Brainscape's Knowledge GenomeTM

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


See full index

Smart Revision > Last min pharm i dont know fuck fuck fuck :P > Flashcards

Last min pharm i dont know fuck fuck fuck :P Flashcards

1
Q

What is the target HbA1c in diabetes?

A

HbA1C = 6.5 – 7.5%

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

Outline the side effects of Metformin

A

Limited weight gain and ↓ CVS events
Side effects include GI symptoms
Lactic acidosis rare
Vitamin B12 deficiency uncommon

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

Outline the mechanism of action of Acrbose. Outline the adverse side effects of it.

A

Acarbose inhibits enzymes (glycoside hydrolases) needed to digest carbohydrates, specifically, alpha-glucosidase enzymes in the brush border of the small intestines and pancreatic alpha-amylase
Inhibition of these enzyme systems reduces the rate of digestion of complex carbohydrates

Less glucose is absorbed because the carbohydrates are not broken down into glucose molecules (x1)
Flatulence (x½) loose stools/diarhhoea (x½)

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

Glitazones. Why are they rarely used nowadays?

A

Concerns regarding weight gain, fluid retention, heart failure, effects on bone metabolism and bladder cancer

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

Describe the adverse side effects of GLP-1 agonists

A

Nausea, loose stools, diarrhoea

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

Describe the mechanism of action of Gliflozin

A

SGLTs are responsible for mediating glucose reabsorption in the kidneys, as well as in the gut and the heart. SGLT-2 is primarily expressed in the kidney on the epithelial cells lining the S1 segment of the proximal convoluted tubule. (x1)
It is the major transport protein that promotes reabsorption from the glomerular filtration glucose back into circulation and is responsible for approximately 90% of renal glucose reabsorption. (x1)
By inhibiting SGLT-2 it prevents renal reuptake from the glomerular filtrate and subsequently lowers the glucose level in the blood and promotes glucosuria (x1)

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

Describe the adverse side effects of Gliflozin

A

Polyuria

UTI’s

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

Describe some of the secondary benefits of statin treatment

A

Anti-inflammatory
Plaque reduction
Improved endothelial cell formation
Reduced thrombotic risk

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

Describe the side effects of Fibric Acid derivatives

A

SE – GI Upset (8%) (x1/2), Cholelithiasis (x1/2), myositis (x1/2), Abnormal LFTs (x 1/2)

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

Describe the contraindications of Fibric Acid derivatives

A

CI – Hepatic or Renal dysfunction (x ½), Pre-existing gallbladder disease (x ½)

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

Describe the adverse effects of Nicotinic Acid

A

Flushing, itching and headache
Hepatotoxicity
Activation of peptic ulcer
Hyperglycaemia and reduced insulin sensitivity

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

What are the contraindications of Nicotinic Acid

A

Active liver disease or unexplained LFT elevations

Peptic Ulcer disease

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

What top remember about exetimibe

A

Circulate enterohepatically

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

Name some of the DNA viruses treated with antiviral agents

A 
Herpes Simplex I 
Herpes Simplex II 
Varicella-zoster  
Cytomegalovirus 
Epstein Barr Virus 
Human Herpes Virus 8 
Hepatitis B
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Name some of the RNA viruses treated with antiviral agents

A 
Influenza (x½)
Human Immunodeficiency Virus (x½)
Hepatitis C (x½)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Name and describe the different types of influenza virus

A

Influenza A – Multiple host species, antigenic drift and shift
Influenza B – No animal reservoir, low mortality
Influenza C – Common cold like

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

Name the M2 Ion Channel Inhibitors and what strain of Influenza they are good for

A

Amantadine and Rimantadine

Limited to Influenza A

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

Describe which M2 Ion Channel Inhibitor has a higher risk of ADR and what the ADR’s for this class of drugs are

A

Amantadine > Rimantidine
Dizziness, GI symptoms and hypotension
Confusion, Insomnia and Hallucinations

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

Name and compare the two current Neuramidase Inhibitors

A

Zanamivir – Given as an aerosol, low bioavailability and can only be used for treatment
Oseltamivir – Prodrug and is well absorbed by contrast, can be used for treatment and prophylaxis

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

What strains of Influenza can neuramindise inhbitors be used for

A

Both Influenza A and B

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

Describe the ADR’s associated with Neuramidase inhibitors

A

GI disturbances, Headache, Nose Bleed

Rarely respiratory depression, bronchospasm (

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

Describe the four different categories that phase three clinical trails of Oseltamivir informed.

A

Symptom severity and dosing – No difference in 75 and 150mg of Oseltamivir, but marked difference between administration and placebo
Initiation of treatment – Earlier treatment, shorter duration of symptoms up. Works up to 48 hours
Mortality - ~70% reduction in mortality
Prophylaxis - Treatment for six weeks with 75 mg significantly reduced incidence of flu in both healthy adults and frail elderly subjects.

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

What is RA?

A

An autoimmune multi-system disease
Initially localised to the synovium
Inflammatory change and proliferation of synovium leading to dissolution of cartilage and bone
Pro-inflammatory cytokines > Anti-inflammatory Cytokines

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

How is RA diagnosed?

A 
Morning stiffness >1 hr 
Arthritis of >3 joints 
Arthritis of hand joints 
Symmetrical Arthritis 
Rheumatoid Nodules 
Serum rheumatoid factor 
X-ray changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the treatment goals in SLE and vasculitis?

