Brainscape's Knowledge GenomeTM

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


See full index

P > P31 > Flashcards

P31 Flashcards

1
Q

Ramipril
Lisinopril
Captopril
Perindopril

A

ACE inhibitors

Antihypertensive!

SE:

  • Dry cough 10-20% secondary to increased bradykinin which is usually inactivated by ACE,
  • Hypotension,
  • Hyperkalaemia (lower aldosterone promotes K+ retention),
  • Worsen renal failure,
  • Angioedema,
  • Other anaphylactoid reactions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Simvastatin
Atorvastatin
Rosuvastatin

A

Statins

HMG-CoA reductase inhibitor [rate-limiting enzyme in cholesterol synthesis]

  • Inhibition reduces hepatic cholesterol synthesis
  • This leads to upregulation of LDL-receptors and increased hepatic removal of LDL from circulation

SE:

  • Headache,
  • Gastrointestinal disturbances,
  • Muscle aches,
  • Myopathy,
  • Rhabdomyolysis (rare),
  • Risk in liver enzymes (ALT) leading to drug induced hepatitis (rare)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Antianginal drug classes

A 
Beta blockers / Ca antagonist
Nicorandil if above not tolerated
Short acting nitrate
Aspirin
Lipid lowering drug
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Antihypertensive drug classes

A
  • ACE Inhibitors
  • Angiotensin receptor blockers
  • Beta blockers
  • Calcium channel blockers
  • Thiazide-like/thiazide diuretics
  • Spironolactone (aldosterone antagonist)
  • Alpha-receptor blockers
  • Loop diuretics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Atenolol
Bisoprolol
Propranolol
Metoprolol

A

Beta-blockers

Anti-anginal

SE:

  • Dizziness, fatigue, cold hands, impotence
  • Hypotension (falls in elderly)
  • Bronchoconstriction (care in asthma)
  • Bradycardia / heart block
  • Masking hypoglycaemia
  • Raynaud’s phenomenon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Diltiazem
Verapamil
Fendiline

A

Non-dihydropyridine calcium channel blockers

SE:

  • Headache
  • Flushing
  • Tachycardia
  • Peripheral oedema
  • Constipation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q 
Glyceryl trinitrate (spray)
Isosorbide dinitrate (tablet)
A

Nitrates

  • Gives rise to NO which activates PKG and reduces contraction.
  • They work on peripheral vessels mainly.
  • Dilates venous vessels to decrease preload.
  • Dilates arterial vessels to decrease afterload.
  • Increases perfusion and oxygenation of cardiac muscle.

SE:

  • Headache,
  • Postural hypotension,
  • Syncope,
  • Flushing,
  • Reflex tachycardia
  • Tolerance with prolonged use,
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Aspirin

A

COX inhibitor

Analgesic, antiplatelet

Irreversibly binds to COX and inhibits prostaglandin + thromboxane formation

SE:

  • GI irritation
  • Ulceration + haemorrhage
  • Bronchospasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

AF drugs

A

Beta blocker

Non-dihydropyrrhidine calcium channel blocker

Digoxin

Amiodarone

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

Amiodarone

A

Anti-dysarrythmic (class III)

Non-selective action sodium and calcium receptors and alpha receptors.

Amiodarone is also used in the management of tachycardias.

IV infusion in stable wide complex tachycardia. After failed cardioversion in unstable wide complex tachycardias.

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

Anticoagulation drug classes

A

LMWH

Directly acting oral anticoagulants – only apixaban and rivaroxaban licenced for use without bridging therapy with LMWH currently

Fondaparinux

Unfractionated heparin (less common now)

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

Warfarin

A

Anticoagulant

  • Inhibits vitamin K epoxide reductase
  • Prevents recycling of Vit K → functional Vit K deficiency
  • Inhibits synthesis of factors 2, 7, 9, 10, C and S
  • Initially procoagulant: protein S is depleted first
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Co-trimoxazole

A

Trimethoprim and sulfamethoxazole

These are used in combination (as co-trimoxazole) because of their synergistic activity (the importance of the sulfonamide group of antibiotics has decreased as a result of increasing bacterial resistance and their replacement by antibacterials which are generally more active and less toxic).

