

95
Q

The antiemetics drugs have an effect on these neurotransmitters:

A

anticholinergic drugs
antihistamines (H-1 receptor blockers)
dopamine antagonists
serotonin blockers (5-HT3 antagonists)

96
Q

Anticolinergic medications

A

The mode of action of anticholinergic antiemetic medications is to block muscarinic receptors and inhibit cholinergic transmission from the vestibular apparatus to the vomiting center. Anticholinergic drugs are muscarinic receptor antagonist.

This group of medications is used primarily to prevent or treat motion sickness.

97
Q

The antihistamine medications block

A

the H-1 receptors in the medulla oblongata. But unfortunately, they also affect the muscarinic receptors elsewhere in the CNS.

H-1 antihistamine drugs are mainly used to treat motion sickness and morning sickness.

Examples of H-1 antagonists include promethazine, cyclizine and doxylamine

98
Q

5-HT3 (serotonin) antagonist drug

A

block 5-HT3 receptors in GIT and CTZ and thus prevent vomiting.

This group of drugs is used to prevent chemotherapy or radiotherapy induced vomiting.

Examples are ondansetron

99
Q

Dopamine antagonists or prokinetic drugs block

A

dopamine D-2 receptors in the CTZ and thus produce an antiemetic action.

These medications drug also enhance the gastrointestinal motility and increases gastric emptying.

Domperidone and metoclopramide belonging to this category.

100
Q

sympathomimetic

A 
agonist 
adrenergic 
simulant
Maci
adrenaline
101
Q

sympatholytic

A

antagonist
anti-adernic
betablocker
a/b antagonist

102
Q

parasympathomimetic

A 
Muscarinic agonits
Cholinergic drug
Parasympathomimetic   drug
Anti-cholinesterase drug
agonist
103
Q

parasympatholytic

A

Parasympatholytic drug
Muscarinic antagonist
Anti-cholinergic drug
antagonist

104
Q

The parasympathetic nervous system is responsible for

A

the body’s rest and digestion response when the body is relaxed, resting, or feeding. It basically undoes the work of sympathetic division after a stressful situation. The parasympathetic nervous system decreases respiration and heart rate and increases digestion.

105
Q

The sympathetic nervous system

A

directs the body’s rapid involuntary response to dangerous or stressful situations. A flash flood of hormones boosts the body’s alertness and heart rate, sending extra blood to the muscles

106
Q

Anaemia is defined as

A

a haemoglobin level below that which would be normal for a person’s age and sex. In pregnancy this means a haemoglobin below 110 mg/L or a ferritin below 15 µmol/L.

107
Q

The most common cause of anaemia is due to

A

low iron intake (iron deficiency).

Anaemia can also be due to vitamin B12 (cyanocobalamin) or B9 (folate) deficiency.

108
Q

Common symptoms of anaemia are due to a reduced amount of oxygen in the blood.
They include

A 
feeling tired or being lethargic
feeling faint or dizzy
pallor
short of breath 
headaches
tachycardia
fingernail changes
109
Q

The median dietary iron intake in pregnant women is

A

14.7 mg/day, due to the extra 2.5 mg required during the 1st trimester and 6.6 mg (max 27 mg) in the 3rd trimester.

110
Q

The NZ Formulary recommends the following

A

Ferrous fumarate - 200mg/3xday, it has less side effects, contains 65 mg elemental of which 30% is available

Ferrous sulfate – 325mg/2xday, contains 105 mg elemental iron, with 30% availability

Ferrous gluconate – 320mg/3xday, contains 20 mg elemental iron with 12% availability

111
Q

Adverse effects include

A

gastrointestinal disturbances such as constipation or diarrhoea, epigastric pain and vomiting.

112
Q

to increase the haemoglobin

A

It takes 3 weeks of therapy

113
Q

Folic acid is a

A

water-soluble vitamin B9 found in green vegetables and liver.

Folic acid is needed for thymidine (thymine) production in DNA synthesis, cell division and growth and neural tube closure. Folic acid removes homocysteine, a protein associated with atherosclerosis.

A lack of folic acid can result in neural tube defects, cleft palate, cardiac and renal abnormmalities and megaloblastic anaemia.

