Session 5 - Group Work Flashcards
Indicate whether the drug increases, decreases or does not affect: LDL-Chol, HDL-Chol, TGs
Statin
LDL-Chol, HDL-Chol, TGs
Decrease, Increase, Decrease
Indicate whether the drug increases, decreases or does not affect: LDL-Chol, HDL-Chol, TGs
Ezetimibe
LDL-Chol, HDL-Chol, TGs
Decrease, Increase, Decrease
Indicate whether the drug increases, decreases or does not affect: LDL-Chol, HDL-Chol, TGs
Nicotinic acid
LDL-Chol, HDL-Chol, TGs
Decrease, Increase, Decrease
Indicate whether the drug increases, decreases or does not affect: LDL-Chol, HDL-Chol, TGs
Cholestyramine
LDL-Chol, HDL-Chol, TGs
Decrease, Increase, Increase
Indicate whether the drug increases, decreases or does not affect: LDL-Chol, HDL-Chol, TGs
Omega 3 FA
LDL-Chol, HDL-Chol, TGs
Increase, Increase, Decrease
Indicate whether the drug increases, decreases or does not affect: LDL-Chol, HDL-Chol, TGs
Fibrates
LDL-Chol, HDL-Chol, TGs
Decrease, Increase, Decrease
1) A 63-year-old man was admitted to CCU with an acute anterior MI. He received the usual treatment with thrombolysis, aspirin, beta blocker and ACE inhibitor.
His total cholesterol was found to be 7mmol/L with TG of 1.1 mmol/L.
a) What is the evidence that lowering cholesterol is likely to be beneficial to this patient?
For every 1 mmol/L you drop it you have 20% reduced risk of CVD.
1) A 63-year-old man was admitted to CCU with an acute anterior MI. He received the usual treatment with thrombolysis, aspirin, beta blocker and ACE inhibitor.
His total cholesterol was found to be 7mmol/L with TG of 1.1 mmol/L.
b) The patient is prescribed a lipid-lowering drug.
What different agents could be used?
Statin Ezetimibe Nicotinic acid Cholestyramine(?) Fibrates
1) A 63-year-old man was admitted to CCU with an acute anterior MI. He received the usual treatment with thrombolysis, aspirin, beta blocker and ACE inhibitor.
His total cholesterol was found to be 7mmol/L with TG of 1.1 mmol/L.
c) Atorvastatin is prescribed.
What is the mechanism of action of this group of drugs and where to they predominantly act?
Competitive inhibition of HMG-CoA reductase – rate controlling enzyme in mevalonate pathway
Upregulation of hepatic LDL receptors
Increased clearance of circulating LDL
1) A 63-year-old man was admitted to CCU with an acute anterior MI. He received the usual treatment with thrombolysis, aspirin, beta blocker and ACE inhibitor.
His total cholesterol was found to be 7mmol/L with TG of 1.1 mmol/L.
d) What advice should the patient receive about statin therapy and explain why it is recommended to be taken NOCTE?
Avoid grapefruit juice (or grapefruit) because it affects CYP 3A4 and take it at night because the circadian rhythm upregulates LDL receptors so it has highest efficacy here
1) A 63-year-old man was admitted to CCU with an acute anterior MI. He received the usual treatment with thrombolysis, aspirin, beta blocker and ACE inhibitor.
His total cholesterol was found to be 7mmol/L with TG of 1.1 mmol/L.
e) Would the absolute level of cholesterol affect the decision to use a lipid-lowering agent?
Yes, full lipid profile should be done and QRISK.
1) A 63-year-old man was admitted to CCU with an acute anterior MI. He received the usual treatment with thrombolysis, aspirin, beta blocker and ACE inhibitor.
His total cholesterol was found to be 7mmol/L with TG of 1.1 mmol/L.
f) Once the treatment is initiated, what is the target cholesterol value?
