Brainscape's Knowledge GenomeTM

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


See full index

Yr 4 - CCC > Cardiology: HTN, CVS Disease & Stable Angina > Flashcards

Cardiology: HTN, CVS Disease & Stable Angina Flashcards

1
Q

What BP readings suggest a diagnosis of HTN?

(both clinical setting and ambulatory/home readings)

A

Clinical –> above 140/90

Confirmed with ambulatory or home readings above 135/85

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

Essential hypertension accounts for 90% of hypertension. What does this mean?

A

This is also known as primary hypertension.

It means a high blood pressure has developed on its own and does not have a secondary cause.

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

Secondary causes of hypertension can be remembered with the “ROPED” mnemonic.

What are these?

A

R - Renal disease
O - Obesity
P - Pregnancy-induced or pre-eclampsia
E - Endocrine
D - Drugs e.g. alcohol, steroids, NSAIDs, oestrogen, liquorice

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

What is the most common cause of 2ary HTN?

A

Renal disease

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

When the blood pressure is very high or does not respond to treatment, what disease should you consider?

A

Renal artery stenosis

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

How can renal artery stenosis be diagnosed (i.e. what investigation)?

A

Diagnosed with duplex US or an MR or CT angiogram.

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

Most endocrine conditions can cause hypertension.

What is an important condition to consider?

A

Hyperaldosteronism (Conn’s syndrome)

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

give some complications of HTN

A
  • Ischaemic heart disease (angina and acute coronary syndrome)
  • Cerebrovascular accident (stroke or intracranial haemorrhage)
  • Vascular disease (peripheral arterial disease, aortic dissection and aortic aneurysms)
  • Hypertensive retinopathy
  • Hypertensive nephropathy
  • Vascular dementia
  • Left ventricular hypertrophy
  • Heart failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which ventricle may become hypertrophied in HTN?

A

Left ventricle - straining to pump blood against increased resistance in the arterial system, so the muscle becomes thicker.

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

What cardio exam findings may there be with LV hypertrophy (think apex beat)?

A

Sustained and foreful apex beat

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

Which investigation is best to diagnose LV hypertrophy?

A

Echocardiogram

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

How often should BP be measured to screen for HTN?

A

Every 5 years (but more often in borderline cases and every year in patients with type 2 diabetes)

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

How often should BP be measured to screen for HTN in patients with T2D?

A

Every year

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

What clinic BP would indicate the need for 24-hour ambulatory blood pressure or home readings?

A

Clinic blood pressure between 140/90 mmHg and 180/120 mmHg

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

Why are home readings required as well as clinc BP readings?

A

White coat syndrome

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

NICE recommend measuring blood pressure in both arms.

If the difference between arms is MORE THAN 15mmHg, which BP reading should you use?

A

Use reading from arm with higher pressure

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

What clinic BP readings define:

1) Stage 1 HTN
2) Stage 2 HTN
3) Stage 3 HTN

What ambulatory or home readings confirm these?

A

1) Above 140/90 –> confirmed with above 135/85 (ambulatory/home)

2) Above 160/100 –> confirmed with above 150/95

3) Above 180/120

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

What is ambulatory blood pressure monitoring?

A

records your blood pressure (BP) readings over a 24-hour period, whether you’re awake or asleep (as you go about your daily life)

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

What investigations should all patients with a new HTN diagnosis have?

A

1) Bloods –> HbA1c, renal function and lipids

2) Fundus exam –> hypertensive retinopathy

3) ECG –> for cardiac abnormalities (including LV hypertrophy)

4) Urine albumin:creatinine ratio (ACR) –> for proteinuria (kidney damage)

5) Urine dipstick –> for microscopic haematuria (assess for kidney damage)

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

For patients with HTN, a QRISK score should be calculated.

What is a QRISK score?

A

Estimates the percentage risk that a patient will have a stroke or myocardial infarction in the next 10 years.

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

If a patient’s QRISK score is above 10%, what should they be offered?

A

Statin –> initially atorvastatin 20mg at night

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

What is starting statin and dose for patients with QRISK of above 10%?

A

Atorvastatin 20mg at night

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

Why should statins be taken at night?

A

Many statins work more effectively when they are taken at night. This is because the enzyme which makes the cholesterol is more active at night.

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

Lifestyle advice in HTN management?

A
  • Smoking cessation
  • Reduce alcohol
  • Regular exercise
  • Reduce caffeine and salt intake
  • Healthy diet
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What medications are used in HTN management?

Think ABCD ARB

A

A - ACEi (e.g. ramipril)
B - beta blocker (e.g. bisprolol)
C - calcium channel blocker (e.g. amlodipine)
D - thiazide like Diuretic (e.g. indapamide)

ARB - angiotensin II receptor blocker (e.g. candesartan)

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

Which medication is recommended 1st line for HTN in patients aged <55 (caucasian)?

A

ACEi

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

Which medication is recommended 1st line for HTN in patients aged <55 (black african or african-caribbean)?

A

Calcium channel blocker

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

Which medication is recommended 1st line for HTN in patients of black african or african-caribbean decent REGARDLESS of age?

A

Calcium channel blocker

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

Which medication is recommended 1st line for HTN in patients with T2D REGARDLESS of age?

A

ACEi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Which medication is recommended 1st line for HTN in patients aged >/=55 (caucasian)?

A

Calcium channel blocker

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

What is stepwise pharmacological management of HTN in those aged <55 or with T2D (regardless of age)?

A
  1. ACEi
  2. Add CCB or thiazide-like diuretic
  3. ACEi + CCB + thiazide
  4. Check potassium:
    a) if </= 4.5mmol/l, add spironolactone
    b) if > 4.5 mmol/l add alpha or beta blocker
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is stepwise pharmacological management of HTN in those aged >/= 55 (with no T2D) or Black African or African-Caribbean ethnicity?

A
  1. CCB
  2. CCB + ARB or CCB + thiazide like diuretic
  3. CCB + ARB + thiazide
  4. Check potassium:
    a) if </= 4.5mmol/l, add spironolactone
    b) if > 4.5 mmol/l add alpha or beta blocker
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Who are ARBs recommended in?

A

Angiotensin receptor blockers (ARBs) are recommended by NICE instead of ACE inhibitors in patients of Black African or African-Caribbean family origin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Can you use ACEi and ARBs together?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

If someone cannot tolerate ACEi (commonly due to dry cough), what can be given instead?

A

ARBs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

If someone cannot tolerate CCBs (commonly due to ankle oedema), what can be given instead?

A

Thiazide-like diuretics

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

What is most common reason for patients not being able to tolerate CBBs?

A

Ankle oedema

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

Step 4 of pharmacological management of HTN depends on the serum potassium level.

What is given if K+ is less than or equal to 4.5 mmol/L?

A

consider a potassium-sparing diuretic, such as spironolactone

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

Step 4 of pharmacological management of HTN depends on the serum potassium level.

What is given if K+ is more than 4.5 mmol/L?

A

consider an alpha blocker (e.g., doxazosin) or a beta blocker (e.g., atenolol)

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

What is important to always check in HTN management?

A

adherence

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

What class of drug is spironolactone?

A

Potassium-sparing diuretic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Mechanism of spironolactone?

A

Blocks action of ALDOSTERONE in the kidneys, resulting in sodium excretion and potassium reabsorption.

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

What does spironolactone increase the risk of?

A

Hyperkalaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What 2 classes of HTN drugs can cause hyperkalaemia?

A
  1. ACEi
  2. K+ sparing diuretics e.g. spironolactone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is important to regularly monitor in patients on spironolactone or ACEi?

A

U&Es

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

What is the BP target for those aged <80 y/o?

A

<140/90 (clinic)

N.B. this is the same for those with T2D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is the BP target for those aged >80 y/o?

A

<150/90

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is malignant HTN?

A

Accelerated hypertension - refers to extremely high blood pressure, above 180/120, with retinal haemorrhages or papilloedema.

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

What BP defines malignant HTN?

A

> 180/120

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

What 2 eye signs may be seen in malignant HTN?

A

1) papilloedema
2) retinal haemorrhages

51
Q

Management of malignant HTN?

A

1) SAME DAY referral
2) Fundoscopy exam –> to look for key findings

52
Q

What is atherosclerosis?

A

A combination of atheromas (fatty deposits in the artery walls) and sclerosis (hardening or stiffening of the blood vessel walls).

53
Q

What is an atheroma?

A

fatty (lipid) deposits in the artery walls

54
Q

What arteries does atherosclerosis affect?

A

Medium and large

55
Q

Cause of atherosclerosis?

A

It is caused by chronic inflammation and activation of the immune system in the artery wall.

56
Q

Pathophysiology behind atherosclerosis?

A

1) chronic inflammation and activation of the immune system in the artery wall

2) this causes the deposition of lipids in the artery wall, followed by the development of fibrous atheromatous plaques.

3) plaques cause stiffening, stenosis & can rupture

57
Q

How does atherosclerosis lead to HTN?

A

Stiffening of the artery walls leads to HTN and STRAIN on the heart as it tries to pump blood against extra resistance.

58
Q

How does atherosclerosis lead to angina?

A

Stenosis leads to reduced blood flow (e.g. in angina).

59
Q

How does atherosclerosis lead to ischaemia?

A

Plaque rupture creates a thrombus that can block a distal vessel and cause ischaemia.

An example is acute coronary syndrome, where a coronary artery becomes blocked.

60
Q

Non-modifiable risk factors for atherosclerosis?

A

Older age
Family history
Male

61
Q

modifiable risk factors for atherosclerosis?

A

Raised cholesterol
Smoking
Alcohol consumption
Poor diet
Lack of exercise
Obesity
Poor sleep
Stress

62
Q

Which 4 medical cobmorbidities can increase the risk of atherosclerosis?

A

1) Diabetes
2) HTN
3) CKD
4) Inflammatory conditions e.g. rheumatoid arthritis

63
Q

Which group of medications can lead to atherosclerosis?

A

Atypical antipsychotic medications

64
Q

Consider risk factors when taking a history from someone with suspected atherosclerotic disease (such as someone presenting with chest pain).

What should you ask about?

A
  • PMH
  • FH
  • Diet
  • Exercise
  • Alcohol
  • Smoking
  • Occupation
  • Medications
65
Q

What are some end results of atherosclerosis?

A
  • Angina
  • MI
  • TIA
  • Stroke
  • Peripheral arterial disease
  • Chronic mesenteric ischaemia
66
Q

Prevention of CVS disease can be split into 1ary and 2ary prevention.

Who is 1ary prevention for?

A

Primary prevention for patients that have NEVER had a diagnosis of cardiovascular disease.

67
Q

Prevention of CVS disease can be split into 1ary and 2ary prevention.

Who is 2ary prevention for?

A

Secondary prevention after a diagnosis of angina, myocardial infarction, TIA, stroke or peripheral arterial disease.

68
Q

Give some dietary recommendations for those with CVS disease

A
  • Total fat is less than 30% of total calories (primarily monounsaturated and polyunsaturated fats)
  • Saturated fat is less than 7% of total calories
  • Reduced sugar intake
  • Wholegrain options
  • At least 5 a day of fruit and vegetables
  • At least 2 a week of fish (one being oily)
  • At least 4 a week of legumes, seeds and nuts
  • Increase fibre
69
Q

What is medication for 1ary prevention of CVS based on?

A

QRISK score

70
Q

Atorvastatin 20mg is offered as 1ary prevention to which 2 groups of patients?

A

1) CKD (eGFR <60)
2) T1D for more than 10 years or are over 40 years

71
Q

Mechanism of statins?

A

Statins reduce cholesterol production in the liver by inhibiting HMG CoA reductase.

72
Q

What enzyme do statins inhibit?

A

HMG CoA reductase.

73
Q

When should lipids be checked after starting statins?

A

After 3 months

74
Q

When should you consider increasing statin dose?

A

Increase the dose to aim for a greater than 40% reduction in non-HDL cholesterol (BUT check adherence)

75
Q

What bloods are required after starting statins?

A

1) Lipids (After 3 months)

2) LFTs (within 3 months, again at 12 months)

76
Q

How can statins affect the liver?

A

Statins can cause a transient and mild rise in ALT and AST in the first few weeks of use.

77
Q

What LFT results would indicate that statins would need to be stopped?

A

If ALT and AST rise is more than 3x the upper limit of normal

78
Q

What are some rare but significant side effects of statins?

A
  • Myopathy (causing muscle weakness and pain)
  • Rhabdomyolysis (muscle damage – check the creatine kinase in patients with muscle pain)
  • Type 2 diabetes
  • Haemorrhagic strokes (very rarely)
79
Q

What blood test is required in patients on statins presenting with muscle pain?

A

Creatine kinase (risk of rhabdomyolysis)

80
Q

Are statins metabolised by P450 enzymes?

