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CARDIOVASCULAR Flashcards

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1
Q

What is primary (essential) hypertension? 1A

A

High blood pressure that doesn’t have a known secondary cause.

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2
Q

How is primary (essential) hypertension diagnosed? 1A

A

Blood pressure tested using a BP monitor.

If high, Doc asks p to check their BP at home using the BP monitor at home at regular intervals.

Normal BP = 120/80.

Stage 1 hypertension = BP readings of = 130-139/80-89

Stage 2 hypertension = BP readings of = higher than 140/ higher than 90.

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3
Q

What are the risk factors associated with primary (essential) hypertension? 1A

A

Diet

Stress

Minimal physical activity

Being overweight

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4
Q

What are the clinical features of primary (essential) hypertension? 1A

A

Generally asymptomatic.

Only symptom tends to be raised blood pressure.

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5
Q

How would primary (essential) hypertension be investigated? 1A

A

Serum U+E = can show evidence of renal impairment. If so, conduct more specific renal investigations -> renal ultrasound + renal angiography).

Urine Stix test - for protein and blood - can indicate renal disease (either cause or effect of hypertension).

Blood glucose, serum lipids + ECG which could show LV hypertrophy or ischaemic disease.

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6
Q

Why are investigations carried out for primary (essential) hypertension? 1A

A

To identify end-organ damage.

And identify those patients with secondary causes of hypertension.

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7
Q

How is primary (essential) hypertension managed if severe? 1A

A

Start meds immediately - before home BP checks.

Examine fundi for hypertensive retinopathy.

Refer if it is accelerated hypertension or phaechromocytoma.

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8
Q

What are the non-pharmacological treatments for primary (essential) hypertension? 1A

A

Weight reduction

Low-fat diet

Low-salt diet

Limited alcohol consumption

Exercise

Increase fruit and veg consumption

Stop smoking if a smoker + eat more oily fish

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9
Q

How is primary (essential) hypertension managed if NOT severe? 1A

A

Under 55? -> ACE inhibitor (e.g. lisinopril) but if not tolerated (e.g. due to cough) then ARB (angiotensin-II receptor antagonist e.g. losartan).

Above 55? And/or Afro-Caribbean? -> CCB (e.g. amlodipine) but if not tolerated (e.g due to oedema) then thiazide-type diuretic (e.g. bendroflumethiazide).

If uncontrolled -> add a CCB to ACE/ARB but if CCB isn’t tolerated then thiazide-type diuretic. Afro-Caribbean? -> add ARB to their CCB/thiazide-type diuretic.

Still uncontrolled? -> review meds + ACE/ARB + CCB + thiazide-type diuretic

Still uncontrolled?! -> low dose spironolactone if K+ = <4.5mmol’L (caution if reduced estimated GFR) or higher dose thiazide-type diuretic if K+ = >4.5mmol’L whilst monitoring.

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10
Q

What is assessed during the annual review for someone with primary (essential) hypertension? 1A

A

Lifestyle + meds (inc adverse effects)

Check BP

Renal function (serum creatinine, electrolytes, estimated GFR + dipstick for proteinuria).

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11
Q

What are the risks of having primary (essential) hypertension? 1A

A

Increases risk of CVD (HF, coronary artery disease, stroke, chronic kidney disease, peripheral arterial disease, vascular dementia). But meds reduce the risks.

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12
Q

What is secondary hypertension? 1B

A

High blood pressure that has a known cause e.g. kidneys, arteries, heart or endocrine.

