Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

RCR1 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Is it correct to talk about ‘thinning the blood’ in reference to anti-coagulant drugs ?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the differences in thrombus formation in veins and in arteries?

A

In arteries Platelets are the dominating mass, in veins there is much more fibrin, and so it will break off much more easily.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the three pathways which contribute to thrombus formation?

A

Fibrinogen to fibrin.

RBC’s.

Collagen to platelet aggregation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What roles do plasmin and plasminogen play?

A

Plasminogen is converted to plasmin and plasmin contributes to thrombolysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is an enzyme amplification cascade?

A

Rapid generation of vast amounts of product by activation of a cascade of inactive precursor enzymes in plasma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the three different pathways that make up the coagulation cascade?

A

Extrinsic pathway

Intrinsic pathway

Common pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the contents of the common pathway that leads to coagulation?

A

Prothrombin -> Thrombin (F2)

Fibrinogen —> Fibrin (F1)

Fibrin mesh.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the contents of the Extrinsic pathway that leads to coagulation?

A

F7 —– (tissue injury) —->F7a

F10 —-> F10a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the contents of the Intrinsic pathway that leads to coagulation?

A

F12 —-> F12a
F11 —–> F11a
F9 —–> F9a
F8 ——> F10 ——> F10a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the role of vitamin K on clotting factors?

A

Helps di-carboxylate glutamate residues on clotting factors especially in factor 7, 10 and prothrombin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does warfarin interfere with the clotting mechanism?

A

It competes with Vitamin K, without any efficacy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is warfarin sodium, how’s it work and what are the antidotes?

A

an oral solution that works in the liver to produce incomplete clotting factors that can’t be activated after their release into the plasma.

Slow onset (2 days) and a slow offset (4-7 days)

Antidotes include Vit. K, plasma and whole blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the disadvantages to warfarin?

A

Has a narrow therapeutic index

The metabolism of warfarin by P450 enzymes is highly variable

Warfarin has lots of drug interactions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Examples of some drug interactions of warfarin?

A

Alcohol and Cimetidine inhibit P450 enzyme, unceasing affect of Warfarin.

phenobarbitone and phenytoin, induce P450 metabolism.

Antibiotics increase the action of warfarin.

Many herbal supplements interact.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is unfractionated heparin?

A

Natural anticoagulant made from animal gut tissue, can only be taken parenterally (not by mouth)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the mechanism of Heparin?

A

Accelerates the activity of anti-thrombin (which inhibits thrombin and factor 10)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is unfractionated heparin and it’s antidote?

A

Continuous Iv infusion of heparin, involves dose-depndent liver elimination.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Side effects of unfractionated heparin?

A

Haemorrhage, Osteoporosis, thrombocytopenia (antibodies cause thrombosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the differences and similarities of low MW heparins to standard heparin?

A

Twice the duration

Still cannot be given orally

Predictable effect, so clotting time monitoring is not necessary

Less risk of Osteoporosis and thrombocytopenia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is an example of a direct thrombin inhibitor and what are there advantages?

A

Lepirudin:

Independent of anti-thrombin III

No thrombocytopenia

No monitoring of clotting time necessary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is an example of a Direct factor Xa inhibitor? and what does it do?

A

Rivaroxaban - it inhibits activated Factor 10, and so prevents conversion of prothrombin to thrombin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Major risk factors for a thromboembolism?

A

Fracture or major surgery of pelvis, hips or legs

Major pelvic or abdominal surgery for cancer

Lower limb paralysis or amputation

Major surgery with history of DVT or PE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Minor risk factors for a thromboembolism?

A

Recent MI, HF, cancer, IBD

Trauma or burns

Aged >40 yrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Clinical uses of heparins and warfarin?

A

Prevention of DVT

Prevention of embolism

Treatment of DVT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How do you monitor clotting time in unfractionated heparin and for warfarin?

A

APTT for unfractionated heparin.

Prothrombin test for warfarin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is an example of an in-vitro anti-coagulant?

