Brainscape's Knowledge GenomeTM

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


See full index

Phase 2 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What are the 7 risk factors for atherosclerosis?

A 
Age 
Smoking 
High serum cholesterol 
Obesity 
Diabetes 
Hypertension 
Family history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where are atherosclerotic plaques found?

A

Peripheral or coronary arteries - Focal distribution along the artery length

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

What harm-dynamic factors govern atherosclerotic plaque distribution

A

Changes In flow and turbulence ie. at bifurcations causes artery to adjust wall thickness leading to neointima development

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

Describe the structural components of a atherosclerotic plaque

A 
Lipid 
Necrotic core 
Connective tissue 
Fibrous cap 
lymphocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What happens if the atherosclerotic plaque occludes a vessel lumen

A

Restricts blood Flow (Angina)

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

What happens if an atherosclerotic plaque ruptures

A

Thrombus formation and death

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

What initiates the formation of an atherosclerotic plaque?

A

Injury to endothelial cells leading to endothelial dysfunction - this causes signals to be sent to circulating leukocytes which accumulate and migrate into vessel wall

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

What stimuli cause inflammation in the arterial wall?

A
  1. LDL passing in and out of arterial wall in excess, accumulate in arterial wall and undergo oxidation and glyceration
  2. Endothelial dysfunction in response to injury hypothesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the role of chemoattractants in the formation of atherosclerotic plaque?

A

Once released from the endothelium, They attract leukocytes through chemotaxis - concentration gradient is created which drives the movement of cells

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

Which inflammatory cytokines can be found in atherosclerotic plaques

A 
IL-1
IL-6
IL-8
IFN-y (Proinflammatory agent) 
TGF-B
Monocyte Chemoattractive Protein-1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the 4 stages of atherosclerosis?

A
  1. Fatty streak formation
  2. Intermediate lesion
  3. Fibrous plaque or advanced lesion
  4. Plaque rupture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

At what age do fatty streaks begin to form

A

<10 years

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

What does a fatty streak consist of?

A

Aggregations of lipid laden macrophages and T lymphocytes within the intimal layer of the vessel wall

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

What are the layers of an intermediate lesion

A 
Foam cells 
Vascular smooth muscle cells 
T-lymphocytes 
Adhesion and aggregation of platelets to vessel wall 
Isolated pools of extracellular lipid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the 4 steps of the adhesion cascade

A
  1. Capture
  2. Rolling - slows cell down for adherence
  3. Adhesion
  4. Transmigration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What mediates the capture and rolling stage of the adhesion cascade?

A

Selectins

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

What mediates the adhesion and transmigration stages of the adhesion cascade

A

Integrins and chemoattractants

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

What are the main concerns with fibrous plaques and advanced lesions?

A

They made impede blood flow or be prone to rupture

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

Which cells secrete the fibrous cap that covers fibrous plaques

A

Smooth muscle cells that overlie the lipid core and the necrotic debris

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

What does a fibrous plaque contain?

A

Smooth muscle cells, macrophages, foam cells and T-lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What does the dense fibrous cap on a fibrous plaque contain

A

ECM proteins including collagen (Strength) and elastin (Flexibility)

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

What occurs in order for a plaque to rupture

A

If the balance is shifted in favour of inflammatory conditions such as increased enzyme activity that causes the cap to become weak hence the cap ruptures

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

What is the result of plaque rupture?

A

Thrombus formation and vessel occlusion

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

What is the treatment for coronary artery disease?

A

Percutaneous coronary intervention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the main issue with percutaneous coronary intervention?

A

Restenosis - artery becomes blocked again once the stent is removed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Name 2 drugs used to prevent restenosis following percutaneous coronary intervention

A

Paclitaxel

Sirolimus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Name three drugs used in the treatment of atherosclerosis

A

Aspirin - anti platelet

Clopidogrel/Ticagreclor

Statins - reduce cholesterol synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is atherosclerosis

A

Hardened plaque in the intimal of an artery - inflammatory process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What can an atherosclerotic plaque cause

A
  1. Heart attack
  2. Stroke
  3. Gangrene
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Which histological layer of an artery may be thinned by an atheromatous plaque

A

Media

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Define angina

A

Angina is a type of IHD - symptom of O2 supply and demand mismatch to the heart experienced on exertion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the 4 types of angina

A

Stable (Induced by effort)
Unstable (Occurs at rest)
Prinzmetal’s (Occurs during rest due to coronary spasm)
Microvascular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are 5 possible causes of angina

A
  1. Narrowed coronary artery (Atherosclerosis)
  2. Increased distal resistance
  3. Reduced O2 carrying capacity (Anaemia)
  4. coronary artery spasm
  5. Thrombosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are 5 modifiable risk factors for angina

A
  1. Hypertension
  2. Smoking
  3. Diabetes
  4. Hyperlipidaemia
  5. Obesity/sedentary lifestyle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Give three non-modifiable risk factors for angina

A
  1. Increasing Age
  2. Gender (Male bias)
  3. Family history/Genetics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Describe the pathophysiology of angina that results from atherosclerosis

A

On exertion there is an increased demand for O2 - coronary blood blood obstructed by atherosclerotic plaque –> Myocardial ischaemia –> Angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Describe the pathophysiology of angina from anaemia

A

On exertion there is increased O2 demand - in someone with anaemia there is reduced O2 transport –> Myocardial ischaemia –> Angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How do blood vessels try and compensate for increased myocardial demand during exercise

A

When demand increases, during exercise, microvascular resistance drops so flow increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Why are the blood vessels unable to compensate for increased myocardial demand in someone with CV disease

A

In CV disease, epicardial resistance is high meaning microvascular resistance has to fall at rest to supply myocardial demand at rest. When the person exercises the microvascular resistance cannot drop more so Flow cant increase to meet metabolic demand = angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

How can angina be reversed?

A

Resting - reduces myocardial demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What three factors can limit blood supply

A
  1. Impairment of blood flow by proximal arterial stenosis
  2. Increased distal resistance
  3. Reduced oxygen carrying capacity of the blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How would you describe the chest pain in angina

A

Crushing central chest pain
Heavy and tight
Patient will often make a fist shape to describe the pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Give 5 symptoms of angina

A
  1. Crushing central chest pain
  2. Pain relieved with rest or GTN
  3. Pain precipitated by exercise, emotion and temperature
  4. Pain may radiate to the arms, neck or jaw
  5. Breathlessness/Nausea/sweating/faintness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

If someone comes claiming chest pain, what characteristics about the pain do you want to determine? (OPQRST)

A 
Onset 
Position (Site)
Quality (Nature/character)
Relationship (With exertion/meals/posture)
Radiation (Anywhere on upper body)
Relieving or aggrevating factors 
Severity 
Timing 
Treatment (Does GTN work immediately)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What conditions would someone with angina most frequently experience symptoms

A

Cold weather
heavy meals
Emotional stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the differential diagnosis for angina

A 
Pericarditis/myocarditis 
Pleural effusion 
PE/Pleurisy 
Pneumonia 
Pneumothorax 
GORD 
Dissection of the aorta 
Musculoskeletal 
Psychological
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What investigations would you do for someone you think might have angina

A
  1. ECG - usually normal (Consider exercise ECG)
  2. Stress Echo (Pictures of heart following dobutamine administration)
  3. Perfusion MRI
  4. CT coronary angiogram
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What might an ECG on someone with angina show

A

ST depression

Flat inverted T waves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What lifestyle changes should someone with angina make?

A

Stop smoking
Weight loss
Increase exercise
Healthy diet (Increase fruit, veg and oily fish)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What treatments may be used in the secondary prevention of angina

A
  1. Aspirin
  2. ACEi
  3. Statins
  4. Antihypertensives
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What three anti-anginal treatments may be used in the treatment of symptomatic angina

A
  1. GTN spray
  2. Beta blocker (Atenolol)
  3. Calcium channel blocker (Verapamil, amlodipine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Describe the action of beta blockers in the treatment of angina

A

Antagonise sympathetic activity so decrease chrontropic (HR) and inotropic (Contractility) heart effects leading to decreased cardiac output and decreased O2 demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the side effects of beta blockers

A 
Bronchospasm
Cold fingers 
Bradycardia 
Tiredness 
Erectile dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

In which individuals are beta blockers contraindicated

A

Asthmatics
Heart failure
Hypotension
Bradyarrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Describe the action of nitrates in the treatment of angina

A

GTN spray is a venodilator –> Reduces venous return –> Reduced preload –> Reduced myocardial work and demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Describe the action of calcium channel blockers in the treatment of angina

A

Arteriodilators –> Cause reduced BP –> Reduced after load –> Reduced myocardial demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Name 2 drugs that might be used in someone with angina or in someone at risk of angina to improve their prognosis

A

Aspirin

Statins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Describe the action of aspirin

A

Irreversibly inhibits COX-1 reducing thromboxane A2 synthesis which reduces platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is a side effect of aspirin

A

Gastric irritation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is the effect of statins

A

HMG CoA inhibitors which reduces cholesterol production by the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Define revascularisation

A

Restore patent coronary arteries and increase flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Name 2 types of revascularisation

A

Percutaneous Coronary Intervention (PCI)

Coronary Artery Bypass Graft (CABG)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Which artery and which veins are commonly used in CABG

A 
Internal mammary artery (To supply LAD)
Saphenous Vein (To supply RCA)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Give 2 advantages and 1 disadvantage of PCI

A

Less invasive
Convenient and acceptable

High risk of restenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Give 1 advantages and 2 disadvantage of CABG

A

Good prognosis after surgery
Very invasive
Long recovery time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are acute coronary syndromes

A

ACS encompasses a spectrum of acute cardiac conditions including unstable angina evolving to MI (STEMI and Non STEMI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is the most common cause of ACS

A

Rupture of an atherosclerotic plaque and subsequent arterial thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are the uncommon causes of ACS

A

Coronary vasospasm
Drug abuse
Coronary artery dissection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Describe the pathophysiology of ACS

A

Atherosclerosis –> Plaque rupture –> Platelet aggregation –> Thrombosis formation –> Ischaemia and infarction –> Necrosis of cells –> Permanent heart muscle damage and ACS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is a type 1 MI

A

Spontaneous MI with ischaemia due to plaque rupture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What is a type 2 MI

A

Secondary to ischaemia due to increased O2 demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What causes an STEMI to develop

A

Complete occlusion of a major coronary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What causes a Non STEMI