A

Symptomatic relief
Reduction in Mortality
Prevention of organ damage
Reduction in long term morbidity

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

Describe the mechanism of action of corticosteroids

A

Prevent IL-1 and IL-6 production by macrophages

Inhibit all stages of T-cell activation

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

Describe the key adverse effects of corticosteroids

A

Weight gain
Glucose intolerance
Cataracts
Avascular necrosis

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

How is Azathioprine used in practice?

A

As maintenance therapy in SLE and Vasculitis
Inflammatory Bowel Disease
Atopic Dermatitis

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

Describe the main adverse effects of Azathioprine

A

Bone marrow suppression
Increased risk of infections
Emergence of malignant cell line

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

WHat does Calcineurin normally do

A

Calcineurin normally exerts phosphatase activity on the nuclear factor of activated T cells. This factor then migrates to the nucleus to start IL-2 transcription

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

Describe the use of calcineurin inhibitors in practice

A

Transplant patients
Inflammatory skin conditions
Selective use in some RA patients

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

Describe the adverse effects of calcineurin inhibitors

A

Nephrotoxicity
Hypertension
Hyperlipidemia
Multiple drug interactions

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

Describe the mechanism of action for Mycophenolate mofetil

A

Inhibits the enzyme inosine monophosphate dehydrogenase (required for guanosine synthesis)
Impairs B and T cell proliferation
Spares other rapidly dividing cells

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

Describe the Mycophenolate mofetil side effects

A

Nausea, vomiting, diarrhea

Most serious is myelosuppression

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

Describe the use of Mycophenolate mofetil in practice

A

Primarily used in transplantation

Good efficacy as induction and maintenance therapy for lupus nephritis

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

Describe the ADRs of Cyclophosphamide

A

Significant toxicity – Increased risk of bladder cancer, lymphoma and leukaemia
Infertility

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

Describe the mechanism of action of Methotrexate

A

Competitively and reversibly inhibits dihydrofolate reductase (DHFR), affinity 1000x more than folate

Catalyses the conversion of dihydrofolate to the active tetrahydrofolate which is the key carrier of one carbon units in purine and thymidine synthesis

Therefore inhibits the synthesis of RNA, DNA and proteins

Cytotoxic during S phase of cell cycle, greater toxic effect on rapidly dividing cells (x1)

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

Describe the adverse effects for Methotrexate

A

Mucositis
Marrow suppression
Hepatitis, cirrhosis

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

Describe the toxicity monitoring of methotrexate

A

ACR and BSR reommendations:
Baseline chest xray
Baseline FBC, LFT, U+E+Creatinine
Monthly checks

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

Describe the effects of Sulfasalazine

A

Relieve pain and stiffness (anti-inflammatory)

And fight infection (sulphonamide)

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

Describe the immunological effects of Sulfasalazine

A

T cells – Inhibition of proliferation, possible t cell apoptosis and inhibition of IL-2 production

Neutrophil – reduced chemotaxis and degranulation

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

Describe the absorption of sulfasalazine and how this is clinically useful

A

Poorly absorbed

Therefore useful for IBD

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

Describe the ADRs of Sulfasalazine

A

Myelosuppression, hepatitis, rash

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

Describe the pathophysiology of asthma

A 
Th2-driven inflammation (x1) leading to:
Mucosal oedema (x1)
Bronchoconstriction and hyper responsiveness (x1)
Mucus plugging (x1)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Describe why Beta agonists should only be used intermittently

A

Potential inhibition of mast cell degranulation if only used intermittently

On regular use of B2 agonists, mast cell degranulation in response to allergen increases

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

Describe the mechanism of action of B2 agonists

A

Act on B2 receptors which are coupled to Gs proteins
This leads to an increase in cAMP levels and consequent decrease in intracellular Ca2+
Reduces binding of Ca2+ by myosin light chain kinase
Increases Ca2+ activated K+ channels
Hyperpolorasis cells and augments bronchodilation

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

When do you begin regular preventer therapy in asthma

A

B2 agonists more than or equal to 3 times a week
Exacerbations 3 or more times a week
Waking once or more times a week
Serious exacerbations requiring oral steroids in the last two years

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

Describe the response to ICS treatment in different types of asthma

A

Patients with eosinophilic asthma have a better treatment response to inhaled corticosteroids than non-eosinophilic patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Describe the mechanism of action of Leukotriene Receptor Antagonists such as Montelukast and Zafirlukast

A

LTC4 release by mast cells and eosinophils can induce bronchoconstriction, mucus secretion, mucosal oedema and promote inflammatory cell recruitment
LRA’s block the effect of cysteinyl leukotrienes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Describe some of the side effects of Leukotriene Receptor Antagonists

A 
Angiodema
Dry Mouth
Anaphylaxis
Arthralgia
Fever
Gastric Disturbances
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Name two Methylxanthines and describe their mechanism of action

A

Theophylline and Aminophylline

Adenosine receptor antagonists
Competitive nonselective phosphodiesterase inhibitor which raises intracellular cAMP, activates PKA, inhibits TNF-alpha and inhibits leukotriene synthesis, and reduces inflammation and innate immunity

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

Describe how the size of the particle determines where they end up in inhaler devices

A

10 micron particles – deposited in mouth and oropharynx
1-5 micron particles – Most effective as they settle in small airways
0.5 microns – Too small, inhaled into alveoli and exhaled without being deposited into the lungs

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

Describe acute severe asthma in adults

A 
Any one of:
Unable to form complete sentences 
Pulse greater than or equal to 110 bpm 
Respiration greater than or equal to 25 a minute 
Peak flow 33-50% of best of predicted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

When does asthma become near fatal?