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13
Q

What are the causes of secondary hypertension? 1B

A

Diabetes -> (damage kidney’s filtering system = high bp)

Polycystic kidney disease -> (cysts in kidneys prevent them from working properly = high bp)

Glomerular disease -> ( glomeruli = swollen = can’t work properly = high bp)

Renovascular hypertension -> (stenosis of arteires leading to kidneys = high bp)

Thyroid problems

Hyperparathyroidism -> (too much parathyroid hormone increases amount of calcium in blood = high bp)

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14
Q

What are the malignant/accelerated causes of secondary hypertension? 1B

A

Cushing syndrome -> (corticosteroid meds or pituitary tumour causes adrenal glands to produce too much cortisol)

Aldosteronism -> (tumour in adrenal glands -> increases growth of normal cells -> excessive release of hormone aldosterone -> kidneys retain salt + water + they lose too much K+ = raised bp)

Pheochromocytoma -> (rare tumour, found in adrenal glands -> increases production of adrenaline + noradrenaline = high bp)

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15
Q

What are the clinical features of secondary hypertension? 1B

A

High bp that does not respond to meds

180/120mmHg bp

Sudden onset of bp before 30yrs

No fam hx of bp

No obesity

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16
Q

How would secondary hypertension be investigated? 1B

A

Same as 1A hypertension

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17
Q

How would secondary hypertension be treated? 1B

A

You treat the underlying medical condition + as 1A hypertension

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18
Q

What are the risks of having secondary hypertension? 1B

A

Damage to heart (HA or stroke)

Aneurysm, HF, weakened + narrowed blood vessels to kidneys

Thickened, narrowed or torn vessels in eyes -> vision loss

Metabolic syndrome

Trouble with memory and understanding

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19
Q

What does phlebitis mean?

A

Inflammation of a vein

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20
Q

What is superficial thrombophlebitis?

A

An inflamed vein near the surface of the skin (usually a varicose vein) caused by a blood clot

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21
Q

How does superficial thrombophlebitis clinically present?

A

Vein looks painful, tender and hard with overlying redness

Usually occurs in the leg

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22
Q

How is superficial thrombophlebitis treated?

A

Simple analgesis -> (e.g. NSAIDs)

Anticoagulation isn’t necessary as embolism does not occur

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23
Q

What are the risk factors for superficial thrombophlebitis?

A

Have varicose veins

Smoker

Overweight

On the pill or hormone replacement therapy

Pregnant

Have previously had a blood clot/ issues with veins

Have a condition that causes blood to clot more easily (thrombophilia), inflammation of the smaller arteries (polyarteritis) or high conc of red blood cells in blood (polycythaemia)

Had drip/injection recently into vein

Have cancer

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24
Q

What is DVT?

