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
what are the possible effects on the morphology of the heart of rhematic heart disease:
- acute? 4
- chronic? 3
acute:
- fibrinous pericarditis
- vegetations on mitral valve/chordae tendinae
- myocardial aschoff body
- inflammation/pancarditis
chronic:
- thickened valves
- commisural fusion of valves
- thick, short chordae tendinae
what are the clinical features of acute rhematic fever? 8
and criteria for diagnosis?
jones criteria:
- evidence of preceeding strep infection
+ 2 major manifestations
or 1 major + 2 minor
major:
- migratory polyarthritis
- pancarditis
- subcutaneous nodules
- erythema marginatum of skin
- sydenham chorea
minor:
- fever
- arthralgia
- elevated acute phase proteins in blood
what clinical signs can be found in a patient with pancarditis? 3
- pericardial frictional rub
- weak heart sounds
- arrythmias
what is sydenham chorea?
collection of symptoms related to inflammation of the nerves
eg:
- involuntary jerking (norm of limbs)
- difficulty with fine movements
- trouble balancing
- unusual emotional outbursts
what are the clinical features of chronic rheumatic heart disease?
appears after many years + depends on which cardiac valves involved
- cardiac murmurs
- cardiac hypertrophy + dilation
- arrythmias
- heart failure
- thromboembolic complications
- infective endocarditis
what are the three main causes of aortic regurgitation?
- rheumatic fever
- infectious
- aortic dilations
what 3 things can lead to aortic diltions?
- syphilis
- rheumatoid arthritis
- marfans (or any other connective tissue disorder)
what are the 5 things which can, most commonly, lead to mitral regurgitation?
which is the most common?
- mitral valve prolapse (most common)
- infectious
- fen-phen (discontinued diet pill)
- papillary muscles, chordae tendinae
- mitral annular calcification
mitral valve prolapse:
- aka?
- cause?
- what is it?
- more common in men or women?
myxomatous degeneration of the mitral valve
cause unknown in most cases (associated with connective tissue disorders)
‘floppy’ valve
females»_space;> males
mitral valve prolapse:
- symptoms?
- auscultation findings?
- sequelae? 4
usually asymptomatic
- occassional chest pain +/or dyspnoea
- mid-systolic ‘click’
- pansystolic murmur
- infective endocarditis
- mitral insufficiency
- arrythmias
- sudden death
nb only seen in 3% of people with MVP, rest have not untoward effects
nb can easily see on echocardiogram
mitral annular calcification:
- what is it?
- possible sequalae? 3
- result in regurgitation or stenosis?
- more males or females?
degenerative calcification of the mitral ‘skeleton’ (annulus)
usually NO dysfunction
- arrythmias + sudden death (deep penetration of Ca deposits on AV conduction system
- infective endocarditis (increased risk)
- embolic stroke (increased risk
- regurgitation usually (but stenosis possible)
females»_space;> males
what does holosystolic murmur mean?
another word for pansystolic
congenital heart defects:
- when does faulty embryogenesis occur?
- overall incidence of births?
- % which have genetic abnormalities?
- most common?
week 3-8 gestation
1% of births
gene abnormalities in 10% of congenital heart defects
ventricular septal defect (42%)
DiGeorge Syndrome:
- genetic abnormality?
- also known as?
Chr 22q11.2 deletion
velocardiofacial syndrome
congenital heart disease:
- which cause L->R shunts? 4
- which cause R->L shunts? 5
L->R shunts: all Ds in their names:
- atrial septal Defect
- ventricular septal Defect
- atrioventricular septal Defect
- patent Ductus arteriosus
R->L shunts: all Ts in their names:
- Tetralogy of fallot
- Transposition of great arteries
- Truncus arteriosus
- Total anomalous pulmonary venous connection
- Tricuspid atresia
“LaRD”
congenital L->R shunts:
- cyanosis?
- most feared sequelae?