A

Developing complete occlusion of a minor or partial coronary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Why do you see increase serum troponin in NSTEMI and STEMI

A

Occluding thrombus causes necrosis of cells and myocardial damage - Troponin is sensitive marker for cardiac muscle injury so is significantly raised to reflect this

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is the issue with looking at troponin for MI

A

It is not specific for acute coronary syndromes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What are three signs of unstable angina

A
  1. Cardiac chest pain at rest
  2. Cardiac chest pain with crescendo patterns
  3. No significant rise in troponin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What are 6 symptoms of an MI

A
  1. Unremitting and severe central chest pain
  2. Pain occurs at rest
  3. sweating
  4. Breathlessness
  5. Nausea
  6. Vomiting
  7. 1/3 occur in bed at night
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What are 5 potential complications of MI

A
  1. HF
  2. Rupture of infarcted ventricle
  3. Rupture of inter ventricular septum
  4. Mitral regurgitation
  5. Arrhythmias
  6. Heart block
  7. Pericarditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What are three non modifiable risk factors for MI

A

Gender (Male)
Age (Older)
Family history

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What are the modifiable risk factors for MI

A
  1. Smoking
  2. Obesity
  3. Hyperlipidaemia
  4. Diabetes
  5. Hypertension
  6. Sendentary lifestyle
  7. Stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What are the signs of an MI

A 
Distress 
Pallor 
Anxiety 
Brady/tachycardia 
High/low BP 
4th heart sounds 
HF sounds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is the differential diagnosis for MI

A 
Pericarditis 
Stable angina 
Aortic dissection 
GORD 
Pneumothorax 
MSK pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What investigations would you do on someone you suspect to have ACS

A
  1. ECG
  2. Blood tests
  3. Chest x-ray (Cardiomegaly, pulmonary oedema, wide mediastinum)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What might an ECG of someone with unstable angina show

A

Might be normal or show some T wave inversion and ST depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What might the ECG of someone with NSTEMI show

A

T wave inversion
ST depression
No Q waves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What might the ECG of someone with a STEMI show

A

ST elevation
Tall T waves
Q waves
T wave inversion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What would the troponin levels be like in someone with unstable angina

A

Normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What would serum troponin levels be like in someone with STEMI/NSTEMI

A

Significantly raised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

In what other conditions might you see in raised troponin

A
  1. gram negative sepsis
  2. Pulmonary embolism
  3. Myocarditis
  4. Heart failure
  5. Arrhythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Other than troponin, what other bloods tests might you do

A

FBC
U/Es
Glucose
Lipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Describe the initial management of ACS

A
  1. Call 999
  2. if STEMI then paramedics should call PCI centre for transfer
  3. Aspirin 300mg
  4. Pain relief (Morphine)
  5. Oxygen if hypoxic
  6. Nitrates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What is the hospital management for a STEMI

A
  1. ECG
  2. O2
  3. IV access for bloods
  4. brief assessment
  5. Antiplatelet
  6. Analgesics
  7. Anti-ischaemic (GTN, Beta-blocker)
  8. Low molecular weight heparin
  9. Primary PCI or thrombolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is the treatment of choice for STEMI

A

PCI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What is the function of P2Y12

A

Amplifies platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What are three side effects of P2Y12 inhibitors

A

Bleeding
Rash
GI disturbance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Describe the secondary prevention therapy for people having a STEMI

A
  1. Aspirin
  2. Clopidogrel (P2Y12 inhibitor)
  3. Statins
  4. Beta blocker
  5. ACE Inhibitor
  6. Modification of risk factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What is dual anti-platelet therapy

A

Aspirin + Clopidogrel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What are the complications of surgical intervention for MI

A

LV dysfunction leading to HF, arrhythmia, pericarditis, ventricular wall thrombus, DVT and PE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What factors affect the response to clopidogrel

A 
Dose 
Age 
Weight 
Disease (Diabetes + CKD)
Drug interactions (Omeprazole)
CYP2C19 loss of function alleles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

ECG - What is the J point

A

Where the QRS complex becomes the ST segment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

ECG - What is the normal axis of the QRS complex

A

-30 degrees to + 90 degrees

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

ECG - what does the P wave represent

A

Atrial depolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

ECG - How long should the pR interval be?

A

120-200ms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

ECG - what might a long PR interval indicate

A

Heart block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

ECG - How long should the QT interval be

A

0.35-0.45s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

ECG - what does the QRS complex represent

A

Ventricular depolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

ECG - What does the T wave represent

A

Ventricular repolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

ECG - where would you place lead I

A

From the right arm to the left arm with the positive electrode on the left arm (Axis = 0 degrees)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

ECG - where would you place lead II

A

From the right arm to the left leg with positive electro on the left leg (Axis 60 degrees)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

ECG - where would you place lead III

A

From the left arm to the left leg with the positive electrode on the left leg (Axis 120 degrees)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

ECG - where would you place lead avF

A

Halfway between the right arm and left arm to the left leg with the positive electrode at the left leg (Axis 90 degrees)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

ECG - Where would you place lead avL

A

From halfway between the right arm and the left leg to the left arm with the positive electrode at the left arm (Axis 30 degrees)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

ECG where would you place lead avR

A

From halfway between the left arm and the left leg to the right arm with the positive electrode being at the right arm 9Axis 150degrees)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What is the dominant pacemaker of the heart

A

SAN (60-100bpm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Ho many seconds should the QRS complex be

A

Less than 110ms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

In which leads would you expect QRS complex to be upright

A

Leads 1 and 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

In which leads are all wave negative

A

AVR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

In which leads must the R wave grow

A

V1-4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

in which leads must the S wave grow

A

From chest leads V1-3. Disappears in V6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

In which leads should T waves and P waves be upright

A

Leads 1,2, V2-V6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What might tall pointed P waves on an ECG suggest

A

Right atrial enlargement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

What might notched M shaped P waves on an ECG suggest (Bifid P waves)

A

Left atrial enlargement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Give 3 signs of abnormal T waves

A
  1. Symmetrical
  2. Tall and peaked
  3. Biphasic or inverted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

What happens to the QT interval when HR increases

A

QT interval decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

What are the symptoms of DVT

A 
Non specific symptoms
Pain 
Swelling 
Tenderness
Warmth 
Discolouration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

What investigations might be done in order to diagnose a DVT

A
  1. Ultrasound compression
    (If vein won’t compress then it is full of clot)
  2. D-dimer (Looks for fibrin breakdown products) - if normal you can exclude DVT - If positive it doesn’t confirm DVT diagnosis (need to go on to do the ultrasound)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What is the treatment for DVT

A
  1. Low molecular weight heparin
  2. Oral warfarin
  3. Compression socks
  4. Treat the underlying cause (Malignancy and thrombosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

What are the 2 types of thrombosis

A

Spontaneous

Provoked

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

What are the 5 risk factors for DVT

A
  1. Surgery, immobility, leg fracture
  2. oral contraceptive pill, Hormone replacement therapy
  3. Long haul flights
  4. Genetic disposition (Thrombophillia)
  5. Pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

How can DVTs be prevented

A
  1. Hydration
  2. Early mobilisation
  3. Compression stockings
  4. Foot pumps
  5. Low molecular weight heparin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Which individuals are at low risk of thromboprophylaxis

A
  1. <40 years
  2. Surgery <30mins
  3. Early mobilisation and hydration
  4. No chemical
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Which individuals are at high risk of thromboprophylaxis

A
  1. Hip and knee surgery

2. Prolonged immobility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

What might be a consequence of a dislodged DVT

A

Pulmonary embolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

How would you describe an arterial thrombosis

A

Platelet rich - white thrombus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

How would you describe a venous thrombosis

A

Fibrin rich - red thrombus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

What are the potential consequences of DVT that breaks off an blocks a pulmonary artery

A

Hypotension, cyanosis, severe dyspnoea, right sided heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

What is the differential diagnosis of PE

A

Musculoskeletal, infection, malignancy, pneumothorax, cardiac, gastro

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

What are the symptoms of PE

A

Breathlessness

pLeuritic chest pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

What are the signs of PE

A

Tachycardia
Tachypnoea
Pleural rub

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

What are the investigations for someone suspected to have a PE

A

CXR (Normal)
ECG (Sinus tachycardia)
Blood gases (Type 1 respiratory failure)
Mainly done to rule out other causes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

What further investigations may be carried out in someone suspected of having a PE

A

D-dimer
Ventilation perfusion scan
Spiral CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

What is the treatment for PE

A

Low molecular weight heparin or oral warfarin
Direct oral anticoagulants
Treat the underlying cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

What are the preventative measures for PE

A

Early mobilisation
Mechanical with stockings
Chemical = LMWH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

How does warfarin work

A

Prevents the synthesis of active clotting factors II, VII, IX and X leading to anti-coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

What is warfarin an antagonist of

A

Vitamin K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

Why is warfarin difficult to use

A

Lots of interactions
Difficult to get into therapeutic range
needs constant monitoring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

Define thrombosis

A

Blood coagulation inside a vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

What are the 3 potential consequences of an arterial thrombus

A
  1. Myocardial infarction
  2. Stroke
  3. Peripheral vascular disease ie gangrene
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

What are the risk factors for atherosclerosis which is a precursor for arterial thrombosis

A 
Smoking 
Diabetes 
Hypertension 
Hyperlipidaemia 
Obesity 
Stress/Type A personality
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

What are the causes of Venous thrombosis

A 
Circumstantial 
Surgery 
Imobilisation 
Oestrogens 
malignancy 
Long haul flights 
Genetic 
Acquired
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

What is the treatment for venous thrombus

A

LMWH
Oral warfarin for 3-6 months
DOAC for 3-6months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

What is a psychosocial factor

A

Factors influencing psychological responses to the social environment and pathophysiological changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

What are the 4 psychosocial factors that increase CHD

A
  1. Type A personality (Hostile, competitive, impatient - identify with questionnaires)
  2. Depression/Anxiety (Measure with MMPI)
  3. Psychosocial work (More than 11hours per day, high demand with low control)
  4. Lack of social support
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

What can doctors do for those with CHD risk

A
  1. Observe behaviour patterns
  2. identify depression/anxiety
  3. Ask questions from assessment tools
  4. Ask about occupation
  5. Liaise with social support services
  6. Vascular screening
  7. Risk reduction through promoting healthier lifestyles
  8. Qrisk2 score
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

How much fluid is in the pericardial space?

