Cardiovascular Flashcards
- Regarding arteries, which is true?
- As vessels become smaller the ratio of wall thickness to lumen diameter becomes greater
- Capillaries are the principal points of physiological resistance to blood flow.
- Capillaries have a media of spirally arranged muscle cells
- In many types of inflammation vascular leakage and leucocyte exudation occur preferentially in pre- capillary venules.
- As vessels become smaller the ratio of wall thickness to lumen diameter becomes greater
- Arterioles are the principal points of physiological resistance to blood flow.
- Capillaries have no smooth muscle in their walls - any dilation is passive due to increased volume/pressure
- In many types of inflammation vascular leakage and leucocyte exudation occur preferentially in post capillary venules.
- Fenestrated endothelial layers are likely to be seen in the capillaries of which organ?
- Spleen
- Liver.
- Lung
- Adrenal gland
Adrenal gland
The liver also contains fenestrae but these are not crossed by transcellular pores (same as glomerular endothelium)
- In atherosclerosis the cells at the centre of the plaque are
- a. Macrophages
- b. Foam cells
- c. Leukocytes
- d. Smooth muscle cells
b. Foam cells
- All of the following are major risk factors for atherosclerosis EXCEPT:
- a. Obesity
- b. Hyperlipidaemia
- c. Smoking
- d. Hypertension
- e. Diabetes
a. Obesity
- Which risk factors have the greatest association with atherosclerosis?
- a. Hypertension, diabetes, smoking, hyperlipidaemia
- b. Hypertension, male, family history
- c. Hypertension, obesity, sedentary lifestyle
- d. Hypertension, female, OCP
- e. Age, family history, sex
a. Hypertension, diabetes, smoking, hyperlipidaemia
atherosclerosis
- a. when advanced is rarely calcified
- b. mainly affects the media of arteries.
- c. commonly affects renal arteries
- d. produces lesions commonly containing neutrophils.
- e. can cause aneurysmal dilation when severe
- a. when advanced is often calcified
- b. mainly affects the intima of arteries
- c. rarely affects renal arteries (or thoracic aorta or upper limb arteries)
- Abdominal aorta, Coronaries, Popliteal, Internal carotid, Circle of Willis (descending order of most commonly affected areas)
- d. produces lesions commonly containing Macrophages
- e. can cause aneurysmal dilation when severe
- Select the true statement concerning atherosclerosis
- a. Congenital absence of LDL cholesterol leads to premature atherosclerosis.
- b. Thoracic aorta is more likely to be involved than the abdominal.
- c. Fatty streaks appear in the aortas of children as young as 1 year
- d. Fatty streaks are destined to become atherosclerotic plaques.
- e. Endothelial disruption always precedes atheroma development
- a. Congenital absence of HDL cholesterol leads to premature atherosclerosis.
- b. Thoracic aorta is less likely to be involved than the abdominal.
- c. Fatty streaks appear in the aortas of children as young as 1 year
- d. Fatty streaks are capable of regression, and are not destined to become atherosclerotic plaques.
- e. Endothelial disruption always precedes atheroma development
- Select the false statement concerning atherosclerosis
- a. Familial hypercholesterolaemia is associated with inadequate hepatic uptake of LDL
- b. CMV has been detected in human atheromatous plaques
- c. Fibrous atheromatous plaques are capable of regression
- d. Foam cells can be considered to be specialized macrophages
- e. Atherosclerosis is associated with medial calcific sclerosis.
e. Atherosclerosis is associated with intimal calcific sclerosis.
- Regarding the plaque in atherosclerosis, which is CORRECT?
- a. Mixture of cells and connective tissue matrix
- b. Rarely causes microemboli
- c. Coronary arteries are the most affected
- d. Thoracic aorta is more affected than the abdominal aorta
a. Mixture of cells and connective tissue matrix
- Regarding atherosclerosis
- a. Coronary arteries equally affected as renal arteries.
- b. Exclusively affects medium and large arteries.
- c. Increased incidence in hypothyroidism.
- d. Decreased incidence in nephritic syndrome
c. Increased incidence in hypothyroidism - as it causes dyslipidaemia
Hyperthyroidism -> increased LDL receptors, so hypo -> fewer LDL receptors -> increased blood LDL levels
- a. Coronary arteries much more commonly affected than renal arteries.
- b. Commonly affects medium and large arteries.
- d. Increased incidence in nephritic syndrome due to hypertension
- Atherosclerotic plaques
- a. Are located within the media.
- b. Involve the coronary arteries most heavily
- c. Contain foam cells that are derived from macrophages and smooth muscle cells.
- d. Are commonly found in arteries of the upper limb
- e. Are rarely found at the ostia of branches of the descending aorta.
- a. Are located within the Intima
- b. Involve the abdominal aorta, then the coronary arteries most heavily
- c. Contain foam cells that are derived from just macrophages
- d. Are rarely found in arteries of the upper limb.
- e. Are commonly found at the ostia of branches of the descending aorta.
- Atherosclerosis
- a. Is initiated by endothelial injury
- b. Is a disease of the media of blood vessels
- c. Predominantly involves arterioles.
- d. Is most common in the internal carotid arteries.
- e. Begins in middle age.
- a. Is initiated by endothelial injury
- b. Is a disease of the media of blood vessels. Intima
- c. Predominantly involves arterioles. Elastic and medium to large muscular arteries
- d. Is most common in the internal carotid arteries. Coronaries
- e. Begins in middle age. First decade of life
- Regarding atherosclerosis
- a. The risk is directly related to HDL (high density lipoprotein) levels.
- b. The current “response to injury” hypothesis considers it to be an acute inflammatory response to endothelial injury of arterial walls.
- c. It typically beings in childhood, but only manifests itself in later life
- d. It involves smaller elastic and larger muscular arteries.
- e. 20% of all deaths in USA are attributable to this disease process.
- a. The risk is inversely related to HDL (high density lipoprotein) levels.
- b. The current “response to injury” hypothesis considers it to be an chronic inflammatory response to endothelial injury of arterial walls.
- c. It typically beings in childhood, but only manifests itself in later life
- d. It involves larger elastic and smaller muscular arteries.
- e. 50% of all deaths in USA are attributable to this disease process.
- In the current view of pathogenesis, atherosclerosis involves:
- a. Smooth muscle migration into adventitia
- b. Chronic endothelial injury
- c. Lymphocytes engulfing lipids
- d. Endothelial cell proliferation.
- e. Collagen degradation.
- a. Smooth muscle migration into Intima
- b. Chronic endothelial injury
- c. macrophages engulfing lipids.
- d. Smooth muscle proliferation
- e. Collagen Deposition
- Regarding complications of atherosclerotic plaques
- Atheroma plaques composing of large amount soft foam cells and lipid, are less likely to rupture than those with smaller amounts of lipid.
- A severely stenotic plaque is required as a precipitating lesion for patients who develop myocardial infarcts.
- In the coronary arteries it is usually around 70% of a fixed occlusion that is required to get stenosis and the signs of angina.
- Haemorrhage into a plaque is considered the most dangerous complication.
- Atheroma plaques composing of large amount soft foam cells and lipid, are more likely to rupture than those with smaller amounts of lipid.
- A severely stenotic plaque is not required as a precipitating lesion for patients who develop myocardial infarcts. - can have thrombosis
- In the coronary arteries it is usually around 70% of a fixed occlusion that is required to get stenosis and the signs of angina.
- Aneursymal rupture is considered the most dangerous complication.
- Of the following arteries, which is least likely to be affected by atherosclerosis?
- Vessels in the Circle of Willis
- Popliteal
- Coronary
- Abdominal aorta
Vessels in the Circle of Willis
- Abdominal aorta
- Coronaries
- Popliteal
- Internal carotid
- Circle of Willis
- Which of the following is not a major risk factor for atherosclerosis?
- Family history
- Cigarette smoking
- Obesity
- Male gender
Obesity
25.Regarding acute plaque change, which is correct?
