Flashcards in Week 8 Cardiovascular 1 Deck (56)
Define Ischaemic heart disease.
Inadequate blood supply to the myocardium
What causes ischaemic heart disease?
Most comminly due to reduced coronary blood flow, almost always due to atheroma +/- thrombus.
Less common cause are due to amyloid accumulation or due to surgical problems
what additional complications can occur with ischeamic heart disease?
myocardial hypertrophy, usually due to systemic hypertension--> mainly left ventricular hypertrophy
What is the pathogenesis of ischaemic heart disease?
Autoregulation of coronary blood flow breaks down if > 75% occlusion
>90% stenosis may be insufficient at rest
low diastolic flow especially subendocardial
myocyte dysfunction/death from ischaemia
Active aerobic metabolism of cardiac muscle
What are the different type of angina pectoris?
typical/stable --. fixed obstruction, predictable relationship to exertion
crescendo/unstable --> often due to plaque disruption
variant/Prinzmetal --> coronary artery spasm
What type of angina pectoris is the most dangerous?
Unstable angina as the angina increasingly gets worse
What are the ischaemic heart disease syndromes?
acute coronary syndrome
sudden cardiac death
chronic ischaemic heart disease
What is acute coronary syndrome?
It refers to a group of conditions due to decreased blood flow in the coronary arteries such that part of the heart muscle is unable to function properly or dies.
Give examples of acute coronary syndrome
acute myocardial infarction (+/- ecg ST elevation)
What occurs in subendocardial myocardial infarction?
The subendocardial myocardium is relatively poorly perfused under normal conditions
How can the subendocardial myocardium infarct without any acute cornary occlusion?
If there is:
Stable athermanous occlusion of the coronary circulation
An acute hypotensive episode
Where is it common to get coronary atheroma and thrombus?
Occur in bifurcation, junctions of the coronary arteries or if there is any abnormalitis.
Due to the shear pressures at the time
What is the morphology of heart after MI within the fisrt 24 hours? Explain both gross and microscopic appearance
Gross appearance --> Normal/dark
Microscopic appearance --> necrosis and neutrophils
What is the morphology of heart after MI within post 1-2 days? Explain both gross and microscopic appearance
Gross appearance -- more necrosis and neutrophils
What is the morphology of heart after MI within post 3-7 days? Explain both gross and microscopic appearance
Gross appearance --> hyperaemic borderm, yellow centre
Microscopic appearance --> macrophages
What is the morphology of heart after MI within post 1-3 weeks? Explain both gross and microscopic appearance
Gross appearance --> red/grey
Microscopic appearance--> granulation tissue
What is the morphology of heart after MI within post 3-6 weeks? Explain both gross and microscopic appearance
Gross --> scar
Microscopic --> collagen scar
What are the different blood markers of cardiac myocyte damage? When can they be detected?
Troponins T & I
detectable 2 – 3h, peaks at 12h, detectable to 7 days
raised post MI but also in pulmonary embolism, heart failure, & myocarditis.
Creatine kinase MB
detectable 2 – 3h, peaks at 10-24h, detectable to 3 days
peak at 2h but also released from damaged skeletal muscle
Lactate dehydrogenase isoenzyme 1
peaks at 3days, detectable to 14days
Also present in liver so less useful as a marker of myocardial damage
Why is creatine kinase not the best marker for MI?
Because creatine kinase is seen in muscles all around the body and not just in the heart.
CK Mb which is mainly found in cardiac is also found in skeletal
What is the prognosis of MI?
20% 1-2h mortality – sudden cardiac death
What are the complications of MI?
Mural thrombus and emboli
arrhythmias, ventricular fibrillation (75-95%) & sudden death
left ventricular failure (60%) & shock (10-15%)
deep leg vein thrombosis & pulmonary embolus (15-40%)
autoimmune pericarditis (Dressler’s syndrome
Contractile dysfunction and chronic cardiac failure
What can be the possible cause of chronic ischaemic heart disease?
coronary artery atheroma produces relative myocardial ischaemia & angina pectoris on exertion
risk of sudden death or MI
possible previous occult MIs
crescendo or unstable angina - evolving plaque
variant angina - coronary arterial spasm
What is familial hypercholesterolaemia?
A genetic disorder characterized by high cholesterol levels, specifically very high levels of low-density lipoprotein
What are the common type of mutation in familial hypercholesterolaemia?
Low density lipoprotein receptor gene (1 in 500)
Apolipoprotein B (1 in 1000)
What are the possible consequence of heterozygote familial hypwecholesterolaemia?
develop xanthomas – tendons, perioccular, corneal arcus – and early atherosclerosis
What is the cause of familial hypercholesterolaemia?
Mutation in genes involved in cholesterol metabolism
Autosomal dominant but variant in penetrance
What is the treatment for heterozygote familial hypercholesterolaemia?
Early primary treatment with statins (hydroxymethyglutaryl CoA reductase inhibitors) is effective
Why is blood pressure physiologically regulated?