A

50ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

What is the function of the serous fluid between the visceral and parietal pericardium

A

Acts as a lubricant so to allow smooth movement of the heart inside the pericardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

What is the function of the pericardium

A

It restrains the filling volume of the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

Define pericarditis

A

Inflammatory pericardial syndrome with or without effusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

What are the causes of pericarditis

A 
Viral (Enterovirus, Herpesviruses)
Bacterial (TB, Staph)
Autoimmune (Sjorgens, RA)
Neoplastic 
Metabolic (Uraemia, hypothyroidism)
Trauma and iatrogenic 
Idiopathic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

How can acute pericarditis be clinically diagnosed?

A

Need 2 of the following

  1. Chest pain
  2. Friction rub
  3. ECG changes
  4. Pericardial effusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

Give 5 symptoms of pericarditis

A
  1. Central chest pain
  2. Dyspnoea
  3. Cough
  4. Hiccups
  5. Skin rash
  6. Viral prodrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

Describe the properties of pericarditis chest pain

A 
Relieved by sitting forward 
Worse when lying down 
Severe 
Sharp 
Pleuritic 
Rapid onset
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

Why might someone with pericarditis have hiccups

A

Irritation of the phrenic nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

What are the differential diagnoses for pericarditis

A

Pneumonia, pleural effusion, PE, GORD, MI, GI inflammation, aortic dissection, pneumothorax, pancreatitis, peritonitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

What investigations might you do on someone with pericarditis

A
  1. ECG
  2. CXR
  3. Bloods (FBC, ESR, CRP)
  4. Echocardiogram
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

What might an ECG look like in someone with acute pericarditis

A

PR depression seen in most leads

Saddle shaped concave ST elevation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

What is the treatment for pericarditis

A
  1. Sedntary lifestyle until symptoms resolve
  2. Ibuprofren
  3. Colchicine (Anti-inflammatory)
  4. Immunosuppressants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

What is pericardial effusion

A

Collection of fluid within the potential space of the serous pericardial sac

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

What can be the effect of large fluid collection in the pericardial sac

A

Causes ventricular filling to be compromised leading to cardiac tamponade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

What are the symptoms of pericardial effusion

A
  1. Soft distant heart sounds
  2. Apex beat obscured
  3. Raised jugular venous pressure
  4. Dyspnoea
  5. Bronchial breathing
  6. Signs of tamponade
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

What are the symptoms of cardiac tamponade

A
  1. High pulse with low Bp
  2. High jugular venous pressure
  3. Muffled 1st and second heart sounds
  4. Kussmauls sign (Raised jugular venous pressure and increased vein distension during inspiration
  5. Pulsus paradoxus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

What is pulsus paradoxes

A

Exaggeration of normal variation in the pulse pressure seen with inspiration such that there is a drop in systolic blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

What investigations are used in the Diagnosis of pleural effusion

A
  1. CXR
  2. ECG
    - low voltage QRS
    - Sinus tachycardia
  3. Echocardiogram (Echo free zone surrounding the heart)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

What investigations are used in the diagnosis of pleural effusion

A
  1. CXR
  2. Becks triad
  3. ECG
    - Low voltage QRS
  4. Echocardiogram
    - echo free zone around the heart
    - Late diastolic collapse of right atrium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

What is Becks triad

A

Falling blood pressure
Rising jugular venous pressure
Muffled heart sounds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

What is the treatment of pleural effusion

A

Treat underlying cause

Most resolve spontaneously

May re-accumulate due to malignancy which requires pericardial fenestration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

what is the treatment for cardiac tamponade

A

Urgent drainage via pericardiocentesis to drain the fluid and relieve the pressure on the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

What is constrictive pericarditis

A

Where the pericardium becomes thick, fibrous and calcified due to TB, bacterial infection and rheumatic heart disease

This causes the pericardium to become inelastic and interfere with diastolic filling of the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

What are the symptoms of constrictive pericarditis

A 
Kussmauls sign
Pulsus Paradoxus 
Diffuse heart sounds 
Ascites 
Oedema 
RHF 
Atrial dilatations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

How would you diagnose constrictive pericarditis

A

CXR
- small heart with or without pericardial calcification

ECG
- Low voltage QRS

Echocardiogram

  • Thickened, calcified pericardium
  • Small ventricular cavities with normal wall thickness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

What is the treatment for constrictive pericarditis

A

Complete resection of the pericardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

Why do we treat hypertension

A

Because it is an important preventable cause of premature morbidity and mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

Hypertension is a major risk factor for what conditions?

A 
Stroke 
MI
HF
Chronic renal disease 
Cognitive decline 
Premature death 
Atrial fibrillation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

What is the criteria for a diagnosis of hypertension

A

Clinic BP of 140/90 mmHg or higher

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

What are individuals with suspected hypertension offered to monitor their blood pressure

A

Ambulatory blood pressure monitoring to confirm the diagnosis of hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

What are the clinic and ambulatory criteria for stage 1 hypertension

A 
clinic = 140/90
Am = 135/85
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

What are the clinic and ambulatory criteria for stage 2 hypertension

A 
clinic = 160/100
Am = 150/95
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

What are the diagnostic criteria for severe hypertension

A

Systolic 180

Diastolic 110

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

What are the treatment options for primary hypertension

A
  1. Lifestyle modification

2. Antihypertensive drug therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

Who is likely to develop secondary hypertension

A

Young individuals
Individuals who are resistant to treatment
Those showing symptoms and signs of the secondary underlying cause (Kidneys, adrenal glands, renal artery stenosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
Q

Who is offered hypertensive treatment?

A

People aged over the age of 80 with stage 1 hypertension who have one or more of the following

  1. Target organ damage
  2. Established CVD
  3. Renal disease
  4. Diabetes
  5. A 10 year cardiovascular risk of 20% or greater

Offer antihypertensive treatment to people of any age with stage 2 hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

What is the BP target for someone under the age of 80

A

<140/90 for clinic

<135/85 for ambulatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
193
Q

What is the BP target for someone over the age of 80

A

<150/90 f0r clinic

<145/85 for ambulatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
194
Q

What are the mechanisms of blood pressure control

A
  1. Cardiac output and peripheral resistance of circulation
  2. Interplay between renin-angiotensin-aldosterone and sympathetic nervous system (Drop in Bp causes noradrenaline release causing vasoconstriction and increased contractility of the heart and increase PR, CO and BP)
  3. Local vascular vasoconstrictor and vasodilator mediators
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
195
Q

What is the driver of chronic hypertension

A

Peripheral resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
196
Q

Describe the renin-angiotensin-aldosterone system

A

Angiotensinogen converted by renin to angiotensin I.

Ang I converted to Ang II by ACE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
197
Q

What are the effects of angiotensin II

A

Vascular hypertrophy and hyperplasia

Aldosterone release leading to sodium reabsorption

Vasoconstriction leading to increased peripheral
resistance and cardiac output

Activates sympathetic nervous system leading to increased noradrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
198
Q

What are the effects of sympathetic NS on RAAS, CO and peripheral resistance

A

Noradrenaline causes renin release

Noradrenaline causes increases peripheral resistance and cardiac output

Noradrenaline is a vasoconstrictor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
199
Q

What are the main clinical indications for the use of ACEi

A

Hypertension
Heart failure
Diabetic nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
200
Q

Give 4 examples of ACEi

A 
End in 'pril'
Ramipril 
Perindopril 
Enalapril 
Trandolapril
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
201
Q

What are the adverse effects of ACEi related to decreased ANG II formation

A

Relate to decreased ANG II formation

  1. Hypotension
  2. Acute renal failure because ANG II helps to perfuse the glomerulus by constricting the artery leaving the kidney
  3. Hyperkalaemia (Due to blocking aldosterone)
  4. Teratogenic effects in pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
202
Q

Why do you get increased bradykinin production with ACEi

A

Because ACE is a non specific enzyme that converts bradykinin into inactive peptides so if you block ACE then you increase the amount of circulating bradykinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
203
Q

What are the adverse effects of ACEi associated with increased kinin formation

A

Persistent dry cough
Rash
Anaphylactoid reactions due to increased bradykinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
204
Q

How do angiotensin II receptor blockers work?

A

Any ANG II produced is blocked from binding to the AT-1 receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
205
Q

What are the main clinical indications for angiotensin II receptor blockers

A

Hypertension
Diabetic nephropathy
Heart failure (When ACE-I contraindicated)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
206
Q

Name some examples of angiotensin II receptor blocker drugs

A

End in ‘sartan’

Candesartan 
Losartan 
Valsartan 
Irbesartan 
Telmisartan
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
207
Q

What are the main adverse effects of angiotensin II receptor blockers

A 
Symptomatic hypotension (Especially in volume depleted patients)
Hyperkalaemia 
Potential for renal dysfunction 
Rash 
Angio-oedema 
Contraindicated in pregnancy 
GENERALLY WELL TOLERATED
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
208
Q

What are the main clinical indications for calcium channel blockers

A

Hypertension
Ischaemic heart disease (Angina)
Arrhythmias (Tachycardia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
209
Q

Name some examples of calcium channel blockers

A 
End in 'pine'
Amlodipine 
Nifedipine 
Felodipine 
Lacidipine 
Diltiazem 
Verapamil
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
210
Q

What is the action of calcium channel blockers

A

To block L-type calcium channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
211
Q

What are the three different categories of calcium channel blocker

A
  1. Dihydropyridines = nifedipine, amlodipine, felodipine, lacidipine
  2. Phenylalkylamines = verapamil
  3. Benzothiazepines = Diltiazem
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
212
Q

Where do dihydropyridine calcium channel blockers preferentially act and what is their M.O.A?