A

PaCO2 greater than 6kPa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Through what pathway are prostaglandins synthesized from? Describe this pathway

A

The arachidonic pathway

Arachidonic acid is produced from phospholipids from the cell membrane mainly via phospholipase A2
Arachidonic acid can then either enter the leukotriene pathway or the prostaglandin pathway
Arachidonic acid is then metabolised by COX 1 and 2 enzymes to produce PGH which can then produce specific prostaglandins

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

Outline the general action of Prostaglandins and the induction of a positive feedback loop

A

Bind to GPCRs
Specific action depends on receptor type binding
Autocoid release will induce the expression of COX-2 and prostaglandins themselves synergise the action of other autacoids, which mean there is a positive feedback loop present

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

Describe how prostaglandins act to induce pain and pyrexia

A

Sensitising peripheral nociception – PGE2 can bind to EP1 (Gαq-type GPCR) in C-fibres which act to inhibit K+ channels, increase Na+ channel expression and also increase neuronal sensitivity to bradykinin, resulting in an increased C-fibre activity

Sensitising central nociception – PGE2 can bind to EP2 (Gαs-type GPCR) in the dorsal horn of the spinal cord The rise in cAMP and subsequent activation of PKAs causes a reduction in glycine receptor binding affinity (where glycine acts as an inhibitor of neuronal activity), leading to increased pain reception

Pyrexia – Macrophage release of IL-1 at inflammatory sites acts on the hypothalamus to stimulate PGE2 release, acting on EP3 (Gαi-type GPCR) which causes a fall in cAMP which eventually causes an increase in CA2+ levels in the neurones regulating temperature, this results in both increased heat production and reduced heat loss

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

Describe the GI related ADR’s of NSAIDS

A

PGE2 stimulates mucus production and also inhibits acid secretion, thus inhibition of PGE2 production will result in damage directly to the stomach on ingestion and systemically
This will lead to ulceration, haemorrhage and perforation

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

Describe the renal related ADR’s of NSAIDS

A

In susceptible individuals (i.e compromised HRH individuals) use of NSAIDS can cause reduced GFR and perfusion of the kidney due to the role PGE2 has in maintaining adequate blood flow

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

Describe the vascular ADR’s of NSAIDS

A

NSAIDS will cause an increased risk of prolonged bleeding time, increased bruising and increased risk of haemorrhage due to NSAIDS inhibiting thromboxane A2 synthesis and thus reducing platelet aggregation

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

What class of patients do you need to be careful when prescribing NSAIDS and why?

A

Asthmatics

In hypersensitivity reactions, asthmatic bronchospasm can sometimes occur

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

Describe how NSAIDS are used therapeutically, specifically in combination therapies. Why do you need to be careful?

A

NSAIDS can be used in combination with low-dose opiates, extending the therapeutic range for treating pain and will also reduce the ADRs seen with increased opiate use
Use of a combination of NSAIDS can increase the risk of ADRs, as they effect one anothers binding of plasma protein

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

Describe specifically which drugs should be monitored carefully when used in combination with NSAIDS

A

Sulphonylurea – Hypoglycaemia
Warfarin– Increased bleeding
Methotrexate – Wide range of issues

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

What other therapeutic uses does aspirin have?

A

Athero-thrombotic disease prevention by acting as an anti-platelet as it prevents thromboxane A2 production
GI cancer prophylaxes

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

Describe paracetamol elimination

A

Displays linear Pharmocokinetics (x1)
90% enters phase 2 metabolism directly (60% glucoronidation and 30% sulphonation) (x1)

10% enters phase 1 oxidation to produce NAPQI (x1)

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

Describe the effects of unconjugated NAPQI

A

Highly nucleophilic
Binds with cellular macromolecules
Loss of hepatic cell function and increase in subsequent cell death as well as potential renal failure

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

Describe the treatment for paracetamol toxicity

A

Treatment given within 8 hours of overdose

If within 0-4 hours, activate charcoal orally can reduce uptake by 50-90%

0-36 hours, agents such as IV N-acetylcysteine or oral methionine can be used, which act to increase glutathione levels

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

Describe endogenous opioids

A

Can be used to modulate a pain response
Produced from precursor molecules and all contain 4 common amino acids (tyr-gly-gly-phe-)

Enkephalins – Produced from proenkephalin
Endorphins – Produced from POMC
Dynorphins – Produced from prodynorphin

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

Describe the mechanism of action of opioids

A

All are GPCRs that act to increase the outward flux of K+ ions to reduce excitability of the neurone
Decrease the influx of Ca2+ directly by inhibiting the ion channels directly Indirectly reducing the influx of Ca2+ by reducing cAMP synthesis
This fall in Ca2+ causes decreased release of neurotransmitter at the synapse

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

Describe how opioids are usually delivered

A

Enterally and parenterally

IV provides the most rapid response and avoids hepatic first-pass metabolism

Intrathecal route is often used for severe pain with the patient controlling the levels of analgesia

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

Outline the pharmacokinetics of morphine

A

M6G is the main active metabolite of morphine and acts to extend its analgesic effect
Any hepatic or renal failure will increase its half life up to 50 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Describe the pharmacokinetics of diamorphine

A

Very lipid soluble molecule so readily crosses BBB

Has to be activated by pseudocholinesterases to become activated by converting it to morphine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

When may you use methadone instead of other options

A

May use instead of other opiods

T1/2 of 15-30 hours so more suitable in chronic pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Describe the pharmacokinetics of codeine

A

Opioid which is metabolised to morphine to become activated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Describe the opioid ADRs

A 
Respiratory depression  – 
MOP mediated action on CO2 sensitivity, only seen in significant use 
Euphoria 
Constipation 
Hypotension and bronchoconstriction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What else can opioids be used to treat?

A

Diarrhoea
Heroin addiction
Following an MI
Naloxone is an opioid antagonist and can be used to for opioid toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Define mild hypertension and how it will be treated

A

140-159/90-99 mmHg

Treated depending on overall cardiovascular profile, usually non-pharmacologically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

When will pharmacological therapies begin?

A

> 160/100mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is Isolated Systolic Hypertension? Who is it common in and why?

A

Low diastolic BP with a high systolic BP (>140mmHg)

Common in increasing age occurring from the loss of compliance of elastic arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Describe how the treatment threshold for hypertension changes in diabetes

A

Threshold is 140/90mmHg

Target of <130/80mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

. What is a major issue in treating hypertension?

A

30% of patients will not take their drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What can individuals who cannot tolerate ACEi be given?

A

Angiotensin-II receptor blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Outline the mechanism of action of Calcium Channel Blockers

A

Bind specifically to the alpha subunit of L-type calcium channels, reducing calcium entry
Vasodilates the peripheral, coronary and pulmonary arteries
May have a rate-limiting effect on the heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Outline the properties of the three groups of calcium channel blockers

A

Dihydropyridines - Anti Hypertnesives
Benzothiazepines - Anti Arthymitics
Phenylalkylamines - Anti Anginals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Dihydropyridines ADRs

A

ADRs include SNS activation (tachycardia and palpitations), flushing, sweating and ankle oedema. Well tolerated (x½)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Phenylalkylamines ADRs

A

ADR’s include constipation, bradycardia and negative inotrophy

87
Q

Benzothiazepines ADRs

A

ADR’s include bradycardia and slight negative inotrophy

88
Q

What is it important to remember about the dosing of thiazide diuretics?

A

Any uptitrating of levels of thiazides will not cause any increase in response (dose-blood pressure response curve flat)
Will only cause an increase in ADRs

89
Q

Describe the ADRs seen with thiazide diuretics

A

Hypokalaemia
Increased urea and uric acid levels (gout)
Impaired glucose tolerance
Cholesterol and triglyceride levels increase

90
Q

Describe the mechanism of action and ADR’s of Alpha-Blockers

A

Act via selective antagonism at post-synaptic apha1 adrenoreceptors and antagonise the contractile effects of noradrenaline, thus reducing TPR
Postural hypotension, dizziness, headache and fatigue, oedema

91
Q

Give some endocrine causes of Hypertension

A

Conns syndrome
Bilateral Adrenal Hyperplasia
Cushings Syndrome
Phaeochromocytoma

92
Q

Give some renal causes of Hypertension

A

Chronic pyelonephritis

Diabetic Renal Disease

93
Q

Give some other causes of hypertension

A 
Pregnancy
OCP
Sleep-apnoea
Drug induced
Aorta coartation
94
Q

How is diagnosis of a phaeochromocytoma diagnosed? How is it initially treated?

A

Urinary catecholamines
Imaging
Non selective alpha-adrenoreceptor antagonists

95
Q

Define a hypertensive emergency

A

> 220/120mmHg

96
Q

Describe treatment and goals of a hypertensive emergency and the consequences of non-treatment

A

BP must be reduced around 20% within 1-2 hours otherwise acute complications such as pulmonary oedema, renal failure or aortic dissection may rapidly develop
Treatment is IV sodium nitroprusside, acting as an endogenous nitric oxide. This causes vasodilation and can produce rapid onset of reduction in BP

97
Q

How is plasmin formed?

A

Circulating plasminogen binds to the fibrin strands within a thrombus
Tissue Plasminogen Activations (regulated by PAI-1) converted plasminogen to plasmin following endothelial damage

98
Q

Describe the mechanism of action of Streptokinase

A

Binds to plasminogen and induces a conformation change to plasmin

99
Q

How is Streptokinase given? What is its half life? What are its ADR’s?

A

Given via IV infusion
15 minutes
Risk of allergic response or transient hypotension

100
Q

Give some examples of recombinant tPA’s. How do they work? How are they administered?

A

Alteplase, Reteplase and Tenecteplase
Same mechanism as natural tPA’s
IV bolus and infusion

101
Q

Describe the contra-indications for fibrinolytic therapies

A 
History of haemorrhagic stroke 
Active bleeding source 
Recent trauma or surgery 
CNS neoplasm 
Aortic Dissection 
Uncontrolled hypertension
102
Q

How should serious bleeding after fibrinolytic therapy be treated?

A

Transfusion of blood or volume expanders
Inhibition of fibrinolytics and administration of tranexamic acid (competitively inhibits the activation of plasminogen to plasmin)

103
Q

Describe the mechanism of action of carbonic anhydrase inhibitors and where they act

A

Act at PCT
Inhibit carbonic anhydrase
Affects the reabsorption rate of NA+ ions

104
Q

Why are carbonic anhydrase inhibitors rarely used nowadays? What are they used?

A

Risk of metabolic acidosis and Hypokalaemia

Used in glaucoma

105
Q

When are loop diuretics used?

A 
Heart failure (also have a slight venodilatory effect) 
Liver Failure
106
Q

What should loop diuretics not be used in combination with and why?

A

Aminoglycosides – Due to the risk of ototoxicity and nephrotoxicity
Digoxin or steroids – Risk of hypokalaemia

107
Q

Describe the mechanism of action of Thiazide diuretics

A

Act on Na+-Cl- symporter

Also promotes Ca2+ reabsorption (so can be helpful in limiting calcium loss and preventing kidney stone formation)

108
Q

X What are the main indications for thiazide diuretics? What else can they be used for?