LDL level should be <2.0 mmol/L and total cholesterol should be <4.0 mmol/L
2) A 25-year-old gentleman presented with vague aches and pains in his arms. Two years before, he was diagnosed with Familial Hypercholesterolemia and had received treatment.
a) What could be the cause of his symptoms?
Adverse drug reaction to the statins - myalgia and rhabdomyolysis
2) A 25-year-old gentleman presented with vague aches and pains in his arms. Two years before, he was diagnosed with Familial Hypercholesterolemia and had received treatment.
b) How would the diagnosis be confirmed?
Take him off the statins and give him an alternative e.g. fibrates or nicotinic acid - check symptoms disappear
If not then serum transaminase and CK levels. K levels LFT and U&E’s.
2) A 25-year-old gentleman presented with vague aches and pains in his arms. Two years before, he was diagnosed with Familial Hypercholesterolemia and had received treatment.
c) What alternative therapy could be used to treat his condition?
Fibrates
Nicotinic acid
Ezetimibe
2) A 25-year-old gentleman presented with vague aches and pains in his arms. Two years before, he was diagnosed with Familial Hypercholesterolemia and had received treatment.
d) How does the mechanism of action differ in this alternative therapy to statins?
This prevents the absorption from the gut rather than the formation of the cholesterol
3) A 30-year-old man was found unconscious in his home and transferred to Casualty. On examination, he was shivering, unresponsive to pain, and breathing rapidly. His skin was dry and veins poorly filled. There was a fluctuant mass in his thigh. His vital signs:
Pulse 110/min
BP 90/55
Respiratory rate 26/min
Temperature 39 C
Blood gases show a pH of 7.01, standard bicarbonate of 15 mmol/L, pCO2 2.1 kPa
Plasma glucose is 25 mmol/L
Creatinine 180 umol/L, Na+ 148 mmol/L, K+ 6.7 mmol/L
a) What treatment should be prescribed as an emergency?
Insulin
Calcium gluconate
Salbutamol - drives potassium into cells (also quicker to get your hands on on a ward)
Calcium resonium - in practice, however, this is rarely given because it is generally an oral tablet, but most patients who are hyperkalaemic are too poorly to take an oral tablet
Abscess - caused by Staphs and Streps, so you need to give him Flucloxacillin
Also need to drain the abscess so the pus can come out
3) A 30-year-old man was found unconscious in his home and transferred to Casualty. On examination, he was shivering, unresponsive to pain, and breathing rapidly. His skin was dry and veins poorly filled. There was a fluctuant mass in his thigh. His vital signs:
Pulse 110/min
BP 90/55
Respiratory rate 26/min
Temperature 39 C
Blood gases show a pH of 7.01, standard bicarbonate of 15 mmol/L, pCO2 2.1 kPa
Plasma glucose is 25 mmol/L
Creatinine 180 umol/L, Na+ 148 mmol/L, K+ 6.7 mmol/L
b) How should his progress and response be monitored?
Regular monitoring of Obs
Sepsis Six Bundle
Hyperglycaemic:
- could be a first presentation of T1DM, where an infection unmasks it
- sepsis
Urine dipstick - looking for elevated glucose, ketones
Man is in DKA (diabetic ketoacidosis)
- treat with sliding scale of insulin
3) A 30-year-old man was found unconscious in his home and transferred to Casualty. On examination, he was shivering, unresponsive to pain, and breathing rapidly. His skin was dry and veins poorly filled. There was a fluctuant mass in his thigh. His vital signs:
Pulse 110/min
BP 90/55
Respiratory rate 26/min
Temperature 39 C
Blood gases show a pH of 7.01, standard bicarbonate of 15 mmol/L, pCO2 2.1 kPa
Plasma glucose is 25 mmol/L
Creatinine 180 umol/L, Na+ 148 mmol/L, K+ 6.7 mmol/L
After 2 days of treatment, he was conscious and afebrile. Blood glucose was 6 mmol/L and he felt hungry. The abscess in his thigh was less tender.
c) What treatment should now be considered?