A

Preferentially affect the vascular smooth muscle where they act as arteriolar vasodilators as calcium plays an important role in vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
213
Q

Where do Phenylalkylamines calcium channel blockers preferentially act and what is their MOA

A

Mainly affect heart calcium channels and are negatively chronotropic (Reduce HR) and negatively ionotropic (Reduce force of contraction

Verapamil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
214
Q

Where do benzodiazepine calcium channel blockers preferentially act and what is their mechanism of action

A

Intermediate heart and peripheral vascular effects

Arteriole vasodilator and -ve chrono and ionotropic

Diltiazem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
215
Q

What adverse effects are associated with dihydropyridines calcium channel blockers

A

Due to peripheral vasodilation

  • Flushing
  • Headache
  • Oedema
  • Palpitations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
216
Q

What adverse effects are associated with verapamil an diltiazem calcium channel blockers

A

Due to the negative chronotropic effects

  • Bradycardia
  • Atrioventricular block
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
217
Q

What adverse effects are associated with verapamil

A

Due to the negative ionotropic effects
Worsening of cardiac failure
bradycardia
Constipation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
218
Q

What are the main clinical indications for the use of beta-blockers

A

Ischaemic heart disease (Angina)
Heart failure
Arrhythmia
Hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
219
Q

Name some examples of beta blockers

A 
Bisoprosol 
Atenolol
Propanolol
Carvediol
Metoprolol
Nadolol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
220
Q

Which beta blockers are B1 selective

A

Metoprolol

Bisoprolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
221
Q

Which beta blocker is non selective

A

Propranolol
Nadolol
Carvediol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
222
Q

What are the adverse effects of beta blockers

A 
Fatigue 
Headache 
Sleep disturbance 
Bradycardia 
Hypotension 
Cold peripheries 
Erectile dysfunction 
Worsening of Asthma (Bronchospasm), PVD, HF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
223
Q

How do diuretics work

A

Increase urine and salt excretion so useful in diseases of congestion

224
Q

What are the main clinical uses of diuretics

A

Hypertension

Heart failure

225
Q

What are the 4 classes of diuretic

A

Thiazides
Loop diuretics
Potassium sparring diuretics
Aldosterone antagonists

226
Q

Where do thiazide drugs work and name some examples

A

Distal tubule
Bendroflumethiazide
Hydrochloromethiazide
Clorthalidone

227
Q

Where do loop diuretics work and name some examples

A

Loop of henle
Furosemide (Blocks NKCC2)
Bumetanide

228
Q

Name some examples of potassium sparing diuretics

A

Spironolactone
Eplerenone
AMiloride
Triameterine

229
Q

What are the adverse effects of diuretics

A 
Hypotension 
Hypovolaemia 
Hypokalaemia 
Hyponatraemia 
hypomagnesaemia 
hypocalcaemia 
Raised uric acid (Gout)
Erectile dysfunction 
Impaired glucose tolerance
230
Q

Name three other antihypertensive medications

A

A1 adrenoceptor blockers (Doxazosin)
Centrally acting antihypertensives (Moxonidine/methyldopa (Used in pregnancy)
Direct renin inhibitors (Aliskiren)

231
Q

What is the front line antihypertensive treatment for individuals under 55 years

A

ACE inhibitor or ANG II receptor blocker

232
Q

What is the front line treatment for over 55’s or afro-caribbean of any age

A

Calcium channel blocker

233
Q

What is the second treatment combination for hypertension

A

ACE-I/ARB + CCB

234
Q

What is the third line treatment combination for hypertension

A

ACE-I/ARB + CCB + Thiazide diuretic

235
Q

What is the treatment options for resistant hypertension

A

Spironolactone
High dose thiazide diuretic
Alpha blocker
Beta blocker

236
Q

Define heart failure

A

Complex clinical syndrome of symptoms and signs that suggest the efficiency of the heart as a pump is impaired

237
Q

What is the most common cause of heart disease

A

Coronary artery disease

238
Q

What is the symptomatic treatment option for HF

A

Diuretics to treat the congestion - usually loop diuretics such as furosemide

239
Q

What are the disease influencing treatment options for HF

A

Inhibition of RAAS (ACEi or ARBs

Inhibition of sympathetic nervous system (Beta blockers

240
Q

Why is it important to titrate medication doses in patients with heart failure

A

Because patients are still reliant on the RAAS and sympathetic nervous system to maintain their hearts

241
Q

What are the alternative treatment options for HF patients who are ACE-I intolerant

A

Aldosterone antagonists such as spirolactone and diparalone

Neprilysin inhibitor

Hydralazine/nitrate combination

Digoxin or ivabradine

242
Q

Why are neprilysin inhibitors used in the treatment of HF

A

Naturietic peptides cause you to lose salt and fluid but these are broken down by neprilysin so inhibit it and you potentiate the effects of neprilysin

243
Q

What are the 2 types of cardiac natriuretic peptides

A

Atrial natriuretic peptide (Atria)

Brain natriuretic peptide (Ventricles)

244
Q

What causes natriuretic peptides to be released

A

Stretching of the atrial and ventricular muscle cells

Raised atrial or ventricular pressure

Volume overload

245
Q

What are the main physiological effects of natriuretic peptides

A

Increase sodium excretion and water excretion

Relax the vascular smooth muscle

Increase vascular permeability

Inhibit the release of aldosterone, ANG II or ADH

246
Q

Name an example of a neprilysin inhibitor

A

Sacubitril

247
Q

What is entresto

A

A combination of sacubitril and valsartan

248
Q

What is the physiological effect of nitrate medication

A

Arterial and venous dilators

Reduce the preload and after load and lower BP

249
Q

What are the main clinical uses of nitrates

A

IHD (Angina)

Heart failure

250
Q

Name some examples of nitrate medication

A

Isosorbide mononitrate (Long acting)
GTN spray
GTN Infusion

251
Q

What are the main adverse effects of Nitrates

A

Headache

GTN syncope

252
Q

What are the treatment options for chronic stable angina

A
  1. Anti-platelet (Aspirin or clopidogrel)
  2. Statins (Atorvastatin)
  3. GTN spray for acute attack
  4. Beta blocker or calcium channel blocker
253
Q

What are the treatment options for acute coronary syndrome (STEMI and NSTEMI)

A
  1. Pain relief (GTN and opioids)
  2. Dual anti platelet therapy (Aspirin + Ticagrelor)
  3. Antithrombin (Fondaparinux)
  4. Glycoprotein IIb IIIa inhibitor
  5. Background angina therapy (Beta blocker, CCB)
  6. Lipid lowering therapy (statins)
  7. Surgical (PCI or CABG)
254
Q

Describe class I anti-arrhythmic drugs

A

Sodium channel blockers used for tachycardia arrhythmias

1a = lengthen the duration of action potential for atrial arrhythmias

1b = Shortens or has no effect on action potential duration for ventricular arrhythmias

1c = no effect on action potential but promotes greater sodium current depression

255
Q

Give an example of class I 1a anti-arrhythmic drug

A

Disopyramide
Quinidine
Procainamide

256
Q

Give an example of Class I 1b anti-arrhythmic drug

A

Lidocaine

Mexilitene

257
Q

Give an example of class I 1c anti-arrhythmic drug

A

Flecainide

Propafenone

258
Q

Describe class II anti-arrhythmic drugs and give some examples

A

Beta-adrenoceptor antagonists
Propanolol, nadolol, carvedilol (Non-selective)
Bisoprolol, metoprolol (B1 selective)

259
Q

Describe class III anti-arrhythmic drugs and give some examples

A

Prolong the action potential as they are potassium channel blockers so they block repolarisation

Amiodarone
Sotalol

260
Q

Describe class IV anti-arrhythmic drugs

A

Calcium channel blockers such as verapamil, dilitiazem

261
Q

What is digoxin and how does it work

A

Cardiac glycoside that inhibits the Na+/K+ pump

262
Q

What are the main effects of digoxin on the heart

A

Bradycardia
Slow of atrioventricular conduction
Increased ectopic activity
Increased force of contraction

263
Q

What are the main side effects of digoxin

A

Nausea, vomiting, diarrhoea, confusion

264
Q

In what diseases is digoxin clinically indicated

A

Atrial fibrillation and severe heart failure

265
Q

Define cardiomyopathy

A

Group of diseases of the myocardium that affect the mechanical and electrical functions of the heart

266
Q

What are the 4 types of cardiomyopathy

A
  1. Hypertrophic (Muscle is thickened)
  2. Dilated (Heart chambers are dilated)
  3. Restricted
  4. Arrhythmogenic (Heart structure abnormality leads to rhythm disturbance)
267
Q

What are the risk factors of a cardiomyopathy

A 
Family history 
High blood pressure 
Obesity 
Diabetes 
Previous MI
268
Q

What is hypertrophic cardiomyopathy

A

Ventricular hypertrophy/thickening of the muscle (Septal hypertrophy) - leads to a smaller ventricular cavity

269
Q

How many people have a hypertrophic cardiomyopathy

A

1 in 500

270
Q

What is the inheritance pattern of hypertrophic cardiomyopathy

A

Autosomal dominant - familial

271
Q

What is the pathophysiology of hypertrophic cardiomyopathy

A

Caused by sarcomeric protein gene mutations leading to hypertrophic non-compliant vesicles that impair diastolic filling and result in reduced SV and CO
Also disarray of cardiac myocytes which affects cinduction

272
Q

What are the symptoms of a hypertrophic cardiomyopathy

A 
Angina and chest pain 
Dyspnoea 
Exertional syncope
Sudden death 
S4
jerky pulse 
Double apex beat 
ESM
273
Q

What are the signs of hypertrophic cardiomyopathy

A

Jerky carotid pulse
Ejection systolic murmur
Double apex beat
S4

274
Q

What 4 investigations would you carry out in someone you believe to have hypertrophic cardiomyopathy

A

ECG - LVH and deep Q waves
Echocardiogram (MR SAM ASH)

  • Mitral Regurgitation
  • Systolic anterior motion
  • Asymmetrical hypertrophy
275
Q

What would the ECG of someone with hypertrophic cardiomyopathy show

A

Left ventricular hypertrophy with progressive T wave inversion and deep Q waves

276
Q

What would the echocardiogram of someone with hypertrophic cardiomyopathy show

(MR SAM ASH)

A

Ventricular hypertrophy with small left ventricle

Mitral regurgitation
Systolic anterior motion
Asymmetrical hypertrophy

277
Q

What is the treatment for hypertrophic cardiomyopathy

A
  1. -ve inotropes ie. B-blockers (Atenolol) and CCB (Verapamil)
  2. Amiodarone (Anti-arrhythmic)
  3. Septal myomectomy
278
Q

What is a dilated cardiomyopathy

A

Where the left ventricle has become dilated so it contracts poorly and has thin muscle

Poorly generated contractile force leads to progressive dilatation of the heart

279
Q

What is the inheritance pattern of dilated cardiomyopathy

A

Autosomal dominant - familial

280
Q

What is the pathophysiology of dilated cardiomyopathy

A

Cytoskeletal gene mutations

281
Q

What are the other causes of dilated cardiomyopathy (DILATES)

A 
Dystrophy 
Infection (Myocarditis) 
Late pregnancy 
Autoimmune SS 
Toxins (EtOH)
Endo = Thyrotoxicosis
282
Q