A

Main – Heart failure Hypertension

Can also be used for kidney stones

109
Q

What drugs should thiazide diuretics not be prescribed alongside?

A

Digoxin or steroids due to risk of hypokalaemia

Beta Blockers due to risk of hyperglycaemia, hyperlipidaemia and hyperuricaemia

110
Q

Outline the mechanism of potassium sparing drugs

A

Act on the ENaC channel in the late DCT and collecting duct

111
Q

What should potassium sparing drugs not be used alongside?

A

ACE inhibitors due to risk of hyperkalaemia

112
Q

Outline the mechanism of action of Aldosterone antagonists

A

Inhibit the action of aldosterone on the mineralocorticoid receptors
Affects Na+-K+-ATPase and ENaC protein synthesis

113
Q

What are the main indications for Aldosterone Antagonists?

A

Heart failure
Hypertension
Liver Failure
Hyperaldosteronism

114
Q

Describe the mechanism of action of Warfarin

A

Prevents the production of vitamin K dependant clotting factors (II, VII, IX and X)
Vitamin K normally acts to carboxylate certain clotting factors and it turn it itself is oxidised and so must be reduced to be re-used again

Warfarin competitively antagonises the reduction of the oxidised vitamin K, meaning these clotting factors cannot be produced

As it is a competitive antagonist, warfarin can be displaced by excessive Vitamin K

115
Q

When is Warfarin used?

A

Anti-coagulant drug for deep vein thrombosis, pulmonary embolism , atrial fibrillation and mechanical prosthetic heart valves

116
Q

Describe how dose levels monitored for Warfarin? Describe the targets

A

INR of 2.0-3.0 for DVT, PE or AF (x½)
INR of 2.5-4.5 for mechanical prosthetic valves, recurrent thrombosis on Warfarin or thrombosis associated with inherited thrombophilia conditions (x½)

117
Q

Describe the main ADRs of Warfarin

A

Haemorrhage – Especially GI

Teratogenic in first trimester of Pregnancy

118
Q

Outline how Low Molecular Weight Heparin works

A

Inhibits only factor Xa and has no effect on thrombin

119
Q

Outline the pharmacokinetics of Unfractionated Heparin

A

Non-linear dose-response
Need to monitor with APTT test
Given parentally
Variable bio-availability (x1)

120
Q

Outline the pharmacokinetics of Low Molecular Weight Heparin

A

Predictable dose-response
Predictable bio-availability
No monitoring needed
Administered SC

121
Q

Describe how monitoring of heparin occurs

A

APTT test
Activated partial thromboplastin time
Measures the efficacy of the coagulation pathway

122
Q

Outline the main ADRs associated with heparin therapy in long term use!

A

Osteoporosis

123
Q

Describe the reversal of heparin therapy

A

Administer Protamine Sulphate

Dissociates heparin from ATII and bind irreversibly to heparin

124
Q

Describe the inhibition of Thromboxane A2

A

Thromboxane A2 is released from activated platelets to promote further platelet aggregation
Aspiring is a COX enzyme inhibitor and so prevents thromboxane A2 production and thus prevents platelet aggregation
Dipyridamole inhibits phosphodiesterase enzymes to inhibit thromboxane A2 production

125
Q

Give some cardiac arrhythmias that are too fast

A

Atrial Fibrillation
Ventricular tachycardia
Torsades de Pointes

126
Q

Give some cardiac arrhythmias that are too slow

A

Sinus Bradycardia

Heart Block

127
Q

What is the most commonly used Class I anti-arrhythmic? Describe its use

A

Flecainide - Class Ic

Used in the treatment and prophylaxis against paroxysmal AF (x1)

128
Q

When should Class II anti-arrhythmic drugs be used?

A

Rate-control in AF

Secondary prevention of VT or VF and heart failure

129
Q

What are the contra-indications for Class II anti-arrhythmic drugs?

A

Asthma

AV-node block

130
Q

Describe when the main Class III drug can be used and its main ADRs

A

Stable VT and SVT
Rate control of AF when other anti-arrhythmics are contra-indicated
Hepatic dysfunction, pulmonary fibrosis, peripheral neuropathy, proximal myopathy and many others

131
Q

Describe the main uses of Class IV anti-arrhythmic drugs

A

Hypertension
Angina
Rate-controlled AF
But only when beta blockers are contra-indicated

132
Q

Describe the main contra-indications of Class IV anti-arrhythmic drugs

A

Heart failure
Bradycardia
AV node block

133
Q

Describe the mechanism of action of Adenosine

A

Acts on the A1-receptor on the AV node
Hyperpolarises the cardiac conducting tissue at the AVN
Induces a transient temporary heart block

134
Q

Describe the half-life and uses of Adenosine

A

Has a half-life of a few seconds
Used to treat SVTs
Can be used to distinguish SVT as if given as the tachycardia continues, then the re-entry loop is likely to occur between the atrium and the ventricles, not at the AVN

135
Q

When can digoxin be used?

A

Used during rapid atrial fibrillation

136
Q

What are the main ADRs of Digoxin?

A

Cardiac toxicity (x1)

137
Q

What is chemotherapy?

A

The administration of cytotoxic drugs

138
Q

Describe how Alkylating Agents work

A 
Platinum compounds (eg cisplatin) 
Allowing covalent bonds to form between DNA strands (intra strand or interstrand) 
Replication cannot occur thus preventing the tumour from growing any further
139
Q

5-Flourouracil moa

A

Activated to 5-FdUMP which acts to inhibit the action of thymidylate synthase , thus preventing pyramidines to be incorporated in DN

140
Q

Methotrexate in chemo MOA

A

Inhibits dihydrofolate reductase which is necessary to form purines and thymine thus resulting in the cells unable to form DNA

141
Q

Describe some of the ADRs of chemotherapy

A

Alopecia
Pulmonary Fibrosis
Cardio toxicity

142
Q

What is the main dose-limiting toxicity in chemotherapy and also the most frequent cause of death from toxicity?