NO cyanosis (though can develop later in disease)
pulmonary hypertension
- want to repair ASAP to prevent permanent damage to lungs
congenital R->L shunts:
- cyanosis?
- most feared sequelae?
yes, cyanosis (‘blue babies’)
venous emboli become systemic (ie instead of going to lungs to form a PE)
= ‘paradoxical’
atrial septal defect:
- what is it?
- three classifications?
- symptoms? 4
abnormal fixed opening in atrial septum caused by incomplete tissue formation that allows communication between left + right atria
- NOT patent foramen ovale!!
cassified according to location:
- secundum (90%)
- primum (5%)
- sinus venosus (5%)
usually asymptomatic ubntil adulthood:
- dyspnoea on exertion
- fatigue
- peripheral oedema
- frequent lung infections
ventricular septal defect:
- most common type?
- prognosis?
90% involve mebranous septum (10% muscular)
small ones often close spontaneously
large ones progress to pulmonary hypertension
tetralogy of fallot:
- embroyologically, why does it occur?
- what 4 things make it up?
- prognosis?
due to anterosuperior displacement of the infundibular septum during embryogenesis
- ventricular septal defect
- overriding aorta
- pulmonary (valve) stenosis
- right ventricular hypertrophy (due to pulm stenosis)
survival depends on severity of pulmonary stenosis
nb can be a ‘pink’ tetralogy is pulm stenosis is small but the greater the obstruction the greater the R->L shunt
what are the 3 types of obstructive congenital heart diseases?
- coarctation of aorta
- pulmonary stenosis/atresia
- aortic stenosis/atresia
what’s the difference between stenosis and atresia?
atresia = absence of opening
stenosis = narrowing of opening
coarctation of aorta:
- more males or females?
- what are the two main types? describe the morphology + symptoms
- half of patients with this also have?
M>F (2:1)
- but females with turner syndrome (XO) often have it
infantile form:
- proximal to PATENT ductus arteriosus
- shunting of deoxygenated blood via PDA
- > cyanosis in lower half of body
- SERIOUS
adult form:
- CLOSED ductus arteriosus
- hypertension in upper extremities
- hypotension, weak pulses + claudication/coldness in lower extremities
- development of collateral circulation via intercostal arteries etc
50% also have bicuspid aortic valve
what is virchov’s triad?
- blood stasis
- vessel wall injury
- hypercoagulability
anything that increases any of these things increases the risk of thrombosis
what are the risk factors for peripheral vascular disease? 7
- smoking
- hypertension
- obese
- hypercholesterolaemia
- diabetes
- increased age
- men/post-menopausal women
what are the 6 clinical signs of acute peripheral vascular occlusion?
the 6 Ps:
- pale
- perishingly cold
- paralysed
- parasthetic
- painful
- pulseless
giant cell arteritis:
- aka?
- what is it?
- what arteries are normally infected?
- what’s seen on biopsy? 3
aka temporal arteritis
chronic autoimmune granulomatous inflammation of large to small arteries primarily in head + neck
- temporal arteries
- opthalmic arteries (can -> permanent blindness)
- nb normally affects predominately branches of external carotid artery
- thickening of tunica intima (reducing lumen diameter)
- granulomatous inflammation
- multinucleated giant cells (in 75%)
giant cell arteritis:
- risk factor? 1
- symptoms? 5
- treatment?
older age >50
- it’s rare though
often quite vague:
- fatigue
- weight loss
- head ache
- facial pain (jaw claudication +/or painful temporal artery)
- blurry or double vision
high dose corticosteroids
nb this is an emergency, risk to vision!! - if you suspect it give steroids, don’t wait to biopsy
infective endocarditis:
- who is most at risk?