To ensure the perfusion of organs sufficient to maintain function
Prevents higher flow that exceeds metabolic demands, increases damage to blood vessels and thus to organs
When is blood pressure high?
Normal = 120/80mmHg”
Abnormal: Sustained diastolic of 90mmHg
Abnormal: Sustained systolic of 140mmHg
95% of cases are “primary”
aka “idiopathic”, “benign”, “essential”,
Dysfunction over a long period of time of what physiological systems cause primary hypertension?
Renin-angiotensin- aldosterone system
Adrenergic receptor system
Autocrine factors produced by blood vessels
Autonomic nervous system
What is the pathway that net set balance causes increase in BP?
Increased intravascular volume and volume delivery to the heart augment cardiac output and therefore blood pressur.
Results in tissue perfusion exceeding metabolic demand --> autoregulation of blood flow which increases vascoconstriction to reduce blood flow.
This results in a steady-state hemodynamic pattern of elevated blood pressure with increased systemic vascular resistance and normal cardiac output.
What are the possible effect of hypertension?
Cardiovascular --> hypertensive heart disease
What occurs in hypertensive heart disease?
Systemic hypertension leads to increased left ventricular blood pressure
Left ventricle hypertrophy without dilatation initially in response to increased work needed to pump blood
When the pressure is too great the left ventricle fails to pump blood at a normal rate and dilates
Whattypes of arterial rupture are consequence of hypertensive cerebrovascular disease?
atheromatous (intracerebral haemorrhage) --> weak vessels with atheroma can rupture
berry aneurysm of the Circle of Willis (subarachnoid haemorrhage)
What is the BP of malignant hypertension?
BP > 180/120 mmhg
What are the signs and symptoms of malignant hypertension?
acute hypertensive encephalopathy
What are the complications of acute hypertensive encephalopathy?
Diffuse cerebral dysfunction:
Confusion, vomiting, convulsions, coma and death
What are the causes pulmonary hypertension?
Loss of pulmonary vasculature
Secondary to left ventricular failure
Systemic to pulmonary artery shunting
Primary or idiopathic in children
What pulmonary vasculature diseases can cause pulmonary hypertension?
Chronic obstructive lung disease
Pulmonary interstitial fibrosis (interstitial lung diseases)
Pulmonary emboli or thrombosis
Under ventilated alveoli
What can be the consequence of pulmonary hypertension?
Increased right ventricular work to pump blood
Right ventricular myocardial hypertrophy initially without dilation
Later dilatation and systemic venous congestion as right ventricular failure develops
What are cardiovascular risk factors?
High blood cholesterol
Low blood high density lipoproteins
Obesity – especially central obesity
High alcohol use
Ethnicity – south Asian
What is the consequence of hypertension on the kidney?
Arterial intimal fibroelastosis
Slow deterioration in renal function leading to chronic renal failure
How does kidney produce aldosterone?
Renin Synthesized, stored in, and released from the juxtaglomerular apparatus in the wall of the afferent arterioles of the kidney
Cleaves angiotensinogen to angiotensin I
Angiotensin I is converted to active angiotensin II in many tissues
Angiotensin II stimulates adrenal cortex to produce aldosterone
What are the effects of angiotensin 11 and aldosterone?
Potent natural vasoconstrictor
Very short half-life
The physiological mineralocorticoid
Renal action causes sodium and thus water retention
Circulating blood volume increases
What disease is caused by excess aldosterone secretion?
What causes excess aldosterone secretion?
Usually due to adrenocortical adenoma
Possibly micronodular hyperplasia
Renal sodium and water retention
Elevated aldosterone, low renin
How is Conn's syndrome diagnosed?
Diagnose by CT scan of adrenals in presence of these metabolic abnormalities
What is phaechromocytoma?
Tumour of the adrenal medulla
Presents due to secretion of vasoconstrictive catecholamines – adrenaline and noradrenaline
What is phaechromocytoma usually presented with?
How do you diagnose and treat phaeochromocytoma?
Diagnosed by 24hr urine collection for adrenaline metabolites
Surgical is the main treatment but usually bilateral so don’t want to take both of your adrenal glands
What is Cushings disease?
Overproduction of cortisol by adrenal cortex
What is the conseuqence of Cushings disease?
Cortisol has several metabolic effects including potentiating sympathetic nervous system activity and it has a mineralocorticoid (aldosterone-like) action on the kidneys, thus causing hypertension
What causes Cushings disease?
An adrenocortical neoplasm usually an adenoma
A pituitary adenoma
A paraneoplastic effect of other neoplasms
What is a common paraneoplastic effect of other neoplasm that causes Cushings disease?
Small cell lung carcinoma producing adrenocorticotrophic hormone that stimulates the zona fasciculata cells of the adrenal cortex to produce cortisol
What is the consequence of renal artery stenosis?
Reduced blood pressure in kidney
Reduced blood pressure in renal afferent arterioles
Juxtaglomerular apparatus stimulated to produce renin
Renin-angiotensin system stimulates adrenal cortex zona glomerulosa cells to produce aldosterone