LRTI

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

Bendroflumethiazide
Chlorthalidone
Indapamide
Metolazone

A

Thiazide diuretics

Inhibits the Na/Cl co-transporter in the luminal membrane of the distal convoluted tubule
- Increases NaCl excretion

Indication: Hypertension,
Chronic heart failure

SE:

  • Hypokalaemia,
  • Hyponatremia
  • Metabolic alkalosis,
  • Hyperuricemia,
  • Increased glucose in DM,
  • Erectile dysfunction!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Compliance

A

Compliance – patient expected to stick to regimen prescribed by doctor, without question

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

Concordance

A

Concordance – a mutually agreed contract between doctor and patient, to take medicines in a way which suits both parties.

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

Adherence

A

Adherence – why a patient may not take medicines in the way agreed between doctor and patient:

Unintentional non-adherence – lack of understanding.

Intentional non-adherence – doesn’t actually agree with what was decided.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q 
Ipratropium
Tiotropium
Glycopyrronium
Aclidinium 
Umeclidinium
A

Muscarinic antagonists (bronchodilators - used in asthma)

Ipratropium (SAMA)
Tiotropium (LAMA)
Glycopyrronium
Aclidinium 
Umeclidinium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Salbutamol

A

Short-acting beta2 agonist (SABA)

Bronchodilator

Asthma

SE:

  • Tachycardia
  • Fine tremor (particularly in the hands);
  • Angioedema;
  • Arrhythmias;
  • Behavioural disturbances;
  • Collapse;
  • Headache;
  • Hyperglycaemia (especially when given intravenously)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Acute asthma medications

A 
Salbutamol
Ipratropium Bromide
Hydrocortisone
Magnesium sulfate
Aminophylline

IV fluids

Magnesium sulphate + aminophylline - should only be given after senior consultation

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

Magneusium sulphate

A

Bronchodilator (unlicensed use)

Severe acute asthma

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

Aminophylline

A

Aminophylline is a methylxanthine bronchodilator composed of theophylline and ethylenediamine.

MoA not completely understood.

Theophylline relaxes smooth muscle in the respiratory tract and suppresses airway stimuli.

SE:

  • Tachycardia,
  • Arrhythmia
  • Nausea/vomiting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Tiotropium

A

LAMA

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

Salmeterol

A

LABA

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

Roflumilast

A

A selective, long-acting inhibitor of the enzyme phosphodiesterase-4.

It has anti-inflammatory properties.

Adjunct to bronchodilators for the maintenance treatment of patients with severe chronic obstructive pulmonary disease associated with chronic bronchitis and a history of frequent exacerbations.

26
Q

Anti-anginal drug classes

A
  • Beta blockers / Ca antagonist
  • Nicorandil (short acting nitrate) if above not tolerated
  • Aspirin
  • Lipid lowering drug (statins)
27
Q

AF medications

A
  • Beta blockers
  • Non-DHP calcium channel blocker (Diltiazem, Verapamil, Fendiline)
  • Digoxin
  • Amiodarone
28
Q

Adrenaline

A

To protect heart and brain by peripheral vasoconstriction

Indicated in cardiac arrest

29
Q

If you suspect a pulmonary embolism what treatment should be initiated before the result of the investigation is available?

A

Low molecular weight heparin

Also could use Direct Factor Xa inhibitor (DOAC) such as apixaban or rivaroxaban.

30
Q

List some anticoagulants

A

LMWH

Directly acting oral anticoagulants (apixaban and rivaroxaban)

Fondaparinux

Unfractionated heparin (less common now)

31
Q

Dalteparin (LMWH)

Enoxaparin (LMWH)

A

Action: Anticoagulant

MOA: accelerates action of antithrombin III by increasing its inactivation of factor Xa

Use: VTE prevention. Treat DVT, PE, MI and unstable angina

Dose calculated via body weight

ADE: given subcut, renally excreted

SE: bleeding. less likely than heparin to cause thrombocytopaenia. Hypersensitivity reactions. Osteoporosis

  • Blood tests prior to starting: APTT, PT, U&Es, platelets
  • No routine monitoring
  • Takes up to 5 days to reach therapeutic range

Do COAG and FBC prior to treatment to ascertain baseline coagulation status and to ensure platelet count is normal before starting a heparin (risk of heparin induced thrombocytopenia).