A

Yes

81
Q

What Abx class can interact with statins?

A

Macrolides (e.g. clarithromycin) –> these are P450 enzyme inhibitors which can lead to accumulation of statins and increased risk of adverse effects (e.g. muscle problems)

82
Q

If a patient taking statins is prescribed clarithromycin or erythromycin, what should they be advised?

A

should be advised to STOP taking their statin whilst taking these antibiotics.

83
Q

Give 3 contraindications for statins

A

1) Hepatic impairment (metabolised by liver)

2) Renal impairment (excreted by kidneys)

3) Pregnancy & breastfeeding (cholesterol is essential for normal foetal development)

84
Q

What are the 3 indications for statins?

A

1) 1ary prevention of CVS events –> in people >40 y/o with a 10 year CVS risk >10% (assessed using QRISK tool)

2) 2ary prevention of CVS events – 1st line alongside lifestyle changes to prevent events in patients with established CVS disease

3) 1ary hyperlipidaemia e.g. 1ary hypercholesterolaemia, mixed dyslipidemia and familial hypercholesterolaemia

85
Q

Name 2 other cholesterol lowering drugs

A
  1. Ezetimibe
  2. PCSK9 inhibitors (e.g., evolocumab and alirocumab) –> these are monoclonal antibodies that lower cholesterol
86
Q

What are some pharmacological options for 2ary prevention of developing CVS disease?

(4 A’s)

A
  1. Antiplatelet medications (e.g., aspirin, clopidogrel and ticagrelor)
  2. Atorvastatin 80mg
  3. Atenolol (or an alternative beta blocker – commonly bisoprolol) titrated to the maximum tolerated dose
  4. ACE inhibitor (commonly ramipril) titrated to the maximum tolerated dose
87
Q

After an MI, what 2 drugs are used in long-term management?

A

1) Aspirin 75mg (indefinitely)

2) Clopidogrel or ticagrelor (generally for 12 months before stopping)

88
Q

What dose of aspirin is given for longterm management following an MI?

A

75 mg

89
Q

What is the antiplatelet of choice in peripheral arterial disease and following an ischaemic stroke?

A

Clopidogrel

90
Q

How is familial hypercholesterolaemia inherited?

A

Autosomal dominant

91
Q

What is familial hypercholesterolaemia?

A

An genetic condition causing very high cholesterol levels. Several genes have the potential to cause the disorder.

Heterozygous –> only one copy of the gene is abnormal.

Homozygous –> both copies of the gene are abnormal (rarer)

92
Q

What criteria is used for making a clinical diagnosis of familial hypecholesterolaemia?

A

The Simon Broome criteria or the Dutch Lipid Clinic Network Criteria

93
Q

What are the 3 important features in making a diagnosis of familial hypecholesterolaemia?

A

1) FH of premature CVS disease (e.g. MI under 60 in a first-degree relative)

2) Very high cholesterol (e.g., above 7.5 mmol/L in an adult)

3) Tendon xanthomata (hard nodules in the tendons containing cholesterol, often on the back of the hand and Achilles)

94
Q

Management of familial hypercholesterolaemia?

A

1) Specialist referral for genetic testing and testing of family members

2) Statins

95
Q

What causes angina?

A

Angina is caused by atherosclerosis affecting the coronary arteries, narrowing the lumen (inside diameter) and reducing blood flow to the myocardium (heart muscle).

During times of high demand, such as exercise, there is an insufficient supply of blood to meet the demand –> symptoms

96
Q

What arteries are affected in angina?

A

Coronary arteries

97
Q

Symptoms of angina?

A

Constricting chest pain, with or without radiation to the jaw or arms.

98
Q

When is angina ‘stable’?

A

Symptoms only come on with exertion AND always relieved by rest of GTN

99
Q

When is angina ‘unstable’?

A

Symptoms appear randomly at rest

This is a type of ACS and requires immediate management!

100
Q

Investigations in angina?

A
  • Physical exam (e.g. heart sounds, signs of HF)
  • O2 sats, BP & HR
  • ECG
  • FBC (anaemia)
  • U&Es (required before starting ACEi etc)
  • LFTs (required before starting statins)
  • Lipid profile
  • TFTs
  • HbA1c and fasting glucose (diabetes)
101
Q

What is cardiac stress testing?

A

Cardiac stress testing involves assessing the patient’s heart function during exertion.

