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cardiology > cardiovascular risk problems > Flashcards

cardiovascular risk problems Flashcards

1
Q

what is the heart derived from

A

The heart is derived from visceral mesoderm. It comes from the cranial end of the embryo and starts as a hoarse shaped structure

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2
Q

the heart tube develops 5 dilations. what are they and what do they develop into in an adult heart

A
  • truncus arteriosus = aorta, pulmonary trunk
  • bulbus cordis = trabeculated part of the right ventricle, outflow part of both ventricles
  • ventricle = trabeculated part of the left ventricle
  • atrium = trabeculated part of both atria
  • sinus venosus = sinus part R.atrium, coronary sinus
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3
Q

what day does the heart begin to loop and fold

A

day 23

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4
Q

in a foetus what do the aortic arches I,II,III,IV,V,VI develop into

A 
I and II = mostly obliterated
III = common carotid artery 
IV = right subclavian 
V = rudimentary or absent 
VI = sprout branches that form pulmonary aa
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5
Q

there are 3 parts to the embryonic venous system what are they

A
  1. vitelline- drain the yolk sac (venous structures relating to draining the gut)
  2. umbilical - from placenta
  3. systemic = the anterior cardinal veins that drain the head and neck and the posterior cardinal veins that drain the trunk
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6
Q

what are modifiable and non modifiable risk factors for cardiovascular disease

A

modifiable = smoking, diet, hypertension, diabetes mellitus, obesity, chromogenic factors, physical inactivity, alcohol consumption

non modifiable = personal history of CHD, family history , age, gender

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7
Q

what should be collected routinely and included in the clinical history for cardiovascular risk?
what should be measured when assessing cardiovascular risk?

A
  • age, sex, lifetime smoking habit, Fox of cardiovascular disease, ethnicity
  • blood pressure, weight and BMI, cholesterol, diabetes, rheumatoid arthritis
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8
Q

for cardiovascular disease what is the primary, secondary and tertiary prevention

A
  • primary = reduce incidence in population
  • secondary = detection and treatment of pre-symptomatic and early disease
  • tertiary = reducing incidence/recurrences of chronic incapability among those with symptomatic disease
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9
Q

how clinically are you likely to come across lipids

A
  • xanthomata (fatty growths develop under skin)
  • xanthelasma ( yellowish deposit of cholesterol under skin ie eyelids)
  • corneal arcus (cholesterol in the peripheral cornea)
  • milky blood/serum
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10
Q

how do statins work

A

Statins fool liver enzymes into thinking they don’t have enough cholesterol by inhibiting an enzyme that’s involved in cholesterol syntheses in the cells (HMG coenzyme reductase). Expresses more LDL receptors on its surface ie increasing LDL clearance

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11
Q

what’s PCSK9s role in the LDL receptor pathway

A
  • exerts control over LDL recycling pathway
  • involved In the recycling of LDL receptors in cell
  • acts as a brake - blocking PCSK9
  • the more PCSK9 there is the more recycling possible
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12
Q

what are some lipid lowering drugs

A
  • Statins
    Pravastatin
    Simvastatin
    Atorvastatin
  • PCSK9 inhibitors
    Alirocumab
    Evolocumab
  • Fibrates
  • Ezetimibe - only for patients who cannot tolerate statins
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13
Q

what are aetiologies of atheroma

A
  • smoking
  • hypertension
  • hyperlipedemia
  • diabeties
  • older age
  • male
  • genetics
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14
Q

how does an atheroma form

A
  1. primary endothelial injury eg smoking, toxins ..
  2. accumulation of lipids and macrophages - increased LDL, reduced HDL. Induces pro inflammatory cytokines (V-CAM, IL-1 and TNF)
  3. migration of smooth muscle cells with growth factors present (PDGF, FGF, TGF alpha)
  4. increase in size - proliferation of smooth muscle with the formation of a layer of cells covering the extracellular lipid separates it from the adaptive smooth muscle thickening in endothelium
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15
Q

when does atheromatous narrowing of an artery likely to produce critical disease

A
  • it is the only artery supplying an organ or tissue ie there is no collateral circulation
  • the artery diameter is small (eg coronary artery vs common iliac artery)
  • overall blood flow is reduced ie cardiac failure
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16
Q

what are some complications of atheroma

A
  • stenosis = when a valve that is narrowed doesn’t open properly. The flaps of a valve may thicken, stiffen or fuse together
  • thrombosis = formation of a blood clot inside a blood vessel of the heart
  • aneurysm - bulge or swelling in the aorta
  • dissection
  • embolism - obstruction that travels from the heart to lodge in a blood vessel
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17
Q

what is arterial stenosis

A

The narrowing of the arterial lumen, reduced elasticity, reduced flow in systole, tissue ischaemia

18
Q

what are clinical effects of cardiac ischaemia

A

reduced exercise tolerance, angina, unstable angina, myocardial infarction, cardiac failure

19
Q

what os cardiac fibrosis

A

loss of cardiac myocytes, replacement by fibrous tissue, loss of contractility, reduced elasticity and filling

20
Q

wha are superadded thrombosis and what can be the clinical effects

A

when plaques rupture thrombus forms over the top and can completely block the arterial lumen in a coronary artery

clinical effects:

  • MI
  • Cerebral infarction
  • Renal infarction
  • Intestinal infarction
21
Q

how is an aneurysm formed and what are the complications

A
  • abnormal and persistent dilation of an artery due to a weakness in the wall
  • mycotic, atherosclerotic, dissecting, congenital, arteriovenous, traumatic
  • commonest site = abdominal aorta

complications = rupture, thrombosis, embolism, pressure erosion of adjacent structures, infection

22
Q

what is arterial dissection

A
  • splitting within the media by flowing blood
  • false lumen filled with blood within the media
  • sudden collapse and high mortality
23
Q

what is an embolism

A
  • both superadded thrombus and plaque material may break off and embolism
24
Q

what is essential hypertension

A

defined as the rise in blood pressure of unknown cause that increases risk for cerebral, cardiac and renal events. blood pressure is greater than 140/90 mmHg. “the level of BP where treatment does more good than harm”

25
Q

how is ABPM used when measuring BP

A

at least 2 measurements an hour during the persons usual waking hours

26
Q

how is HBPM used when measuring BP

A

2 consecutive seated measurements, 1 minute apart. BP is recorded twice a day for at least 4 days and preferably 7 days. Measurements on the first day are discarded - average value of all remaining is used

27
Q

define: stage 1 hypertension
stage 2 hypertension
severe hypetension

A
  • stage 1 hypertension - clinic BP is 140/90 mmHg or higher and ABPM or HBPM daytime average is 135/85 mmHg or higher
  • stage 2 hypertension - clinic BP 160/100 mmHg or higher and an ABPM or HBPM daytime average of 150/95 mmHg
  • severe hypertension - clinic BP of 180 mmHg or higher or clinic diastolic BP of 110mmHg or higher
28
Q

what are the recommendations for assessing cardiovascular risk

A
  • estimation of CV risk to discuss prognosis and heathcare options

for all with hypertension offer to:

  • test urine for presence of protein
  • take blood to measure glucose, electrolytes, creatinine, estimated glomerular filtration rate and cholesterol
  • examine funds for hypertensive retinopathy
  • arrange a 12- lead ECG
29
Q

what are the Keith, Wagner and Barker classifications of hypertensive retinopathy

A

grade 1 = slight or modest narrowing of the retinal arterioles, with an arteriovenous ratio > 1:2

grade 2 = modest to severe narrowing of retinal arterioles with an arteriovenous ratio of <1:2 or arteriovenous nickling

grade 3 = bilateral soft exudates or flame shaped haemorrhages

grade 4 = bilateral optic nerve oedema

30
Q

what are some blood pressure reducing drugs

A
  • Thiazide diuretic
  • ACE inhibitor
  • Calcium channel blocker
  • Beta channel blocker
  • Spironolactone, Alpha blockers, centrally acting older drugs
31
Q

what would you prescribe a patient less than 55 years with hypertension

A

step 1 = ACE inhibitor
step 2 = ACE inhibitor and calcium channel blocker
step 3 = ACE inhibitor , calcium channel blocker and diuretic
step 4 = add further diuretic therapy or alpha blocker or beta blocker

32
Q

what would you prescribe a patient over 55 with hypertension

A

step 1 = calcium channel blocker or diuretic
step 2 = ACE inhibitor and calcium channel blocker or ACE inhibitor and diuretic
step 3 = ACE inhibitor, calcium channel blocker
step 4 = add further diuretic therapy or alpha blocker or beta blocker

33
Q

how to use spironolactone for resistant hypertension

A
  • start low and go slow
  • caution: diabetes and low GFR
  • 12.5mg/day
  • liquid available
  • tolerate 25% rise in K+ and Creat
34
Q

what is haemostasis and what are the stages

A

the arrest of blood loss from a damaged vessel - at the site of injury involves in sequence:
1. vascular wall damage exposing collagen and tissue factor (Thromboplastin)

  1. primary haemostasis causing local vasoconstriction, platelet adhesion, activation and aggregation (by fibrinogen). the activated platelets synthesise and release thromboxane A2 (TXA2)
  2. TXA2 binds to: platelet GPCR TXA2 receptors causing mediator release and adenosine diphosphate (ADP). Vascular smooth muscle cell TXA2 receptors causing vasoconstriction that is augmented by mediator 5-HT binding to smooth muscle GPCR 5-HT receptors
  3. ADP binds to platelet GPCR purine receptors (P2Y12) that:
    - act locally to activate further platelets
    - aggregate platelets into a soft plug act the site of lung injury. TXA2 acts similarly
    - expose acidic phospholipids on the platelet surface that initiate coagulation of blood and solid clot formation
  4. activation of blood clotting (coagulation) and the formation of stable clot (by fibrin enmeshing platelets)
35
Q

what is thrombosis

A

pathological haemostasis - a haematological plug in the absence of bleeding.

  • injury to vessel wall
  • abnormal blood flow
  • increased coagulability of the blood
36
Q

what is an arterial thrombus vs a venous thrombus

A

arterial thrombus

  • white thrombus: mainly platelets in fibrin mesh
  • forms an embolus if it detaches from its site of origin
  • primarily treated with antiplatelet drugs

venous thrombus

  • red thrombus: white head, jelly like red tail, fibrin rich
  • if detached forms an embolus that usually lodges in the lung
  • primarily treated by anticoagulants
37
Q

what are the sites of action of anticoagulant drugs

  • warfarin
  • rivarociban
  • heparin and LMWH
  • dabigatran
A
  • warfarin - blocks modification of factors X and II essential for their function
  • rivaroxiban - directly inhibits factor Xa
  • heparin/ LMWH - inactivates factor Xa via antithrombin III
  • dabigatran - inhibits factor IIa
38
Q

what is the function of anticoagulant Warfarin

A
  • Structurally related to vitamin K with which it competes for binding to hepatic vitamin K reductase preventing production of the active hydroquinone
  • renders factors II, VII, IX, X inactive
  • blocks coagulation in vivo, not in vitro
  • is administered orally and is very well absorbed
  • has a slow onset of action (2-3 days) whilst unmodifiable factors replace y-carboxylated factors
  • long half life
  • difficult to strike the balance between anticoagulant effect and haemorrhage - low therapeutic index
  • factors that increase the risk of haemorrhage = liver disease, high metabolic rate, drug interactions
39
Q

what is the role of antithrombin III

A

inhibits coagulation which neutralises all serine protease factors in the coagulation cascade by binding to their active site in a 1:1 ratio

heparin binds to antithrombin III increasing its affinity for serine protease clotting factors to greatly increase their rate of their inactivation

40
Q

what are adverse effects of heparin and LMWH

A
  • osteoporosis
  • hypoaldosteronism
  • hypersensitivity reactions
41
Q

what is the function of aspirin

A
  • Main anti platelet agent - irrevesibly blocks cycloxygenase in platelets, preventing TXA2 synthesis, but also COX in endothelial cells inhibiting production of antithrombotic prostaglandin I2 (PGI2)
  • used orally or rectally in high dose for thromboprophylaxis is patient at high cardiovascular risk and for treatment of acute coronary syndrome and acute ischaemic stroke
  • main adverse effect is gastrointestinal bleeding and ulceration
42
Q

what is the use of Clopidogrel

A
  • Anti platelet drug
  • links to P2Y12 receptor by a disulphide bond producing irreversible inhibition of ADP binding
  • can be used alone for patients intolerant to aspirin
  • administered orally when combined with aspirin

cardiology (13 decks)

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