32
Q

When is it safe to stop LMWH when switching to warfarin?

A

After 5 days provided the INR has been therapeutic above 2 for a minimum of 48 hours.

33
Q

High INR managment

A

Major bleeding—stopwarfarin sodium; givephytomenadione(vitamin K1) by slow intravenous injection; givedried prothrombin complex(factors II, VII, IX, and X); if dried prothrombin complex unavailable, fresh frozen plasma can be given but is less effective; recombinant factor VIIa is not recommended for emergency anticoagulation reversal

INR >8.0, minor bleeding—stopwarfarin sodium; givephytomenadione(vitamin K1) by slow intravenous injection; repeat dose ofphytomenadioneif INR still too high after 24 hours; restartwarfarin sodiumwhen INR <5.0

INR >8.0, no bleeding—stopwarfarin sodium; givephytomenadione(vitamin K1) by mouth using the intravenous preparation orally [unlicensed use]; repeat dose ofphytomenadioneif INR still too high after 24 hours; restart warfarin when INR <5.0

INR 5.0–8.0, minor bleeding—stopwarfarin sodium; givephytomenadione(vitamin K1) by slow intravenous injection; restartwarfarin sodiumwhen INR <5.0

INR 5.0–8.0, no bleeding—withhold 1 or 2 doses ofwarfarin sodiumand reduce subsequent maintenance dose

34
Q

Ezetimibe

A

Actions: inhibits absorption of cholesterol from intestine. Decreases LDL

MOA: Blocks sterol carrier protein in brush border of enterocytes. Decrease biliary and dietary cholesterol delivered to liver

Use: hypercholesterolaemia, usually adjunct to statin

SE: few. GI upsets. Headaches. Rashes. Myalgia

35
Q

Fenofibrate

Bezafibrate

A

Actions: marked decrease in plasma VLDL and triglyceride. Modest decrease in LDL and small increase in HDL

MOA: increase transcription for genes for lipoprotein lipase and apoproteins apoA1 and apoA5. Increased LDL uptake by receptors.

Use: mixed dyslipidemia.

SE: GI upset. Rash. Moderate increase in gallstones. myositis

Do not give with a statin

36
Q

Co-trimoxazole

A

Combination of:

  • Trimethoprim and
  • Sulfamethoxazole

These are used in combination (as co-trimoxazole) because of their synergistic activity (the importance of the sulfonamide group of antibiotics has decreased as a result of increasing bacterial resistance and their replacement by antibacterials which are generally more active and less toxic).

Use: pneumonia, bronchitis, infections of the urinary tract, ears, and intestines

37
Q

Causes of hyponatraemia?

A

Urinary sodium >20 mmol/L:

  • Addison’s disease
  • Thiazide + loop diuretics
  • SIADH
  • Hypothyroidism

Urinary sodium <20mmol/L:

  • Vomiting, diarrhoea
  • Burns
  • Psychogenic polydipsia
  • Renal failure
  • Secondary hyperaldosteronism: liver cirrhosis. heart failure
38
Q

Causes of hypernatraemia

A
  • Diabetes insipidus
  • Primary aldosteronism
  • Dehydration
  • Excess IV saline
  • Osmotic diuretics
39
Q

Causes of hyperkalemia

A
  • Acute renal injury
  • Metabolic acidosis
  • Addison’s disease
  • Rhabdomyolysis
  • Massive blood transfusion
  • Type 4 renal tubular acidosis
  • Drugs (ACEi, ARBs, spironolactone, amiloride, ciclosporin, heparin)
40
Q

Causes of hypokalemia

A

Haemolysis!