Prescribe insulin regime
3) A 30-year-old man was found unconscious in his home and transferred to Casualty. On examination, he was shivering, unresponsive to pain, and breathing rapidly. His skin was dry and veins poorly filled. There was a fluctuant mass in his thigh. His vital signs:
Pulse 110/min
BP 90/55
Respiratory rate 26/min
Temperature 39 C
Blood gases show a pH of 7.01, standard bicarbonate of 15 mmol/L, pCO2 2.1 kPa
Plasma glucose is 25 mmol/L
Creatinine 180 umol/L, Na+ 148 mmol/L, K+ 6.7 mmol/L
After 2 days of treatment, he was conscious and afebrile. Blood glucose was 6 mmol/L and he felt hungry. The abscess in his thigh was less tender.
d) Who should be involved in his education?
Himself
Family/NOK in case it happens again (emergency)
Diabetic nurse - how to manage it day-to-day; e.g. sick day rules - if you’re poorly and can’t eat
(Endocrinologist at some point)
3) A 30-year-old man was found unconscious in his home and transferred to Casualty. On examination, he was shivering, unresponsive to pain, and breathing rapidly. His skin was dry and veins poorly filled. There was a fluctuant mass in his thigh. His vital signs:
Pulse 110/min
BP 90/55
Respiratory rate 26/min
Temperature 39 C
Blood gases show a pH of 7.01, standard bicarbonate of 15 mmol/L, pCO2 2.1 kPa
Plasma glucose is 25 mmol/L
Creatinine 180 umol/L, Na+ 148 mmol/L, K+ 6.7 mmol/L
After 2 days of treatment, he was conscious and afebrile. Blood glucose was 6 mmol/L and he felt hungry. The abscess in his thigh was less tender.
e) What advice should he be given regarding his prescription?
Sick day advice
Check his feet
Alcohol
Fasting/exercise
4.1) An Asian man attended his GP surgery complaining of recent weight loss, polyuria blurring of vision, and tingling in his feet. On examination, he was obese, his BP was 164/84 mmHg, loss of sensation in a glove and stocking distribution and fundoscopy revealed hard exudates in both eyes.
Please use the NICE guidelines (NG28) for type 2 diabetes in adults to help answer the questions below:
https://www.nice.org.uk/guidance/ng28
a) What is the likely cause of all these symptoms?
Type 2 diabetes mellitus
4.1) An Asian man attended his GP surgery complaining of recent weight loss, polyuria blurring of vision, and tingling in his feet. On examination, he was obese, his BP was 164/84 mmHg, loss of sensation in a glove and stocking distribution and fundoscopy revealed hard exudates in both eyes.
Please use the NICE guidelines (NG28) for type 2 diabetes in adults to help answer the questions below:
https://www.nice.org.uk/guidance/ng28
b) How would you plan this man’s management? Answers should include non-pharmacological approaches.
Pharmacological:
- Metformin
- ACE inhibitor
- Statin
- Ezetimibe
- Anti-platelet (warfarin)
- Refer to podiatry and optometry
Non-pharmacological:
- Lose weight (diet and exercise)
- Exercise
4.1) An Asian man attended his GP surgery complaining of recent weight loss, polyuria blurring of vision, and tingling in his feet. On examination, he was obese, his BP was 164/84 mmHg, loss of sensation in a glove and stocking distribution and fundoscopy revealed hard exudates in both eyes.
Please use the NICE guidelines (NG28) for type 2 diabetes in adults to help answer the questions below:
https://www.nice.org.uk/guidance/ng28
c) How would you monitor his progress?
- Glucose diaries
- HbA1c (long-term marker of compliance to treatment)
- GP appointments
- Regular check ups, blood tests
- Diabetic foot clinics
4.1) An Asian man attended his GP surgery complaining of recent weight loss, polyuria blurring of vision, and tingling in his feet. On examination, he was obese, his BP was 164/84 mmHg, loss of sensation in a glove and stocking distribution and fundoscopy revealed hard exudates in both eyes.