A

Haematological toxicity

Sepsis associated with haematological suppression is the most common cause

143
Q

How is chemotherapy monitored?

A

Radiological imaging
Tumour marker blood tests
Bone marrow tests
Drug levels monitored and organ damage should be checked for

144
Q

Define a seizure

A

A convulsion or transient abnormal event from episodic discharge of high frequency electrical activity in the brain

145
Q

Define epilepsy

A

The continuing tendency to have seizures, even if a long interval separates attacks

146
Q

Describe the mechanism of a seizure

A 
Large groups of neurones are activated repetitively, unrestrictedly and hyper synchronously, with inhibitory neurones failing 
A partial (focal) seizure is confined to one area of the cortex, yet can spread to cause a secondary generalisation 
Generalised seizures can also occur as a focal seizure, this can also be a primary generalised major convulsion
147
Q

Describe a tonic-clonic seizure (grand mal seizure)

A

Warning signs
Tonic phase commences – Body becomes rigid and patient falls to the floor, tongue is bitten, incontinence of urine and faeces
Clonic phase begins – Generalised convulsion, frothing at the mouth and rhythmic jerking of the muscles
Normally self-limiting and followed by drowsiness, confusion or a coma for several hours

148
Q

Describe a Typical Absence Seizure (petit mal seizure)

A

Generalised epilepsy that occurs in childhood
Patient will stare, eyelids may twitch and a few muscles jerk
Normal activity resumes
Children with typical absence attacks are more likely to develop generalised grand mal seizures as adults

149
Q

Give some examples of other partial seizure types

A

Jacksonian (focal motor seizures)

Temporal Lobe Seizures (jamais vu or déjà vu)

150
Q

Describe status epilepticus.

A

Continuous seizures without a recovery period of consciousness
Defined as a single convulsion lasting more than 30 minutes or convulsions occurring back to back with no recoqvery between them
High mortality rate

50% of cases occur without previous history of epilepsy

151
Q

How does untreated status epilepticus cause damage?

A

Physical injury relating to a fall/crash
Hypoxia
SUDEP (Sudden Death in Epilepsy)
Other dangers can include varying degrees of brain dysfunction, cognitive impairment, serious psychiatric disease

152
Q

What are the two main classes of prescribed AEDs and give some examples of each

A

Voltage-Gated Sodium Channel Blockers – Carbamazepine, Phenytoin and Lamotrigine

Enhanced GABA Mediated Inhibition – Valproate Sodium and Benzodiazepines (x1)

153
Q

Describe the action of Voltage-Gated Sodium Channel Blockers

A

Bind to the internal face of an inactivated sodium channel
Act preferentially on the neurones causing the high-frequency discharge that occurs in an epileptic fit, whilst not interfering with the low-frequency firing neurones in their normal state
Depolarisation of a neurone increases the proportion of the sodium channels in the activated state, and VGSC blockers bind preferentially to the channels in this state, preventing them from returning to a resting state where they could continue to depolarise the neurone (x1)
Thus reducing the number of functional channels available to generate action potentials

154
Q

Describe the pharmacokinetic profile of Carbamazepine

A

Strong inducer of CYP450, which metabolises it, so initial t1/2 is 30 hrs, yet with repeated use the t1/2 becomes 15hrs (x1)

155
Q

Describe the ADRs of Carbamazepine

A

CNS – drowsiness, dizziness, ataxia, motor disturbances, paraesthesia, anaesthesia
GI – nausea and vomiting
CVS – variation in BP
Other – Rashes and bone marrow suppression

156
Q

Describe the pharmacokinetic profile of phenytoin

A

Acts as a CYP450 inducer

Has non-linear PK at therapeutic levels

157
Q

Describe the ADRs of Phenytoin

A

CNS – dizziness, ataxia, headaches and nystagmus
Gingival hyperplasia (20%)
Hypersensitivity rashes

158
Q

Describe the Drug-Drug Interactions of phenytoin

A

Competitive binding with Valproate to increase plasma levels
Reduce levels of oral contraceptive
Increase cimetidine levels

159
Q

Describe the ADRs of Lamotrigine

A

CNS effects – Dizziness, Ataxia and Somnolence
Nausea
Potential for skin rashes

160
Q

Describe the drug-drug interactions of Lamotrigine

A

Adjunct therapy with other AEDs
Oral contraceptives reduce Lamotrigine plasma levels
Valproate increases levels in plasma due to competitive binding

161
Q

Describe the ADRs of Valproate Sodium

A

CNS – Ataxia and tremor

Hepatic – Increases transaminases

162
Q

Describe the DDIs of Valproate Sodium

A

Aspirin binds against it

Antidepressants and antipsychotics antagonise the action of valproate

163
Q

Outline the mechanism of Benzodiazepines and what are its uses

A

Used for status epilepticus and absence seizures

164
Q

Why are Benzodiazepines not used in first line therapy?