What are the symptoms of dilated cardimyopathy

A 
Arrhythmias
dyspnoea 
fatigue 
HF 
Thromboembolism
283
Q

What are the signs of dilated cardiomyopathy

A

Increased jugular venous pressure
Decreased blood pressure
S3 gallop
Displaced Apex beat

284
Q

What investigations would you conduct in someone suspected to have dilated cardiomyopathy

A

CXR (Cardiomegaly, Pulomonary oedema)

ECG (Tachycardia, T wave inversion)

ECHO (Globally dilated heart with decreased ejection fraction)

Cathether and biopsy (Myocardial fibre disarray)

285
Q

What are the treamtne options for dilated cardiomyopathy

A

Bed rest

Diuretics, ACEi, digoxin for the HF

286
Q

What is restrictive cardiomyopathy

A

Poor dilation of the heart restricts the hearts ability to take on blood and pass it to the rest of the body due to a rigid myocardium

287
Q

What are the causes of restrictive cardiomyopathy (MiSSHAPEN

A 
Sarcoid 
Systemic Sclerosis 
Haemochromatosis 
Amyloidosis 
Primary end-myocardial fibrosis 
Eosinophilia 
Neoplasia
288
Q

What is the clinical presentation of restive cardiomyopathy

A 
Dyspnoea 
Fatigue 
Embolic symptoms 
Elevated jugular venous pressure 
Hepatic enlargement 
Third and fourth heart sounds
289
Q

What investigations would yo carry out in someone with restrictive cardiomyopathy

A

CXR, ECHO and ECG are abnormal but non specific so carry out cardiac catheterisation

290
Q

What is the treatment for restrictive cardiomyopathy

A

No treatment with poor prognosis

Consider transplant

291
Q

What is arrhythmogenic cardiomyopathy

A

Progressive genetic cardiomyopathy characterised by progressive fatty and fibrous replacement of ventricular myocardium

292
Q

What is the inheritance pattern of arrhythmogenic cardiomyopathy

A

Autosomal dominant but in incomplete penetrance it can be recessive

293
Q

What is the pathophysiology of arrhythmogenic cardiomyopathy

A

Desmosome (Holds cardiac cells together) gene mutation

294
Q

What is the clinical presentation of arrhythmogenic cardiomyopathy

A

Cardiac cells are not held as closely together due to desmosome mutation leading to arrhythmias

Syncope

295
Q

What investigations would you conduct in an individual you suspect to have arrhythmogenic cardiomyopathy

A

ECG may show T wave inversion, be abnormal for right ventricle and show epsilon waves

ECHO may be normal but in advanced disease might show right ventricular dilatation

Genetic testing

296
Q

What is the treatment for arrhythmogenic cardiomyopathy

A

Beta blockers for patients with non life-threatening symptoms

Amiodarone for patients with more severe symptoms

297
Q

What is Naxos disease

A

Fibro-fatty infiltration of the heart and ventricular arrhythmias

298
Q

What is the clinical presentation of Naxos disease

A

Plantar keratoderma due to cell separation
Wooley hair
Recessive disease

299
Q

What is a channelopathy

A

Inherited arrhythmia caused by ion channel protein gene mutations usually related to K+,Na+ and Ca2+

300
Q

Name some examples of channelopathies

A 
Long QT 
Short QT 
Brugada 
Catecholamingeric polymorphic ventricular tachycardia 
Wolff Parkinson White
301
Q

What may channelopathies lead to?

A

Sudden arrhythmic death syndrome

302
Q

What is the clinical presentation of channelopathies

A

Structurally normal heart but recurrent syncopes

303
Q

What is familial hypercholesterolaemia

A

Inherited abnormality of cholesterol metabolism due to mutation in the LDL receptor which normally removes cholesterol from the circulation - causes 100x increase in risk of heart attack

304
Q

What are the clinical manifestations of hypercholesterolaemia

A

Lipid seen in the hands and the eyes

305
Q

Name some aorto-vascular syndromes

A

Marfan
Loeys-dietz
Ehler danlos

306
Q

What is the pathophysiology of sort-vascular syndromes

A

Abnormalities in fibrillar which is densely located at the base of the aorta making that area more susceptible to rupture

307
Q

What is the clinical presentation of patients with aortovascular syndromes

A

Tall and lanky with arm span wider than height
Changes in palate and height
Can develop aortic aneurysm

308
Q

What is heart failure

A

When cardiac output is inadequate to deliver blood and O2 at a rate that meets the requirements of metabolising tissue in the body despite adequate filling pressures

309
Q

What is the pathophysiology of compensated heart failure

A
  1. Starling effect causes the heart to dilate to enhance contractility
  2. This leads to remodelling mainly hypertrophy
  3. RAAS and ANP/BNP release
  4. Sympathetic activation
310
Q

What is the pathophysiology of decompensated heart failure

A
  1. Progressive dilatation leads t impaired contractility
  2. Hypertrophy leads to myocardial ischaemia
  3. Activation of RAAS leads to Na+ and H2O retention and increased venous pressure which leads to oedema
  4. Sympathetic excess leads to increased afterload and decreased cardiac output
311
Q

What is systolic cardiac failure

A

Impaired contraction

312
Q

What is diastolic cardiac failure

A

Impaired filling

313
Q

What are the risk factors for heart failure

A 
65 or older 
African Descent 
Men 
Obesity 
Previous MI
314
Q

What are the causes of right sided HF

A

LVF
Cor Pulmonale
Tricuspid or pulmonary valve disease

315
Q

What are the symptoms of right sided heart failure

A

Anorexia and nausea

316
Q

What are the signs of right sided heart failure

A

Increased jugular vein pressure and distension

Hepatomegaly and splenomegaly

Pitting oedema

Ascites (Fluid build up in the peritoneal space)

317
Q

What are the 4 main causes of left sided heart failure

A
  1. Ischaemic heart disease
  2. Dilated cardiomyopathy
  3. Sustained hypertension
  4. Restrictive and hypertrophic cardiomyopathy
  5. Mitral and aortic valve disease
318
Q

What are the symptoms of left sided heart failure

A

Fatigue
Exertional dyspnoea
Orthopnoea (Difficulty breathing when lying down)
Nocturnal cough (with pink frothy sputum)
Wt loss and muscle wasting

319
Q

What are the signs of left sided heart failure

A 
Cold peripheries
Cyanosis 
Cardiomegaly 
S3 and tachycardia 
Wheeze 
Displaced apex beat
320
Q

Define acute heart failure

A

New onset or decompensation of chronic

Peripheral or pulmonary oedema

Evidence of peripheral hypo perfusion

321
Q

Define chronic heart failure

A

Develops slowly

Venous congestion common

322
Q

Outline the New York Heart Associated classification of heart failure

A
  1. No limitation of activity (asymptomatic)
  2. Comfortable at rest by dyspnoea on ordinary activity
  3. Marked limitation of normal activity
  4. Dyspnoea at rest and activity
323
Q

What investigations would you carry out in an individual excepted to have heart failure

A
  1. Bloods - looks for natriuretic peptide
  2. CXR
  3. ECG
  4. ECHO
324
Q

What would you expect to see in the bloods of someone with heart failure

A

BNP secreted from the ventricles in response to increased pressure and myocardial stretch so BNP marker of heart failure

325
Q

When analysis a CXR of a heart failure patient, what are you looking for

A 
Alveolar shadows
Karley B lines 
Cardiomegaly 
Upper lobe divisions
Pleural effusions 
Fluid in fissures
326
Q

What might the ECG of someone with HF suggest

A

Ischaemia

Hypertrophy of LA/LV

327
Q

What would you expect to see on the ECHO of someone with HF

A

Ejection fraction normally 60%

Hypertrophy

328
Q

What is the primary prevention for HF

A 
Stop smoking 
decrease salt intake 
Optimise weight 
Aspirin 
Statins
329
Q

What is the specific front line treatment for heart failure

A

ACEi/ARB + Diuretic + Beta blocker

via neurohumoral blockade (RAAS-SNS)

330
Q

What is the second treatment for heart failure

A

Spironolactone
ACEi+ ARB
Vasodilators (Hydralazine)

331
Q

What is the third line treatment option for heart failure

A

Digoxin

Cardiac resynchronisation therapy (Pacemaker)

332
Q

What are the 5 causes of heart failure

A
  1. Comment is IHD
  2. Hypertension
  3. Cardiomyopathy
  4. Excessive alcohol
  5. Obesity
333
Q

Briefly describe the pathophysiology of heart failure

A

When the heart fails, compensatory mechanisms attempt to maintain CO but as HF progresses these mechanism become exhausted and become pathophysiological

334
Q

What are the compensatory mechanisms in HF

A
  1. Sympathetic system
  2. RAAS
  3. Natriuretic peptides
  4. Ventricular dilation
  5. Ventricular hypertrophy
335
Q

Explain how the sympathetic system is compensatory in heart failure and give one disadvantage of sympathetic activation.

A

The sympathetic system improves ventricular function by increasing HR and contractility = CO maintained.
BUT it also causes arteriolar constriction which increases after load and so myocardial work

336
Q

Explain how RAAS is compensatory in heart failure and give one disadvantage of RAAS activation.

A

Reduced CO leads to reduced renal perfusion; this activates RAAS. There is increased fluid retention and so increased preload.
BUT it also causes arteriolar constriction which increases after load and so myocardial work.

337
Q

Give 3 properties of natriuretic peptides that make them compensatory in heart failure

A
  1. Diuretic.
  2. Hypotensive.
  3. Vasodilators.
338
Q

What are the 3 cardinal symptoms of HF?