- common routes of entry + causative organism? 6
anyone with any sort of structural abnormality of valves/myocardium/cardiac implants
dental disease or procedures
- strep viridans
vascular catheters or IVDU
- staph aureus, (candida, rare)
bowel malignancy
- strep bovis (rare!)
genitourinary disease or procedures
- enterococci
soft tissue infections (esp in diabetes, IVDU + long-term intravascular catheters)
- staphylococci
valve replacement surgery
- staph aureus or epidermis (<60 days post surgery)
- strep viridans or staph aureus (>60 days post surgery)
nb almost always bacterial cause
signs + symptoms of infective endocarditis? 8
“FROM JANE”
F - Fever
R - Roth spots
O - Osler’s nodes
M - Murmurs (can be just of underlying abnormality though!)
J - Janeway lesions
A - Anaemia
N - Nail (splinter) haemorrhage
E - Emboli (septic)
- nb fever is most common symptom but can be absent in elderly
- non-specific flu-like syndrome and maybe weight loss
nb 90% of infective endocarditis is left-sided
what are:
- splinter haemorrhages?
- janeway lesions?
- osler’s nodes?
- roth spots?
what are they all signs of?
splinter haemorrhages:
- red lines/tiny bleeds under nails
janeway lesions:
- red, flat, non-tender lesions on palms
osler’s nodes:
- red, swollen, painful finger tips
roth spots:
- retinal haemorrhages in the eyes
all due to microemobli from infective endocarditis
what is a complication of infective endocarditis?
immunologically mediated conditions eg glomerulonephritis
pericarditis:
- what is it?
- what tends to be most common cause?
- what chronic sequalae can it lead to?
- what is the treatment for the sequalae?
inflammation of the pericardial sac
infection
chronic pericarditis
- aka adhesive pericarditis/constrictive pericarditis
- fibrosis/stringy adhesions obliterates pericardial cavity
- heart can become encased in fibrous scar, limits cardiac function
surgery to remove ‘shell’ around heart
nb can also cause mediastinopericarditis
causes of acute pericarditis:
- infections? 5
- autoimmune? 5
- other? 5
infections:
- viral
- bacteria
- TB (caseous)
- fungi
- parasites
autoimmune:
- rheumatic fever
- SLE
- scleroderma
- Dressler’s syndrome
- drug hypersensitivity
other:
- post-MI
- uraemia
- neoplasia
- trauma
- radiation
what virus is most likely to cause pericarditis?
coxsackie B
what is Dressler’s syndrome?
a type of pericarditis believed to be caused by an immune response after damage to heart tissue or the pericardium from events such as MI, surgery or trauma
acute pericarditis:
- description of classical chest pain presentation?
- other signs/symptoms? 3
- possible sequalae?
sharp central chest pain:
- exacerbated by: movement, respiration, lying flat
- relieved by: sitting forward
- radiates: shoulder/neck
- pericardial friction rub
- fever
- leucocytosis
pericardial effusion
-> cardiac tamponade -> acute heart failure
can also lead to chronic pericarditis
what is a cardiomyopathy?
what is a major risk factor for most?
what are the 4 types?
what are symptoms normally due to?
literally a ‘heart muscle disease’ and strictly speaking of uncertain cause (is a diagnosis of exclusion)
genetics
- dilated
- hypertrophic
- restrictive
- arrythmogenic right ventricular
- heart failure
- emboli (virchov’s triad)
- arrythmias
dilated cardiomyopathy:
- pathogenesis?
- main associations/causes? 3
- age most commony affected?
- signs/symptoms?
progressive dilation -> contractile (systolic) dysfunction
- myocyte hypertrophy with fibrosis
- genetic (20-50%)
- alcohol + other toxins (eg chemo)
- others (SLE, scleroderma, thiamine def, acromegaly, hyperthyroidism, diabetes…)
20-5-years (but affects all ages)
slow proggressive signs of heart failure
- SOB, fatigue, poor exertional capacity etc
hypertrophic cardiomyopathy:
- pathogenesis?
- cause?
- signs/symptoms? 2
thick-walled myocardium which is poorly compliant - basically stiff ventrivle which doesn’t fill properly
- so low stroke volume
nb if LVH with no high BP or valve disease: think this!
