Cardio Week 3 Flashcards

1
Q

what is atherosclerosis

A

progressive disease characterised by build up of plaque

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

what is the normal level for triglycerides

A

2.3mmol/l

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

what is the role of HDL

A

protective effect for risk of atherosclerosis and CHD

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

what are markers of high cholesterol

A

xanthelasma (xanthomas of eyelids), tendon xanthomas, tuberous xanthomas or eruptive xanthomas (small reddish-yellow pauples)

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

what is the events leading up to the formation of a fatty streak or plaque

A

damage - productive of adhesion molecules - attachment of monocytes and T cells - migration to sub endothelial space - macrophages take up oxidised LDL - forms lipid rich foam cells

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

what diseases are attributable to hypertension

A

aortic aneurysm, HR, LVH, MI, CHD, cerebral haemorrhage, preeclampsia, stroke, chronic kidney disease, blindness

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

what is the risk factors for CVD that most hypertensives have

A

dyslipidemia, diabetes, age, male gender, smoking, family history

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

what lifestyle modifications can be made to reduce risk of CVD

A

lose weight, limit alcohol intake, increase physical activity, reduce salt intake, stop smoking, limit intake of foods rich in fat and cholesterol

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

what is hypertension a risk factor for

A

cerebral haemorrhage, atheroma, renal failure, sudden cardiac death

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

what is primary hypertension

A

90% of cases, no obvious cause, increase in dietary salt leads to increase in BP

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

what is secondary hypertension

A

underlying disease implicated

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

what are common causes of secondary hypertension

A

renal disease (salt and water overload), sleep apnoea, aldosteronism, Reno-vascular disease

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

what are uncommon causes of secondary hypertension

A

cushings (excess corticosteroids), pheochromocytoma (excess noradrenaline) hyperparathyroidism, aortic coarctation (congenital narrowing)

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

what is benign hypertension

A

life threatening, asymptomatic, incidental finding, eventually causes LVH, congestive cardiac failure, increases atheroma, aneurysm rupture and renal disease

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

what is the process behind left ventricular hypertrophy

A

increased LV load - poor perfusion - interstitial fibrosis - micro infarcts - diastolic dysfunction results in cardiac death or failure

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

what is the cause of hypertensive atherosclerosis

A

blood vessel wall changes (esp in retina and kidney), thickening of media and hyaline arteriosclerosis where plasma proteins forced into vessel wall

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

what is malignant hypertension

A

serous, diastolic >130, can develop from either benign primary or secondary hypertension or arise de-novo - urgent treatment needed

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

causes of malignant hypertension

A

cerebral oedema (seen as papillodema), acute renal failure, acute heart failure, headache and cerebral haemorrhage

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

what is the consequence of pregnancy associated hypertension and proteinuria

A

pre-eclampsia - obstetric emergency and the hypertension is secondary to silent renal or systemic disease

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

what is the virchows triad that leads to thrombosis

A

endothelial injury, turbulent blood flow, hypercoaguable blood

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

what causes endothelial injury

A

hypertension, autoimmune disease (eg primary vasculitis)

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

thrombus via intravascular coagulation is caused by what two things

A

platelet activation and fibrin production via coagulation cascade

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

what is special about activated platelets

A

more sticky, attract and aggregate with other platelets, aggregate with fibrin (fibrin is end point of coagulation cascade)

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

what happens when endothelial damage occurs and endothelium is lost

A

collagen exposed, binds to Ia/IIb on platelets as does vWF, there is increase in platelet integrins, IIb/IIIa binds fibrogen and activated platelets release granules to attract other platelets (vWF, platelet activating factor PAD, TXA2 and ADP)

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

what is the common intrinsic pathway

A

XII-XII-IV-VIII

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

what is common extrinsic pathway

A

tissue factor joins factor VII

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

what is the complications of atherosclerosis

A

thrombosis, narrowed coronary artery (may be asymptomatic if myocardial O2 demand met), exercised induced angina (stable) or plaque rupture (unstable angina)

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

what is homeostasis

A

constant clotting and constant clot lysis

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

what are anti clotting proteins

A

protein C and S (degrades factor V and VIII) and antithrombin III (degrades II, IX and X)