A

Calcium chelators, this works because Ca2+ is essential for F10. e.g. oxalate, citrate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the differences in asthma and COPD?

A

Asthma is bronchoconstriction caused by exposure to an allergen or non-specific stimuli such as cold air.

COPD is bronchoconstriction caused by long-term exposure to irritants such as cigarette smoke, air pollution and isocyanates.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What two receptors influence the contraction of bronchial smooth muscle? what can be given to relax the smooth muscle?

A

ß-adrenoceptors, ß-agonists can be given

Muscarinic receptors, muscarinic antagonists can given.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Difference in adrenaline and noradrenaline?

A

Adrenaline is a potent stimulus for both a and ß adrenoceptors

Noradrenaline is only potent for a adrenoceptors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is given in status asthmaticus (severe asthma attack) when there is respiratory failure.

A

Adrenaline.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is Adrenaline’s effect on the heart? (3)

A

Increased Force of contraction

Increased Heart Rate

Reduced Cardiac efficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Advantages and disadvantages of ß-2 adrenoceptor agonists? and example?

A

Rapid action
Relaxes smooth muscle regardless of stimulus

Does not affect underlying airways inflammation.

Salbutamol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Effects of too much salbutamol?

A

Skeletal muscle Tremor.
Hyperglycaemia in diabetic patients
Cardiovascular effects - arrhythmias acutely and in the long term potentially myocardial ischaemia.
Hypokalaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is an example of a longer acting ß-2 agonist?

A

Salmeterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Why are ß-antagonists (beta blockers) not given to asthmatics?

A

The antagonise ß2 adrenoceptors and can cause severe bronchoconstriction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Why are muscarinic antagonists effective? Give two examples.

A

Some irritants such as cigarette smoke can activate the Parasympathetic nervous system through muscarinic receptors and cause bronchoconstriction.

Ipratropium and oxitropium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is a better for asthma Muscarinic antagonists or ß2 agonists?

A

ß2 agonists.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Why are muscarinic antagonists of limited use in asthma, and more use in COPD?

A

They take 20-30 minutes to act and last over 4-6 hours.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Advantages and disadvantages for muscarinic antagonists?

A

Not absorbed into systemic circulation so side effects are minimal

Care has to be taken when prescribing to patients with glaucoma or prostate/bladder conditions

Side effects can include constipation and rarely tachycardia and atrial fibrillation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What other drugs (apart from ß2 agonists) can be used for asthma?

A

Xanthines
Steroids
Anti-leukotrienes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Where is the anatomical location of the adrenal gland?

A

Sitting just above the kidneys.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the four zones of the adrenal gland that synthesise hormones and what hormones do they synthesise?

A

Zona glomerulosa: Mineralcorticoids (aldosterone)

Zona fasciculata: Glucocorticoids (cortisol)

Zona reticularis: Androgens - sex hormones (testosterone)

Adrenal medulla: adrenaline (not steroids)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the precursor to all Mineralcorticoids, Androgens and Glucocorticoids?

A

Cholesterol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is cholesterols role in cell membranes?

A

Present next to phospholipids, almost one cholesterol to every phospholipid.

Makes membrane less deformable and less water-permeable.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How is cholesterol transported in the body?

A

In lipoproteins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How is cholesterol derived and synthesised in the body?

A

Derived from the diet or synthesised in hepatocytes by HMG CoA reductase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is Low-density Lipoprotein (LDL)’s role in Coronary artery disease?

A

Deposits cholesterol in fatty deposits to form atheroma’s.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the main mechanisms of action of corticosteroids?

A

Prepare for a period of starvation and dehydration:

  • Mobilising energy stores into glycogen and glucose
  • Conserving water (less urine production)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Most common Glucocorticosteroid in the body? what are it’s main actions?

A

Cortisol (hydrocortisone)

  • Mobilising nutrients (metabolism)
  • Anti-inflammatory
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Four synthetic Glucocorticosteroids (GCS) and what they are used to treat?

A

Prednisolone and dexamethasone (systemic arthritis)

Betamethasone (eczema) - topical

Fluticasone (asthma) - inhaled

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the hypothalamo-pituitary-adrenal (HPA) axis, and what is the effect of cortisol on it?

A

The combination of the hypothalamus, pituitary and adrenal cortex, cortisol inhibits their action and prepares the body for a period of starvation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are the effects of cortisol?

A

Catabolic: Hyperglycaemia, mobilisation of lipids, breakdown of proteins.

Anti-inflammatory: Decreased leucocyte activity, decreased inflammatory mediators.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the cellular mechanism of action of GCS’s?

A

They bind to cytoplasmic GCS receptors (GRs) and then modulate the transcription of many inflammatory genes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are some of the genes that GCS effects? (just need some)

A

Blocks pro-inflammatory genes:

  • Cycloxygenase-2 (source of prostaglandins)
  • Adhesions molecules, complement components.
  • Immunoglobulins (IgG and IgE)
  • Cytokines

Induces anti-inflammatory genes:

  • Ribonucleases (breaks down inflammatory mRNA)
  • Interleukin 10
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Downsides to glucocorticosteroids?

A

Slow in onset, slow in offset.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Some examples of uses of GCS (glucocorticosteroids)?

A

Asthma
Allergic diseases (eczema)
Rheumatoid Arthritis
Oedema e.g. cerebral oedema.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What can be used to inhibit metabolic OVER-production of cortisol?

A

Metyrapone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What condition is caused by over-use of GCS’?

A

Cushing’s syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Symptoms of Cushing’s syndrome?

A

Tinning of skin
Hypertension
Poor wound healing
Increased abdominal fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How are GCS drugs withdrawn?

A

By tapering the dose (removing slowly)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

In what situation is aldosterone (mineralocorticoid) released into the body, what is it’s mechanism of action and the molecular mechanism behind this?

A

Released in response to low plasma Na+ and by renin-angoitensin system.

It Acts on Mineralocorticoid Receptors (MR) in the cytoplasm of kidney tubule epithelial cells, and increases gene transcription of Na+ channels.

Increasing Na resorption and therefore water resorption. K+ and H+ are secreted instead.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is Fludrocortisone and when is it used?

A

It is an MR agonist and is used in replacement therapy in adrenal insufficiency.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is Spironolactone and when is it used?

A

Competitive MR antagonist, it has diuretic and K+ sparing actions, used with other diuretics to reduce blood volume.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

How do GCS’ achieve their anti-inflammatory effects? (3)

A

They are inhibitors of Phospholipase A2, which is the enzyme that catalyses the production of arachidonic acid. Therefore production of prostaglandins and leukotrienes is reduced.

They reduce the activity of inflammatory leucocytes

They also reduce oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Two types of asthma?

A

Extrinsic: Identifiable external trigger causing allergic reaction.

Intrinsic: No obvious trigger, tends to be more severe and difficult to control.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What can trigger asthma?

A

Inflammation: Respiratory infections, allergens

Constriction: Exercise, cold air, strong odours.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is the pathophysiology of asthma and of early and late phase asthma?

A

Early phase caused by mast cell degranulation and release of prostaglandins and leukotrienes.

Late phase caused by eosinophil granules, cytokines and leukotrienes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are the two main pharmacological approaches to asthma?

A

Relievers and preventers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What are the two main reliever drugs and how do they act on the autonomic nervous system controlling the lungs?

A

Anti-muscarinics inhibit the parasympathetic nervous system, B2 agonists stimulate the sympathetic nervous system causing bronchodilation and reduced secretions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Three types of ß2 agonists and their acting time?

A

Rimiterol 2hrs
Salbutamol 4-5hrs
Salmeterol 12-24 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Side effects of salbutamol?

A

Skeletal muscle tremor
Hypokalaemia
Arrhythmia

72
Q

How do Salmeterol and formoterol became long acting ß2 agonists?

A

Salmeterol - binds to an exposed site via a flexible tail and repeatedly stimulates the receptor

Formoterol - Dissolves into the plasma and then dissolves out to stimulate the receptor.