100% genetic (mutations in sarcomeric proteins)
- exertional dyspnoea
- systolic ejection murmur
what are 5 complications of hypertrophic cardiomyopathy?
- AF
- mural thrombus formation -> embolus/stroke
- heart failure
- ventricular arrhythmias
- sudden death (most common cause of sudden death in athletes)
restrictive cardiomyopathy:
- pathogenesis/morphology?
- causes? 5
nb this is rare!!
primary decrease in ventricular compliance
- impaired ventricular filling during diastole
- ventricles normal size/slightly enlarged
- myocardium is firm and non-compliant
idiopathic or secondary (infiltration):
- fibrosis
- amyloidosis
- sarcoidosis
- metastatic tumours
- deposition of metabolites (inborn errors of metabolism
arrythmogenic right ventricular cardiomyopathy:
- pathogenesis?
- cause?
- symptoms?
RV dilation/myocardial thinning then fibrofatty replacement of RV walls -> interferes with conduction -> weird arrythmias etc
AD genetic disease
(disorder of cell-cell desmosomes)
often silent
- syncope
- chest pain
- palpitations
- sudden cardiac death (young/exercise)
causes of myocarditis:
- infections? 7
- immune mediated? 5
- others? 2
infections:
- viruses (coxsackie A+B, echo, influenza, HIV, CMV)
- bacteria (diptheria, meningococcus, lyme disease)
- fungi (candida, histoplasma)
- protozoa (chagas disease)
- helminths (trichonosis)
- chlamydiae
- rickettsiae (type of bacteria)
immune mediated:
- post-viral
- rheumatic fever
- SLE
- drugs (methyldopa, sulfonamides)
- transplant rejection
others:
- sarcoidosis
- giant cell myocarditis
don’t bother learning all of these just get the gist!
myocarditis:
- pathogenesis?
- possible clinical presentations? 5
infection or inflammatory trigger
- > cytokines, cytotoxic damage, damage myocytes
- > myocytes +/or endothelium malfunction
- > electrical/mechanical/clotting problems
- asymptomatic
- chest pain
- heart failure
- arrythmias
- sudden death
what is bacteraemia?
NOT a diagnosis
(always secondary to some other infection)
simply means there is bacteria in the blood
bacteraemia + symptoms/sign of infection = bloodstream infection
what are the three types of bacteraemia?
what sort of things tend to cause them?
transient
- mostly asymptomatic
- post teeth brushing/dental procedure
intermittent
- pneumonia, pyelonephritis, abscess, meningitis etc
continuous
- endocarditis, mycotic aneurysm, pacing lead infection, infected DVT
when should you take blood cultures when you suspect bacteraemia?
take blood cultures at least 3 times (even if positive)
as otherwise intermittent bacteraemia can be missed
best time to take is when patient has fever/is symptomatic
what are the three types of presentation of infective endocarditis?
non-specific illness
- lethargy
- malaise
- night sweats
- anorexia
- weight loss
heart failure
- SOB
- orthopnoea
- paroxysmal nocturnal dyspnoea
results of extra-cardiac foci of infection
- back pain from haematogenous vertebral osteomyelitis (HVO)
- stroke
- abdo pain/ splenomegaly from splenic infarct
nb symptoms are often caused by toxins produced by bacteria
what are the three groups of bacteria which are most likely to cause infective endocarditis?
- staphylococci
- streptococci
- enteroccocci
mycotic aneurysms:
- definition?