A
  1. Shortness of breath.
  2. Fatigue.
  3. Peripheral oedema
339
Q

What is primary hypertension

A

When the cause is unknown (95% of cases)

340
Q

What is secondary hypertension

A

When the cause is known

341
Q

What is stage 1 hypertension

A

Clinic BP >140/90

AM BP >135/85

342
Q

What is stage 2 hypertension

A

Clinic BP >160/100

AM BP > 150/90

343
Q

What is severe hypertension

A

Clinic BP >180/110

344
Q

What is malignant hypertension

A

Clinic BP >180/110 + papilloedema and or retinal haemorrhage

345
Q

What are the causes of hypertension (remember PREDICTION)

A

Primary (95%)

Renal (Glomerularnephritis, PCKD)

Endo (Cushing’s, Conns, Phaeo, acromegaly

Drugs (Cocaine, NSAIDs, Amphetamines, alcohol, oral contraceptive pill

Intra-cranial pressure increase

CoA

Toxaemia of pregnancy

increased viscosity

Overload with fluid

Neurogenic

346
Q

What is the end organ damage caused by hypertension (remember CANER)

A

Cardiac (IHD, LVH –> CCF, AR, MR)

Aortic (Aneurysm, dissection)

Neuro (Encephalopathy, CVA)

Eyes (hypertensive retinopathy)

Renal (Proteinuria)

347
Q

What investigations would you carry out in a patient you expected to be hypertensive

A

24hr ambulatory BPM

Urine (Haematuria, ALB: creatine ratio, protein)

Bloods (FBC, U+E, eGFR, glucose)

ECG

Calculate 10yr CV risk

Echo for LVH

Fundoscopy for retinal haemorrhage or papilloedema

348
Q

What lifestyle interventions are important in the treatment of hypertension

A 
Increase exercise 
Decrease smoking 
Decrease alcohol
Decrease salt 
Decrease caffeine
349
Q

What are the indications for commencing the pharmacological management of hypertension

A

<80 years with stage 1 hypertension
(End organ damage or CV risk of >20%)

Anyone with stage II

Anyone with severe/malignant hypertension

350
Q

What are the blood pressure targets following pharmacological management

A

Under 80 = <140/90

Over 80 = <150/90

351
Q

What is the 1st line anti-hypertensive treatment for someone under the age of 55

A

ACEi/ARB

352
Q

What is the 1st line anti-hypertensive treatment for someone over the age of 55 or are black

A

CCB or thiazide diruretic

353
Q

What is the second line treatment for hypertension

A

ACEI/ARB + CCB

354
Q

What is the third line treatment for hypertension

A

ACEi/ARB + CCB + Diuretic

355
Q

What is the treatment options for someone with resistant hypertension

A

ACEi + CCB + Diuretic + Beta blocker

356
Q

What is cor pulmonate

A

RV hypertrophy and dilatation due to pulmonary hypertension

357
Q

Name 5 conditions that hypertension is a major risk factor for

A
  1. MI
  2. Stroke
  3. Heat failure
  4. Chronic renal disease
  5. Dementia
358
Q

Will anti-hypertensives make someone feel better?

A

Anti-hypertensives won’t necessarily make someone feel better as there are few symptoms associated with high BP although headache symptoms may improve.

359
Q

Name 4 valvular heart diseases

A
  1. Aortic stensis
  2. Aortic regurgitation
  3. Mitral regutgitation
  4. Mitral stenosis
360
Q

Briefly describe aortic stenosis

A

A disease where the aortic orifice is restricted so the LV cannot eject blood properly in systole leading to pressure overload

361
Q

What are the causes of aortic stenosis

A
  1. Senile calcification
  2. Congenital bicuspid valve
  3. Rheumatic fever
362
Q

Describe the pathophysiology of aortic stenosis

A

Aortic orifice is restricted so the pressure gradient between the LV and aorta increases. This increases afterload and leads to subsequent ventricular hypertrophy and ischaemia - this culminates in LVF

363
Q

When does aortic stenosis become symptomatic

A

when the valve is 1/3 its normal size

364
Q

What are the three main symptoms of aortic stenosis

A

Angina
Dyspnoea
Syncope

365
Q

What are three signs of aortic stenosis

A

Slow rising carotid pulse with decreased pulse amplitude

Narrow pulse pressure

Soft or absent S2 heart sound

Crescendo-decrescendo ejection systolic murmur

366
Q

What are the investigations to carry out in someone with suspected aortic stenosis

A 
Bloods 
ECG - LVH 
CXR - LVH and calcified AV
Echo and doppler 
(Thickened calcified cusps, pressure gradient >40, jet velocity >4 and valve area >1)
Cardiac catheterisation
367
Q

What is the definition of severe aortic stenosis

A

Pressure gradient >40mmHg
Jet velocity >4m/s
Valve area <1cm2

368
Q

What is the management for someone with aortic stenosis

A
  1. Ensure good dental hygiene
  2. Infective endocarditis prophylaxis
  3. Aortic valve replacement or trans catheter aortic valve implantation
369
Q

Who should be offered aortic valve replacement

A

Severe symptomatic patients with AS

Severe asymptomatic AS with decreasing ejection fraction

Severe AS undergoing CABG

370
Q

What is aortic regurgitation

A

Aortic valve is not competent and blood leads back into the LV during diastole due to caption of aortic cusps

371
Q

What are the causes of aortic regurgitation

A
  1. infective endocarditis
  2. Aortic dissection (Type A)
  3. Congenital bicuspid aortic valve
  4. Connective tissue disease such as Marfans or Ehler’s Danlos
372
Q

Describe the pathophysiology of aortic regurgitation

A

Pressure and volume overload in the LV leads to compensatory LV dilatation and LVH - LVF

373
Q

What are 3 symptoms of aortic regurgitation

A
  1. Exertional dyspnoea
  2. Orthopnoea
  3. Angina
  4. Palpitations
  5. Syncope
374
Q

What are the signs of aortic regurgitation

A
  1. Collapsing pulse (Corrigans sign)
  2. Wide pulse pressure
  3. Displaced apex beat
  4. Ejection diastolic murmur
  5. Soft/Absent S2 heart sounds
375
Q

What investigations might you carry out in someone with suspected aortic regurgitation

A

ECG - LVH

CXR (Cardiomegaly, dilated ascending aorta, pulmonary oedema)

ECHO (Aortic structure and function and evidence of infective endocarditis

376
Q

What are the management options for someone with aortic regurgitation

A

IE prophylaxis. Vasodilators e.g. ACEi. Regular echo’s to monitor progression. Surgery if symptomatic.

377
Q

What is mitral stenosis

A

Obstruction of LV inflow that prevents proper filling from the LA during diastole

378
Q

What are the causes of mitral stenosis

A
  1. Rheumatic heart disease
  2. Prosthetic valve
  3. Congenital
  4. Infective endocarditis
  5. Calcification
379
Q

Describe the pathophysiology of Mitral stenosis

A
  1. LA dilation = pulomonary congestion
  2. Increased transmitral pressure = LA enlargement and AF
  3. Pulmonary venous hypertension causes RHF symptoms
380
Q

Give 3 symptoms of mitral stenosis

A

Dyspnoea
Haemoptysis
Fatigue
Chest pain

381
Q

What are the signs of mitral stenosis

A
  1. Malar flush
  2. a wave in jugular venous pulsations
  3. Diastolic murmur
  4. Loud 1st heart sound
382
Q

What investigations might you do in seomone with mitral stenosis

A
  1. ECG - atrial fib and LA enlargement
  2. CXR - LA enlargement, mitral calcification, pulmonary oedema
  3. ECHO and Doppler
383
Q

What is the diagnostic criteria for severe mitral stenosis

A

Valve orifice <1cm2
Pressure gradient >10mmHg
Pulmonary artery systolic presssure >50mmHg

384
Q

What is the management for mitral stenosis

A

in AF rate control e.g. beta blockers/CCB. Anticoagulation if AF. Balloon valvuloplasty or valve replacement. IE prophylaxis.

385
Q

Why does medication not work for mitral and aortic stenosis?

A

The problem is mechanical and so medical therapy does not prevent progression.

386
Q

What is mitral regurgitation

A

Backflow of blood from the left ventricle to the LA during systole leading to LV volume overload

387
Q

What are the causes of mitral regurgitation

A
  1. Mitral valve prolapse
  2. Rheumatic heart disease
  3. Infective endocarditis
    4
    Annular calcification
388
Q

What is the pathophysiology of mitral regurgitation

A

LV volume overload leading to compensatory LA enlargement, LVH and increased contractility.- progressive LV volume overload leads to dilatation and progressive HF

389
Q

What are the symptoms mitral regurgitation

A
  1. Dyspnoea on exertion
  2. AF
  3. Pulmonary congestion
390
Q

What are the signs of mitral regurgitations

A
  1. Pansystolic murmur
  2. Soft 1st heart sound
  3. 3rd heart sound
    4, displaced apex beat
391
Q

What investigations for Mitral regurgitation

A

Bloods
CXR
ECHO
ECG

392
Q

What is the management of mitral regurgitation

A

Rate control for AF e.g. beta blockers. Anticoagulation for AF. Diuretics for fluid overload. IE prophylaxis. If symptomatic = surgery.

393
Q

What is infective endocarditis

A

Cardiac valves and endocardial lined structures develop vegetations composed of bacteria

394
Q

What are the risk factors for infective endocarditis

A

Abnormal valve regurgitation

Prosthetic valves

Dental caries

Post-Op wounds

Rheumatic fever

395
Q

What are the different types of IE

A
  1. Left side native
  2. Left side prosthetic
  3. Right sided
  4. Device related IE
396
Q

What is infective endocarditis commonly caused by

A

Staphylococcus aureus
Pseudomonas Aeruginosa
Streptococcus viridian’s (Dental problems)

397
Q

Describe the epidemiology of infective endocarditis

A

Now a disease of

  1. Elderly
  2. Young drug abusers
  3. Young with congenital heart defects
  4. Anyone with prosthetic heart valves
398
Q

What are the clinical signs of infective endocarditis

A

Signs of sepsis (Fever, sweats, wt loss, clubbing, splenomegaly

Immune complex lesions
(Vasculitis, Roth spots, splinter haemorrhages, oslers nodes, janeway lesions

399
Q

Which diagnostic criteria is used to diagnose infective endocarditis

A

Duke criteria

400
Q

Describe the duke criteria

A

2 major criteria

(i) +ve blood culture
(ii) Endocardium involved (+ve echo or new valvular regurgitation

5 Minor criteria

  1. Predisposition
  2. Fever
  3. Vascular phenomena
  4. Immune phenomena
  5. Equivocal blood cultures

Definitive IE = 2 major/ 1 major + 3minor or 5 minor

401
Q

What are Roth spots

A

Boat shaped retinal haemorrhages

402
Q

What are janeway lesions

A

Painless Palmer macule

403
Q

What are Osler’s nodes

A

Painful purple maculae’s on finger pulps

404
Q

What investigations might you carry out in someone with suspected IE

A

Bloods - normochromic, normcytic anaemia
ECG - AV block
Urine = microhaematuria
Echo
(i) Transthoracic detects vegetation >2mm
(ii) Transoesophageal is more sensitive