73
Q

What are methyxanthines, and what is their mechanism of action?

A

Bronchodilator used in asthma. They inhibit PDE which is am enzyme involved in turning cAMP to AMP, which is produced after ß-2 stimulation. there is then more cAMP which causes bronchodilation.

74
Q

Two Methyxanthines?

A

Theophylline

Aminophylline

75
Q

Features of theophylline?

A

Oral administration only

Variable gut absorption and hepatic metabolism.

Narrow therapeutic index.

76
Q

Three main anti-muscarinic asthma drugs?

A

Ipratropium

Oxitropium

Tiotropium

77
Q

Features of anti-muscarinic drugs?

A

Inhaled M1/3 antagonists

Block the parasympathetic nervous system

Few side effects as they are poorly absorbed from the lungs.

78
Q

Main drugs used to prevent asthma by treating underlying airways inflammation?

A

Corticosteroids.

79
Q

Ways in which corticosteroids reduce the symptoms of asthma?

A

Reduce the numbers of inflammatory cells such as mast cells and eosinophils

Reduces the cytokine secretion of T-lymphocytes and macrophages

Decrease mucus secretion

Increase ß2 receptors on epithelium.

80
Q

Some Corticosteroids used in the treatment of asthma?

A

Fluticasone most common oral inhaler

Oral prednisolone in severe asthma

In status asthmaticus, IV hydrocortisone can be used.

81
Q

How are side-effects of inhaled corticosteroids reduced?

A

Giving the lowest possible dose, effective inhaler technique, using drugs such as fluticasone that are inactivated by first-pass metabolism.

82
Q

What are the receptors for Ach at skeletal muscle fibres and at smooth muscle fibres?

A

Skeletal: N2

Smooth: Muscarinic

83
Q

How is the action of suxamethonium and of vecronium terminated?

A

Suxamethonium: plasma cholinesterases

Vecronium: Through redistribution and metabolism

84
Q

Side effects of Vecronium and suxamethonium?

A

Suxamethonium: Post-op muscle pain

Vecronium: no after-effects

85
Q

Side effects of neostigmine?

A

Nausea, increased salivation, sweating, nystagmus, due to stimulation of both somatic and autonomic nervous system.

86
Q

How could you reverse the effects of neostigmine?

A

Atropine (Ach antagonist)

87
Q

What drugs are used to treat organophosphate poisoning?

A

Pralidoxime and atropine later

88
Q

What would a drug such as edrophonium be used for?

A

Diagnosis of myasthenia gravis.

89
Q

True/False: suxamethonium is two molecules of Ach joined together.

A

False it is three.

90
Q

Is the duration of action of suxamethonium longer or shorter than vecronium?

A

Shorter.

91
Q

What are the main types of adverse drug reactions?

A

Type A - Augmented, dose related, due to known pharmacological action of the drug.

Type B - unpredicatable dose related reactions

92
Q

Three type A adverse drug reaction mechanisms?

A
  • exaggerated therapeutic response at target site
  • desired pharmacological effect at another site
  • additional pharmacological action
93
Q

Two main types of Type B drug reactions?

A

Type I - IgE effects on mast cells, and basophil reactions.

Type IV - Lymphocyte mediated.

94
Q

What kind of effects can Type B, I reactions cause?

A

Asthma, angiodema

95
Q

Examples of effects of Type B II reactions?

A

Skin effects, Topical epidermal necrolysis.

96
Q

How can ADR’s be diagnosed?

A

History of administered drugs

Clinical and histological examination

In vivo and in vitro lab tests.

97
Q

How can ADR’s be managed?

A

Withdrawing of the drug may be enough

Steroids can be helpful

98
Q

What are cromones?

A

Dry powder inhaler used as prophylaxis for asthmatics.

99
Q

What is the method of action of anti-leukotrienes?

A

Antagonist of Cys-LT receptor on smooth muscle and eosinophils.