A

Wide range of ADRs
Include sedation, tolerance with chronic use, confusion, impaired coordination, aggression, act as abrupt withdrawal seizure triggers and respiratory and CNS depression

165
Q

Describe the basic management steps of epilepsy

A

Valproate Sodium as first line therapy from primary generalise seizures

Carbamezepine for partial seizures (although can be used for general)

Lamotrigine can be used for both generalised and partial seizures and is probably drug of choice for woman of childbearing age (due to reduced teratogenic effects and effects on OCP)

Benzodiazeines or Phenytoin for acute life-threatening status epilepticus

166
Q

Describe the classic triad of Idiopathic Parkinsons Disease

A

Tremor
Rigidity
Bradykinesia

167
Q

Describe how Myasthenia Gravis is treated and what over treatment can lead to, as well as side effects of the treatment

A

Treated with acetylcholinesterase inhibitors

Acute exacerbations can cause a Myasthenic crisis

Over treatment can lead to a cholinergic crisis (a flaccid paralysis and respiratory failure)

Side effects = SSLUDGE = Salivtion, Sweating, Lacrimation, Urinary Incontinence, Diarrhoea, GI hypermobility and Emesis (x1)

168
Q

Describe the synthesis of dopamine

A

Synthesised in the cytosol of neurones (mainly in their cell body)

L-Tyrosine → L-DOPA (x1) → Dopamine (→ Noradrenaline → Adrenaline)

169
Q

Describe how Levodopa works, and why it has minimal effect in advanced IPD. How is it ensured that Levodopa is crosses the BBB and has minimal peripheral effects?

A

Dopamine cannot cross the BBB directly, L-DOPA can and can be taken up by dopaminergic cells in the Substantia Nigra and converted to dopamine
In advanced IPD, not enough dopaminergic neurones are left so does not work
Commonly administered with a peripheral DOPA decarboxylase inhibitor so more L-DOPA crosses the BBB, rather than getting broken down

170
Q

Side effects of L-Dopa

A

side effects (N&V, hypotension, psychosis or tachycardia)

Causes involuntary movements and can cause motor complications

171
Q

Describe how Anticholinergics effect L-DOPA

A

Acetylcholine may have an antagonistic effect to dopamine

Therefore anticholinergics can have a minor role in the treatment of IPD, especially treating a tremor

No effect on bradykinesia and have side effects of confusion, drowsiness and anti-cholinergic side effects (

172
Q

What are the three core symptoms of depression?

A

Low mood
Anhedonia (lacking pleasure from anything)
Decreased energy

173
Q

Name some Selective Serotonin Reuptake Inhibitors (SSRIs) and outline how they work

A

Fluoxetine, Citalopram, Paroxetine

Act by preventing the reuptake of serotonin by the presynaptic membrane, increasing the serotonin concentration in the synaptic cleft

174
Q

Describe the main ADRs of SSRIs

A

Anorexia
Nausea
Diarrhoea
Mania and extrapyramidal syndromes

175
Q

Give some examples of Tricyclic Antidepressents and outline their mechanism of action

A

Amitriptyline or Clomipramine

Blocking both the re-uptake of serotonin and noradrenaline at the presynaptic membranes

176
Q

Why do TCAs have limited clinical use?

A

Affect multiple systems and cause multiple side effects
CNS – Sedation and impaired psychomotor function

Max.
Mark ANS – Reduced glandular secretions and eye accommodation block (x1)
CVS – Tachycardia, postural hypotension and sudden cardiac death (x1)

177
Q

Name a Serotonin-Noradrenaline Reuptake Inhibitor and describe how they work

A

Venlafxine

Cause reuptake of noradrenaline too

178
Q

Describe the ADRs of SNRIs

A

Same ADRs as SSRIs
+ Sleep disturbances, increased BP, dry mouth and hyponatraemia
Relatively short half life so may produce a withdrawal syndrome on discontinuation

179
Q

Name the positive symptoms of Schizophrenia

A

Hallucinations (a perception in the absence of an external auditory or olfactory and visual stimulus)
Disturbances of thinking
Delusions
Behavioural changes

180
Q

Name the negative symptoms of Schizophrenia

A

Social withdrawal

Unusual speech and thought

181
Q

Name the cognitive symptoms of Schizophrenia

A

Selective attention
Poor memory
Reduced abstract thought

182
Q

Name the affective symptoms of Schizophrenia

A

Anxiety

Depression

183
Q

What is the main pathophysiological theory behind the onset of Schizophrenia at the moment? What are the main CNS pathways?

A

Excess of dopamine being released by the brain
Meso-limbic pathways Meso-cortical pathway
Nigrostiatal pathways
Tubero-hypophyseal pathways

184
Q

X What is the main method of schizophrenia medication? Describe the effects

A

D2 antagonism, blocking pathways

Therapeutic responses, alongside enhanced negative and cognitive symptoms, potential dyskinesia and hyperprolactinaemia

185
Q

Give some examples of typical anti-psychotics, and describe why they are not used much clinically. When are they used?

A

Haloperidal and Chloropromazine
Regularly cause extra-pyramidal symptoms and tardive dyskinesia, thus are not used much now clinically
Haloperidal is used in acute emergency setting for sedation and tranquilisation

186
Q

Name some Atypical Anti-Psychotics

A

Olanzipine, Ripseridone, Clozapine and Quetiapine

187
Q

What will all the anti-psychotics produce in a few hours after administration?

A

Sedation and tranquilisation

188
Q

What are the main ADRs of antipsychotics?

A

Excessive weight gain – Olanzapine
Increased prolactin secretion – Ripseridone
Extra-pyramidal side effects – (Typical Anti-Psychotics)
Postural hypotension and Cardiac Toxicity leading to long QT syndrome

189
Q

How do benzodiazepines work? Why are they rarely prescribed?

A

Act on GABA receptors
Significant dependence, drowsiness, dizziness, psychomotor impairment, toxic during pregnancy
Overdose is rare but can be treated with Flumazenil

190
Q

What are the main drugs to treat bipolar?