Please use the NICE guidelines (NG28) for type 2 diabetes in adults to help answer the questions below:
https://www.nice.org.uk/guidance/ng28
He deteriorates further and you are unable with initial treatment to achieve fasting blood glucose under 9 mmol/L
d) What further treatment would you consider?
- Sulfonylurea if the metformin doesn’t work
- Conventional diet; if not low-calorie diet (600-800 calories)
4.1) An Asian man attended his GP surgery complaining of recent weight loss, polyuria blurring of vision, and tingling in his feet. On examination, he was obese, his BP was 164/84 mmHg, loss of sensation in a glove and stocking distribution and fundoscopy revealed hard exudates in both eyes.
Please use the NICE guidelines (NG28) for type 2 diabetes in adults to help answer the questions below:
https://www.nice.org.uk/guidance/ng28
He deteriorates further and you are unable with initial treatment to achieve fasting blood glucose under 9 mmol/L
e) What side effects should you warn this man about?
- Weight gain because it stimulates appetite
- Hypoglycaemia
4.1) An Asian man attended his GP surgery complaining of recent weight loss, polyuria blurring of vision, and tingling in his feet. On examination, he was obese, his BP was 164/84 mmHg, loss of sensation in a glove and stocking distribution and fundoscopy revealed hard exudates in both eyes.
Please use the NICE guidelines (NG28) for type 2 diabetes in adults to help answer the questions below:
https://www.nice.org.uk/guidance/ng28
He deteriorates further and you are unable with initial treatment to achieve fasting blood glucose under 9 mmol/L
f) What other therapies should you consider, in order to prevent future cardiovascular complications of the disease?
Statins
4.2) See stem for q4
Calculating CVD risk often forms part of screening and decision making regarding the course of action in patients presenting with co morbidities and or risk factors. Using the patient data below calculate the CVD risk for this patient. Consider why changing the parameters in parentheses alters the calculated risk making associations with the underlying pathology and public health evidence.
a) Male
An important take home message here is that CVD risk is not fixed, it is modifiable both through pharmacological and lifestyle interventions. Although there is considerable familial association with some of the contributing risk factors, many can be targeted and reduced.
https: //qrisk.org/three/index.php
33. 6%
4.2) See stem for q4
Calculating CVD risk often forms part of screening and decision making regarding the course of action in patients presenting with co morbidities and or risk factors. Using the patient data below calculate the CVD risk for this patient. Consider why changing the parameters in parentheses alters the calculated risk making associations with the underlying pathology and public health evidence.
b) 69 years old (50 years old)
An important take home message here is that CVD risk is not fixed, it is modifiable both through pharmacological and lifestyle interventions. Although there is considerable familial association with some of the contributing risk factors, many can be targeted and reduced.
69 years old = 33.6%
50 years old = 17%
4.2) See stem for q4
Calculating CVD risk often forms part of screening and decision making regarding the course of action in patients presenting with co morbidities and or risk factors. Using the patient data below calculate the CVD risk for this patient. Consider why changing the parameters in parentheses alters the calculated risk making associations with the underlying pathology and public health evidence.
c) White
An important take home message here is that CVD risk is not fixed, it is modifiable both through pharmacological and lifestyle interventions. Although there is considerable familial association with some of the contributing risk factors, many can be targeted and reduced.
33.6%
4.2) See stem for q4
Calculating CVD risk often forms part of screening and decision making regarding the course of action in patients presenting with co morbidities and or risk factors. Using the patient data below calculate the CVD risk for this patient. Consider why changing the parameters in parentheses alters the calculated risk making associations with the underlying pathology and public health evidence.
d) LE1 7RH (try your family home postcode)
An important take home message here is that CVD risk is not fixed, it is modifiable both through pharmacological and lifestyle interventions. Although there is considerable familial association with some of the contributing risk factors, many can be targeted and reduced.
