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Pharmacology > Systemic pharmacology > Flashcards

Systemic pharmacology Flashcards

1
Q

What is Haemostasis?

A

The arrest of blood loss from damaged blood vessels

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2
Q

How is haemostasis obtained endogenously?

A

A haemostatic plug is fomed involving adhesion and activation of platelets andd activation of clotting factors

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3
Q

What is thrombosis?

A

A pathological condition related to the formation of a haemostatic plug associated with arterial disease or stasis of the blood in the veins/atria of the heart

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4
Q

What is an embolus?

A

Portion of a thrombus that breaks away into the circulation

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5
Q

Where does an embolus from the veins commonly lodge?

A

In the lungs

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6
Q

Where does an embolus from the left heart commonly lodge?

A

Brain

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7
Q

What aspect related to blood flow is normally targeted in disease?

A

Therapy to promote haemostasis is rarely employed

Therapy of thromboembolic disease are extensively used due to the prevalence in the developing world.

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8
Q

Examples of drugs used to treat thromboembolic disease

A

Anticoagulants

Antiplatelets

Fibronolytic drugs

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9
Q

Example of procoagulant drug

A

Vitamin K

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10
Q

How does vitamin K increase coagulation?

A

Activates coagulation factors through y-carboxylation of glutamic acid residues

Coagulation factors targeted: II, VII, IX, X

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11
Q

What do anticoagulants target?

A

The activation of clotting factors

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12
Q

What do antiplatelets target?

A

Platelet adhesion, activation and aggregation

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13
Q

What do fibrinolytic agents target?

A

Activate plasminogen to the active enzyme plasmin

Plasmin degrades fibrin

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14
Q

What are the two forms of administering anticoagulants?

A

Injection - heparin

Oral - warfarin

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15
Q

Explain the mechanism of action of heparin

A

Accelerates the action of antithrombin II

Inactivates pro-coagulant factors

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16
Q

What form of heparin is more frequently administered

A

Low-molecular weight heparins

Due to their longer half-life

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17
Q

Advantages of injectable anticoagulants

A

Acts immediately upon intravenous administration

Acts after 1 hour following subcutaneous administration

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18
Q

Disadvantages of anticoagulants

A

Bleeding

Thrombocytopenia

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19
Q

Explain the mechanism of action of warfarin

A

Inhibits the reduction of vitamin K

Vitamin K is necessary to activate coagulation factors

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20
Q

How long does it take for the effects of warfarin to take place

A

Days

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21
Q

Examples of antiplatelet drugs

A

Aspirin

Clopidrogel

Dipyrimadole

GPIIb

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22
Q

Explain the mechanism of action of aspirin

A

Irreversibly inhibits cyclooxygenase

COX is an enzyme which forms TXA2 in platelets and PGI2 in endothelium

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23
Q

Why must the dose of aspirin be carefully controlled?

A

In platelets, COX successfully blocks TXA2 formation, promoting anticoagulation

In endothelial cells, PGI2 is useful in preventing coagulation as well

Therefore, a dose must be given which inhibits TXA2 formation in platelets whilst allowing endothelial cells to produce PGI2

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24
Q

What type of binding does aspirin make with platelets?

A

Irreversible

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25
Q

When does the effect of aspirin on TXA2 end?

A

Due to irreversible binding, the platelet cannot make more TXA2 once aspirin has carried out its effect

So platelet TXA2 is only restored when they are replaced

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26
Q

Explain the mechanism of action of Clopidogrel

A

Inhibits ADP-induced aggregation in platelet cells

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27
Q

How are fibrinolytic drugs administered?

A

Intravenously

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28
Q

Which anticoagulant drug is used for long-term therapy?

A

Warfarin

Heparin and LMWH - short term administration

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29
Q

When are drugs inhibiting thromoemboli given?

A

Myocardial infarction

Unstable angina

Coronary surgery

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30
Q

What are the main disorders of the respiratory system?

A

Asthma

Chronic obstructive pulmonary disease

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31
Q

Which NT-receptor interactions commonly cause constriction of the airway smooth muscle?

A

Upper airways = ACh acting on M3 receptors

Lower airways = NANC

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32
Q

How can lower airway smooth muscle be relaxed?

A

Inhibitory NANC transmitters

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33
Q

Innervation of blood vessel smooth muscle

A

Sympathetic innervation only

Relaxed mainly by circulating adrenaline

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34
Q

What stimulates mucus secretions from glands?

A

Parasympathetic system

Inflammatory mediators

Chemical and physical stimuli

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35
Q

What inhibits mucus secretions from glands?

A

Sympathetic system

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36
Q

Underlying physiological mechanisms of asthma

A

Reversible airway obstruction caused by inflammatory reactions

Causes bronchoconstriction and mucus secretion

Occurs in response to stimuli that are not noxious

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37
Q

Symptoms of an asthma patient

A

Difficulty breathing out

Wheezing

Coughing

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38
Q

Risk factors for development of asthma

A

Genes

Allergens

Viral infections

Pollutants

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39
Q

What are the two phases of asthma?

A

Immediate - release of spasmogens (histamine) and chemotaxins

Delayed - influx and activation of inflammatory cells which release further mediators

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40
Q

What reverses the immediate phase of an asthma attack?

A

B2-adrenoreceptor agonists

Xanthines

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41
Q

What reverses the delayed phase of an asthma attack?

A

Glucocorticoids

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42
Q

What is the aim of the drugs targeting the immediate phase of asthma attacks?

A

Reduce the bronchoconstriction

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43
Q

What is the aim of the drugs targeting the delayed phase of asthma attacks?

A

Reduce the bronchoconstriction an

Reducing the bronchial inflammation

Reducing the mucus concentration/secretion

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44
Q

Precipitating factors of an asthma attack

A

Allergens

Respiratory viral infections

Air pollutants

Exercise

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45
Q

Two types of drugs used in the treatment of asthma

A

Bronchodilators

Anti-inflammatory agents

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46
Q

Difference between first-and second-line drugs

A

First-line drugs are the most recommended drug

Second-line drugs are good alternatives

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47
Q

Examples of first-line bronchodilators

A

B2-adrenoceptor agonists

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48
Q

Examples of second-line bronchodilators

A

Xanthine compounds

Muscarinic receptor antagonists

Cysteinyl leukotriene receptor antagonists

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49
Q

Describe the mechanism of action of B2-adrenoceptor agonists

A

Physiological antagonist to spasmogenic mediators

Can be short-acting (emergency) or long-acting (preventative)

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50
Q

Examples of B- adrenoceptor agonist drugs

A

Salbutamol

Salmeterol

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51
Q

Describe the mechanism of action of xanthine compounds

A

Inhibits PDE (breaks down cAMP into AMP)

Increases cAMP and cGMP concentrations

Leads to smooth muscle relaxation

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52
Q

Why is xanthine a second line drug in the treatment of asthma?

A

Narrow therapeutic index

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53
Q

How do muscarinic receptor antagonists work?

A

Binds to muscarinic receptor subtypes and decreases acetylcholine mediated spasm

Reduces mucus secretion

Increases ciliary clearance of bronchial secretion

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54
Q

Example of a cysteinyl leukotriene receptor antagonist

A

Montelukast

Blocks leukotrienes from binding to their receptor

Inhibits the inflammatory effect of leukotrienes

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55
Q

Common anti-inflammatory agents given to asthma patients

A

Glucocorticoids

Cromoglycate

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56
Q

What phase of an asthma attack do glucocorticoids target?

A

The inflammatory component of the delayed phase

57
Q

Explain the mechanism of action of glucocorticoids

A

Reduce activation of inflammatory cells

Reduce the release of cytokines

Through blocking the transcription of inflammatory mediators

58
Q

Explain the mechanism of action of sodium cromoglycate

A

Known to block mediator release from mast cells

Reducing IgE release

But unknown effect in asthma phase

Given prophylactically by inhalation of an aerosol or powder

59
Q

What is COPD?

A

Common condition caused by chronic inflammation of the airways

Gives rise to cough

At first intermittent, then chronic

60
Q

What is the treatment of COPD?

A

Palliative

Muscarinic receptor antagonists

61
Q

What is a cough normally caused by?

A

Irritation in the bronchi and bronchioles

62
Q

To which subjects are antitussive drugs like codeine not recommended?

A

Asthma patients

Chronic bronchitis - can cause sputum retention

63
Q

What are the main functions of the kindey?

A

Excretion of waste products

Salt and water regulation

Maintain an acid-base balance

64
Q

What is the main active transport mechanism in the kidney tubule?

A

Na+/K+ ATPase

65
Q

Describe the process that occurs within the kidney during filtration

A
  1. In the renal corpuscule (glomerulus + Bowman’s capsule) ultrafiltration causes a solution without cells, proteins and large molecules to enter the Bowman’s Space
  2. The ultrafiltrate passes down to the PCT, loop of Henle and DCT, where reabsorption takes place
  3. During reabsorption, solutes and water are removed from the tubular fluid and transported into the blood
  4. Most water is reabsorbed in the collecting tube
66
Q

What is reabsorbed in the PCT?

A

50% salt and 50% water

67
Q

What is reabsorbed in the PST?

A

20 % salt and 20% water

68
Q

What is reabsorbed in the descending loop of Henle?

A

5% water

69
Q

What is reabsorbed in the thick ascending loop of Henle?

A

20% sodium

70
Q

What is reabsorbed in the DCT?

A

5% sodium

71
Q

What is reabsorbed in the collecting duct?

A

4% salt

19% water

72
Q

What is the reabsorption like in the collecting duct?

A

Highly regulated

73
Q

What is the main factor providing the osmotic gradient for AHD-mediated water reabsorption?

A

The hypertonicity of the interstitium produced by the reabsorption of salt in the thick ascending loop

74
Q

How do diuretics work?

A

Block channels reabsorbing ions like sodium

Increasing the sodium concentration in the tubules

And therefore increasing the water excretion

Water loss is secondary to salt loss

75
Q

Pharmacological actions of diuretics

A

Increase the flow of urine

Loss of K+ and H+,

Decreased excretion of uric acid (high concentration of acid in tubule)

Moderate vasodilator effects

76
Q

Differences in pharmacological action between loop and thiazide diuretics

A

Loop diuretics - Increased excretion of Ca2+ and Mg2+

Thaizide duiretics - decreased excretion of Ca2+ and increased excretion of Mg2+

77
Q

Unwanted effects of diuretics

A

Hypokalaemia due to K+ loss

Metabolic alkalosis due to H+ loss

Increased plasma uric acid

78
Q

Examples of loop diuretics

A

Furosemide

Bendolumethiazide

79
Q

What are potassium-sparing diuretics?

A

Act in the collecting tubules

Block the ENAC channels, and therefore indirectly the ROMK channels

Less potassium is secreted into the urine, and more is pumped back into the blood

Mechanisms of action include:

  • Inhibiting aldosterone’s Na+-retaining, K+-excreting effect (reduce gene expression of eNAC)
  • Inhibiting Na+ reabsoprtion and reducing K+ excretion
80
Q

Unwanted effects of potassium-sparing diuretics

A

Hyperkalaemia

Acidosis

81
Q

Mechanism of action of osmotic diuretics

A

Inert compounds pass into the tubules in the glomerulus, increasing the osmotic pressure of the filtrate

Overall effect = increase water excretion

82
Q

Which part of the nephron do osmotic duiretics primarily work on?

A

Proximal tubule

83
Q

What are the principle unwanted effects of osmotic diuretics?

A

Temporary expansion of the extracellular fluid compartment

Hyponatraemia

84
Q

What are the main physiological aspects of the GI tract?

A

Gastric acid secretion

Motility of the bowel

Excretion of the bowel contents

85
Q

What are the main pathophysiological aspects of the GI tract?

A

Peptic ulcers

Vomiting

Disturbances of excretion

Gallstones

86
Q

What leads to peptic ulcer formation?

A

Alteration of the balance between mucosal-damaging processes and mucosal-protective mechanisms

87
Q

Important factors which increase mucosal damage

A

H. Pylori

Non-steroidal inflammatory drugs

88
Q

3 main ways to treat peptic ulcers

A

Reduce acid secretion

H. pylori infection treatment

Protecting the gastric mucosa

89
Q

Pharmacological methods of reducing acid secretion

A

Histamine antagonists or proton pump inhibitors

Selective muscarinic antagonists

Antacids

PGE2 analogues

90
Q

Why are histamine antagonists and proton pump inhibitors effective at treating peptic ulcers?

A

Histamine binds to H2 receptors on parietal cells, inducing gastric acid secretion through activating the respective ion pumps

Proton pumps are essential for the movement of H+ out of the parietal cells using K+/H+ antiporter, so it can combine with Cl- and form gastric acid

91
Q

Treatment of H. pylori infection

A

Combination of proton pump inhibitor/ H2 antagonist with 2 antibiotics

Amoxicillin and metronidazole

92
Q

Pharmacological approach to protecting the gastric mucosa

A

Give compounds like Sucralfate which form complex gels on the mucosa and have a protective effect

93
Q

Unwanted effects of H2 antagonists

A

Potentiate the actions of many drugs

94
Q

Unwanted effects of drugs protecting the gastric mucosa

A

Reduce absorption of other drugs

95
Q

What stimulates acid secretion in the stomach?

A

Histamine receptors acting through Gs receptors

Acetylcholine acting on muscarinic receptors

Gastrin acting on gastrin receptors

96
Q

What are the two ways in which ACh and gastrin cause gastric acid secretion?

A

Directly through increasing the calcium concentration in parietal cells

Indirectly via the stimulation of histamine release by mast cells

97
Q

Which pathway inhibits HCl secretion?

A

Prostaglandin receptor

98
Q

Underlying physiology of vomiting

A

Complex response

Involves the coordinated activity of the involuntary muscles of the GI tract and the somatic respiratory and abdominal muscles

99
Q

Which part of the brain control vomiting?

A

Two centers in the medulla:

  • the vomiting center
  • the chemoreceptor trigger zone (CTZ)
100
Q

What stimuli activate the CTZ?

A

Disorientating motion

Toxins/drugs

Stimuli from pharynx/stomach

101
Q

What stimuli activate the vomiting center?

A

Repulsive experiences

Stimuli from pharynx/stomach

102
Q

What is the importance of the vestibular nuclei?

A

Relay the stimulus of disorientation to the CTZ

103
Q

Anti-emetics targeting the vestibular nuclei

A

H1 antagonists

Muscarinic antagonists

104
Q

Anti-emetics directly targetting the CTZ

A

D2 antagonists

5HT3 antagonists

Cannabinoids

105
Q

Anti-emetics targeting the local gut stimuli

A

H1 antagonists

Muscarinic antagonists

106
Q

What is the role of Neurokinin?

A

Control chemotherapy emesis

107
Q

What is the difficulty of oral administration of emetics?

A

Vomiting of the drugs reduces their efficacy

108
Q

What are the unwanted effects of anti-emetics?

A

Anti-histamines = drowsiness

Anti-muscarinics = dry mouth, blurry vision

D2 antagonists = extrapyramidal effects on movement, increased release of prolactin

GI imbalances

109
Q

Clinical uses of antiemetic drugs

A

5HT3 antagonists = chemotherapy

Muscarinic antagonists = motion sickness

Cannabinoids = emesis caused by cytotoxic drugs

110
Q

What, apart from emesis and peptic ulcers, are other common GI conditions?

A

Diarrhoea

Constipation

Gallstone

111
Q

Treatment for diarrhoea

A

If caused by infections = antibiotics

Replacement of fluid and electrolytes

Opiates and muscarinic antagonists = reduce motility

112
Q

Treatment for constipation

A

Bulk laxatives = not digested, stimulate peristalsis through increasing the mass of material in the gut lumen

Osmotic purgatives = retain water and increase peristalsis

Stimulate purgatives = increase mucosal secretion and stimulate enteric nerves

113
Q

Treatment for gallstones

A

Non-calcified cholesterol gallstones can be dissolved by bile acid

114
Q

What are the two main thyroid hormones?

A

T3

T4

115
Q

Compare T3 and T4

A

T3 has a faster turnover rate

T3 is found intracellularly, T4 is found in the circulation

T3 is found in target organs, T4 is bound to thyroxine-binding globulin

116
Q

Functions of thyroid hormone

A

Important for

  • growth and development
  • energy metabolism
117
Q

What is the functional unit of the thyroid?

A

The follicle

Contains a single layer of epithelial cells around the follicle unit

Containing a thick colloid composed of thyroglobulin

118
Q

What is the action of TH in metabolism?

A

Increases basal metabolic rate through increasing oxygen consumption and increasing heat production

Modulates glucocorticoids, catecholamines, insulin and glucagon
= increasing metabolism

119
Q

What is the action of TH in growth and development?

A

Potentiates growth hormones

Essential for maturation of the CNS and skeletal development

120
Q

Describe the cellular action of TH

A

T4 converts to T3 which binds to receptors on DNA

When unbound, these receptors repress basal transcription

T3 activates transcription, resulting in mRNA and protein synthesis

121
Q

Describe the release of TH

A

Stimulus (cold, trauma, stress) stimulates the hypothalamus to release thyrotrophin-releasing hormone

TRH activates the anterior pituitary to release thyrotrophin

Thyrotrophin acts on the thyroid to release T4 and T3

T4 and T3 inhibit the anterior pituitary through negative feedback, to prevent the release of T3 and T4

122
Q

Symptoms of hyperthyroidism

A

Loss of weight

Increase in temperature

Sweating

Nervousness

Tremor

Tachycardia

123
Q

Two common types of hyperthyroidism

A

Diffuse toxic goitre (Grave’s disease)

Toxic nodular goitre

124
Q

Characteristic signs of Grave’s disease

A

Exophthalmos

Increased sensitivity to catecholamines

125
Q

What is toxic nodular goitre?

A

A benign tumour

126
Q

Types of hypothyroidism

A

Myxoedema

Cretinism

Hashimoto’s thyroiditis

Radioiodine therapy induced hypothyroidism

127
Q

Signs of Myxoedema

A

Low metabolic rate

Slow speech

Mental impairment

128
Q

What is cretinism?

A

Hypthyroidism in childhood

Manifestations include retardation in growth and mental deficiency

129
Q

Features of simple non-toxic goitre

A

Hypothyroidism caused by deficiencies in iodine

Leads to a rise in thyrotrophic hormone

Increases the size of the gland

Hypothyroidism can occur

130
Q

What are the main drugs used to treat hyperthyroidism?

A

Thioureylenes

Radioiodine

Iodine

Other miscellaneous drugs

131
Q

Mechanism of action og Thioureylenes

A

Decrease the thyroid hormone output

Inhibit T4 to T3 breakdown or inhibit the oxidation of iodine

132
Q

How long do Thioureylenes take to work?

A

Weeks

Due to the iodine stores

133
Q

Unwanted effects of Thioureylenes

A

Rashes

Granulocytopenia

Headache

Nausea

Jaundice

134
Q

Mechanism of action of Radioiodine

A

Taken up by the thyroid gland similarly to iodide ions

Incorporated into the thyroid

The b-rays the iodine emits causes destruction of the nearby thyroid cells

135
Q

Unwanted effect of Radioiodine

A

Causes hypothyroidism

Will need replacement therapy with synthetic T4

136
Q

Mechanism of action of iodine

A

Temporarily reduces TH secretion

137
Q

How can other miscellaneous drugs be used to treat hyperthyroidism?

A

B-adrenoceptor antagonists decreases signs and symptoms like tachycardia, dysrhythmias, tremor and agitation

138
Q

What drugs are used to treat hypothyroidism?

A

Levothyroixine

Liothyronine

Have same actions as the natural hormones

139
Q

What are unwanted effects of Levothyroixine and Liothyronine?

A

Increase heart rate and output

Dysrhythmias

Pharmacology (13 decks)

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