A

A blood clot that forms in the deep veins of the body, usually in the leg

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25
How does DVT clinically present?
Often asymptomatic Leg may be warm + swollen with calf tenderness + superficial vein distention
26
How would DVT be investigated?
If Wells score is less than 3 then measurement of serum D-dimer = initial investigation. If D-dimers = normal then no further investigation needed. All other patients -> venous compression ultrasonography = indicated. Above = reliable test for iliofemoral thrombosis but not for calf vein thrombosis. Repeat scanning 1 week later + interim heparin treatment = indicated if initial scan = negative + high index of clinical suspicion.
27
How is DVT treated?
Injection of heparin if waiting to undergo an ultrasound scan to confirm DVT Coagulation screen + platelet count before starting treatment to rule out pre-existing thrombotic tendency LMWH - Enoxaparin - 1.5mg/kg subcut injec every 24 hrs, for at least 5 days till oral anticoagulation is confirmed Warfarin + heparin at same time Warfarin dose adjusted to maintain INR @ 2/3x control value Hep+War overlapped for min 5 days + continued till INR = in therapeutic range Anticoagulation for 6 weeks should be sufficient after their first thrombosis with precipitating cause - if there are no risk factors But long-term anticoagulation is needed for those with repeated episodes or continuing risk factors EXTRA -> Inferior vena cava filter (IVC filter) may be inserted in order to prevent a PE (pulmonary embolism) if anticoagulants are deemed unsuitable Elastic support stockings to prevent post-thrombotic syndrome
28
How is a DVT treated in pregnancy?
Heparin injections from diagnosis till 6 weeks after baby is born
29
What are the risks of having a DVT?
Could lead to a PE Post-thrombotic syndrome (permanent pain, swelling, oedema and potentially venous eczema) + recurrence of thrombosis.
30
What are the risk factors of developing DVT?
Aged over 60 1 or more significant co-morbidities e.g. HD Obesity Major abdominal/pelvic surgery Active cancer Pregnancy Oestrogen containing contraception/HRT Significant immobility Varicose veins with phlebitis Diabetic coma Personal hx/ first-degree relative with hx of venous thromboembolism Thrombophilia, IBD, Nephrotic syndrome
31
What are the side effects of having DVT treatment - specifically heparin therapy?
Bleeding + thrombocytopenia. Platelet count should be measured if patient is receiving heparin for more than 5 days.
32
What is a pulmonary embolism (PE)?
A condition where one or more emboli (typically from a thrombus formed in veins) are lodged in + obstruct the pulmonary arterial system = severe respiratory dysfunction
33
Whar is the pathophysiology of a PE?
The embolism means that lung tissue is still ventilated but not perfused -> leading to impaired gas exchange.
34
How would a PE clinically present?
Small/medium PE's -> breathlessness, pleuritic chest pain + haemoptysis (coughing up blood or blood-stained mucous) if there's pulmonary infarction On examination - patient may be tachypnoeic (abnormal rapid breathing) + have a pleural rub + an exudative pleural effusion can develop Massive PE's -> medical emergency - patient has severe central chest pain - suddenly becomes shocked, pale + sweaty, marked tachypnoeia + tachycardia -> syncope + death may follow rapidly On examination - patient is shocked with central cyanosis - elevation of jugular venous pressure + right ventricular heave + accentuation of second heart sound + gallop rhythm (acute right heart failure) Multiple recurrent PE's -> symptoms + signs of pulmonary hypertension developing over weeks to months
35
How would a PE be investigated?
Clinical pre-test probability score is used prior to investigation - Chest X-ray, ECG + blood gases = may all be normal with small/medium emboli + any abnormalities with massive emboli = non-specific. - Chest X-ray may show decreased vascular markings + raised hemidiaphragm (due to loss of lung volume). With pulmonary infarction - a late feature = wedge shaped opacity adjacent to pleural edge - sometimes with pleural effusion. ECG findings - sinus tachycardia or may be new onset of atrial fibrillation + non-specific ST segment + T-wave abnormalities, right axis deviation, incomplete/complete right bundle branch block. Arterial blood gases may show hypoxaemia + hypocapnia with massive PE's.
36
How would suspected PE be treated?
Wells score of more than 4 points = PE likely so hospital admission for CTPA + other testing e.g. D-dimer testing, ABG, chest X-ray, ECG, lower limb compression venous ultrasound, ventilation perfusion + echocardiography. If delay in patient getting CTPA -> give immediate low molecular weight heparin (LMWH) + arrange hospital admission. Pre-test clinical probability = low -> D-dimer testing -> negative? Look for differential diagnosis. Positive? CTPA -> PE present? Warfarin!
37
How is confirmed PE treated?
Pre-test clinical probability = intermediate/high - > Start LMWH - > Do CTPA - > PE present -> start warfarin
38
What other treatmenrs could be given alongside warfarin for treatment of PE?
High flow oxygen if hypoxaemic Thrombolysis for massive PE with persistent hypotension Analgesia - morphine - relieves pain/anxiety IV fluids (to raise filling pressure) for patients with moderate/severe embolism. Preventing further thrombi? - LMWH + oral warfarin
39
What is the initial investigation for suspected PE in pregnancy?
Compression ultrasonography of the legs. CTPA = needed if ultrasound = normal + delivers a lower dose of radiation to foetus than lung VQ scan. Warfarin = teratogenic so PE in pregnancy is treated by LMWH.
40
What are the risk factors for PE?
DVT Previous VTE Active cancer Recent surgery Significant immobility Lower limb trauma/fracture Pregnancy - 6 weeks postpartum Other risk factors as listed for DVT
41
What are the risks of having PE?
Death Cardiac arrest Pleural effusion Pulmonary infarction Arrythmia
42
What is angina?
Central chest tightness/pain caused by myocardial ischaemia.
43
What are the two types (we've learnt) of angina?
Stable Unstable
44
How does angina (both types) clinically present?
Tightness or heaviness in chest on exertion/rest /emotion/cold/heavy meals. May radiate to one or both arms, neck, jaws or teeth. Other Symptoms: Dyspnoea, nausea, sweatiness, faintness
45
Note on stable angina
Induced by effort, relieved by rest
46
Note on unstable angina
Increasing severity/frequency Minimal exertion, ^^risk of MI
47
Pathophysiology of both types of angina
Atheroma obstructing or narrowing coronary vessels (rarely; others such as anaemia)
48
Cause of both types of angina
Atheroma
49
Diagnostic test for both types of angina
ECG: usually normal, some ST depression, flat or inverted T waves.
50
Treatment of both types of angina
Modify risk factors, aspirin, B Blockers, Nitrates (isosorbide mononitrate or GTN spray), Long-acting calcium channel blocker, K+ channel activator
51
Sequelae of both types of angina
Might indicate higher risk of MI
52
What is a myocardial infarction?
Death of heart tissue due to an ischaemic event
53
What are the two types of myocardial infarction?
STEMI NSTEMI
54
How does myocardial infarction clinically present?
Crushing chest pain, radiating to left arm. Sweating, nausea, vomiting, dyspnoea, fatigue, and/or palpitations. Signs: Fever, hypo/hypertension, 3rd/4th heart sound, signs of congestive heart failure
55
Note on STEMI MI
ST elevated. Medical emergency
56
Note on NSTEMI MI
Non-ST elevated. Medical emergency.
57
Pathophysiology of myocardial infarction
Blockage of a coronary artery by a thrombus. This leads to ischaemia in cardiac tissue. The location of necrosis is determing by the coronary artery and where within it the blockage occurs."
58
Cause of myocardial infarction
Atheroma
59
Epidemiology of myocardial infarction
600/100,000 for men. 200/100,000 for women
60
Diagnostic test for myocardial infarction
Don't delay treatment. ECG: ST elevation (if STEMI), Initially peaked T waves and then T wave inversion, New Q waves, New conduction defects. FBC: Rules out anaemia. Cardiac enzymes: Troponins T and I are markers for cardiac damage
61
Treatment of myocardial infarction
Thrombolytic (aspirin). Percutaneous transluminal coronary angioplasty. Possibly CABG, if PCI fails. Follow up clopidogrel (antiplatelet) for 30 days.
62
Complications of myocardial infarction
Ischaemic: Recurrent infarct. Post-infarction angina. Mechanical: Left ventricular dysfunction -> Heart failure. Ventricular septal rupture (life threatening). Free wall rupture -> Pericardial bleed -> Cardiac tamponade. False aneurysm in ventricular wall. Acute mitral regurgitation (caused by ischaemic damage to papillary muscle). Arrhythmias: Ventricular tachycardia, ventricular fibrillation and total AV block. Bradycardia. Thrombotic/Embolus: Thrombus can form in ventricular wall. DVT and PE possible, but low risk. Pericarditis: Common after anterior infarct. Dressler's syndrome (presents as pericarditis). Depression: 20% of patients following MI.
63
Sequelae of myocardial infarction
Shock, heart failure, pericardiitis
64
What is cardiac failure?
Cardiac output inadequate for the body requirements
65
Types of cardiac failure
Left Right
66
How does cardiac failure (eft) clinically present?
Dyspnoea, tachypnea, crackles in the lungs (base -> the rest), wheezing, cyanosis (late occuring). Frothy pink sputum Signs: Laterally displaced apex beat, 'gallop' rhythm. Heart murmurs possible.
67
How does cardiac failure (right) clinically present?
Peripheral oedema, ascites, liver enlargement, raised JVP
68
Pathophysiology of cardiac failure (eft)
Blood backs up into the pulmonary circulation
69
Pathophysiology of cardiac failure (right)
Blood backs up into the systemic circulation
70
Cause of cardiac failure
Systolic: Ischaemic heart disease, MI, cardiomyopathy Diastolic: Tamponade, constrictive pericarditis, systemic hypertension
71
Epidemiology of cardiac failure
1-3/100 general pop, 10% of elderly. Poor prognosis (25-50% die in first 5yrs of diagnosis)
72
Diagnostic test for cardiac failure
ECG, CXR (Bat wing alveolar oedema, Kerley B lines, cardiomegaly, dilated prominent upper lobe vessels, pleural effusion) and BNP. If abnormal -> Echocardiography
73
Treatment of cardiac failure
Stop smoking, eat healthily and exercise. Chronic: Loop and potassium sparing diuretics for fluid overload, ACEI, Beta-blockers Acute: Oxygen, monitor ECG, diamorphine, furosemide, GTN spray LOON: Loop, Oxygen, Opioid Nitrates
74
What is valvular heart disease?
Disease process affecting the valves of the heart.
75
What are the four types of valvular heart disease?
Mitral stenosis Mitral regurgitation Aortic stenosis Aortic regurgitation
76
How does mitral stenosis clinically present?
Pulmonary hypertension -> dyspnoea, pink frothy sputum, left atrial dilatation, right ventricular hypertrophy, palpitations. Malar flush due to low CO. Opening snap and diastolic murmur.
77
How does mitral regurgitation clincally present?
Variable haemodynamic effects. Pansystolic murmur. Mid-systolic click and late systolic murmur in mitral prolapse. Deviated apex beat.
78
How does aortic stenosis clinically present?
Ejection systolic murmur. Left ventricular hypertrophy. Syncope, angina, dyspnoea (SAD)
79
How does aortic regurgitation clinically present?
Early diastolic murmur. Wide pulse pressure, collapsing pulse, angina, left ventricular failure. Austin flint murmur: Fluttering of anterior mitral valve cusp due to regurgitant stream
80
Note on mitral stenosis
Mid-diastolic murmur
81
Note on mitral regurgitation
Pansystolic murmur
82
Note on aortic stenosis
Early systolic murmur
83
Note on aortic regurgitation
Early diastolic mumur
84
Pathophysiology of mitral stenosis
Inflammation -> Mitral valve thickened/calcified obstructing normal flow. Raised LA pressure -> LA hypertrophy and dilatation -> palpitations. Raised LA pressure -> pulmonary hypertension -> RV hypertrophy and failure
85
Pathophysiology of mitral regurgitation
Mitral valve fails to prevent reflux of blood. Regurgitation into the LA -> increased LA pressure -> increased pulmonary pressure -> pulmonary oedema
86
Pathophysiology of aortic stenosis
Aortic valve thickened/calcified obstructing normal flow. Obstructed LV outflow -> Increased LV pressure -> Compensatory LV hypertrophy -> Relative ischaemia -> Angina, arrythmia and LV failure -> Reduced cardiac output.
87
Pathophysiology of aortic regurgitation
Aortic valve fails to prevent reflux of blood. LV hypertrophy to maintain cardiac output -> Reduced diastolic blood pressure -> relative ischaemia. Eventually leads to left ventricular failure.
88
Cause of mitral stenosis
Rheumatic valvular disease (usually Strep pyogenes)
89
Cause of mitral regurgitation
Dilatation of mitral valve annulus. Mitral valve prolapse. Infective endocarditis. Rheumatic valvular disease. Marfan's and Ehler-Danlos
90
Cause of aortic stenosis
Calcific degeneration. Rheumatic valvular disease. Congenital bicuspid valve.
91
Cause of aortic regurgitation
Aortic root dilatation. Infective endocarditis, rheumatic fever. Some rheumatological disorders. Ascending aortic dissection possible.
92
Epidemiology of mitral regurgitation
Second most common valvular condition requiring surgery
93
Epidemiology of aortic stenosis
Most common valvular condition requiring surgery. Mostly in the elderly.
94
Epidemiology of aortic regurgitation
Moderate or severe common after transcatheter aortic valve replacement.
95
Diagnostic test for mitral stenosis
Echocardiography. ECG: AF, LA enlargement, RV hypertrophy Echocardiography: Definitive diagnosis; measure mitral orifice.
96
Diagnostic test for mitral regurgitation
Echocardiography
97
Diagnostic test for aortic stenosis
Echocardiography. ECG: LV hypertrophy
98
Diagnostic test for aortic regurgitation
Echocardiography. ECG: LV hypertrophy
99
Treatment of mitral stenosis
Diuretics (furosemide), rate control + anticoagulation. Valvotomy. Excise segments of valve, or valve replacement. Infective endocarditis prophylaxis (amoxicillin?)
100
Treatment of mitral regurgitation
Repair preferred over replacement
101
Treatment of aortic stenosis
Valve replacement, Balloon valvuloplasty, Transcatheter aortic valve replacement, Surgical valvuloplasty
102
Treatment of aortic regurgitation
Treat underlying cause. Possibly vasodilators or inotropes. Diuretics. Valve replacement.
103
Complications of valvular disease
Valve replacements can cause clotting. Anticoagulants prescribed with them. Endocardititis
104
Sequelae of aortic stenosis
Left sided heart failure. Sudden death.
105
Sequelae of aortic regurgitation
Left sided heart failure.
106
What is atrial fibrillation?
Irrergularly irregular ventricular pulse and loss of association between cardiac apex beat and radial pulsation.
107
How does atrial fibrillation clinically present?
Breathlessness, palpitations, syncope, chest discomfort, stroke/TIA. Irregularly irregular pulse.
108
Pathophysiology of atrial fibrillation
Artial activity is chaotic and mechanically ineffective. Stagnation of blood in the atria -> thrombus formation and a risk of embolism -> stroke. Reduction in cardiac output -> Heart failure
109
Cause of atrial fibrillation
Hypertension, coronary artery disease, valvular heart disease (particularly mitral valve stenosis), cardiac surgery
110
Epidemiology of atrial fibrillation
Most common sustained arrhythmia.
111
Diagnostic test for atrial fibrillation
ECG: variability in the R-R intervals, absent p waves.
112
Treatment of atrial fibrillation
Control arrhythmia; rate: Beta blockers, Calcium antagonists rhythm: cardioversion. Thromboprophylaxis to prevent strokes. Treat underlying cause.
113
What is peripheral vascular disease?
Narrowing of arteries distal to the aortic arch.
114
How does peripheral vascular disease clinically present?
Varying symptoms: Asymptomatic -> Intermittent claudication (on exercise) -> rest pain (critical limb ischaemia) -> skin ulceration and gangrene. Signs: Absent femoral, popliteal or foot pulses. Cold white legs.
115
Note on peripheral vascular disease
50% mortality at 5 years 70% at 10 years. Gradual progression -> Sudden deterioration.
116
Pathophysiology of peripheral vascular disease
Atherosclerosis causing stenosis of arteries.
117
Cause of peripheral vascular disease
Atherosclerotic damage. Risk Factors: Classical atheroma risk factors.
118
Epidemiology of peripheral vascular disease
Affects 4-12% of people between 55-70, and 15-20% of 70+
119
Diagnostic test for peripheral vascular disease
ECG: 60% of claudication patients have evidence of coronary artery disease. Doppler ultrasonography: Confirm diagnosis. Site, degree and length.
120
Treatment of peripheral vascular disease
Modify risk factors.
121
Complications of peripheral vascular disease
Acute limb ischaemia -> Amputation, gangrene, infection, poor healing, ulceration.

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