- four most common patterns of pathogenesis?
any aneurysm resulting from, or secondarily infected by, microorganisms
haematogenous seeding
- eg secondary to IE
trauma to arterial wall + direct contamination
- eg norm IVDU
extension from a contiguous focus
secondary to septic microemboli
- eg secondary to IE
what is dukes criteria used for?
criteria for diagnosisng infective endocarditis
nb this is NOT dukes STAGING system which is used to stage colorectal cancer
what are the two types of echocardiography used to visualise the heart?
transthoracic
- less invasive
- less clear
transoesophageal
- done via endoscope
- more clear (esp left side of heart)
what is the typical presentation of a mycotic aneurysm?
usually systemic symptoms of infection + variable symptoms from aneurysm, depending on location:
- no localising symptoms
- painless swelling
- painful swelling
- symptoms caused by rupture (eg intracerebral haemorrhage, collapse)
mycotic aneurysms:
- 2 most common causative organisms?
salmonella spp
- about 50%
staph aureus
- about 20%
infected DVT:
- 2 routes of pathogenesis?
- signs/symptoms?
- common causative organisms in IVDU?
- seeded with bacteria during bacteraemia (from any cause)
- directly infected (norm IVDU injecting into femoral vein)
signs/symptoms of DVT + systemic infection
and/or
resp symptoms (from infective PE)- incl consolidation
- staph aureus
- streptococci
- anaerobes
what are the four main different PRIMARY types of infection of the CNS?
- meningitis
- encephalitis
- brain abscess
- subdural empyema
what are three main classifications of infective meningitis? + their causes
acute pyogenic:
- usually bacterial
aseptic:
- usually viral
chronic:
- TB
- spirochetes (neurosyphilis)
- cryptococcus
‘chronic’ tends to have less severe symptoms and sub-acute onset
- not a medical emergency
- diagnose properly THEN treat
- in acute presentations: treat THEN diagnose properly
nb can also get non-infective causes
- underlying malignancies, drugs, autoimmune + trauma can also cause meningitis
what is kernigs sign?
if positive, what is it a sign of?
have person lying on back and passively flex knee + hips at right angles
- then passively extend at knee
if this extension is painful + resisted then sign is positive
meningitis or meningism (eg sub arach haemorrhage)
nb not very sensitive
what is nuchal rigidity?
what is it a sign of?
inability to flex neck muscles (move head down)
(if can flex neck but its painful then not nuchal rigidity)
meningitis or meningism
nb not very sensitive
what are some early signs of meningitis in infants/young children?
- isn’t feeding well
- fever
- bulging frontal fontanelle in infants
what two infections tend to enter the CNS by travelling up peripheral nerves?
rabies virus
herpes zoster virus
what are the typical clinical features suggesting meningitis? 8
which groups of people may have non-typical presentations?
- headache
- neck stiffness
- photophobia
- irritable
- rash
- fever
- vomitting
- varying levels of conciousness
- neonates
- elderly
- immunosuppressed
what are the top three bacterial causes of neonatal meningitis?
- strep B
- e coli
- listeria
what are the top 2 causes of bacterial meningitis in children/adults?
S. pneumoniae
N. meningitidis
(nb also H. influenzae)
nb this is in immunocompetent people!
what CSF abnormalities are seen in these different types of infective meningitis:
- bacterial?
- aseptic (viral)?
- chronic (TB)?
- appearance?
- cells/cu mm? + types
- protein?
- glucose?
normal CSF:
- clear, colourless
- 0-5 lymphocytes
- protein: norm
- glucose: norm
bacterial:
- cloudy, turbid
- 100-2000 polymorphs/neutrophils
- protein: high
- glucose: low
viral:
- clear, slightly cloudy
- 10-500 lymphocytes
- protein: low
- glucose: high
TB:
- clear, slightly cloudy
- 10-500 lymphocytes
- protein: high
- glucose: low
“bacteria eat glucose, viruses don’t!”
what are the most common causes of viral meningitis?
enteroviruses:
- echo
- Coxsackie A, B
(also paramyxovirus, herpes simplex, VXV, adeno viruses and others)
symptoms of encephalitis? 6
- headache
- seizures
- fever
- focal neurological deficits
- behavioural changes
- altered level of consciousness
most common cause of encephalitis?
herpes viruses (esp HSV 1)
- often reactivation!