Bronchodilator

Anti-inflammatory

100
Q

What is anti-IgE used to treat and how does it work?

A

Used to treat moderate-severe asthma, works by bonding to IgE in plasma and doesn’t cause mast cell degranulation.

101
Q

How do you treat status asthmaticus?

A
  • oxygen
  • nebulised β₂-agonist
  • Oral prednisolone or Hydrocortisone

If no improvement in 20 minutes:

  • Continued oxygen and β₂-agonist
  • Ipratropium
  • Mg²+
  • admit to hospital
102
Q

Steps of asthma therapy?

A

Mild - Short acting β₂ agonist

Mild persistent - Low-dose inhaled GCS

Moderate persistent - High dose inhaled GCS and salmeterol/Anti LT/Ipratropium/theophylline/cromone.

Severe persistent - Oral GCS

103
Q

Main reasons asthma treatment fails?

A

Not asthma.

Non-adhereance

Poor inhaler technique/drug interaction.

104
Q

Main two methods of pathogenesis of COPD?

A

1.

  • oxidative stress can lead to inactivation of α₁-antitrypsin
  • increase in proteases and breakdown of elastin.

2.

  • Smoke as an irritant increases mucus production
  • leads to neutrophils being recruited/infection
  • Neutrophils release elastase
105
Q

Pharmacological treatment of COPD?

A

Anti-muscarinics
β₂ agonists
Methylxanthines
Steroids

106
Q

Reasons for intentional non-adhereance?

A

Patient feels better and stops taking the drug

Patient experiences side-effects and stops taking the drug

Patient doesn’t feel the drug is working

Cost

107
Q

How can the contractility of heart be regulated in the short and long term?

A

Short term - Sympathetic drive

Long Term - Hypertrophy

108
Q

How is sympathetic down-regulation of the heart achieved?

A

Reduction in number of β₁ adrenoceptors

109
Q

What receptors on the heart can dopamine affect at different therapeutic levels?

A

What DA₁ and DA₂

With increased dosage it can affect β1 and α receptors

110
Q

What receptors on the heart can Dobutamine affect?

A

β₁ adrenoceptors.

111
Q

What is the mechanism of action of Digoxin?

A

Na and Ca exchangers blocked increasing intracellular levels of Na and Ca.

Leads to increased storage of Ca in SR, leading to increased contractility.

112
Q

What is Digoxin used to treat?

A

Heart arrhythmias e.g. Atrial fibrillation and flutter.

113
Q

What are the Neurohormonal effects of Digoxin?

A

Decreased sympathetic nervous system activity

Decreased RAAS (renin system) activity

Increased Vagal tone

114
Q

What are the haemodynamic effects of digoxin?

A

Increased Cardiac output

Increased LV diastolic pressure

Increased secretion of sodium in the kidneys (natriuresis)

115
Q

Long-term effects of Digoxin in heart failure?

A

Survival similar to placebo

Less hospital admissions

Improved exercise tolerance

More serious arrhythmias

More MI’s

116
Q

Effects of increased vagal tone caused by digoxin?

A

Slows SA node discharge

Slows AV node conduction, increases refractory period

117
Q

What is the half life for Digoxin and what does this mean for administration?

A

Half Life of 36 Hours

Long meaning a loading dose is normally required.

118
Q

Unwanted effects of Digoxin?

A

Narrow Therapeutic Index:

Anorexia
Fatigue
Arrhythmias or heart block

119
Q

When would you expect to use Digoxin?

A

In Atrial Fibrillation, with rapid ventricular response

Short term in heart failure with sinus rhythm.

120
Q

What is heart failure?

A

Any condition in which the heart cannot maintain sufficient blood flow around the body to meet the bodies needs.

121
Q

How do ACE inhibitors work and what are their effects?

A

Block the Conversion of Angiotensin I to II, blocking the RAAS pathway. They improve exercise tolerance and reduce symptoms.

122
Q

What are Angiotensin Receptor blockers and how do they work?