405
Q

What is the treatment for IE

A

Antimicrobials IV for around 6 weeks

406
Q

When do you consider surgery for infective endocarditis

A

Heart failure
Emboli
Valve obstruction
Prosthetic valve

407
Q

What is an arrhythmia

A

Abnormality of cardiac rhythm

408
Q

What do arrhythmias causes

A 
Sudden death 
Syncope 
HF
Chest pain 
Dizziness 
Palpitations 
Can be asymptomatic
409
Q

What are the two types of arrhythmia

A

Bradycardia

Tachycardia

410
Q

Define bradycardia

A

HR low

<60

411
Q

What are the causes of bradycardia

DIVISION

A

Drugs

  • antiarrhythmics
  • B-blockers
  • CCB
  • Digoxin

Ischaemia (Inferior infarct)

Vagal hypertonia (Athlete)

Infection (IE, RF)

Sick sinus syndrome

Infiltration (Dilated cardiomyopathy)

O = Hypothermia, thyroid and kalaemia

Neurogenic

412
Q

What are the two types of bradycardia

A

Sinus node disease

AVN/Distal conduction problems (Heart block)

413
Q

Define tachycardia

A

HR fast

>100

414
Q

What are the two types of tachycardia

A

Supraventricular tachycardias

Ventricular tachycardias

415
Q

What is the treatment for bradycardia

A

If asymptomatic and HR >40 then not required

If <40bpm then treat the underlying cause

Medical options = atropine and isoprenaline or pacing

416
Q

What is heart block

A

AVN blockage leading to bradycardia

417
Q

What is 1st degree heart Blok

A

Delayed AV contraction leading to a fixed prolonged PR interval

418
Q

What is second degree heart block

A

When some contractions from the atria fail to pass through the AVN and reach the ventricles so there are more P waves than QRS waves

419
Q

What is third degree heart block

A

Atrial contractions do not pass through the AVN so Atrial and ventricle rhythms are independent

420
Q

What are the causes of heart block

A

Coronary Artery Disease
Cardiomyopathy
Conducting tissue fibrosis

421
Q

What are narrow complex tachycardias

A

Supraventricular tachycardias
Rate >100bpm
QRS width <120ms

422
Q

What are the 4 types of supraventricular tachycardia

A 
Sinus Tachycardia 
Atrial
 - flutter
 - fibrillation 
 - tachycardia

AV nodal re-entry tachycardia

AV re-entry tachycardia

423
Q

What is sinus tachycardia

A

When there is excessive activation of the SAN leading to shortened RR intervals

424
Q

What are the causes of sinus tachycardia

A

Exercise
Fever
Thyrotoxicosis

425
Q

What are the risk factors for SVT

A

MI
Rheumatic heart disease
Pericarditis

426
Q

What are the causes of SVT

A 
Drugs 
Alcohol
Smoking 
Congenital WPW
MI
427
Q

What are the symptoms of SVT

A

Paroxymal attacks, palpitations
Syncope
tachycardia

428
Q

What features would you see on an ECG of someone with AV nodal re=entry tachycardia

A

P wave absent or immediately before or after QRS

Normal QRS

429
Q

What would you seen on the ECG of someone with AV re-entry tachycardia

A

P waves between QRS complexes

QRS narrow or wide

430
Q

What ECG features would you see with atrial tachycardia

A

Abnormal shaped P waves

Normal QRS
Rate >150bpm

431
Q

What ECG features would you see in atrial flutter

A

Saw toothed baseline as atria contract

narrow QRS

432
Q

What ECG features would you seen in atrial fibrillation

A

No P waves

Irregularly irregular QRS

433
Q

What is atrial fibrillation

A

Chaotic irregular atrial rhythm

434
Q

What is the heart rate in atrial tachycardia

A

125-250

435
Q

What is the heart rate in atrial flutter

A

250-350

436
Q

What is the heart rate in atrial fibrillation

A

350+

437
Q

What are the causes of atrial fibrillation

A 
IHD
Rheumatic heart disease 
Thyrotoxicosis 
Hypertension 
Mitral valve stenosis 
Alcohol 
PE 
Post OP
438
Q

What are the symptoms of atrial fibrillation

A 
Asymptomatic 
Chest pain 
Palpitations 
Dyspnoea 
Faintness 
Syncope
439
Q

What are the signs of atrial fibrillation

A

Irregularly irregular pulse

Pulse deficit

440
Q

How do we manage atrial fibrillation

A

CCB
BB
Digoxin for rate control
Cardioversion for rhythm control

441
Q

What is the definition of broad complex tachycardias

A

Rate >100bmp

QRS width >120ms

442
Q

What are the causes of ventricular tachycardia

A 
Infraction 
Myocarditis 
QT interval increases 
Valve abnormality 
Iatrogenic (Digoxin, antiarrhytmics)
Cardiomyopathy 
Hypokalaemia
443
Q

What ECG features do you see in ventricular tachycardia

A

No p waves
Broad regular QRS
No T waves

444
Q

What ECG features do you see in Ventricular fibrillation

A

Shapeless rapid oscillations with no organised complexes

445
Q

What ECG features do you see in WPW

A

Accessory conducting bundle
Short PR interval
Slurred upstroke of QRS called delta wave

446
Q

What ECG features do you seen in hyperkalaemia

A

Tall tented T waves
Widened QRS
Absent P waves

447
Q

What ECG features do you see in hypokalaemia

A

Small T waves
ST depression
Prolonged QT interval

448
Q

What ECG features do you see in pericarditis

A

PR depression and saddle shaped ST elevation

449
Q

What ECG features do you see in hypercalcaemia

A

QT shortening

450
Q

What ECG features do you see in hypocalcaemia

A

QT lengthening

451
Q

Define shock.

A

When the cardiovascular system is unable to provide adequate substrate for aerobic cellular respiration.

452
Q

Give 7 signs/symptoms of shock.

A
  1. Pale.
  2. Sweaty.
  3. Cold.
  4. Pulse is weak and rapid.
  5. Reduced urine output.
  6. Confusion.
  7. Weakness/collapse.
453
Q

What can cause hypovolemic shock?

A
  1. Loss of blood e.g. acute GI bleeding, trauma, post-op, splenic rupture.
  2. Loss of fluid e.g. dehydration, burns, vomiting, pancreatitis.
454
Q

Classification of shock: describe the vital signs in class 1 e.g. blood loss, pulse, blood pressure, pulse pressure, respiratory rate and urine output.

A
  1. 15% blood loss.
  2. Pulse < 100 bpm.
  3. Blood pressure - normal.
  4. Pulse pressure - normal.
  5. Respiratory rate: 14 - 20.
  6. Urine output > 30ml/h.
455
Q

Classification of shock: describe the vital signs in class 2 e.g. blood loss, pulse, blood pressure, pulse pressure, respiratory rate and urine output.

A
  1. 15-30% blood loss.
  2. Pulse > 100 bpm.
  3. Blood pressure - normal.
  4. Pulse pressure - decreased.
  5. Respiratory rate: 20 - 30.
  6. Urine output: 20 - 30ml/h.
456
Q

Classification of shock: describe the vital signs in class 3 e.g. blood loss, pulse, blood pressure, pulse pressure, respiratory rate and urine output.

A
  1. 30-40% blood loss.
  2. Pulse > 120 bpm.
  3. Blood pressure - decreased.
  4. Pulse pressure - decreased.
  5. Respiratory rate: 30 - 40.
  6. Urine output: 5 - 15ml/h.
457
Q

What can cause cardiogenic shock?

A
  1. Cardiac tamponade.
  2. Pulmonary embolism.
  3. Acute MI.
  4. Fluid overload.
458
Q

What is septic shock?

A

A systemic inflammatory response associated with an infection (bacterial endotoxins).

459
Q

What is anaphylactic shock?

A

An intense allergic reaction associated with massive histamine release = haemodynamic collapse. The patient may be breathless, wheezy and have a rash.

460
Q

What is the treatment for anaphylactic shock?

A

Adrenaline and supportive therapy e.g. O2 delivery, fluid replacement.

461
Q

What is VSD?

A

An abnormal connection between the two ventricles.

462
Q

Would a baby born with VSD be cyanotic?

A

No. There is a higher pressure in the LV than the RV and so blood is shunted from the left to right meaning there is an increased amount of blood going to the lungs; not cyanotic.

463
Q

Give 4 clinical signs of a large VSD.

A
  1. High pulmonary blood flow.
  2. Breathless, poor feeding, failure to thrive.
  3. Increased respiratory rate,
  4. Tachycardia.
  5. Requires surgical repair.
464
Q

What syndrome might VSD lead on to?

A

Eisenmengers syndrome.

Infective endocarditis

465
Q

Briefly describe the physiology of Eisenmengers syndrome.

A

High pressure pulmonary blood flow damages pulmonary vasculature -> there is increased resistance to blood flow (pulmonary hypertension) -> RV pressure increases -> shunt direction reverses (RV to LV) -> CYANOSIS!

466
Q

What are the risks associated with Eisenmengers syndrome?

A
  1. Risk of death.
  2. Endocarditis.
  3. Stroke.
467
Q

What are the causes of VSD

A

Congenital

Acquired post MI

468
Q

What is the clinical presentation of a small VSD

A

Loud systolic murmur

Systolic thrill

469
Q

What is the treatment for VSD

A

Surgical closure is symptomatic

470
Q

What might you see on CXR for a small VSD and a large VSD

A

Small = mild pulmonary plethora

Large = cardiomegaly and marked pulmonary plethora

471
Q

What is ASD?

A

An abnormal connection between the two atria; it is fairly common.

472
Q

Would a baby born with ASD be cyanotic?

A

No. There is a higher pressure in the LA than the RA and so blood is shunted from the left to right, therefore not cyanotic. - blood flow increased to the right heart and the lungs

473
Q

Give 5 clinical signs of a large ASD.

A
  1. Significant increase in blood flow through the right heart and lungs - pulmonary flow murmur.
  2. Enlarged pulmonary arteries.
  3. Right heart dilatation.
  4. SOBOE.
  5. Increased chest infection.
  6. Delayed pulmonary valve closure
  7. Pulmonary hypertension
474
Q

What are the complications of ASD

A

Paradoxical emboli

Eisenmenger’s syndrome

475
Q

What would you see on the CXR of someone with ASD

A

Cardiomegaly and pulmonary plethora

476
Q

Treatment of ASD

A

Surgical

477
Q

What is ASVD

A

Atrio-ventricular septal defects. Basically a hole in the very centre of the heart.