The normal serum folic acid level is 5-40 nmol/L.

114
Q

Supplementation

A

400 µg/day starting 4 weeks preconception and continue till the end of 1st trimester or take 5mg tablet weekly
or start ASAP if pregnant
give 800 µg/day if there is a history of neural tube defects
add vitamin C to the regime to increase absorption

115
Q

Vitamin B12 = cynacolabalmin

A

Vitamin B12 has an important function in myelin sheath and DNA synthesis. It is also needed for normal blood and neuron function.

Vitamnin B12 absortion requires the presence intrinsic factor and pepsin to digest proteins which will help to release vitamin B12.

Vitamnin B12 is only found in animal products and is this a problem for vegans

116
Q

Treatment

A

The pregnancy needsare 2.6-4 µg/day or 1mg every 3 months.

117
Q

Analgesic medications are medicinal agents which

A

relieve or reduce pain.
This is achieved by increasing the pain threshold level in a body, interrupting the pain transmission or altering the sensory interpretation. Analgesics act both on the central and peripheral nervous systems.

118
Q

Narcotic

A

The narcotic analgesics are the medications that have an analgesic effect but also cause central nervous system depression eg loss of consciousness or respiratory depression.

Narcotic analgesics have the addictive properties of opioids and other CNS depressant agents.

The opioid analgesics are the most frequently used narcotic analgesics and they are effective for severe pain.

The examples are morphine, codeine, pethidine, and fentanyl.

119
Q

The non-narcotic analgesic medications are also called

A

non-opioid analgesics. They have an analgesic effect and may also have other properties, such as antipyretic and anti-inflammatory effects.

The non-narcotic analgesic medications do not cause physical dependencies and are available over-the-counter (OTC).

These drugs are used in the management of mild to moderate pain.

120
Q

The non-narcotic analgesics can be further subdivided.

A

Non-steroidal anti-inflammatory drug (NSAID)

121
Q

Non-steroidal anti-inflammatory drug (NSAID)

A

The non-steroidal anti-inflammatory drugs have different modes of action and varying analgesic, antipyretic and anti-inflammatory properties.

These drugs work mainly by inhibiting the cyclooxygenase (COX) enzymes but not the lipooxygenase enzymes.

The examples are ibuprofen, indomethacin and diclofenac.

122
Q

Aspirin does not fall in the NSAID group although the action is on the COX enzymes. Aspirin also works on

A

the lipooxygenase enzymes.

123
Q

Paracetamol is not an NSAID because

A

it does not have anti-inflammatory properties. The mode of action of paracetamol is on the COX enzymes.

124
Q

The NSAID have analgesic, anti-inflammatory, and antipyretic properties and their pharmacological action (mode of action) is in the peripheral and central nervous system.

These medications are

A

anti-prostaglandins or anti-histamines.

125
Q

Practice points when using NSAIDs.

A

Always take NSAIDS with food or immediately after food, to prevent stomach upset.
Use the lowest dose for the shortest possible time to provide pain relief.
Do not take more than the recommended dose and avoid using over-the-counter NSAIDs for longer than a few days without checking with a doctor or pharmacist.
Avoid taking more than one NSAID at a time.
Check all other medicines to see if they contain NSAIDs.
Tell a doctor or pharmacist about all prescribed medicines before buying any type of pain relief.
If hypertensive, check the blood pressure regularly while taking NSAIDs.
NSAIDs may not be suitable for elderly people, those with stomach, liver or kidney problems.
NSAIDs should not be taking when pregnant or if there is underlying asthma.

126
Q

Paracetamol is a

A

weak COX-inhibitor but is not an NSAID.

Paracetamol is an analgesic and antipyretic but does NOT have anti-inflammatory properties.

The clinical indication is for mild to moderate pain or fever.

The pharmacological ac–tion is mainly in the brain on the COX-3 enzymes. Here it increases the pain threshold and thermostat.

127
Q

Aspirin is a

A

pro-drug and is converted to salycilic acid.

Apirin is an irreversible COX-1 inhibitor at low doses but a COX-2 inhibitor at higher doses.

The therapeutic effect is anti-inflammatory, analgesic, antipyretic and antiplatelet.

128
Q

Local anaesthetic medications are

A

aromatic compounds, where one end is lipid-soluble and the the other end is water-soluble. They are weak bases.

The most commonly used medications are lignocaine and bupivacaine.

129
Q

The pharmacological action is by stopping the depolarization of neurons by blocking sodium channels.

A

The effect is on both sensory and motor neurons but the pain fiber are affected first because they are thinner and unmyelinated.

130
Q

The naturally occurring corticosteroids include

A

the glucocorticoids which suppress inflammation and immunity. They are also responsible for breaking down carbohydrates, fats and proteens. An example is hydrocortisone.

131
Q

The synthetic corticosteroids are

A

agonists of naturally occurring corticosteroids. These medications are used to replace corticosteroids or higher doses are used to treat immune system disorders.

132
Q

The endogenous opioids

A

(enkephalins, endorphins) stimulate the opioid receptors (mu, kappa) which affects pain transmission in the central nervous system to alter pain perception and the emotional response.

Although the opioid receptors are similar at cellular level, they have different distributions in the body and different sensitivities to the various opioid drugs, which leads to markedly different pharmacologic reactions.

133
Q

Other than the analgesic effects, opioids also cause

A

depression of vital centres – respiratory and vasomotor centers, cough center
smooth muscle relaxation – uterus (prolongs labour), urinary retention, constipation, pupil constriction
stimulation of the chemoreceptor trigger zone
decreased hypothalamic effect on the autonomic system

134
Q

Opioid receptors

A

The main receptors are called μ (mu), δ (delta) and κ (kappa). Generally, opioid analgesics are μ-agonists

135
Q

The opioids medications bind to

A

the opioid receptors on the cell membrane and this activates the cAMP and G-proteins. The result is potassium efflux and closure of the calcium channels. This causes hyperpolarisation of the post-synaptic membrane and less neuro-excitability with reduced pain transmission and altered perception and interpretation.

136
Q

Morphine has a considerably higher affinity for

A

μ-receptors than for other opioid receptors.

137
Q

Morphine is a naturally occurring derivative from chemicals in the opium poppy.

A

Morphine is the standard drug against which all other opioids are compared.

Dose: Morphine can be given orally, intramuscularly (IM), intravenously (IV), subcutaneously (SC), rectally, epidurally and intrathecally.

The intramuscular dose is 0.1-0.2 mg/kg, peak effect is reached in 30-60 minutes and the duration of action is 3-4 hours. Intravenous administration should be titrated (usually 1-2 mg boluses), but the total dose is similar. The low lipid solubility results in slow penetration of blood-brain barrier.

Pharmacokinetics: Morphine is extensively metabolised by the gut wall and the liver. Some of the metabolites are 10-20 times more potent than morphine.

Neonates are more sensitive than adults to morphine due their immature livers. Because the elderly have less body water, the peak plasma level of morphine is higher compared to younger patient.

Effects: The main effects are mediated through the mu receptors. While morphine is effective against nociceptive pain (pain resulting from tissue damage), it is also able to reduce the affective or psychological part of pain perception.

Morphine is a potent analgesic with good sedative and anxiolytic properties. It may cause cough suppression, constipation, itching. Morphine has minimal effects on cardiovascular system.

138
Q

Pethidine is a synthetic substance, with analgesic and sedative properties, but only one-tenth the potency of morphine.

A

Pharmacokinetics: Pethidine has a more rapid onset and a shorter duration of action than morphine.

Pethidine is extensively metabolised in the liver into a pharmacologically active metabolite and is thus not recommended for use in chronic pain. It can also cause central excitation and convulsions.

Effect: Unlike morphine, pethidine does not appear to delay labour.

Tolerance can be developed to pethidine and there is a high addiction potential.

The antidote for pethidine is also naloxone.

139
Q

Oxycodone hydrochloride is an opioid analgesics. It is commonly prescribed to relieve moderate to severe pain. However, there is increasing concern about the risks of using oxycodone for a long time.

A

Dose: Oxycodone comes in different forms including capsules, tablets, liquid and suppositories. It also comes in a variety of strengths with an average dose of 5- 60 mg twice daily.

Pain relief
Dizziness or faintness,  tiredness
Confusion and difficulty concentrating
Euphoria or negative mood, restlessness
Blurred vision
Stiff muscles, constipation
Dry mouth,  stomach ache and nausea
Difficulty urinating

Oxycodone comes in oral dosage forms and controlled-release tablets. Studies have demonstrated marked interindividual variation in the pharmacokinetics of oxycodone. Oral oxycodone has a higher bioavailability and a slightly longer half-life than morphine.

The pharmacokinetics of oxycodone varies considerable depending on the route of administration and the patient characteristics.

140
Q

Tramadol is an analogue of codeine and a weak agonist at all opioid receptors.

A

It also inhibits neuronal noradrenaline reuptake and potentiates the release of serotonin. The effect is inhibition of nociception.

Dose: Oral and parenteral dosage requirements are similar, 50-100 mg 4 hourly.

Pharmacokinetics: Tramadol has high oral bioavailability which can reach 100%. It has low protein binding is metabolized in the liver. in to a number of metabolites.

Effects: Tramadol has the same analgesic effect per dose as morphine. The advantage of tramadol is, it produces less constipation, respiratory and cardiovascular depression than morphine.

141
Q

Fentanyl is a synthetic phenylpyperidine derivative and has an efficacy x100 more than morphine.

A

Fentanyl is used for analgesic effects during minor surgery and it augments the effect of local anesthetics in spinal and epidural analgesia.

Dose: It comes as a solution for injection containing 50 µg/ml. It has rapid onset and short duration of action. Fentanyl can be used as a transdermal patch for chronic pain conditions and as lollipop to premedicate children.

Pharmacokinetics: Fentanyl is 500 times more lipid soluble than morphine, consequently it is rapidly and extensively distributed in the body (volume of distribution 4 L/kg). At small doses (1-2µg/kg), plasma and CNS concentration fall below an effective level during rapid distribution phase. However, following prolonged administration or with high doses, its duration of action is significantly prolonged. In these circumstances, the distribution phase is complete while the plasma concentration is still high. Recovery from the effect of the drug then depends on its slow elimination from the body (terminal half life 3.5 hours). Fentanyl is predominantly metabolised in the liver to norfentanyl which is inactive. The metabolite is excreted in the urine over few days.

Effects: Fentanyl has many properties that are similar to morphine. It produces respiratory depression in a dose-dependent manner. Large doses (50-100 µg/kg) have been used for cardiac surgery to reduce the metabolic stress response. Thus at high doses, sedation is profound and unconsciousness may occur, muscular rigidity of the chest wall may affect ventilation.

142
Q

Codeine is a natural opioid and one of the principal alkaloids of opium. It has very low affinity for opioid receptors.

A

dose: Can be given orally and IM. The dose for an adult is 30-60 mg by either route and can be repeated at 6 hours interval. Varying doses of codeine can be incorporated with NSAIDs to treat mild to moderate pain. Codeine is also used in antitussive and antidiarrhoeal preparations.

Pharmacokinetics: Oral bioavailability of codeine is 50%. About 10% of codeine is metabolised to morphine and the remainder is metabolised into inactive compounds.

Effects: Codeine causes little euphoria and thus has a low abuse potential. Codeine is less sedative effects and is less likely to cause respiratory depression than morphine.

Codeine can cause disorientation and excitement, as well as constipation.

143
Q

Naloxone is a pure opioid agonist and will reverse opioid effects at mu, kappa and delta receptor

A

Naloxone is the drug of choice for the treatment of opioid induced respiratory depression.

Dose: The dose is 200-400 µg IV. Smaller doses are used to reverse unwanted effects of the drug.

The duration of effective antagonism of naloxone is limited to around 30 minutes. Caution must be used in opioid addicts as giving naloxone may cause an acute withdrawal state with hypertension, pulmonary oedema and cardiac arrhythmias.

Effect: Naloxone is an opioid antagonist and thus has a blocking the effects on oipioid receptors.

There is an exogenous effect of stopping the exogenous opiod effect.

Adverse effects of naloxone include insomnia, anxiety, headaches and nausea.
Naloxone can save lives.

midwifery (1 decks)

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