A

Block AT1 receptors, which bind to angiotensin II and are probably equivalent to ACE inhibitors

123
Q

Effects of Digitalis Glycosides, in heart failure?

A

Reduces symptoms
Increases exercise tolerance
Decreases risk of HF progression
Does not improve survival

124
Q

Differences in thrombosis in arteries and in veins?

A

In arteries it is a streamlined shape with mostly platelets.

In veins it is mostly fibrin due to a long fibrin tail.

125
Q

Antidote to heparin?

A

Protamine (fish protein)

126
Q

What are platelets?

A

Non-nucleated fragments of megakaryocytes, with a lifespan of 5-9 days

127
Q

What activates platelets?

A 
Von Willibrand Factor
Collagen
Thrombin
ADP
Thromboxane
128
Q

What inhibits platelets?

A

NO
ADPase
Prostacyclin (PGI₂)

129
Q

How does LOW dose aspirin work to inhibit platelet aggregation?

A

Low dose aspirin inhibits COX-1.

In platelets COX-1 goes on to produce thromboxane, which promotes aggregation. Because platelets are non-nucleated this is irreversible

In the endothelium COX-1 produces PGI₂, which is anti-aggregatory, a low dose will not permanently inhibit this.

130
Q

When would you prescribe low-dose aspirin?

A

After an MI or angina

No-prven benefits for patients without atheromatous disease

131
Q

Risks associated with low-dose aspirin?

A

Risk of GI bleed.

132
Q

What is clopidogrel?

A

A pro-drug, non-competitive antagonist of platelet ADP receptors, this reduces expression of gpIIb/IIIa and reduces aggregation.

133
Q

When would you clinically use clopidogrel?

A

Prevention of MI or stroke in symptomatic patients

After MI, and if patient is intolerant of low-dose aspirin

134
Q

Side effects of clopidogrel?

A

Severe neutropenia

GI bleeds

135
Q

An example of a gpIIb/IIIa antagonist? What is it?

A

Abciximab, immunoglobulin against gp IIb/IIIa, short plasma half-life, Given intravenously

136
Q

When would you use Abciximab?

A

In an angioplasty procedure.

137
Q

Pharmacological treatment of acute MI?

A

Angelsia: Oxygen, GTN, Heroin,

Reperfusion: Clopidogrel, streptokinase (thrombolytic), Heparin

Protect myocardium: Beta blocker, ACE inhibitor,

Prevention: low does aspirin, Statin.

138
Q

Mechanism of action of statins?

A

Inhibit HMG Co A reductase

Blocks cholesterol synthesis

Causes an increase in Hepatic LDL receptors

Less LDL in periphery as it is reuptaken by the kidney

139
Q

Possible side effects of statins?

A

Myalgia (Muscle Pain)

Rhabdomyolysis (muscle break down)

140
Q

How do Fibrates work?

A

Decrease synthesis of VLDL, Stimulate Lipoprotein Lipase.

Reduce Plasma TG by 20-50%

LDL decreased and HDL increased.

141
Q

How does nicotinic acid work?

A

Reduces VLDL release leading to reduced Plasma TG and LDL.

142
Q

What causes Corneal arcus and xanthelesmata?

A

Hypercholesterolaemia

143
Q

Why is GTN taken sublingually?

A

Because it is inactivated in First-pass metabolism.

144
Q

What is diamorphine and why is it given with cyclizine?

A

Heroin, cyclizine is an anti-emitic and will stop him throwing up due to the diamorphine.

145
Q

Normal tests for MI?

A

Blood Troponin I and ECG.

146
Q

What cells are present in Chronic and `Acute inflammation?

A

Neutrophils in acute

Macrophages in Chronic

147
Q

Where is the DVT if the whole leg is swollen?

A

At the bottom.

148
Q

What is the SOB in an Mi due to?

A

Pulmonary Oedema

149
Q

What’s a mural thrombus?

A

Thrombus in actual heart

150
Q

What’s Empyema?

A

Pus in the pleural cavity.

151
Q

What’s the difference in an obstructive and restrictive lung condition?