- more dangerous than other causes
also viral cause (lots of viruses can cause) is a lot more common than bacterial cause
nb HSV2 is more likely to cause meningitis
Rabies:
- what is it?
- pathogenesis?
acute, progressive viral encephalitis
virus enters through bite/scratch
- grows at trauma site for a week
- then enters peripheral nerve endings + advances into CNS
- infection cycle complete when virus replicates in salivary glands
what are the 4 clinical stages of rabies?
prodromal stage:
- fever
- nausea/vomitting
- headache
- fatigue
- pain/burning/tingling at wound site
furious phase:
- agitation
- disorientation
- seizures
- twitching
- hydrophobia
dumb phase:
- paralysed
- disorientated
- stupurous
coma phase
- coma -> death
nb 100% of people die once get clinical symptoms of rabies
neurosyphilis:
- what % of people with syphilis will develop this?
- early symptomatic forms? 2
- late symptomatic forms? 2
- diagnosis?
30-40%
- nb more in immunocomprimised people
early symptomatic forms (months to a few years post primary infection):
- acute meningitis
- meningovascular (stuttering stroke)
late symptomatic forms (>2 years):
- general paresis
- tabes dorsalis
blood and CSF serology
nb a high degree of suspision + good history taking is needed for neurosyphillis
brain abscess:
- 4 common forms of pathogenesis?
- causative organisms?
- treatment?
direct spread
- eg from ear 40%, sinuses, teeth
haematogenous spread (often multiple abscesses) - eg endocarditis, bronchiectasis
trauma
- eg open cranial fracture, post-neurosurgery
cryptogenic
- no focus is recognised (20%)
depends on primary source of infection
- often mixed (polymicrobial)
- streptococci (60-70%)
- staph aureus (10-15%) (most common post trauma/surgery)
- drainage of abscess (to decrease ICP)
- antibiotics (which cross BBB)
symptoms of brain abscess? 7
- headache (most)
- focal neurological deficit (30-50%)
- seizures
- fever (<50%)
- nausea, vomitting
- neck stiffness
- papilloedema (raised ICP)
antibiotics which cross the blood-brain barrier at therapeutic doses? 5
- ampicillin
- penicillin
- cefotaxime
- ceftazidime
- metronidazole
“so remember penicillins, cephalosporins METROnidazole because it’s like a METRO train getting through the little tunnels/gaps to go through the BBB”
what are three common differentials for a history of fever, night sweats + breathlessness?
- infective endocarditis
- malignancy (esp haematological)
- pulmonary TB
what are the two types of replacement heart valves? when are each used?
metallic heart valves
- high risk of clots
- but last a lifetime
bioprosthetic (animal) heart valves
- low risk of clots
- only last 10-20 years (so usually reserved for elderly)
why do people with infective endocarditis often get shortness of breath?
due to back pressure from the heart due to regurgitation -> pulmonary oedema which presents as breathlessness
nb also get fine inspiratory crackles at bases of lungs
what sort of murmur would be present with:
- aortic stenosis?
- aortic regurgitation?
aortic stenosis
- systolic
- turbulent flow is present during systole
aortic regurgitation
- diastolic
- turbulent flow is present during diastole
what are some differential diagnoses for an elderly man with central abdo pain radiating to his back who is tachycardic and hypotensive? 8
cardiovascular:
- ruptured AAA
- (cardiac ischaemia or heart failure)
GI:
- bowel ischaemia +/or perforation
- pancreatitis
- peptic ulcer disease
- appendicitis
Urinary:
- renal colic
- pyelonephritis
what is the definition of an aneurysm:
- true aneurysm?
- pseudo aneurysm?
localised dilation of an artery to over 1.5 times its normal diameter
true = involves all 3 layers of arterial wall
pseudo
= blood enters between layers of artery wall (aka dissection)
= outer wall of aneurysm is formed by surrounding tissue
which arteries tend to be muscular and which elastic?
larger arteries (eg aorta) are elastic whereas smaller arteries are muscular
“aorta have to be elastic to deal with changes in pressure during systole”
who is screened for aortic aneurysms in the UK? when? how?
ultrasound scan for all MEN in the year they turn 65
if negative, no further screening, if positive, then further watch and wait until big enough to require stenting
what are the main risk factors for AAA development? 5
- male
- older age
- smoking
- hypertension
- hypercholesteraemia
nb diabetes mellitus seems to be protective but don’t know why
what are some common differential diagnoses for sudden onset central chest pain:
- cardiovascular? 3
- resp? 2
- GI? 4
- musculoskeletal? 2
- other? 1
cardiovascular:
- angina
- MI
- aortic dissection
resp:
- PE
- pneumothorax
GI:
- perforated ulcer
- cholecystitis
- reflux
- oesophageal spasm
musculoskeletal:
- costochondritis
- trauma
other:
- panic attack
what does an acute ischaemic stroke look like on a CT scan?
black (death) in area supplied by occluded artery (the thrombus itself is white)
nb the area is less well circumcised than in haemorrhage
also haemorrhage is pale/white (though goes darker later)
what is another anti-platelet drug? aside from aspirin
clopidogrel
the risk of haemopericardium is greatest how long after an acute MI?
1 week
what is the most common clinical presentation of heart failure?
fatigue
what 5 medications should you give immediately following an MI?
- morphine
- antiplatelets (aspirin +/or clopidogrel)
- nitrates (dilate arteries)
- B blockers (makes heart beat slowly + with less force, reduce demand)
- statins
what’s the definition of a minor stroke?
recovery without significant deficit within one week
what is Amaurosis fugax?
what causes it?
painless temporary loss of vision in one or both eyes
occlusion of opthalmic artery
- due to tia or stroke
‘like a curtain coming down over your eye’
nb it’s iPSilateral to side of embolus
which artery supplies the lower gyri of the temporal lobe?
POSTERIOR cerebral artery
NOT middle cerebral
what are lacunar strokes?
what can it lead to?
strokes which occur in the small arteries deep in the brain. affecte area of less than 1.5cm area
repeated lacunar infarcts can lead to vascular dementia
occlusion of which artery leads to lateral medullary syndrome?
PICA
in which coronary artery do most MIs occur in?
left anterior descending (LAD)
aka anterior interventricular artery
a blood clot in which coronary artery is most likely to result in arrythmias? why?
right coronary artery
as this supplies areas of myocardium where sinoatrial and AV nodes are
what is the histological findings in a:
- STEMI?
- NSTEMI?
STEMI = transmural infarct (full-thickness)
NSTEMI = subendocardial infarct (inner third only)
describe the pathogenesis of a the formation of a fatty streak and how that leads to plaque
damage to endothelium, eg smoking
- > LDLs go to damage
- > macrophages follow LDLs and consume as much of them as they can until they die -> foam cells
- when macrophages die they release cytokines attracting more macrophages
= fatty streak
platelets come to the fatty streak and release PDGF (platelet derived growth factor)
-> stimulates smooth muscle cells to migrate and form fibrous cap
fatty streak + fibrous cap = plaque
what is the frank-starling mechanism and why is it relevant to heart failure?
if there is a larger pre-load then the heart adapts by contracting more forcefully therefore as the pre-load increases, the force of the heart increases
this occurs, up to a point when the heart then gets ‘overwhelmed’ and can no longer increase the force with which it contracts, essentially heart failure
basically think of it like an elastic hair band, the more you stretch it (increasing the preload), the greater force it bounces back with, until you stretch it too much and it starts to go lax
what are the differences in symptoms between right and left heart failure?
left heart failure:
- fluid backs up to the LUNGS
- > SOB, orthopnoea, cough (blood tinged) etc
right heart failure:
- fluid backs up to BODY
- > peripheral oedema, hepatosplenomegaly, ascites
nb these often occur together as it’s a closed circuit so eventually one will cause the other
