Brainscape's Knowledge GenomeTM

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


See full index

Pharmacotherapeutics Theory 1 > Endocarditis, Hypertension and Dyslipidaemia CUE CARDS > Flashcards

Endocarditis, Hypertension and Dyslipidaemia CUE CARDS Flashcards

1
Q

Describe a Simplistic CVD Pathophysiological Overview

A

> Normal Blood Vessels

> Plaque starts building up on the blood vessels leading to vascular disease (Stroke [TIA] and Peripheral Disease [Claudication])

> Angina (becomes symptomatic CVD)

> Atrial Fibrillation (Stroke)

> Death

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

Prevention of CVD

How do we Treat CVD (HTN and Dyslipidaemia)?

What’s the difference between Primary and Secondary Prevention?

A

Does the patient have Symptomatic CVD?

NO: Primary Prevention - Taken in healthy person, consider use of meds, to prevent them to go on and develop symptomatic CVD

YES: Secondary Prevention - Taken by patients who have symptomatic CVD to stop them from having another CV event

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

CV Risk Assessment: If an individual already has CVD, what’s their risk?

A

Absolute

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

CV Risk Assessment: What factors, both modifiable and non-modifiable, influence the probability of progressing through the CVD pathway?

A

Modifiable: smoking status, blood pressure, serum lipids, BMI, waist circumference, nutrition, physical activity level, alcohol intake

Non-Modifiable: Age, Gender, Family Hx of premature CVD, social hx including cultural identity, ethnicity and socioeconomic status

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

Endocarditis:

What is Endocarditis?

What are the Symptoms?

How can the infection occur?

A

> An infection of the endocardial surface of the heart

> Symptoms: Fever and chills, Heart Murmurs, Congestive Heart Failure, Secondary Embolic Phenomena

> Bacteria enter bloodstream (via surgical procedure, valve replacement, IV drug use) and lodge on abnormal heart valves or other damaged heart tissue

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

Endocarditis:

What are the causative organisms dependent upon?

What are the most likely causative organisms?

A

> Causative organism dependant upon site leading to bacteria in the blood

> Gram +ve: staphylococcus, enterococcus, streptococcus

> Gram -ve: HACEK Group

> Fungal: Candida

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

Endocarditis Treatment:

What is the purpose of combining two penicillins (flucloxacillin and benzylpenicillin)?

Why is gentamicin also used?

Is there a benefit of vancomycin over penicillin?

Is there a risk of using vancomycin instead of penicillin?

A

> Flucloxacillin provides good staphylococcus aureus cover and benzylpenicillin covers other gram +ve organisms such as strep. Gentamicin covers gram negative organisms

> Only a benefit in those who are likely to have MRSA

> Unnecessary use promotes the development of resistance to this important abx

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

Endocarditis: Directed Therapy

Discuss directed therapy of endocarditis caused by strep

A

> The sensitivity of organism will determine drug choice which will then influence things like duration

> If less sensitive, may have to treat for longer

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

Gentamicin in Endocarditis

Discuss the use of Gent in directed therapy and its dosing in Endocarditis caused by strep

A

> Gentamicin isn’t there for gram -ve cover, it’s there to enhance the effects of benzylpenicillin

> When Gent is being use to enhance the effects of benzylpenicillin, it’s given tds (very low dose)

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

Endocarditis Prophylaxis

What is the main message regarding endocarditis prophylaxis and abx choice?

A

The main message is to give the abx before the procedure (in patients with cardiac condition/previous endocarditis), to allow it to be circulating the blood stream and therefore kill bacteria as it enters (if it enters) the bloodstream, to prevent infection

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

Endocarditis Prophylaxis

What are the risks and benefits of endocarditis prophylaxis?

A

Risks include adverse reactions and abx resistance

Benefits determined by the likelihood of surgical procedure resulting in bacteraemia and the nature of existing cardiac defect

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

Endocarditis Prophylaxis

Why is this practice less common than it was in the past?

A

Less common than it was is the past as the benefit may not be as significant as once thought - needs to be balanced with the risks

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

Endocarditis Prophylaxis

The decision about whether or not to use prophylaxis is determined by what?

A

Determined by the probability of the patients developing endocarditis

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

Endocarditis Prophylaxis

The choice of abx is determined by what?

A

The choice of abx is determined by procedure site (determines what type of bacteria will enter bloodstream)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Rheumatic Heart Disease:

What is Acute Rheumatic Fever?

Where does ARF affect?

What is Rheumatic Heart Disease?

A

> ARF is an autoimmune consequence of infection with Group A Streptococci

> ARF is a generalised inflammatory response and an illness that selectively affects the heart, joints, brain and skin - the involvement of the cardiac valves is RHD

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

Rheumatic Heart Disease:

Discuss the Frequency of Benzathine Penicillin G dosing, when would this change?

A

> The concentrations at the end of the standard frequency dosing (4 weekly) are quite low

> For patients who are at high risk of breakthrough, we may need to shorten the interval (3 weekly) to make sure that they’re maintained the protection

17
Q

HTN:

What are the types of HTN?

A

> Primary (Essential) HTN: don’t have a cause

> Secondary HTN: have a cause and if you can identify the cause, manage that first - Causes include renal disease, Cushing’s, hyperthyroidism, pregnancy

18
Q

HTN:

What are the risks of not treating HTN?

A

> CV risk factor
Target organ damage including eyes (retinopathy, optic neuropathy), brain (haemorrhagic stroke, encephalopathy), kidneys, heart (left ventricular hypertrophy)

19
Q

HTN:

How do you measure someone’s blood pressure?

A

> Patient seated and relaxed with limited recent exertion (avoidance of stimulants ~2hrs prior)

> Cuff fit easily around upper arm at heart level

> Measure both arms initially, then use arm with highest BP

> Calculate average of 2 measurements and remeasure after 5 minutes if differ more than 10mmHg

> Confirm at subsequent visit

20
Q

HTN:

What lifestyle advice can you give to reduce BP?

A 
> Reduce weight
> Reduce salt intake
> Increase physical activity
> Modify diet
> Limit alcohol intake
21
Q

HTN:

What is antihypertensive drug choice based on?

A

Based on patient age, comorbidities and drug toxicity

22
Q

HTN:

What are the benefits or antihypertensive drugs?

What benefits do specific MOA have?

A

> Covering BP reduces CV risk and end-organ damage (benefit determined by BP value)

> Specific mechanisms of action may have additional benefits for the management of comorbidities

23
Q

HTN:

What are the targets of BP for Antihypertensives?

A

> Generally treat initially to a goal of <140mmHg and if treatment is well tolerated, proceed to a target goal of <130mmHg (age 50-74 yrs) - if they respond well, can lower further

> At age <50yrs, goal is 120/80mmHg

24
Q

HTN:

What risks are associated with the use of antihypertensive drugs?

A

> Side effects: All drugs that lower BP may cause dizziness until the baroreceptors reset

> Drug Interactions

> Cost

25
Q

HTN:

Discuss the Triple Whammy Effect

When does this not occur?

A

> ACE inhibitor dilates the efferent arteriole and reduces GFR
Diuretics reduce plasma volume and GFR
NSAIDs constrict blood flow into the glomerulus via the afferent arteriole and reduce GFR

  • GFR severely reduced, potentially causing renal failure

> Usually not a problem with low dose thiazide + ACEi + low dose aspirin

26
Q

HTN:

What are the 2 drug dosing strategies with antihypertensives and LLT?

What are the benefits and risks associated with them?

A

> Conservative: Start low and slowly uptitrate according to response. Risk that response may take longer and this may not be safe for patient in that time period. Because dose started low, adverse effects minimised

> Aggressive: Start high and down titrate according to response. Benefit is that you may achieve rapid control. Because you started at high dose, may experience adverse reaction

27
Q

HTN:

What are the acute benefits and risks of drug dosing in hypertension if we drop too quickly?

How do we usually control these?

When would the risks outweigh the benefits?

A

> Benefit: No acute benefits, long term reduction in CV risk and target organ damage

> Risk: Acute risk of hypotension, assorted long term risks (barrier to compliance)

> Control by starting with low dose and up-titrating dose or additional therapy according to response

> Risks would outweigh benefits in hypertensive emergency

28
Q

HTN:

What are hypertensive emergencies?

What are the causes?

Are there symptoms associated with it?

A

> Severe elevations in BP (>220/140 mmHg) that require immediate admission and BP reduction

> Causes: head trauma, vascular disorders, stimulant drugs, antihypertensive withdrawal (clonidine)

> Symptomatic due to HTN - rapid damage to tissue - progressive target organ dysfunction. Symptoms include headache, confusion and visual disturbances

29
Q

HTN:

For urgent short-term use in an Hypertensive Emergency, what drug would you give in ICU?

What is the main message regarding drugs used in hypertensive emergencies?

A

> In ICU, use sodium nitroprusside (direct acting vasodilator). Can adjust infusion to achieve desired BP

> The main message is the idea that no matter what drug, we can usually tailer the dose to adjust BP accordingly

30
Q

HTN in Pregnancy:

What is pre-eclampsia, when is it a concern?

What can it present in the mother as?

How does it affect the fetus?

A

> A disorder of placental dysfunction leading to a syndrome of endothelial dysfunction with associated vasospasm (major concern after 20 weeks gestation)

> Can present in mother as rapid weight gain, edema, pulmonary edema

> Affect fetus via decreased utero-placental blood flow

31
Q

HTN in Pregnancy:

What is first line drug used in HTN in pregnancy?

What other drugs can be used?

What is the risk of using ACEi in pregnancy?

A

> Methyldopa is first-line

> Beta blockers can also be used (labetalol, oxprenolol)

> ACEi can decrease kidney function, during pregnancy: reduced amniotic fluid and fetus is exposed to pressure of uterus wall (flattened ears, nose and big head)

32
Q

Dyslipidaemia:

What dietary modification should be adopted for patients?

A

> Mainly plant-based foods e.g. fruits, vegetable, whole-grains

> Moderate amounts of reduced, low or no fat dairy products

> Moderate amounts of lean unprocessed meats, poultry and fish

> Moderate amounts of polyunsaturated and monounsaturated fats (e.g. olive oil, canola oil)

33
Q

Dyslipidaemia:

How is LLT initiated?

Discuss the use of LLT in high CV risk compared to moderate CV risk. Compare this to low CV risk

What end-point are you trying to achieve?

A

> The initiation of LLT is based upon calculated CV risk rather than just lipid levels

> In patients with high CV risk, start LLT immediately, whereas in patients with moderate CV risk, patients should modify their lifestyle for 3-6 months to try and lower the risk (risk may be underestimated e.g. obesity, family hx)

> In patients with low CV risk, LLT isn’t generally appropriate

> End point: Reduction in CV risk

34
Q

Dyslipidaemia:

Discuss:

Lipophilicity of Pravastatin compared to Atorvastatin and Rosuvastatin

Metabolism of Rosuvastatin compared to Atorvastatin and Simvastatin

Metabolising CYP enzymes of Simvastatin, Rosuvastatin and Atorvastatin

A

> Pravastatin has the least lipophilicity compared to the other statins. Lipophilicity may influence the risk of muscle toxicity. In patients with hx of myalgia, can justify pravastatin

> Rosuvastatin is metabolised in bile, whereas simvastatin and atorvastatin are metabolised by the liver. This causes a difference in clearance mechanism, ultimately causing a difference in drug interactions

> Simvastatin and Atorvastatin are metabolised by CYP3A4. If patient on other drugs, may be likely that they may be CYP3A4 inhibitors. In this case, justify rosuvastatin as likely less drug interactions

35
Q

Dyslipidaemia:

Discuss the comparisons between atorvastatin and rosuvastatin compared with other statins e.g. fluvastatin

A

> Atorvastatin and Rosuvastatin are both high potency statins that have a longer half-life when compared to simvastatin and pravastatin

> Because of the short half-lives, patients must take simvastatin and pravastatin at night time as the body synthesises more cholesterol at night - patients are less likely to remember this

> Rosuvastatin and atorvastatin have longer half-lives so it doesn’t matter when you take

36
Q

Dyslipidaemia:

What strategies can be used to manage drug interactions with statins?

A

> If initiating: choose a drug that doesn’t inhibit statin metabolism

> Switch to a statin that is cleared via an alternate path

> Hold the statin for duration of treatment with other interacting drug (e.g. erythromycin - hold statin for 1 week - can lead to rhabdomyolysis) - risk: patient may forget to restart LLT

Pharmacotherapeutics Theory 1 (17 decks)

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