- Only haemodynamically significant lesions result in acute transformation
- Plaque rupture always results is occlusive thrombosis
- Statins have a beneficial effect by reducing plaque inflammation and therefore increasing stability
- Plaque composition is stable once formed
Statins have a beneficial effect by reducing plaque inflammation and therefore increasing stability
- Malignant hypertension
- a. 75% recover with no loss of renal function
- b. is associated with abnormal renin levels
- e. affects 1-5% of HT sufferers.
e. affects 1-5% of HT sufferers.
R&C: ‘as much as 5% of HT patients show a rapidly rising BP that if untreated leads to death within 1-2 years’
- possible causes of secondary hypertension include
- a. hypothyroidism. Listed in R&C 9th but hyperthyroidism is much more common
- b. reduced intracranial pressure.
- c. Increased serum renin
- d. addison’s disease
- e. glomerulonephritis
c. Increased serum renin (nick)
e. glomerulonephritis (me)
as per R&C both renin-secreting tumours and acute glomerulonephritis can cause it
Hyperthyroidism and raised ICP also can
- Regarding hypertension
- Hypertension is defined as either sustained diastolic pressure > 100mmHg or sustained systolic pressure > 180mmHg
- 10%of the general population are hypertensive
- 5% of hypertensive patients develop malignant hypertension
- Hypertension is twice as common in white skinned people compared to black patients
5% of hypertensive patients develop malignant hypertension
- Aortic dissection
- a. Occurs most commonly in women.
- b. Is most commonly caused by atherosclerosis.
- c. Can be associated with inherited connective tissue disorders
- d. Most commonly causes death by disruption of the aortic valve.
- e. Is most commonly preceded by an internal tear occurring in areas of atherosclerotic plaque.
- a. Occurs most commonly in Men
- b. Is most commonly caused by Hypertension
- c. Can be associated with inherited connective tissue disorders
- d. Most commonly causes death by Rupture
- e. Is Not associated with atherosclerosis
- With regard to aortic dissection, which is INCORRECT?
- a. It tends to occur in 40-60 year old men
- b. Approximately 90% of non-traumatic cases occur in patients with antecedent hypertension
- c. It is usually associated with marked dilation of the aorta
- d. It is unusual in the presence of substantial atherosclerosis
- e. It is usually caused by an intimal tear within 10cm of the aortic valve
c. It is usually associated with marked dilation of the aorta
- false aneurysms
- a. remain in the confines of the circulatory system.
- b. include berry aneurysms.
- c. can be fusiform or saccular.
- d. are produced by a leak at the junction of a vascular graft with a natural artery
- e. are commonly caused by syphilis
- a. do not remain in the confines of the circulatory system - they communicate with extravascular haematoma
- b. include berry aneurysms -? True
-
c. can be fusiform or saccular.
- These describe the morphology but can be due to any cause (note saccular – only a small length of vessel involved, fusiform = longer
- d. are produced by a leak at the junction of a vascular graft with a natural artery??
- e. are commonly caused by syphilis??
- The most common cause of aortic dissection in the elderly
- a. Hypertension
- b. Marfan’s syndrome
- c. Connective tissue disorders
- d. Ischaemic heart disease
- e. Aortic valvular disorders
a. Hypertension
2.In aneurysms
- HT is the most common condition associated with aneurysms of the descending aorta.
- Atherosclerosis is the most common condition associated with aneurysms of the ascending aorta.
- Berry aneurysms are typically seen in the Circle of Willis
- All the above are true
Berry aneurysms are typically seen in the Circle of Willis
Ascending aorta = hypertension
Descending aorta = atherosclerosis
- Abdominal aortic aneurysms are
- Common above the renal arteries.
- Common in Marfans syndrome.
- Caused by intimal weakness.
- A source of atheroemboli to the kidneys
- Rare above the renal arteries.
- Thoracic aneurysm are Common in Marfans syndrome.
- Caused by medial weakness.