LE3 7RH
4.2) See stem for q4
Calculating CVD risk often forms part of screening and decision making regarding the course of action in patients presenting with co morbidities and or risk factors. Using the patient data below calculate the CVD risk for this patient. Consider why changing the parameters in parentheses alters the calculated risk making associations with the underlying pathology and public health evidence.
e) Ex-smoker
An important take home message here is that CVD risk is not fixed, it is modifiable both through pharmacological and lifestyle interventions. Although there is considerable familial association with some of the contributing risk factors, many can be targeted and reduced.
4.2) See stem for q4
Calculating CVD risk often forms part of screening and decision making regarding the course of action in patients presenting with co morbidities and or risk factors. Using the patient data below calculate the CVD risk for this patient. Consider why changing the parameters in parentheses alters the calculated risk making associations with the underlying pathology and public health evidence.
f) Type 2 diabetes (non diabetic)
An important take home message here is that CVD risk is not fixed, it is modifiable both through pharmacological and lifestyle interventions. Although there is considerable familial association with some of the contributing risk factors, many can be targeted and reduced.
4.2) See stem for q4
Calculating CVD risk often forms part of screening and decision making regarding the course of action in patients presenting with co morbidities and or risk factors. Using the patient data below calculate the CVD risk for this patient. Consider why changing the parameters in parentheses alters the calculated risk making associations with the underlying pathology and public health evidence.
g) On blood pressure treatment
An important take home message here is that CVD risk is not fixed, it is modifiable both through pharmacological and lifestyle interventions. Although there is considerable familial association with some of the contributing risk factors, many can be targeted and reduced.
4.2) See stem for q4
Calculating CVD risk often forms part of screening and decision making regarding the course of action in patients presenting with co morbidities and or risk factors. Using the patient data below calculate the CVD risk for this patient. Consider why changing the parameters in parentheses alters the calculated risk making associations with the underlying pathology and public health evidence.
h) Cholesterol/HDL ratio 4.5 (3)
An important take home message here is that CVD risk is not fixed, it is modifiable both through pharmacological and lifestyle interventions. Although there is considerable familial association with some of the contributing risk factors, many can be targeted and reduced.
4.2) See stem for q4
Calculating CVD risk often forms part of screening and decision making regarding the course of action in patients presenting with co morbidities and or risk factors. Using the patient data below calculate the CVD risk for this patient. Consider why changing the parameters in parentheses alters the calculated risk making associations with the underlying pathology and public health evidence.
i) Systolic blood pressure 150 mmHg (140)
An important take home message here is that CVD risk is not fixed, it is modifiable both through pharmacological and lifestyle interventions. Although there is considerable familial association with some of the contributing risk factors, many can be targeted and reduced.
4.2) See stem for q4
Calculating CVD risk often forms part of screening and decision making regarding the course of action in patients presenting with co morbidities and or risk factors. Using the patient data below calculate the CVD risk for this patient. Consider why changing the parameters in parentheses alters the calculated risk making associations with the underlying pathology and public health evidence.
j) Height 170 cm
An important take home message here is that CVD risk is not fixed, it is modifiable both through pharmacological and lifestyle interventions. Although there is considerable familial association with some of the contributing risk factors, many can be targeted and reduced.
4.2) See stem for q4
Calculating CVD risk often forms part of screening and decision making regarding the course of action in patients presenting with co morbidities and or risk factors. Using the patient data below calculate the CVD risk for this patient. Consider why changing the parameters in parentheses alters the calculated risk making associations with the underlying pathology and public health evidence.
k) Weight 85 kg
An important take home message here is that CVD risk is not fixed, it is modifiable both through pharmacological and lifestyle interventions. Although there is considerable familial association with some of the contributing risk factors, many can be targeted and reduced.
