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What is the target HbA1c in diabetes?

HbA1C = 6.5 – 7.5%


Outline the side effects of Metformin

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


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

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)


Glitazones. Why are they rarely used nowadays?

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


Describe the adverse side effects of GLP-1 agonists

Nausea, loose stools, diarrhoea


Describe the mechanism of action of Gliflozin

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)


Describe the adverse side effects of Gliflozin



Describe some of the secondary benefits of statin treatment

Plaque reduction
Improved endothelial cell formation
Reduced thrombotic risk


Describe the side effects of Fibric Acid derivatives

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


Describe the contraindications of Fibric Acid derivatives

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


Describe the adverse effects of Nicotinic Acid

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


What are the contraindications of Nicotinic Acid

Active liver disease or unexplained LFT elevations

Peptic Ulcer disease


What top remember about exetimibe

Circulate enterohepatically


Name some of the DNA viruses treated with antiviral agents

Herpes Simplex I
Herpes Simplex II
Epstein Barr Virus
Human Herpes Virus 8
Hepatitis B


Name some of the RNA viruses treated with antiviral agents

Influenza (x½)
Human Immunodeficiency Virus (x½)
Hepatitis C (x½)


Name and describe the different types of influenza virus

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


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

Amantadine and Rimantadine
Limited to Influenza A


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

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


Name and compare the two current Neuramidase Inhibitors

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


What strains of Influenza can neuramindise inhbitors be used for

Both Influenza A and B


Describe the ADR’s associated with Neuramidase inhibitors

GI disturbances, Headache, Nose Bleed
Rarely respiratory depression, bronchospasm (


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

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.


What is RA?

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 is RA diagnosed?

Morning stiffness >1 hr
Arthritis of >3 joints
Arthritis of hand joints
Symmetrical Arthritis
Rheumatoid Nodules
Serum rheumatoid factor
X-ray changes


What are the treatment goals in SLE and vasculitis?

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


Describe the mechanism of action of corticosteroids

Prevent IL-1 and IL-6 production by macrophages
Inhibit all stages of T-cell activation


Describe the key adverse effects of corticosteroids

Weight gain
Glucose intolerance
Avascular necrosis


How is Azathioprine used in practice?

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


Describe the main adverse effects of Azathioprine

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


WHat does Calcineurin normally do

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