A

Restrictive - Cannot fully fill their lungs.

Obstructive - Can’t get air through the bronchi.

152
Q

Is emphysema Obstructive or restrictive?

A

Obstructive.

153
Q

How do most anti-anginal drugs act?

A

Reducing myocardial oxygen demand.

154
Q

What drug is often given at the time of an acute anginal attack? how does it work?

A

GTN, given sublingually, it works by mostly reducing preload, through vasodilation of the capacitance veins, can also improve collateral coronary circulation.

155
Q

Prophylactic treatment of Angina?

A

Long acting form of GTN e.g. Isosorbide

β-Blocker e.g. atenolol, to reduce cardiac work

Non-Dihydropyridine Ca+ Channel Blocker

Dihydropyridine Ca+ Channel Blocker

K+ channel opener, will dilate arterioles.

156
Q

What’s the difference in Non and Normal Dihydropyridine Ca+ channel antagonists.

A

A Dihydropyridine Ca+ channel antagonist will have effects on the peripheral circulation, causing arterial vasodilation.

A non-Dihydropyridine Ca+ channel antagonist will supplement these effects with actions on the cardiac muscle decreasing contractility, and on the SA/AV node slowing conduction.

157
Q

Difference in angina and myocardial infarction?

A

Angina is due to ischaemia for a short period (20-30mins

158
Q

How does aspirin work to reduce thrombosis?

A

It works to inhibit COX-1 in both the endothelial cells and in the platelets.

This inhibits production of thromboxane in platelets, and inhibit production of prostacylin in the endothelium.

Thromboxane: prothrombosis

Prostacyclin: platelet inhibiting (anti-thrombosis)

Platelets cannot produce anymore as they have no nucleus, however endothelial cells can produce more. if the dose is low.

159
Q

Uses for diuretics?

A

Diabetes insipidus

Kidney stones

Polycystic ovary syndrome

Osteoporosis

Hugh blood pressure

Heart failure

160
Q

Where do the CA inhibitor diuretics work?

A

upper PCT

161
Q

Where do Osmotic Diuretics work?

A

PCT, thin descending limb

162
Q

Where do loop diuretics work?

A

Thick ascending limb

163
Q

Where do thiazide diuretics work?

A

DCT

164
Q

Where do potassium sparing diuretics work?

A

start of the collecting tubule

165
Q

How do loop diuretics work?

A

Inhibit the Na+/K+/Cl- resorption in the thick ascending limb of the loop of henle

166
Q

When would you use a loop diuretic?

A

Peripheral and pulmonary oedema

Congestive heart failure.

167
Q

S/E of a loop diuretic?

A

Osteoporosis calcium loss

Hypokalaemia

168
Q

When would you use a thiazide diuretic?

A

Mild Heart failure

Hypertension

Oedema

may protect against osteoporosis

169
Q

How do thiazide diuretics work?

A

Inhibit the Na+/Cl- transporter in the DCT.

170
Q

S/E of thiazide diuretics?

A

Hypokalaemia

Hyperuricaemia (uric acid in joints - gout)

171
Q

S/E of potassium sparing diuretics?

A

Hyperkalaemia

Hyponatraemia

172
Q

How do potassium sparing diuretics work?

A

Aldosterone antagonists: Inhibits aldosterone and so less Na+/K+ transports on the basolateral membrane in the collecting tubule.

Potassium sparing: blocks the Na+ channels in the collecting tubule

173
Q

Why do loop and thiazide diuretics cause hypokalaemia?

A

They block transporters that pump K+ into the interstitium.

174
Q

How do carbonic anhydrase inhibitors work?

A

Block the H+/Na+ transporters in the proximal convoluted tubule so there is more Na+ in the lumen and less H+

175
Q

How do osmotic diuretics work?

A

e.g. Mannitol is a non-metabolised sugar which is filtered but not reabsorbed and therefore increases the osmotic concentration of the fluid in the lumen an so increase H2O diffusion into the lumen.

RCR1 (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions