Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

BDS2 BASICS > Cardiovascular Medicine > Flashcards

Cardiovascular Medicine Flashcards

1
Q

Risk factors of CV disease?

A
  • irreversible, age sex family history
  • reversible, smoking obesity diet exercise
  • reversible (medical), hypertension hyperlipidaemia diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Approach to prevention for CV disease?

A
  1. lifestyle changes
  2. control total cholesterol (statin treatment)
  3. control hypertension (reduce BP to target of <140/85)
  4. anti platelet drugs - aspirin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

relation between dental team and cardiac prevention?

A
  • opportunity for general health education and promotion of good OH
  • diet and lifestyle and offer advice (smoking cessation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

(drugs used in the cardiovascular system) drugs which prevent further disease

A

= anti platelet drugs
= lipid lowering drugs
= anti=arrhythmics
= anticoagulants
= diuretics - furosemide
= ace - inhibitors

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

(drugs used in the CV system) drugs which reduce symptoms of current disease

A
  • diuretics
  • anti-arrhythmics
  • nitrates
  • calcium channel blockers
  • ace -inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Name 3 anti-platelet drugs?

A

= aspirin
= clopidogrel
= dipyridamole

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

How does aspirin work?

A

=inhibits platelet aggregation

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

Why are anti-platelet drugs used in combination?

A

to increase the effect

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

What do anti-platelet drugs do?

A

= significantly reduce chance of a heart attack or stroke

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

relation between anti-platelet drug and dental extractions

A

prolong the bleeding time following dental extraction

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

Name 5 oral anticoagulants?

A

= warfarin
= rivaroxiban
= apixaban
= dabigatran
= edoxaban

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

describe warfarin ?

A

= coumarin based anticoagulant
= inhibits synthesis of vit K dependant clotting factors
- 2,7,9,10 - slow 2 days
- protein C & S - quick
= initial hyper-coagulation
- anticoagulation takes 2-3 days
- often HEPARIN used concurrently initially

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

How is warfarin monitored?

A

INR test- aim for 2-4
prothrombin time

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

With regards to dental treatment, if the INR is out-with 2-4 what should you do?

A
  • refer for medical advice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

with regards to dental treatment if IRN is within 2-4 range ?

A

no alteration needed for dental care

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

What injection should you avoid if a patient taking warfarin ?

A

ID block

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

Name 4 NOACS?

A

= apixiban - twice
= dabigatran - twice
= rivaroxiban - once
= edoxaban - once

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

why is there no anticoagulant test used for NOACs?

A

bioavailability predictable

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

When is best time to undertake an extraction for a patient taking NOACs?

A

just before dose is due (maximum chance for blood clot to form)

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

Other drugs preventing CV disease?

A
  • statins
  • beta-adrenergic blockers
  • diauretics
  • calcium channel blockers
  • ACE inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is a statin?

A

Lipid lowering drugs

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

How do statins work?

A

= Inhibit cholesterol synthesis in the liver

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

What can statins interact with?

A

= omit statin when prescribing anti-fungal treatment (fluconazole)

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

Examples of statins

A

= simvastatin
= atorvastatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Examples of B blockers
= atenolol = propranolol
26
What do B-blockers do?
= stop arrhythmias leading to cardiac arrest = reduced heart muscle excitability
27
What are diuretics and what are some examples?
= antihypertensive and for heart failure = thiazide diuretics (bendroflumethiazide) and loop diuretics (frusemide)
28
2 examples of nitrates and their use?
= glyceryl trinitrate (GTN) - short acting- emergency management of angina pectoris = isosorbide mononitrate - long acting - prevention of angina pectoris
29
How do nitrates work?
= dilate veins = dilate resistance arteries = dilate colateral coronary artery supply
30
What are calcium channel blockers used for?
= hypertension treatment = migraine treatment
31
With regards to dentistry, what can calcium channel blockers lead to?
gingival hyperplasia - dependant of good OH
32
Examples of ACE inhibitors (-pril)
= ramapril = lisinopril = enalapril
33
How do ACE inhibitors work?
= inhibit conversion of angiotensin I to angiotensin II
34
What do ACE inhibitors stand for?
= angiotensin converting enzyme inhibitors
35
What do ace inhibitors do?
= reduce blood pressure = reduce excess salt and water retention
36
Oral reaction of ACE inhibitors
= angio-oedema = lichenoid reaction
37
Pathology revision of acute coronary syndromes- what are the 2 processes
- blood vessel narrowing - blood vessel occlusion
38
What happens in blood vessel narrowing?
- inadequate oxygen delivery for tissue needs - cramp in affected tissue/muscle - no residual deficit at first
39
What happens in blood vessel occlusion?
= no oxygen delivery - tissue death = more severe pain = loss of function of tissue
40
ACS possibilities: stable angina
increased demand in setting of a stable atherosclerotic plaque (vessel unable to dilate enough to allow adequate blood flow0
41
ACS possibilities: unstable angina
the plaque ruptures and a thrombus forms around ruptured plaque - partial occlusion of vessel
42
ACS possibilities: NSTEMI
= plaque rupture and thrombus forms and causes partial occlusion of vessel- causes injury and infarct- rise in troponins
43
ACS possibilities: STEMI
= complete occlusion of blood vessel lumen, transmural injury and infarct to myocardium - ECG changes and rise is troponins
44
Biomarker of ACS diagnosis
troponin
45
What is angina pectoris? (def, claaical, stable, what do all describe?)
= reversible ischaemia of heart muscle = 'classical' angina worse with exercise no biomarkers = ' unstable' angina symptoms at rest no biomarkers =all describe central crushing chest pain - radiation to arm, back, jaw possible
46
Angina- investigations
= ECG- resting and exercise = eliminate other disease- thyroid, anaemia and valve = echocardiography = angiography
47
Angina- treatment
= reduce oxygen demands of the heart - reduce afterload and preload - correct mechanical issues = increase oxygen delivery to the tissues - dilate blocked/narrowed vessels - bypass blocked/ narrowed vessels (Coronary Artery Bypass Grafting (CABG))
48
Non-drug therapy of angina
- explanation of illness - modify risk factors = smoking =graded exercise programme = diet
49
Drug therapy for patients with angina
= reduce MI risk- Aspirin = hypertension- diuretics, ace inhibitors, b blockers = reduce heart filling pressure - nitrates = emergency treatment - GTN spray
50
Surgical therapy for angina patient
= CABG Coronary artery bypass grafting = angioplasty and stenting (risk of vessel rupture)
51
What is peripheral vascular disease?
= angina of the tissues = claudication pain on limb on exercise = managed in same was as angina
52
What can happen as a result of peripheral vascular disease?
= limitation of function = poor wound healing = can lead to necrosis and gangrene = aggravated by CV risk factors
53
How can ischaemia lead to infarction?
= atheroma in vessels = thrombosis can enlarge rapidly to block vessel = plaque surface/ platelets detach
54
What is the strategy for infarction?
= reduce tissue loss from necrosis (open blood flow to ischaemic tissue) =prevent further episode = RF management and aspirin
55
Symptoms and signs of MI?
= pain nausea pale sweaty = going to die = silent MI's
56
How can MI be diagnosed?
= history = ECG findings STEMI NSEMI = Biomarkers (troponin mainly low)
57
MI treatment?
=PRIMARY CARE analgesia aspirin reassurance BLS =hospital treatment - up to 3 hours from onset of symptoms - Primary PCI = prevent recurrence
58
What is the best option for delayed admission?
Thombolysis (6hrs after symptoms)
59
How does angioplasty and stent work?
= catheter inserted through artery = moved to site of blockage under x-ray control = balloon inflated to open blockage = mental stent clicks rigid to hold vessel open and allow blood flow
60
Complications of MI
= death =post MI arrhythmias = heart failure = ventricular hypofunction and mural thrombosis = DVT and pulmonary emolism
61
How to prevent next MI?
= risk modification and aspirin = B blocker = ace inhibitor
62
How to treat complications of ..???
= heart failure = arrhythmias = psychological distress
63
What is the primary prevention of CV disease?
= smoking cessation, diet and exercise = encourage fruit and veg, fewer processed
64
What is atherosclerosis?
thickening or hardening of the arteries caused by a build-up of plaque in the inner lining of an artery - medicated with statins

BDS2 BASICS (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions