cardio (+ CNS) Flashcards
what is the definition of ischaemic heart disease?
what are the two types of aetiology?
generic designation for a group of syndromes resulting from myocardial ischaemia
(an imbalance between demand and supply of oxygenated blood to the heart)
reduced supply (almost always) - norm coronary artery atherosclorosis
increased demand (sometimes) - myocardial hypertrophy
what are the 4 main syndromes which come under the umbrella of ischaemic heart disease (IHD)?
- MI
- angina pectoris
- chronic IHD with heart failure
- sudden cardiac death
what are the 3 different types of angina?
stable angina
unstable angina
prinzmetal (aka variant) angina
- due to vasospasm NOT atherosclerosis
- only about 2% of angina
- occurs in younger people with few/no atherosclerotic risk factors
what are the 3 main clinical differences between stable and unstable angina?
stable:
- pain on exertion/stress
- pain begins slowly and gets worse over minutes
- pain relieved by rest or medication
- nb seems to be a predictable pattern as to the onset and timing of pain
unstable:
- attacks of pain occur randomly, with or without exertion
- pain is sudden + severe
- pain not relieved by rest or medication
nb in prinzmetal/variant angina you tend to pain radomly at rest
nb stable angina can develop into unstable angina
what are the 3 things which make up acute coronary syndrome?
- unstable angina
- MI
- sudden cardiac death
in terms of testing blood levels for cholesterol what is the most useful measuring for predicting risk of IHD?
a high total cholesterol:HDL ratio is BAD
does coronary heart disease affect more men or more women
more men
nb stroke affects more women
what are the three main modifiable risk factors for IHD?
- smoking
- poor diet
- low physical activity
nb alcohol (in moderation) is cardioprotective
describe the pathogenesis of myocardial ischaemia
Myocardial ischemia is a consequence of reduced blood flow in coronary arteries, due to a combination ofFIXED VESSEL NARROWINGandABNORMAL VASCULAR TONEas a result ofATHEROSCLEROSISandENDOTHELIAL DYSFUNCTION. This leads to an imbalance between myocardial oxygen supply and demand
in the pathogenesis of IHD, when does it become chronic IHD?
when more than 75% of the lumen of the coronary artery is occluded
after this level of occlusion the artery can no longer autoregulate and vasodilate + permanent chronic damage can occur = chronic IHD
what is the definition of myocardial infarction?
what are the 2 histological types?
death of cardiac muscle from prolonged ischaemia
subendocardial
- inner one third of wall (least well perfused)
transmural
- full thickness of myocardium
what is the pathophysiology of a stable atherosclerotic plaque leading to an MI?
- acute plaque changes/rupture of fibrous cap
- > platelet aggregation
- > thrombus formation
- > occlusion of coronary artery
- > infarction
histologically what changes are seen in the myocardium: <24hrs post-MI? - 1-2 days post-MI? - 3-4 days post-MI? - 1-3wks post-MI? - 3-6wks post-MI?
<24hrs post-MI:
- normal
1-2 days post-MI:
- pale
- oedema
- myocyte necrosis
- neutrophils
3-4 days post-MI:
- yellow with haemorrhagic edge
- myocyte necrosis
- macrophages
1-3wks post-MI:
- pale
- thin
- granulation tissue then fibrosis
3-6wks post-MI:
- dense fibrous scar
what are the main complications of MI? 7
- arrythmias
- cardiogenic shock
- heart failure
- pericarditis (if infarction occurs in pericardium as well)
- ventricular aneurysm
- cardiac tamponade
- thromboembolism
why can an MI lead to arrythmias?
- either directly or due to limited perfusion to the conduction system structures (SA node etc)
how can an MI lead to heart failure? 2
what are two synonyms for heart failure?
- contractility dysfunction
- papillary muscle infarct -> severe mitral regurgitation
- congestive cardiac failure
- congestive heart failure
what is the definition of cardiogenic shock?
Cardiogenic shock is defined by sustained low blood pressure with tissue hypoperfusion despite adequate left ventricular filling pressure
(so basically there is enough blood but the heart isn’t pumping it so no oxygen/nutrients is getting to tissues)
what is cardiac tamponade?
describe how an MI can cause it?
when fluid builds up in the pericardial sac around the heart + subsequently compresses the heart
full thickness (transmural) MI -> myocardium so weak that it ruptures + blood goes into pericardium + compresses heart from outside
nb cardiac tamponade has lots of acute + chronic causes, not just MI
what are the 5 main blood markers of IHD?
what can they also be raised in?
- troponins T & I
- –also raised in PE, heart failure + myocarditis
- creatine kinase
- – also raised in skeletal muscle and brain damage
- myoglobin
- – also released from damaged skeletal muscle
- lactate dehydrogenase isoenzyme 1
- – can also be raised in liver damage
- aspartate transaminase
- – also present in liver so less useful
what is creatine kinase?
in which 3 places is it specifically found in the body?
what are the 3 isoenzymes?
which is most specific to myocardium?
an enzyme
chiefly found in:
- brain
- skeletal muscles
- myocardium
CK-BB
CK-MM
CK-MB
CK-MB is the one found mainly in myocardium (bit in skeletal muscle as well though!)
what is the arbritary definition of hypertension? systolic + diastolic
a sustained systolic pressure greater than 140mmHg and/or sustained diastolic pressure greater than 90mmHg
what are the main features of metabolic syndrome? 4
what 3 conditions are most commonly caused by metabolic syndrome?
- high BP
- high blood sugar
- excess body fat around the waist
- high/abnormalchlesterol +/or triglyceride levels
- heart disease
- stroke
- diabetes
what are the main modifiable environmental risk factors for primary/essential hypertension? 5
- obesity
- alcohol
- smoking
- stress
- Na+ intake
what % of the UK adult population has high BP?
about 1/3
what 2 main general factors affect blood pressure?
BP = cardiac output x peripheral resistance
anything which affects either of those two things will have an effect on BP
describe what happens in the body when there is a drop in blood pressure (RAAS system)
drop in BP/fluid volume
- > renin released from kidney
- > renin cleaves angiotensinogen -> angiotensin I
ACE (angiotensin converting enzyme) converts angiotensin I -> angiotensin II
what organ produces:
- angiotensinogen?
- angiotensin-converting enzyme (ACE)?
angiotensinogen
= liver
ACE = lungs
what are the effects of angiotensin II? 7
- vasoconstriction (via AII receptors)
- acts directly to increase water + salt retention
- acts on adrenal cortex -> releases ALDOSTERONE which increases water + salt retension
- stimulates the release of vasopressin (aka ADH) which increases fluid retention
- stimulates thirst centres in the brain
- facilitates noradrenaline release from sympathetic nerves + inhibits noradrenaline reuptake by nerve endings -> enhanced sympathetic function
- stimulates cardiac + vascular hypertrophy
where is ADH released from?
posterior pituatory gland
what % of hypertension is secondary?
ie NOT primary/essential
5-10%
name 4 endocrine conditions which can lead to secondary hypertension.
cushing syndrome
- because cortisol stimulates the symp nervous system + has an aldosterone like action on the kidneys
- “stress leeds to high BP”
acromegaly
- excess growh hormone
hyper OR hypothydroidism
hyperparathyroidism
- as parathyroid hormone increases blood calcium which increases fluid retention(?)
name 3 adrenal conditions which cause secondary hypertension
adrenal hyperplasia
pheochromocytoma
- tumour produces catecholamines
primary hyperaldosteronism
what is another name for primary hyperaldosteronism?
conn’s disease
name 5 renal conditions which can cause secondary hypertension
- diabetic nephropathy
- chronic glomerulonephritis
- adult polycystic disease
- chronic tubulointerstitial nephritis
- renal vascular disease
basically anything causes chronic damage to kidney parencyma has potential to lead to high BP because kidney is involved with so much of RAAS
name three conditions of the CVS which can lead to secondary hypertension. why?
- aortic coarctation
- renal artery stenosis
- polyarteritis nodosa
all of these things have the potential to reduce blood flow to the kidneys which leads to the kidneys ‘thinking’ that the systemic BP is lower than it actually is -> inappropriate release of renin
what part of the kidneys is stimulated to produce renin?
juxtaglomerular apparatus
what is polyarteritis nodosa?
an idiopathic inflammation of medium sized arteries
thought to be linked to hep B but don’t know
what is malignant hypertension?
clinical signs? 3
BP >180/120mmHg
- acute hypertensive encephalopathy
- and/or nephropathy
- with retinal haemorrhages/papilloedema
medical emergency, requires urgent treatment to preserve organ function
what are 3 chronic complications of hypertension?
- hypertensive renal disease/nephropathy (‘flea bitten kidney’)
- hypertensive cerebrovascular disease
- hypertensive heart disease
what is systemic hypertensive heart disease?
- incl 2 diagnostic criteria
aka left-sided hypertensive heart disease
hypertension -> pressure overload -> hypertrophy of myocardium (adaptive response), can -> moyocardial dilation, heart failure + sudden death
criteria for diagnosis:
- left ventriculare concentric hypertrophy
- history or pathological evidence for hypertension
what is cor pulonale? what causes it?
pulmonary (right sided) hypertensive heart disease
RV hypertrophy, dilation + potentially heart failure secondary to pulmonary artery hypertension caused by disorders of the lung/pulmonary vasculature
nb RV hypertrophy secondary to disease of the LV + congenital heart defects are generally excluded from diagnosis of cor pulmonale
- nb LV hypertrophy often causes RV hypertrophy
what are the 4 broad types of causes of Cor Pulmonale?
diseases of pulmonary parenchyma
diseases of pulmonary vessels
disorders affecting chest movement
disorders inducing pulmonary arterial compression
what is pickwickian syndrome?
aka?
obesity hypoventilation syndrome
short and shallow breathing (due to obesity) leading to low blood O2 (especially during night) and high blood CO2 (especially during day)
often get obstructive sleep apnoea as well
if weight is not lost can lead to cor pulmonale + heart failure
what is the definition of an aneurysm?
a localised abnormal dilation of a blood vessel OR the wall of the heart
what is the difference between a true and false (aka pseudo) aneurysm?
true:
- when the aneurysm is bounded by all layers of the artrial/ventricular wall
false/pseudo:
- when there is a breach in the vascular/ventricular wall -> extravascular haematoma (contained by the surrounding tissues) that freely communicates with the intravascular space (‘pulsating haematoma’)
name 5 diseases of pulmonary parenchyma which can lead to cor pulmonale
- COPD
- diffuse pulmonary interstitial fibrosis
- pneumoconiosis
- cyctic fibrosis
- bronchiectasis
name 7 diseases of pulmonary vessels which can lead to cor pulmonale
- primary pulmonary hypertension
- arteritis
- drugs
- toxins
- radiation
- recurrent PEs
- tumour microemboli
name 3 disorders affecting chest movement which can lead to cor pulmonale
- kyphoscoliosis
- marked obesity (pickwickian syndrome)
- neuromuscular diseases
name 4 disorders inducing pulmonary arterial compression which can lead to cor pulmonale
- metabolic acidosis
- hypoxemia
- chronic altitude sickness
- obstruction to major airways
what do you call an true aneurysm which only affects one side of the artery?
what do you call a true aneurysm which affects the whole circumfrence of the artery?
one side:
- saccular (“forms a little SAC”)
full circumfrence:
- fusiform (“two sides FUSE together to form a ring”)
what is arterial dissection?
when there is a tear in the tunica intima and blood flows between the tunica intima and the outer layers of the blood vessel wall
nb can lead to transient or permanent occlusion of artery and/or embolism
nb symtpoms depend on artery affected, eg aorta, carotid artery
nb can be caused by external trauma to artery or other causes too
aortic dissection:
- risk factors? 5
- 3 types?
- main symptom?
- HYPERTENSION
- male
- increased age
- smoking
- connective tissue disorders (eg marfan)
- type A (Ascending aorta)
- type B (Descending aorta)
- chronic dissection (double barrelled aorta)
sudden high intensity ‘ripping’ pain in chest
what are the three main signs of chronic heart failure?
- breathlessness (due to fluid backing up)
- – inc dyspnoea, orthopnoea, PND
- fatigue (due to lack of O2/nutrients to tissues)
- peripheral oedema
what is orthopnea?
breathlessness when lying down flat, relieved by sitting/standing up
what is azotemia?
it means there is high levels of nitrogen containing compounds in the blood, eg urea, creatinine etc
why can reduced kidney perfusion in heart failure lead to worsening of heart failure?
because reduced kidney perfusion leads to activation of RAAS system which increases fluid retention, increasing the cardiac preload, putting more strain on it
what can advanced cardiac failure lead to?
cerebral hypoxia:
- irritability
- restlessness
- stupor
- coma
what are the two broad causes of right sided heart failure?
- left sided heart failure
- cor pulmonale
what are the signs/symptoms of right sided heart failure? 5
- hepatosplenomegaly
- ascites
- peripheral oedema
- elevated JVP
- fatigue
what are the 2 broad types of valvular heart disease? what’s the difference?
stenosis
- failure of valve to open completely, impending forward flow -> pressure overload of heart
- pretty much always chronic
regurgitation
- failure of valve to close completely allowing reverse flow -> fluid overload of heart
- chronic or acute
what are the three main causes of aortic stenosis?
- age -related calcification of anatomically normal valve
- rhematic heart disease
- other causes (congenital abnormalities in anatomy, bicuspid semi lunar valves, endocarditis)
what is the only known cause of mitral stenosis?
rheumatic heart disease
what is the most common valvular abnormality?
what are 5 main risk factors for this?
age-related calcification of aorta (can spread a bit to mitral valve)
- bicuspid semilunar valves (earlier onset)
- increased age
- hyperlipidaemia
- hypertension
- inflammation
what are the sequelae for aortic stenosis?
left ventricular hypertension due to aortic regurgitation
-> cardiac decompensation -> angina
also extra work for heart eventually -> congestive heart failure and can get secondary pulm hypertension and pulm oedema
what are the three layers of the heart?
what is it called if all three layers are inflammed?
- endocardium
- myocardium
- pericardium
pancarditis
what is the mechanism of rhematic heart disease? incl causative organism
which valves does it normally affect?
what age do people normally get it?
strep A throat infection
immune response produces antibodies to strep A and fights off infection but these antibodies also happen to target cells of the heart (called cross-reactions), thus damaging them
- just mitral valve 70%
- mitral + aortic 25%
(- rarely can affect other 2)
nb MV always involved
between 5-15 years
nb rare in developed world now