Cardio Week 3 Flashcards
what is atherosclerosis
progressive disease characterised by build up of plaque
what is the normal level for triglycerides
2.3mmol/l
what is the role of HDL
protective effect for risk of atherosclerosis and CHD
what are markers of high cholesterol
xanthelasma (xanthomas of eyelids), tendon xanthomas, tuberous xanthomas or eruptive xanthomas (small reddish-yellow pauples)
what is the events leading up to the formation of a fatty streak or plaque
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
what diseases are attributable to hypertension
aortic aneurysm, HR, LVH, MI, CHD, cerebral haemorrhage, preeclampsia, stroke, chronic kidney disease, blindness
what is the risk factors for CVD that most hypertensives have
dyslipidemia, diabetes, age, male gender, smoking, family history
what lifestyle modifications can be made to reduce risk of CVD
lose weight, limit alcohol intake, increase physical activity, reduce salt intake, stop smoking, limit intake of foods rich in fat and cholesterol
what is hypertension a risk factor for
cerebral haemorrhage, atheroma, renal failure, sudden cardiac death
what is primary hypertension
90% of cases, no obvious cause, increase in dietary salt leads to increase in BP
what is secondary hypertension
underlying disease implicated
what are common causes of secondary hypertension
renal disease (salt and water overload), sleep apnoea, aldosteronism, Reno-vascular disease
what are uncommon causes of secondary hypertension
cushings (excess corticosteroids), pheochromocytoma (excess noradrenaline) hyperparathyroidism, aortic coarctation (congenital narrowing)
what is benign hypertension
life threatening, asymptomatic, incidental finding, eventually causes LVH, congestive cardiac failure, increases atheroma, aneurysm rupture and renal disease
what is the process behind left ventricular hypertrophy
increased LV load - poor perfusion - interstitial fibrosis - micro infarcts - diastolic dysfunction results in cardiac death or failure
what is the cause of hypertensive atherosclerosis
blood vessel wall changes (esp in retina and kidney), thickening of media and hyaline arteriosclerosis where plasma proteins forced into vessel wall
what is malignant hypertension
serous, diastolic >130, can develop from either benign primary or secondary hypertension or arise de-novo - urgent treatment needed
causes of malignant hypertension
cerebral oedema (seen as papillodema), acute renal failure, acute heart failure, headache and cerebral haemorrhage
what is the consequence of pregnancy associated hypertension and proteinuria
pre-eclampsia - obstetric emergency and the hypertension is secondary to silent renal or systemic disease
what is the virchows triad that leads to thrombosis
endothelial injury, turbulent blood flow, hypercoaguable blood
what causes endothelial injury
hypertension, autoimmune disease (eg primary vasculitis)
thrombus via intravascular coagulation is caused by what two things
platelet activation and fibrin production via coagulation cascade
what is special about activated platelets
more sticky, attract and aggregate with other platelets, aggregate with fibrin (fibrin is end point of coagulation cascade)
what happens when endothelial damage occurs and endothelium is lost
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)
what is the common intrinsic pathway
XII-XII-IV-VIII
what is common extrinsic pathway
tissue factor joins factor VII
what is the complications of atherosclerosis
thrombosis, narrowed coronary artery (may be asymptomatic if myocardial O2 demand met), exercised induced angina (stable) or plaque rupture (unstable angina)
what is homeostasis
constant clotting and constant clot lysis
what are anti clotting proteins
protein C and S (degrades factor V and VIII) and antithrombin III (degrades II, IX and X)
what is the primary causes of hypercoaguability
Factor V lieden (mutation at point in factor V targeted by protein C and S: results in C, S and antithrombin III deficiency)
what secondary causes of hypercoaguability
prolonged immobility, significant tissue injury, autoimmune, MI, AF, cancer (activate coagulation cascade through tumour produced TF) and many cancer therapies injure endothelium
what are low risk secondary causes of hypercoagubility
the pill, smoking, renal disease (nephrotic syndrome) and cardiomyopathy
what happens to organs which are distal to branching arteries
more susceptible to embolism and infarction eg stroke and small bowel infection
what do you need to ensure when using ABPM (ambulatory BP monitoring) to confirm diagnosis
at least two measurements per hour during the persons usual waking hours
what do you need to ensure when using HBPM (home blood pressure monitoring) to confirm diagnosis
two consecutive seated measurements, 1 minute apart, BP recorded twice a day for at least 4 days - measurements on first day are discarded
what is stage 1 hypertension
140/90 or higher
what is stage 2 hypertension
160/100 or higher
what is severe hypertension
180/110 or higher
how can CV risk and organ damage be assessed
urine (protein), blood (glucose, electrolytes, creatine, estimated glomerular filtration rate and cholesterol) fundi (hypertensive retinopathy) and arrange 12 lead ECG
what is the care pathway for stage 1 hypertension
if organ damage present or high risk - hypertensive drugsif <40 yrs - consider specialist referral offer lifestyle interventions
what is care pathway for stage 2 hypertension
offer anti-hypertensive drug treatment
what information is given in patient education and adherence
provide info about benefits of drugs and side effects, details of patient organisation and annual review of care
first line treatment for aged under 55 years
ACE inhibitor or low cost angiotensin II receptor blocker ARB
first line treatment for over 55 years or black person of african or caribbean family origin of any age
calcium channel blocker
second line treatment for all
ace inhibitor/arb and calcium channel blocker
third line treatment for all
ACE/ARB and CCB and thiazide like diuretic
what is the treatment for resistant hypertension
ACE/ARB and CCB and thiazide like diuretic and consider further diuretic or alpha or beta blocker
vessel damage exposes collagen, what binds to this collagen
platelets which then become activated and extend pseudopia (temporary cytoplasm-filled projection of eurkaryotic cell membrane) and synthesise and release thromboxane A2 (TXA2)
what does TXA2 bind to
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)
ADP binds to platelet GPCR purine receptors (P2Y12) that does what
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
what is the key events in a complex, amplifying, cascade in which proenzymes are converted to active enzymes
production of protease thrombin (factor IIa) that cleaves fibrinogen to fibrin to form a solid clot
what is an arterial thrombus
white thrombus (mainly platelets in fibrin mesh), forms embolus if it detaches and primarily treated with anti platelet drugs
what is a venous thrombus
red thrombus (white head, jelly like red tail, fibrin rich) if detaches normally lodges in lung (PE) and treated with anticoagulants
what are examples of anti-coagulants
warfarin, orally active inhibitors, heparin
when are anticoagulants used
DVT, prevention of post operative thrombosis, patients with artificial heart valves and atrial fibrillationall carry risk of haemorrhage
how does warfarin work
orally - competes with vitamin K for binding to hepatic vitamin K reductase - renders clotting factors II, VII, IX and X inactive and blocks coagulation
what are the warnings associated with warfarin
difficult to stoke balance between anticoagulant effect and haemorrhage - overdose treated with vitamin K1 (phytomenadione) or concentrate of plasma clotting factors (IV)
what are factors that potentiate warfarin action (risk of haemorrhage increased)
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)
what are factors which lessen warfarin action (risk of thrombosis increased)
pregnancy, hyperthyroidism, vitamin K consumption, and agents that increase hepatic metabolism of warfarin
how does heparin work
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
what are examples of LMWH
enoxaparin and dalteparin
LMWH are now preferred except in when
renal failure since they are eliminated by renal excretion
how to LMWH work
inhibit factor Xa but not thrombin IIa
what is adverse effects of heparin
haemorrhage (sulphate IV inctivates heparin), osteoporosis (long term treatment), hyposensitivity reactions
what are examples of orally active inhibitors
inhibitors or thrombin (dabigatran etexilate) or factor Xa (rivaroxaban, apixaban)
when are orally inactive inhibitors used
to prevent venous thrombosis in patients undergoing hip and knee replacements
what are examples of anti-platelet drugs
aspirin, clopidogrel and tirofiban
when are anti-platelet drugs mainly used
treatment of arterial thrombosis
how does aspirin work
orally - irreversibly blocks COX in platelets, preventing TXA2 synthesis
when is aspirin used
thromboprophylaxis in patients at high CV risk
what is adverse effects of aspirin
GI bleeding and ulceration
how does clopidogrel work
orally - links to p2y12 receptor (produces glycoprotein IIb/IIIa) producing irreversible inhibition - often used in patients intolerant to aspirin
when is tirofiban used
IV in short term treatment to prevent MI in high risk patients with unstable angina (with aspirin and heparin)
when is an example of fibrinolytic drugs
streptokinase
when are fibrinolytic drugs used
principally to reopen occluded arteries in acute MI or stroke - less frequently life threatening venous thrombosis or PE
how does streptokinase work
IV or intracoronary - protein extracted from streptococci which reduces mortality in acute MI but action blocked after 4 days by antibodies
what is adverse effects of streptokinase
may cause allergic reaction (not to be given to patients with recent strep infections)
what are examples of plasminogen drugs
alteplase and duteplase
how do alteplase and duteplase work
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
what signs could suggest pleural malignancy
hoarse voice and dysphagia (difficulty swallowing), reduced air entry and dull to percussion
what areas can the mediastinum be divided into
superior inferior (divided into anterior, middle and posterior)
where is thoracic inlet (opening at top of thoracic cavity)
bounded by ribs 1, T1 vertebra and jugular notch
where is the transverse thoracic plane (divides superior into inferior) located
between sternal angle and t4/t5
where is anterior mediastinum located and what does it contain
between sternum and fibrous pericardium contains thymus (produces T cells in childhood - becomes adipose tissue after puberty)
what does middle mediastinum contain
pericardium and heart
what parts of the great vessels connect to heart
inferior part of SVC, superior part of IVC, pulmonary trunk and arteries, pulmonary veins and ascending aorta
what does the posterior mediastinum contain
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
where does azygous vein arch
anteriorly, superiorly to the lung root to drain into SVC and can be ruptured in chest trauma
what is the branches of the arch of aorta
left side - left subclavian and left common carotid right side - brachiocephalic trunk which bifurcates into right subclavian and right common carotid
what are the branches of the ascending aorta
left and right coronary arteries
what are branches of thoracic aorta (in descending order)
bronchial arteries, mediastinal arteries, oesophageal arteries, pericardial arteries, phrenic arteries and intercostal and subcostal arteries
where does abdominal aorta begin and where does it terminate
begins at T12, ends at L4 where it bifurcates into right and left common iliac arteries that supply lower body
where does right lymphatic duct drain lymph
right venous angle
where does thoracic duct drain lymph
left venous angle (left sternoclavicular joint)
what does bronchopulmonary lymph nodes surround
main bronchus at lung root
what does tracheobronchial lymph nodes surround
bifurcation of aorta
what is the cisterna chyli
swollen start of thoracic duct in abdomen
what is the role of the right phrenic nerve
pass through diaphragm with IVC to supply diaphragm from inferior aspect
what is the role of left phrenic nevre
pierces through left dome of diaphragm to supply it from inferior aspect
what is the contents of superior mediastinum anteriorly to posteriorly
brachiocephalic veins and SVC, arch of aorta, trachea, oesophagus and thoracic duct
what is the contents of superior mediastinum lateral to medial
phrenic nerves, vagus nerves, recurrent laryngeal nerves
what are central veins
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
what creates the pressure wave which can be seen in internal jugular vein
atrial contraction then filling of right atrium against closed tricuspid valve causes double pulsation that is conducted in retrograde direction
at 45o the JVP should be no more than what height above sternal angle
3cm
which recurrent laryngeal nerves enter chest
Left (hooks under arch of aorta)right does not!! (hooks under right subclavian)
what are the phrenic nerves a somatic sensor to
mediastinal parietal pleura, fibrous pericardium, diaphragmatic parietal pleura, diaphragmatic parietal peritoneum
where does pain from diaphragm get referred to
more superficial structure (skin over shoulder tip) due to supraclavicular nerves entering spinal cord at same level as phrenic nevre
what does vagus nerves contain
somatic sensory nerves (palate, laryngopharynx and larynx), somatic motor nerves (pharynx and layrnx) and autonomic parasympathetic nerves (organs and abdominal organs)
what are the branches of vagus nerves which supply pharynx and larynx
recurrent laryngeal nerves - once vagus nerves have given off their recurrent laryngeal branches they contain only parasympathetic fibres
where is pulse felt in neck
bifurcation of the common carotid (also site for auscultating carotid bruits)anterior to sternocleidomastoid muscle at level of superior border of thyroid cartilage
where is brachial artery located
medial to biceps brachii tendon in cubital fossa
where is radial artery located
lateral to tendon of flexor carpi radialis
where is femoral artery located
inferior to midpoint of inguinal ligament
where is popliteal artery located
in popilteal fossa - immediately posterior to knee joint
where is posterior tibial artery located
between posterior border of medial malleolus and Achilles tendon
where is dorsalis pedis artery located
medial to tendon of extensor hallucis longus on dorsum of foot
where can arterial access (left side of heart) take place
radial artery (cannulation for BPM or ABG)subclavian artery (insertion of cardiac pacing wire under ultrasound guidance)femoral artery (intravascular interventions)
where can central venous access (right side of heart) take place
femoral vein (insertion of central line and intravascular interventions)internal jugular vein (insertion of central line under ultrasound guidance)