102
Q

What are 2 methods of cardiac stress testing?

A

1) exercise e.g. treadmill

2) medication to stress heart e.g. dobutamine

103
Q

What are the methods of assessing the heart in cardiac stress testing?

A
  • ECG
  • Echo
  • MRI
  • Myocardial perfusion scan (nuclear medicine scan)
104
Q

How can CT coronary angiography be used in assessing cardiac function?

A

involves injecting contrast and taking CT images timed with the heart contractions to give a detailed view of the coronary arteries, highlighting the specific locations of any narrowing.

105
Q

What is invasive coronary angiography?

A

An invasive procedure performed in a catheter laboratory (cath lab).

1) A catheter is inserted into the patient’s brachial or femoral artery

2) directed through the arterial system to the aorta and the coronary arteries under x-ray guidance

3) where contrast is injected to visualise the coronary arteries and identify any areas of stenosis using x-ray images.

106
Q

What is considered the gold standard for determining coronary artery disease?

A

Invasive coronary angiography

107
Q

what are the 5 principles of management of stable angina?

Pneumonic RAMPS

A

R - Refer to cardiology

A - Advise them about the diagnosis, management and when to call an ambulance

M - Medical treatment

P - Procedural or surgical interventions

S - Secondary prevention

108
Q

Who are stable angina referrals usually sent to?

A

rapid access chest pain clinic (RACPC)

109
Q

What are the three aims of medical management of stable angina?

A

1) Immediate symptomatic relief during episodes of angina

2) Long-term symptomatic relief

3) Secondary prevention of cardiovascular disease

110
Q

What is used for immediate symptomatic relief during episodes of angina?

A

Sublingual glyceryl trinitrate (GTN) in the form of a spray or tablets.

111
Q

Mechanism of GTN?

A

Vasodilation –> improving blood flow to the myocardium

112
Q

When are patients advised to take GTN?

A

When symptoms start

113
Q

How many doses of GTN spray can patinets take?

A

3, then need to call ambulance

1) First dose when symptoms start
2) Take a second dose after 5 minutes if the symptoms remain
3) Take a third dose after a further 5 minutes if the symptoms remain
4) Call an ambulance after a further 5 minutes if the symptoms remain

114
Q

How soon after the 1st dose of GTN can you take the 2nd?

A

5 minutes

115
Q

What are the 2 key side effects of GTN?

A

1) headaches
2) dizziness

116
Q

What is used for the medical long term symptomatic relief in stable angina?

A

Either, or a combination of:

1) Beta blocker (e.g., bisoprolol)

2) Calcium-channel blocker (e.g., diltiazem or verapamil – both avoided in heart failure with reduced ejection fraction)

117
Q

What are the 2 surgical options in stable angina?
Who are these offered to?

A

Surgical procedures are generally offered to patients with more severe disease and where medical treatments do not control symptoms.

2 options:
1) Percutaneous coronary intervention (PCI)
2) Coronary artery bypass graft (CABG)

118
Q

What does PCI involve?

A

1) Involves inserting a catheter into the patient’s brachial or femoral artery under xray guidance to the coronary arteries.

2) Contrast is inserted to visualise the coronary arteries and identify areas of stenosis

3) Areas of stenosis can be treated by dilating a balloon to widen the lumen (angioplasty) and inserting a stent to keep it open.

119
Q

What does a CABG involve?

A

1) This involves opening the chest along the sternum, with a midline sternotomy incision

2) A graft vessel is attached to the affected coronary artery, bypassing the stenotic area.

120
Q

What are the 3 main options for graft vessels in CABG?

A

1) Saphenous vein (harvested from the inner leg)
2) Internal thoracic artery, also known as the internal mammary artery
3) Radial artery

121
Q

Scar in CABG?

A

Midline sternotomy

122
Q

Generally, short and medium-term outcomes are similar between PCI and CABG.

What are the advantages of PCI over CABG?

A

1) Faster recovery

2) Lower rate of strokes as a complication

3) Higher rate of requiring repeat revascularisation (further procedures)

123
Q

When examining a patient that you think may have coronary artery disease in your OSCEs, what scars should you check for?

A

1) midline sternotomy scar (previous CABG)

2) scars around the brachial and femoral arteries (previous PCI)

3) along the inner calves (saphenous vein harvesting scar)

124
Q
A

Yr 4 - CCC (54 decks)

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