Hypokalemia with hypertension:

  • Cushing’s syndrome
  • Conn’s syndrome (primary hyperaldosteronism)
  • Liddle’s syndrome
  • 11-beta hydroxylase deficiency

Hypokalaemia without hypertension:

  • Thiazide diuretics
  • GI loss (diarrhoea, vomiting)
  • Renal tubular acidosis (type 1 and 2)
  • Bartter’s syndrome
  • Gitelman syndrome
41
Q

Causes of hypocalcemia

A
  • Primary hyperparathyroidism
  • Malignancy induced: bone metastases, myeloma, PTHrP from SqCC
  • Sarcoidosis
  • Vitamin D intoxication
  • Acromegaly
  • Thyrotoxicosis
  • Milk-alkali syndrome
  • Drugs: thiazides, calcium containing antacids
  • Dehydration
  • Addison’s disease
  • Paget’s disease of the bone
  • Multiple endocrine neoplasia type I
42
Q

Causes of hypocalcemia

A
  • Bisphosphonates toxicity
  • Vitamin D deficiency
  • Magnesium deficiency
  • Hypoparathyroidism
  • Pseudohypoparathyroidism
  • Rhabdomyolysis
  • Chronic kidney disease
43
Q

Hyponatremia treatment?

A

Give IV fluids to correct any hypovolaemia (0.9% NaCl or Hartmann’s)

44
Q

Beta-blocker + verapamil?

A

Can interact to cause serious bradycardia

45
Q

Antibiotics most frequently implicated in predisposition to C. difficile associated diarrhea (CDAD)?

A

Fluoroquinolones,

Clindamycin,

Broad-spectrum penicillins (amoxicillin) and cephalosporins.

46
Q

List 3 types of healthcare acquired infections that use of broad spectrum antibiotics predispose one to?

A

C difficile

MRSA

ESBL - Extended-spectrum beta-lactamases (ESBL) are enzymes that confer resistance to most beta-lactam antibiotics, including penicillins, cephalosporins, and the monobactam aztreonam.

Carbapenem resistant enterococci

47
Q

Compliance vs concordance vs adherence?

A

Compliance – patient expected to stick to regimen prescribed by doctor, without question!

Concordance – a mutually agreed contract between doctor and patient, to take medicines in a way which suits both parties.

Adherence – why a patient may not take medicines in the way agreed between doctor and patient:
Unintentional non-adherence – lack of understanding.
Intentional non-adherence – doesn’t actually agree with what was decided.

48
Q

What factors could improve medication adherence and concordance?

A

Simplification / rationalise therapy

Assessment

  • Fuller’s Self-medication screening risk assessment
  • Self medication schemes
  • Medication review service

Aids

  • Reminder charts
  • Nomad / Dosette boxes
  • Medication Record Charts
49
Q

Terbutaline

A

Short-acting beta-2 agonist

Actions: bronchodilation. Relaxes uterine smooth muscle.

MOA: decreased calcium mediated contraction in bronchioles. Increased cAMP which activates PKA. PKA inhibits myosin light chain kinase - mediator of contraction

Use: asthma. Acute attacks. COPD

Side effects: tremors, tachycardia, dysrhythmias, peripheral dilation.

Note: hypertensive crisis if used with MAO inhibitor.

50
Q

When should a low dose of ICS be started in asthma treatment?

A

A low dose of inhaled corticosteroid should be started if

  • Inhaled short-acting beta2 agonist used 3+ times a week
  • Waking at night due to asthma symptoms at least once a week.
  • BTS/SIGN (2016) also recommend initiation in patients who have had an asthma attack in the last 2 years, and starting inhaled corticosteroids at a dose appropriate to the severity of asthma.
51
Q

5 steps in asthma management

A

Step 1:
- SABA

Step 2:

  • SABA
  • ICS

Step 3:

  • SABA
  • ICS/LABA combo

Step 4:

  • SABA
  • ICS/LABA combo
  • High dose ICS

Step 5:
- Everything in step 4 plus additional treatments (montelukast)

52
Q

Montelukast

A

Class: leukotriene receptor antagonist (LTRA)

Indication: maintenance treatment of asthma and to relieve symptoms of seasonal allergies.