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

what is the primary causes of hypercoaguability

A

Factor V lieden (mutation at point in factor V targeted by protein C and S: results in C, S and antithrombin III deficiency)

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

what secondary causes of hypercoaguability

A

prolonged immobility, significant tissue injury, autoimmune, MI, AF, cancer (activate coagulation cascade through tumour produced TF) and many cancer therapies injure endothelium

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

what are low risk secondary causes of hypercoagubility

A

the pill, smoking, renal disease (nephrotic syndrome) and cardiomyopathy

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

what happens to organs which are distal to branching arteries

A

more susceptible to embolism and infarction eg stroke and small bowel infection

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

what do you need to ensure when using ABPM (ambulatory BP monitoring) to confirm diagnosis

A

at least two measurements per hour during the persons usual waking hours

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

what do you need to ensure when using HBPM (home blood pressure monitoring) to confirm diagnosis

A

two consecutive seated measurements, 1 minute apart, BP recorded twice a day for at least 4 days - measurements on first day are discarded

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

what is stage 1 hypertension

A

140/90 or higher

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

what is stage 2 hypertension

A

160/100 or higher

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

what is severe hypertension

A

180/110 or higher

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

how can CV risk and organ damage be assessed

A

urine (protein), blood (glucose, electrolytes, creatine, estimated glomerular filtration rate and cholesterol) fundi (hypertensive retinopathy) and arrange 12 lead ECG

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

what is the care pathway for stage 1 hypertension

A

if organ damage present or high risk - hypertensive drugsif <40 yrs - consider specialist referral offer lifestyle interventions

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

what is care pathway for stage 2 hypertension

A

offer anti-hypertensive drug treatment

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

what information is given in patient education and adherence

A

provide info about benefits of drugs and side effects, details of patient organisation and annual review of care

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

first line treatment for aged under 55 years

A

ACE inhibitor or low cost angiotensin II receptor blocker ARB

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

first line treatment for over 55 years or black person of african or caribbean family origin of any age

A

calcium channel blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

second line treatment for all

A

ace inhibitor/arb and calcium channel blocker

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

third line treatment for all

A

ACE/ARB and CCB and thiazide like diuretic

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

what is the treatment for resistant hypertension

A

ACE/ARB and CCB and thiazide like diuretic and consider further diuretic or alpha or beta blocker

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

vessel damage exposes collagen, what binds to this collagen

A

platelets which then become activated and extend pseudopia (temporary cytoplasm-filled projection of eurkaryotic cell membrane) and synthesise and release thromboxane A2 (TXA2)

49
Q

what does TXA2 bind to

A

platelet GPCR TXA2 receptors (mediator release and ADP)vascular smooth muscle cell TXA2 receptors (vasoconstriction that is augmented by mediator 5-HT binding to smooth muscle GPCR 5HT receptors)

50
Q

ADP binds to platelet GPCR purine receptors (P2Y12) that does what

A

activate further platelet, aggregate platelets into soft plug (via increased glycoprotein receptors that bind fibrinogen) and expose acidic phospholipids on the platelet surface that initiate coagulation of blood and solid clot formation

51
Q

what is the key events in a complex, amplifying, cascade in which proenzymes are converted to active enzymes

A

production of protease thrombin (factor IIa) that cleaves fibrinogen to fibrin to form a solid clot

52
Q

what is an arterial thrombus

A

white thrombus (mainly platelets in fibrin mesh), forms embolus if it detaches and primarily treated with anti platelet drugs

53
Q

what is a venous thrombus

A

red thrombus (white head, jelly like red tail, fibrin rich) if detaches normally lodges in lung (PE) and treated with anticoagulants

54
Q

what are examples of anti-coagulants

A

warfarin, orally active inhibitors, heparin

55
Q

when are anticoagulants used

A

DVT, prevention of post operative thrombosis, patients with artificial heart valves and atrial fibrillationall carry risk of haemorrhage

56
Q

how does warfarin work

A

orally - competes with vitamin K for binding to hepatic vitamin K reductase - renders clotting factors II, VII, IX and X inactive and blocks coagulation

57
Q

what are the warnings associated with warfarin

A

difficult to stoke balance between anticoagulant effect and haemorrhage - overdose treated with vitamin K1 (phytomenadione) or concentrate of plasma clotting factors (IV)

58
Q

what are factors that potentiate warfarin action (risk of haemorrhage increased)

A

liver decrease (decrease clotting factors), high metabolic rate (increased clearing of clotting factors) and drug interactions (aspirin, other NSAIDs that inhibit platelet function and drugs that inhibit reduction of vitamin K)

59
Q

what are factors which lessen warfarin action (risk of thrombosis increased)

A

pregnancy, hyperthyroidism, vitamin K consumption, and agents that increase hepatic metabolism of warfarin

60
Q

how does heparin work

A

IV - bind to antithrombin III (inhibitor of coagulation which neutralises clotting factors) increasing its affinity for clotting factors to greatly increase their rate of inactivation elimination zero orderGiven in hospital when immobile

61
Q

what are examples of LMWH

A

enoxaparin and dalteparin

62
Q

LMWH are now preferred except in when

A

renal failure since they are eliminated by renal excretion

63
Q

how to LMWH work

A

inhibit factor Xa but not thrombin IIa

64
Q

what is adverse effects of heparin

A

haemorrhage (sulphate IV inctivates heparin), osteoporosis (long term treatment), hyposensitivity reactions

65
Q

what are examples of orally active inhibitors

A

inhibitors or thrombin (dabigatran etexilate) or factor Xa (rivaroxaban, apixaban)

66
Q

when are orally inactive inhibitors used

A

to prevent venous thrombosis in patients undergoing hip and knee replacements

67
Q

what are examples of anti-platelet drugs

A

aspirin, clopidogrel and tirofiban

68
Q

when are anti-platelet drugs mainly used

A

treatment of arterial thrombosis

69
Q

how does aspirin work

A

orally - irreversibly blocks COX in platelets, preventing TXA2 synthesis

70
Q

when is aspirin used

A

thromboprophylaxis in patients at high CV risk

71
Q

what is adverse effects of aspirin

A

GI bleeding and ulceration

72
Q

how does clopidogrel work

A

orally - links to p2y12 receptor (produces glycoprotein IIb/IIIa) producing irreversible inhibition - often used in patients intolerant to aspirin

73
Q

when is tirofiban used

A

IV in short term treatment to prevent MI in high risk patients with unstable angina (with aspirin and heparin)

74
Q

when is an example of fibrinolytic drugs

A

streptokinase

75
Q

when are fibrinolytic drugs used

A

principally to reopen occluded arteries in acute MI or stroke - less frequently life threatening venous thrombosis or PE

76
Q

how does streptokinase work

A

IV or intracoronary - protein extracted from streptococci which reduces mortality in acute MI but action blocked after 4 days by antibodies

77
Q

what is adverse effects of streptokinase

A

may cause allergic reaction (not to be given to patients with recent strep infections)

78
Q

what are examples of plasminogen drugs

A

alteplase and duteplase

79
Q

how do alteplase and duteplase work

A

IV - tissue plasminogen activator (rt-PA) which forms plasmin which is capable of breaking cross-links between fibrin molecules, which provide the structural integrity of blood clots more effective on fibrin bound plasminogen than plasma plasminogen

80
Q

what signs could suggest pleural malignancy

A

hoarse voice and dysphagia (difficulty swallowing), reduced air entry and dull to percussion

81
Q

what areas can the mediastinum be divided into

A

superior inferior (divided into anterior, middle and posterior)

82
Q

where is thoracic inlet (opening at top of thoracic cavity)

A

bounded by ribs 1, T1 vertebra and jugular notch

83
Q

where is the transverse thoracic plane (divides superior into inferior) located

A

between sternal angle and t4/t5

84
Q

where is anterior mediastinum located and what does it contain

A

between sternum and fibrous pericardium contains thymus (produces T cells in childhood - becomes adipose tissue after puberty)

85
Q

what does middle mediastinum contain

A

pericardium and heart

86
Q

what parts of the great vessels connect to heart

A

inferior part of SVC, superior part of IVC, pulmonary trunk and arteries, pulmonary veins and ascending aorta

87
Q

what does the posterior mediastinum contain

A

azygous vein (blood from intercostal veins to SVC), sympathetic chain, thoracic duct (carries lymph to left venous angle), trachea and 2 main bronchi, thoracic aorta, oesophagus and vagal trunks

