Facts Learnt In Practice Flashcards
(24 cards)
What is the fast acronym for stroke
Face weakness: Can the person smile? Has their mouth or eye drooped?
Arm weakness: Can the person raise both arms fully and keep them there?
Speech problems: Can the person speak clearly and understand what you say? Is their speech slurred?
Time to call 999: if you see any one of these signs.
What were the findings of the CTT meta analysis of statins in 2010?
for every 1mmol/L reduction in LDL cholesterol, there is a 22% reduction in major vascular events.
Why are antihistamines often prescribed in liver failure
Causes itchy skin
Why do you need to be cautious of drugs that cross the BBB in renal impairment
When patients have Renal dysfunction they also have altered BBB
increased BBB permeability
Cautious of drugs that cause CNS side effects
Why would patients with hepatic dysfunction have to be assessed in more depth for VTE prophylaxis
Clotting factors are made in the liver, if liver works less then more likely to bleed
Why is Iv iron used in heart failure instead of oral and why is oral iron no longer multiple daily dosing
• Heart failure is often associated with gut edema and reduced gut perfusion, which impair oral iron absorption.
• Additionally, inflammation in chronic disease raises hepcidin levels, which further blocks iron absorption from the gut.
• Oral iron doses stimulate hepcidin production, especially when taken frequently (e.g. TDS). • Hepcidin peaks around 6–24 hours after a dose and can block further iron absorption from subsequent doses. • So, with TDS dosing, the body may absorb less iron overall due to consistently elevated hepcidin levels.
What key information is there regarding Vanc and Fidaxomycin treatment for C.Diff
- SEs
- Bioavailabbility
- Use
Fidaxomycin is given for C.Diff reoccurence according to NICE guideline. However the hospital sometimes use it 1st line in pts at higher risk of reoccurence such as elderly or immunocompromised.
Fidaxomycin and Vancomycin have minimal systemic side effects when used to treat C. Diff because they are taken orally. They both have poor bioavailabilty and therefore have minimal absorbance systemically. therefore SEs like Nephrotoxicity and Ototoxicity are not prevalent in C.diff treatment with Vanc.
Fodaxomycin reduces likelihood of C.diff reoccurence, however is much more expensive than Vanc.
If Fidaxomycin is not effective at preventing reoccurence when used previously then it is not used routinely again as C.diff infections reoccurence increases with each infection. Only get one Pop with fidoxy basically.
What method did Danielle teach you to remember the difference between stroke and Acute coronary syndrome treatment
3 As, a B and a C
Aspirin, ACE, Atorvastatin, Betablocker and Clopidogrel.
Double As
Aspirin, Atorvastatin
What is a key reason that paroxetine is a less favourable SSRI?
The half life is extremely short so even a patient only misses one day they can experience withdrawal symptoms
WHy dont some people on clozapine feel constipated?
Clozapine strongly blocks muscarinic (M1–M5) receptors, which:
Slows intestinal peristalsis (gut movement).
Reduces visceral sensation, so patients may not feel bloated or uncomfortable despite severe constipation.
What value should the trough of gentamicin always be below in order to work out future doses
Below 1
Why does salbutamol cause tachycardia and tremor
Cross reactivity with B1 cells
Causes similar affects to Adrenaline
What are the three criteria for calculating apixaban dosing in AF
Age - 80years
Creatinine - 133
Weight - 60kg
CrCl - less than 30
What is the difference between methylprednisolone sodium succinate and methylprednisololne acetate
- Methylprednisolone Sodium Succinate (e.g. Solu-Medrone®)
Formulation: Water-soluble salt
Route: IV or IM
Onset: Rapid
Use:
Emergency or acute settings (e.g. acute asthma, anaphylaxis, severe Crohn’s disease)
Systemic conditions requiring immediate high-dose corticosteroids
Absorption: Rapid absorption and onset of action
Duration: Shorter compared to acetate (due to rapid metabolism)
- Methylprednisolone Acetate (e.g. Depo-Medrone®)
Formulation: Lipid-soluble suspension
Route: IM, intra-articular, intralesional (not IV)
Onset: Slower
Use:
Long-acting steroid effect
Chronic inflammatory conditions (e.g. rheumatoid arthritis, allergic disorders)
Used when prolonged action is needed but IV access isn’t required
Absorption: Slow release from injection site
Duration: Longer (days to weeks depending on dose and route)
Explain the physiology of Angina
Think of the blood vessels endothelium as a New Table, if you pour oil over the table because its new it will be easy to clean up. This is what the endoleium should be like.
However over time different factors such as HTN, Diabetes, Smoking, High lipids, Alcohol cause irritation to this endothelial lining.
This is like with the table, overtime irritation will cause crevices. This then would mean that the oil would be harder to clean up.
therefore atherosclerotic plaques are able to build up.
When exercising the body increases heart rate, blood pressure any oxygen demands. To increase the blood pressure the body causes vasoconstriction to the blood vessels.
If a plaque is present and the blood vessels constrict then this reduces blood flow through.
This then reduces the amount of oxygen that is able to make it to the muscles of the heart.
angina occurs when the heart muscle (myocardium) doesn’t get enough oxygen-rich blood, usually due to reduced blood flow through the coronary arteries. This imbalance between oxygen supply and demand leads to chest pain or discomfort, often triggered by physical activity or stress, when the heart needs more oxygen.