It is usually administered orally.

MoA: Montelukast blocks the action of leukotriene D4 on the cysteinyl leukotriene receptor CysLT1 in the lungs and bronchial tubes. This reduces bronchoconstriction otherwise caused by the leukotriene, and results in less inflammation.

Because of its method of operation, it is not useful for the treatment of acute asthma attacks.

53
Q

Formoterol vs salmeterol?

A

Formoterol and salmeterol are both long-acting bronchodilators that are effective in the treatment of asthma.

Formoterol has a rapid onset of action, whereas salmeterol causes bronchodilation in a somewhat slower manner.

Formoterol has higher intrinsic activity than salmeterol, which means that it is a full agonist, whereas salmeterol is a partial agonist on the beta2-receptor.

54
Q

SE of beta-2 agonists? (e.g. Salbutamol)

A

Tremor and tachycardia are the most frequent side effects seen in clinical practice.

  • Angioedema;
  • Arrhythmias;
  • Behavioural disturbances;
  • Collapse;
  • Fine tremor (particularly in the hands);
  • Headache;
  • Hyperglycaemia (especially when given intravenously);
  • Hypersensitivity reactions;
  • Hypokalaemia (with high doses);
  • Hypotension; ketoacidosis (especially when given intravenously);
  • Muscle cramps;
  • Myocardial ischaemia;
  • Nervous tension;
  • Palpitation;
  • Paradoxical bronchospasm (occasionally severe);
  • Peripheral vasodilation;
  • Rash;
  • Sleep disturbances;
  • Tachycardia;
  • Urticaria
55
Q

Acute asthma medications

A
  • Short-acting beta2 agonist (salbutamol)
  • Ipratropium bromide: antimuscarinic bronchodilator (LAMA)
  • Hydrocortisone
  • Magnesium sulfate: bronchodilator effect
  • Aminophylline
  • IV fluids to correct dehydration and perhaps reduce tenacity of mucous airway secretions
56
Q

Acute asthma treatment.

A

Acute asthma management is based on:

  • Assessing severity (mild/moderate, severe or life-threatening) while starting bronchodilator treatment immediately
    administering oxygen therapy, if required, and titratingoxygen saturation to target of92–95% (adults) or at least 95% (children)
    completing observations and assessments (when appropriate, based on clinical priorities determined by baseline severity).
  • Administering systemic corticosteroids within the first hour of treatment.
  • Repeatedly reassessing response to treatment and either continuing treatment or adding on treatments, until acute asthma has resolved, or patient is transferred to an intensive care unit or admitted to hospital.
  • Observing the patient for at least 1 hour after dyspnoea/respiratory distress has resolved, providing post-acute care and arranging follow-up.
57
Q

Roflumilast

A

MoA: Selective, long-acting inhibitor of the enzyme phosphodiesterase-4.

It has anti-inflammatory properties.

Indication: Adjunct to bronchodilators for the maintenance treatment of patients with severe chronic obstructive pulmonary disease associated with chronic bronchitis and a history of frequent exacerbations

58
Q

List SABAs

A
  • Bitolterol
  • Carbuterol
  • Fenoterol
  • Pirbuterol
  • Procaterol
  • Reproterol
  • Rimiterol
  • Salbutamol (albuterol)
  • Levosalbutamol
  • Terbutaline
  • Tulobuterol
59
Q

List LABAs

A
  • Bambuterol
  • Clenbuterol
  • Formoterol/Arformoterol
  • Salmeterol
  • Salmefamol
60
Q

List is LAMAs

A
  • Aclidinium bromide
  • Glycopyrronium bromide
  • Ipratropium bromide
  • Oxitropium bromide
  • Tiotropium bromide
  • Umeclidinium bromide
61
Q

List leukotriene antagonists

A
  • Montelukast
  • Pranlukast
  • Zafirlukast
62
Q

List corticosteroids used in asthma

A
  • Beclometasone
  • Betamethasone
  • Budesonide
  • Ciclesonide
  • Flunisolide
  • Fluticasone propionate
  • Mometasone
  • Triamcinolone

P (19 decks)

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