88
Q

where does azygous vein arch

A

anteriorly, superiorly to the lung root to drain into SVC and can be ruptured in chest trauma

89
Q

what is the branches of the arch of aorta

A

left side - left subclavian and left common carotid right side - brachiocephalic trunk which bifurcates into right subclavian and right common carotid

90
Q

what are the branches of the ascending aorta

A

left and right coronary arteries

91
Q

what are branches of thoracic aorta (in descending order)

A

bronchial arteries, mediastinal arteries, oesophageal arteries, pericardial arteries, phrenic arteries and intercostal and subcostal arteries

92
Q

where does abdominal aorta begin and where does it terminate

A

begins at T12, ends at L4 where it bifurcates into right and left common iliac arteries that supply lower body

93
Q

where does right lymphatic duct drain lymph

A

right venous angle

94
Q

where does thoracic duct drain lymph

A

left venous angle (left sternoclavicular joint)

95
Q

what does bronchopulmonary lymph nodes surround

A

main bronchus at lung root

96
Q

what does tracheobronchial lymph nodes surround

A

bifurcation of aorta

97
Q

what is the cisterna chyli

A

swollen start of thoracic duct in abdomen

98
Q

what is the role of the right phrenic nerve

A

pass through diaphragm with IVC to supply diaphragm from inferior aspect

99
Q

what is the role of left phrenic nevre

A

pierces through left dome of diaphragm to supply it from inferior aspect

100
Q

what is the contents of superior mediastinum anteriorly to posteriorly

A

brachiocephalic veins and SVC, arch of aorta, trachea, oesophagus and thoracic duct

101
Q

what is the contents of superior mediastinum lateral to medial

A

phrenic nerves, vagus nerves, recurrent laryngeal nerves

102
Q

what are central veins

A

those close enough to heart such that pressure within them is said to reflect pressure in right atrium:internal jugular, subclavian vein, brachiocephalic vein, SVC, IVC, iliac veins and femoral veins

103
Q

what creates the pressure wave which can be seen in internal jugular vein

A

atrial contraction then filling of right atrium against closed tricuspid valve causes double pulsation that is conducted in retrograde direction

104
Q

at 45o the JVP should be no more than what height above sternal angle

A

3cm

105
Q

which recurrent laryngeal nerves enter chest

A

Left (hooks under arch of aorta)right does not!! (hooks under right subclavian)

106
Q

what are the phrenic nerves a somatic sensor to

A

mediastinal parietal pleura, fibrous pericardium, diaphragmatic parietal pleura, diaphragmatic parietal peritoneum

107
Q

where does pain from diaphragm get referred to

A

more superficial structure (skin over shoulder tip) due to supraclavicular nerves entering spinal cord at same level as phrenic nevre

108
Q

what does vagus nerves contain

A

somatic sensory nerves (palate, laryngopharynx and larynx), somatic motor nerves (pharynx and layrnx) and autonomic parasympathetic nerves (organs and abdominal organs)

109
Q

what are the branches of vagus nerves which supply pharynx and larynx

A

recurrent laryngeal nerves - once vagus nerves have given off their recurrent laryngeal branches they contain only parasympathetic fibres

110
Q

where is pulse felt in neck

A

bifurcation of the common carotid (also site for auscultating carotid bruits)anterior to sternocleidomastoid muscle at level of superior border of thyroid cartilage

111
Q

where is brachial artery located

A

medial to biceps brachii tendon in cubital fossa

112
Q

where is radial artery located

A

lateral to tendon of flexor carpi radialis

113
Q

where is femoral artery located

A

inferior to midpoint of inguinal ligament

114
Q

where is popliteal artery located

A

in popilteal fossa - immediately posterior to knee joint

115
Q

where is posterior tibial artery located

A

between posterior border of medial malleolus and Achilles tendon

116
Q

where is dorsalis pedis artery located

A

medial to tendon of extensor hallucis longus on dorsum of foot

117
Q

where can arterial access (left side of heart) take place

A

radial artery (cannulation for BPM or ABG)subclavian artery (insertion of cardiac pacing wire under ultrasound guidance)femoral artery (intravascular interventions)

118
Q

where can central venous access (right side of heart) take place

A

femoral vein (insertion of central line and intravascular interventions)internal jugular vein (insertion of central line under ultrasound guidance)