(RHYS - cardiology pharmacist)
How do ACE inhibitors and betablockers affect left ventricular remodelling in ACS
ACE inhibitors and beta-blockers both play key roles in preventing and reversing left ventricular (LV) remodeling after an acute coronary syndrome (ACS), especially myocardial infarction (MI). Here’s how each works:
🫀 Left Ventricular Remodeling in ACS:
After a myocardial infarction (MI), damaged heart muscle undergoes structural changes — this is LV remodeling. It involves:
Dilation of the LV
Wall thinning
Shape distortion
Progressive loss of function, leading to heart failure
This process is driven by:
Neurohormonal activation (especially RAAS and sympathetic nervous system)
Mechanical stress on the heart
🟦 1. ACE Inhibitors (e.g., ramipril, lisinopril)
📌 Mechanism of action:
Inhibit the renin-angiotensin-aldosterone system (RAAS)
↓ Angiotensin II → less vasoconstriction, aldosterone release, and hypertrophy
↓ Afterload and preload → reduced stress on the heart
Reduce fibrosis and myocardial cell death
💡 Effect on LV remodeling:
Prevent ventricular dilation and fibrosis
Improve survival and reduce heart failure progression
Best started early after MI, especially in anterior MI, LV dysfunction, or heart failure
🟩 2. Beta-Blockers (e.g., bisoprolol, metoprolol, carvedilol)
📌 Mechanism of action:
Block β1-adrenergic receptors → ↓ heart rate and contractility
Reduce myocardial oxygen demand
Inhibit harmful effects of excess sympathetic activity
Antioxidant and anti-apoptotic effects (especially carvedilol)
💡 Effect on LV remodeling:
Reduce myocardial wall stress and infarct size
Help preserve LV function
Lower risk of arrhythmias, re-infarction, and mortality
Also best started early unless contraindicated (e.g., bradycardia, hypotension, acute heart failure)
When is Troponin elevated and when is BNP elevated?
HF in acute status - causes raised BNP
Heart attack of Myocardial injury causes raised troponin
Why do individuals with heart failure get pulmonary oedema and ankle swelling?
In Heart failure due to the reduced ejection fraction not all of the blood leaves the left ventricles.
- Blood Pooling in the Left Ventricle
Because the ventricle doesn’t contract properly, some blood remains in the left ventricle after each beat.
This increases end-diastolic volume and pressure, leading to left ventricular dilation over time.
- Backward Pressure to the Left Atrium and Pulmonary Circulation
The increased pressure backs up into the left atrium and then into the pulmonary veins.
This elevated pulmonary venous pressure pushes fluid from the blood vessels into the lung tissue, causing pulmonary oedema.
Symptoms: breathlessness, orthopnoea, paroxysmal nocturnal dyspnoea.
- Progression to Right Heart Involvement
If pressure continues to rise, it can affect the right side of the heart (cor pulmonale).
This results in systemic venous congestion, causing:
Peripheral oedema (e.g. ankle swelling)
Hepatic congestion
Jugular venous distension
- Valve Regurgitation
Chronic volume overload and dilation of the heart chambers can cause functional valve regurgitation (e.g., mitral regurgitation), worsening heart failure symptoms. - Management with Diuretics (e.g., Furosemide)
Furosemide, a loop diuretic, is used to relieve fluid overload symptoms.
It promotes diuresis, reducing pulmonary and peripheral oedema.
However, it does not improve mortality – it’s mainly for symptomatic relief.
Why does orthopnoea occur in heart failure?
Orthopnoea is shortness of breath that occurs when lying flat and improves when sitting or standing upright. It’s a classic symptom of left-sided heart failure.
🫁 Why does it happen?
When a person with heart failure lies flat, the following occurs:
Increased venous return to the heart
Lying down causes redistribution of fluid from the lower body and abdominal circulation back into the chest (thoracic circulation).
This increases preload (volume returning to the heart).
The failing left ventricle can’t handle the extra volume
In heart failure, the left ventricle is already struggling to pump blood effectively.
The increased preload causes blood to back up into the pulmonary circulation.
Pulmonary congestion worsens
Fluid builds up in the alveoli and interstitial spaces of the lungs.
This impairs gas exchange and leads to shortness of breath.
Sitting upright helps
In the upright position, gravity pulls fluid down to the bases of the lungs and lower extremities.
This reduces venous return, decreases pulmonary pressure, and relieves symptoms.
How does cancer affect thrombotic risk
Increases it
How do crohns and IBD affect thrombotic risk
Increases it
Which antiemetic causes a high in some patients
Cyclizine
What are the rules with new diabetic medications being bought to market
They have to be able to prove cardiovascular benefit/safety as well as glucose lowering effects
What is the sponge analogy for the pancreas and sulphonylureas vs Metformin
🧽 Pancreas as a Sponge: The Analogy
Think of the pancreas as a sponge filled with insulin. When squeezed, it releases insulin into the bloodstream.
⸻
💊 Sulfonylureas: Squeezing the Sponge
• Sulfonylureas (e.g. gliclazide, glibenclamide) work by directly stimulating insulin release from the beta cells of the pancreas — like squeezing the sponge, regardless of whether the body actually needs more insulin or not.
• This action is glucose-independent, meaning they will stimulate insulin even if blood glucose is normal or low.
🔴 Result: Can lead to too much insulin, dropping blood glucose too low → risk of hypoglycaemia.
⸻
💊 Metformin: Making the Body Use Water Better
• Metformin doesn’t squeeze the sponge. Instead, it works by:
• Reducing liver glucose production
• Increasing insulin sensitivity (helping muscles use glucose more effectively)
• Reducing glucose absorption in the gut
• Importantly, metformin does not stimulate insulin release at all.
✅ Result: No extra insulin = no risk of hypoglycaemia on its own.