A

Lithium (main)

Sodium valproate and carbamazepine

191
Q

Describe some of the ADRs of the main treatment and prophylaxis of bipolar

A

Memory problems, thirst, polyuria, tremor and acts as a nephrotoxin

192
Q

Describe the signaling involved and the process of acid secretion in the stomach

A

Acid secretion occurs at the parietal cells, which contain proton pumps on their apical membranes and act to pump H+ ions into the canaliculus
Stimulated by the action of gastrin on CCK-B receptors
Histamine on H2 receptors
Ach on M3 Muscarinic receptors

193
Q

What will happen if one of the receptors involved in acid secretion are blocked?

A

The others will be upregulated

Except if you block H2 receptors

194
Q

Describe how H+ ions are produced and moved.

A

Carbonic anhydrase produces HCO3- an H+ from CO2 + H2O
Produced in mitochondria of the cell
Proton pump is H+K+ATPase
HCO3- ions are transported out the basolateral membrane in exchange for Cl- ions, producing a slight elevation in blood pH

195
Q

Name the primary four H2-Receptor Antagonists

A

Cimetidine, Ranitidine, Famotidine and nizatidine

196
Q

ADRs H2-Receptor Antagonists

A

cause diarrhoea, dizziness, muscle pain and rashes

Cimetidine associated with gynaecomastia

197
Q

Name the primary four Proton Pump Inhibitors

A

Omeprazole, Ianzaprazole, Rabeprazole and

198
Q

Describe the ADRs of PPIs

A

Headache, Diarrhoea and rashes

Increased levels of Gastrin

199
Q

Describe the treatment of Helicobacter Pylori

A

1 week of clarithromycin, amoxicillin and omeprazole

Stop any NSAIDS and re-endoscopy and biopsy 6 weeks later

200
Q

Describe the process behind emesis (Vomiting)

A

Closing of the pyloric sphincter

Relaxing of cardia and oesophagus

Closure of glottis and elevation of the palate to prevent entry of the gastric contents into the trachea or nasopharynx respectively

Gastric contents being propelled by the contraction of the abdominal wall muscles and diaphragm (x1)

201
Q

Describe the neurotransmitters involved in emesis control and where they can be found

A

Vestibular Apparatus – ACh and H1
Medullary Centre – ACh, H1 and 5-HT
Vomiting Centre - Dopamine

202
Q

Describe the classification of anti-emetic drugs

A 
Dopamine D2 receptor antagonists 
5-HT3-receptor antagonist 
Anti-muscarinics 
H1-receptor antagonists 
Other
203
Q

What class does Domperidone belong to? Describe its mechanism of action. Describe its use and ADRs

A

Dopamine D2 receptor antagonist
Acts on the postrema on the floor of the 4th ventricle and also on the stomach to increase gastric emptying
Used in acute nausea and vomiting episodes
Main ADR is excessive prolactin release, producing galactorrhoea

204
Q

What class does Ondansetron belong to? Describe its mechanism of action. Describe its use and ADRs

A

5-HT3-receptor antagonist
Acts on medullary centres and reducing vagal afferent nerves from the GI tract
Given via IV administration, indicated in radiation sickness and chemotherapy treatment
ADRs are headaches, constipation and flushing

205
Q

What class does Metoclopramide belong to? Describe its mechanism of action. Describe its use and ADRs

A

D2 antagonist
Acting on the postrema on the floor of the 4th ventricle, as well as some anti-cholinergic effects and blocks vagal afferents
Normally considered first line and is safe and easy to administer
Main ADR is extra-pyramidal reactions, so should be avoided in PD

206
Q

What class does Cyclizine belong to? Describe its mechanism of action. Describe its use and ADRs

A

H1-Receptor Antagonist
Acute nausea and vomiting
Can be administered via Oral, IV or IM
ADR of prolonging QT interval

207
Q

Describe the two different types of constipation and how they will be treated

A

Soft faeces – Stimulant laxative

Hard faeces – Osmotic laxative or bulk laxative

208
Q

What could excessive use of laxatives lead to?

A

Hypokalaemia

209
Q

Describe how Bulk Laxatives work. Describe its main ADR and contra-indications

A

Bulk Laxatives – Act as a non-degradable fibre, giving bulk to the gut in order to aid peristalsic action Takes a few days to work

Main ADR is flatulence
Should not be given to any patients with any ulcerations or adhesions

210
Q

Describe how Osmotically Active Laxatives work and give an example. When are they used?

A

Movicol
Cause water retention in the small and large bowel to increase peristalsis
Normally given PR and can act quickly and severely, so should be only be used for any ‘resistant’ constipation or urgent relief

211
Q

Describe how stimulant laxatives work and give an example. Describe when they are used. What can abuse lead to?

A

Senna, Bisacodyl
Excite the sensory nerve ending leading to water and electrolyte retention and thus a peristalsic action
Used for rapid treatment such as faecal impaction or surgical preparation. Act within 6-8 hrs so are administered overnight
Any abuse can lead to melanosis coli

212
Q

Describe how Anti-Motility Drugs work in the pharmacological treatment of Diarrhoea. Give an example and when it is used and its contraindication

A

Loperamide
Opiate analogue to reduce GI motility
Good for chronic diarrhoea
Should be avoided in IBD due to risk of toxic megacolon

213
Q

Describe how Bulk Formin Agents work in the pharmacological treatment of Diarrhoea. Give an example and when it is used.

A

Ispaghula
Increase water absorption by the gut to influence the faecal composition
Particularly useful for patients with IBS and those with an ileostomy

Smart Revision (7 decks)

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