478
Q

What heart structures are involved in an ASVD

A

Ventricular septum
Atrial septum
Mitral valve
Tricuspid valve

479
Q

Give 2 clinical signs of AVSD.

A
  1. Breathless.
  2. Poor feeding and poor weight gain
  3. Torrential pulmonary flow
480
Q

What is PDA?

A

Patent ductus arteriosus.

481
Q

Give 4 clinical signs of PDA.

A
  1. Torrential flow from the aorta to the pulmonary arteries can lead to pulmonary hypertension and RHF.
  2. Breathless.
  3. Poor feeding, failure to thrive.
  4. Risk of endocarditis.
482
Q

What is the treatment of PDA

A

Surgical/percutaneous
Local anaesthetic and venous approach
Indomethacin that decreases prostaglandin 2 levels

483
Q

Describe the pathophysiology behind coarctation of the aorta.

A

Excessive sclerosing that normally closes the ductus arteriosus extends into the aortic wall leading to narrowing.

484
Q

What are the signs of aortic coarctation

A

Weak femoral pulse
Hypertension in right arm
Systolic murmur/ bruit heard over left scapula

485
Q

What are the complications of aortic coarctation

A

HF
Aneurysm
Hypertension

486
Q

What is the treatment for aortic coarctation

A

Balloon dilation and stenting
Subclavian flap repair
Coarctation angioplasty

487
Q

What is pulmonary stenosis?

A

Narrowing of the RV outflow tract.

488
Q

What are the symptoms of pulmonary stenosis

A

RVF
RVH
Collapse
Poor pulmonary blood flow

489
Q

Treatment of pulmonary stenosis

A

Balloon valuloplasty
Open valvotomoy
Shunt

490
Q

Name 3 congenital heart defects that are not cyanotic.

A
  1. VSD.
  2. ASD.
  3. PDA.
491
Q

Name a congenital heart defect that is cyanotic.

A

Tetralogy of Fallot.

Right to left shunt.

492
Q

What are the issues with a bicuspid aortic valve

A

Develop stenosis more quickly
Degenerate quicker
Develop regurgitation quicker

493
Q

What is tetralogy of Fallot

A

Abnormal separation of trunks arterioles into aorta and pulmonary arteries

  • VSD
  • Pulmonary stenosis
  • RVH
  • Overriding aorta
494
Q

What is the presentation of tetralogy of fallot in children and adults

A

Children - cyanotic episodes, clubbing

Adults - Asympto, cyanosis

495
Q

What is the treatment for tetralogy of fallot

A

Surgical (usually before a year)

Closure of the VSD and correction of the pulmonary stenosis

496
Q

Where do supra-ventricular tachycardia’s arise from?

A

They arise from the atria or atrio-ventricular junction.

497
Q

Do supra-ventricular tachycardia’s have narrow or broad QRS complexes?

A

Supraventricular tachycardias are often associated with narrow complexes.

498
Q

Where do ventricular tachycardia’s arise from?

A

The ventricles.

499
Q

Do ventricular tachycardia’s have narrow or broad QRS complexes?

A

Ventricular tachycardias are often associated with broad complexes.

500
Q

What pathophysiological mechanism can cause atrial flutter?

A

The re-entry mechanism - there is blockage of the normal circuit. Another pathway forms, takes a different course and re-enters the circuit -> tachycardia.

501
Q

What is the commonest supra-ventricular tachycardia?

A

AV node re-entry tachycardia (AVNRT).

502
Q

Do you see P waves in AVNRT?

A

No - the P waves are within the QRS complex.

503
Q

Give 4 symptoms of AVNRT.

A
  1. Sudden onset/offset palpitations.
  2. Neck pulsation.
  3. Chest pain.
  4. Shortness of breath.
504
Q

Describe the acute treatment of AVNRT.

A

Acute treatment: vagal manoeuvre and adenosine.

505
Q

What drugs might you give to someone to suppress future episodes of AVNRT?

A

Beta blockers, CCB, flecainide.

506
Q

Describe the pathophysiology of accessory pathway arrhythmias.

A

Congenital muscle strands connect the atria and ventricles - accessory pathway. This can result in pre-excitation of ventricles.

507
Q

Describe the pathophysiology of focal atrial tachycardia.

A

Another area of the atrium becomes more autonomic than the sinus node and so sinus node function is taken over -> focal atrial tachycardia.

508
Q

What might you see on an ECG taken from someone with focal atrial tachycardia.

A

Abnormal P waves appear before a normal QRS.

509
Q

What is the treatment for ventricular tachycardia in an urgent situation?

A

DC cardioversion.

510
Q

What is the long term treatment for ventricular tachycardia in high risk patients?

A

Implantable defibrillator.

511
Q

What are ectopic beats?

A

Very common, generally benign arrhythmias caused by premature discharge. The patient may complain of symptoms of ‘skipped beats’.

512
Q

Give 3 causes of long QT syndrome.

A
  1. Congenital.
  2. Electrolyte disturbances e.g. hypokalaemia and hypocalcaemia.
  3. A variety of drugs.
513
Q

Give 2 signs of long QT syndrome.

A
  1. Palpitations.

2. Syncope.

514
Q

Give 4 causes of sinus bradycardia.

A
  1. Ischaemia.
  2. Fibrosis of the atrium.
  3. Inflammation.
  4. Drugs.
515
Q

Types of second degree AV block: describe Mobitz type 1.

A

PR interval gradually increases until AV node fails and no QRS is seen.

516
Q

Types of second degree AV block: describe Mobitz type 2.

A

There is a sudden unpredictable loss of AV conduction and so loss of QRS. PR interval is constant but every nth QRS complex is missing.

517
Q

What are the complications of atherosclerotic plaques

A 
Haemorrhage
Plaque rupture/fissures 
Overlying thrombosis
Dissection 
Aneurysm
518
Q

What is the proper name for arterial debris

A

Embolism

519
Q

What is the proper name for arterial narrowing

A

stenosis

520
Q

What is the proper name for arterial blockage

A

Occlusion

521
Q

What is the pathology of an aortic aneurysm

A

Degradation of the elastic lamina leading to permanent >50% dilatation of the aorta

522
Q

What are the causes of aortic aneurysm

A

Atherosclerotic and collagen diseases (Marfans and vascular Ehlers danlos

523
Q

Risk factors for aortic aneurysm

A

Smoking, High BP, atherosclerosis, family Hx, COPD and sedentary lifestyle

524
Q

What are the symptoms of an abdominal aortic aneurysm

A

Asymptomatic may be some abdominal/back pain

525
Q

What are the symptoms of a thoracic aortic aneurysm

A

Chest and neck pain, compression symptoms

526
Q

What happens when an aortic aneurysm ruptures

A

Hypotension, collapse and death

527
Q

Investigations for aortic aneurysm

A

Abdominal ultrasound

528
Q

What is the management of an aortic aneurysm

A

Surgery or supportive stent implant

  • Open aneurysm repair
  • Endovascular aneurysm repair
529
Q

What is the pathophysiology of aortic dissection

A

Tear in the aortic intima –> High blood pressure into the aortic wall forms a haematoma which separates the intimal from the adventitia creating a false lumen

530
Q

What are the risk factors for aortic dissection

A

Atherosclerosis, high BP, cocaine, aortic aneurysm and smoking

531
Q

What are the symptoms of an initial aortic tear

A

Sudden severe chest pain, pulse loss and diastolic murmur

532
Q

What are the later symptoms of aortic dissection

A

Aortic branch occlusion

533
Q

What investigations would you do for someone with suspected aortic dissection

A

ECG and CXR

534
Q

What is the treatment for aortic dissection

A

Stenting

Surgery if the dissection is progressing

535
Q

What is the treatment for peripheral vascular disease

A

Clopidogrel

536
Q

What is the pathophysiology of peripheral vascular disease

A

Atherosclerosis –> Stenosis of peripheral arteries
Partial blockage of leg or peripheral vessels by atherosclerotic plaque and resulting thrombus resulting in insufficient t perfusion of lower limb resulting in lower limb ischamia

537
Q

What are the symptoms of peripheral vascular disease

A

Critical leg ischaemia (Rest pain, ulceration, gangrene)

Acute limb ischaemia (Pain, pale, paralysis, paraesthesia, perishing cold, pulseless)

Carotid artery disease (Stroke and TIA)

Abdominal aortic aneurysm (Asymptomatic until rupture occurs)

538
Q

What diagnostic test confirms peripheral vascular disease

A

Doppler ultrasonography

539
Q

What is the treatment of peripheral vascular disease

A

Modify risk factos

  • Exercise and weight control
  • Control (Hypertension, hyperlipidaemia, diabetes, anti platelet, smoking cessation)

Revascularisation for critical ischaemia

Amputation

540
Q

Saddle shaped and PR depression are associated with what condition

A

Pericarditis

541
Q

Tall tented T waves and pathological Q waves are associated with what condition

A

Hyperkalaemia

542
Q

ST elevation is associated with what condition

A

STEMI

543
Q

Absent P waves is associated with what condition

A

Atrial fibrillation

544
Q

ST depression is associated with which condition

A

Angina

545
Q

Pain when lying down but alleviated by leaning forward is associated with what condition

A

Acute pericarditis pain

546
Q

Early diastolic murmur is associated with what condition

A

Mitral stenosis

547
Q

Early systolic click murmur is associated with what condition

A

Mitral valve stenosis

548
Q

Ejection systolic crescendo decrescendo murmur is associated with what condition

A

Aortic stenosis

549
Q

Pansytolic murmur is associated with what condition

A

Mitral regurgitation

550
Q

increasing cGMP and reducing intracellular Ca2+ is the Mechanism for which drug class

A

Calcium channel blockers

551
Q

Inhibition of COX and thromboxane A2 is the mechanism for which drug class

A

NSAIDs

552
Q

Inhibition of vitamin K production is the mechanism for which drug class

A

Warfarin

553
Q

Inhibition of thrombin and factor Xa is the mechanism of which drug class

A

heparin

554
Q 
In infective endocarditis, which of the following is not seen on the hands 
Roth spots 
Janeway lesions 
Oslar nodes 
Splinter haemorrhage 
Clubbing
A

Roth spots

555
Q

What is the diagnostic test for HF

A

BNP as levels increase when you have ventricular dysfunction

556
Q

What compound is responsible for the cough associated with ACE inhibitors

A

Bradykinin

Phase 2 (16 decks)

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