- A source of atheroemboli to the kidneys
18.Regarding aortic dissection
- The most common cause of death is dissection involving the coronary arteries
- Usually commences with an intimal tear within 10cm of the aortic valve
- Men aged > 60years with antecedent HT constitute one of the most common at-risk groups
- Cystic medial degeneration is a rare pre exsisting histological lesion
Usually commences with an intimal tear within 10cm of the aortic valve
Common risk: Men 40-60 with HTN, smokers
Most common death = ruptur
Cystic medial degeneration is a common pre-existing histo lesion
- Regarding giant cell arteritis, which statement is INCORRECT?
- a. Affects medium arteries
- b. Affects small arteries including vertebral
- c. Affects small arteries including ophthalmic
- d. Has an increased prevalence of HLA-DR4
- e. Has no gastrointestinal manifestations
e. Has no gastrointestinal manifestations
- Which is associated with medium vessel vasculitis?
- Kawasaki disease
- Takayasu disease
- Churg –Strauss
- Wegners granulomatosis
Kawasaki disease
- In Giant cell arteritis
- It only affects the temporal arteries
- Is an uncommon vasculitis in the elderly in USA
- Thought to be a T cell mediated immune response against an unknown agent
- A negative biopsy rules out the diagnosis
Thought to be a T cell mediated immune response against an unknown agent
- Thromboangiitis obliterans is commonly associated with
- Female gender
- Old age
- Obesity
- Cigarette smoking
Cigarette smoking
- Regarding Raynaud’s disease (primary Raynaud’s phenomenon)
- Usually associated with a connective tissue disorder
- Is associated to smoking
- Is common in young males
- It is rare to see ulceration
It is rare to see ulceration
Cor pulmonale may be caused by
- Congenital heart disease
- Mitral stenosis
- Left ventricular failure
- Primary pulmonary hypertension.
- Aortic regurgitation
Primary pulmonary hypertension.
Cor pulmonale = RVH/RVF/dilation secondary to lung disease
eg disease of parenchyma, PE, extra-thoracic causes of restrictive lung disease (neuromuscular disorders, obesity)
Heart failure will lead to increased levels of
- Renin
- Aldosterone
- ADH
- ANP
- All of the above
All of the above
Activates the RAAS system due to systemic hypoperfusion -> renin, aldosterone, ADH
ANP will rise because of fluid overload -> atrial stretch
Regarding cardiac failure
- The kidneys compensate for oedema by increasing water and salt excretion
- Hypertrophy protects the myocytes from injury
- Left sided failure causes hepatic cardiac sclerosis
- The mechanism of decompensation is well understood
- ATN is a recognized sequela
ATN is a recognized sequela
‘Pre-renal azotemia’ as worded in R&C
- The kidneys compensate for oedema by increasing water and salt excretion
- Opposite - they retain fluid and salt due to neurohumoral signals in response to systemic hypoperfusion, in an ill-fated attempt to improve CO
- Hypertrophy protects the myocytes from injury
- More likely to lead to ischaemic injury as there is not a corresponding increase in number of capillaries
-
Right sided failure causes hepatic cardiac sclerosis
- Congestion -> necrosis -> fibrosis in centrilobular regions
- The mechanism of decompensation is poorly understood
In heart failure
- Compensatory mechanisms act to maintain the performance of the heart, but can be eventually exceeded
- Systolic dysfunction is where there is failure of the heart chamber to relax to accommodate an adequate ventricular blood volume
- Compensatory mechanisms include hypertrophy and hyperplasia
- Ventricular hypertrophy and dilation are typical of pressure overload
- The ventricles show cardiac hypertrophy, increase capillary density and deposition of fibrous tissue
Compensatory mechanisms act to maintain the performance of the heart, but can be eventually exceeded
- Diastolic dysfunction is where there is failure of the heart chamber to relax to accommodate an adequate ventricular blood volume
- Compensatory mechanisms include hypertrophy, but NOT hyperplasia (muscle cannot undergo hyperplasia. Thats day 1 of study stuff)
- Ventricular hypertrophy and dilation are typical of volume overload
- Pressure overload -> hypertrophy and wall thickening
- The ventricles show cardiac hypertrophy and deposition of fibrous tissue, but no increase in capillary density (which increase risk of ischaemic decompensation)
One of the basic mechanisms for cardiogenic shock is
- Loss of arteriolar tone
- Loss of venous return to the heart
- Increased cardiac work secondary to volume overload
- Disorganized contraction of myocytes
- Inadequate plasma volume
Disorganized contraction of myocytes
(Increased cardiac work secondary to volume overload - need to clarify this one, maybe because it isnt directly shock-related ie occurs with any degree of heart failure)
As in VF
Others are all examples of hypovolemic or distributive shock
a man is brought to the ED with heart failure and has a cardiac index of 81, which is most likely to have caused this
- thiamine deficiency
- myocardial ischaemia
- Vit B6 deficiency
- B12 deficiency
- Arrhythmia
c) thiamine deficiency
Thiamine deficiency causes high-output HF (along with hyperthyriodism, anaemia, pregnancy)
Normal CI is about 3.2/m2/min = ~210+ for a 70kg man
81 is about 1.1
Below 2.2 can suggest cardiogenic shock according to Wikipedia
I think the numbers are just a bit confusing/dont have units, but thiamine is the odd one out
A deficiency of which can cause heart failure
- Pyridoxine
- Vitamin D
- Vitamin C
- Zinc
- Thiamine
Thiamine
Causes ‘wet beriberi’ which is cardiac dysfunction.
High-output failure
Thiamine helps produce ATP
In compensated cardiac hypertrophy, changes include
- Diffuse fibrosis
- Hyperplasia.
- Decreased sarcomeres.
- Increased capillary density.
- Increased capillary/myocyte ratio.
Diffuse fibrosis
- Hyperplasia - Myocytes can not divide
- Decreased sarcomere - Same number or increased
- reduced capillary density
- reduced capillary/myocyte ratio
patients who have a normal BP post MI must have
- increased CO
- increased systolic filling pressure
- increased right atrial pressure
As per Nick, increased CO (I’m not so sure)
MAP = TPR x CO
MI shouldnt change the TPR, so CO should be the same
(unless CO falls off, so TPR rises to maintain perfusion, but that would cause the opposite)
I would think increased HR or contractility etc to compensate for reduced pump performance, but those arent options.
On another question Nick also raises the point that increasing CO implies there is a reduction in TPR which is not consistent with the texts or pathology as we understand it.
An adult make with an ejection of 80% could be due to
- MI
- Arrhythmia
- Thiamine deficiency.
Thiamine deficiency.
This causes high-output HF
causes of peripheral oedema in CCF, which is false
- increased renin
- increased GFR.
- increased angiotensin II
- increased aldosterone
increased GFR.
CCF -> reduces renal blood flow -> reduced GFR, which initiates the renin system
Ang II leads to increased GFR at low levels of efferent arteriole constriction but at higher levels of constriction can reduce RBF, which opposes GFR
Others all cause fluid retention through RAAS system
- The cause of fluid retention peripherally with congestive cardiac failure is
- a. Increased renin
- b. Increased GFR
- c. Increased angiotensin II
- d. Increased aldosterone
d. Increased aldosterone
Promotes fluid retention in kidneys
Activates basal Na/K/ATPase in tubules -> salt retention and K loss
Increased Na channels in collecting ducts -> increased Na and water retention
Other mechanisms in GI tract etc
- All of the following are cardiac compensatory responses that occur in heart failure except:
- a. Cardiac muscle fibre stretching
- b. Increased adrenergic receptors on cardiac cells
- c. Chamber hypertrophy
- d. Decreased heart rate
- e. Increased vasopressin levels
d. Decreased heart rate
Would expect a tachycardia as the heart attempts to increase/maintain CO
- In compensated heart failure
- a. Right atrial pressure drops.
- b. Maximum cardiac output is unchanged
- c. Resting cardiac output is unchanged
- d. Renin level eventually drops below premorbid level.
- e. Fluid retention plays no role.
c. Resting cardiac output is unchanged
If it was reduced, it would be decompensated
- a. Right atrial pressure Rises due to fluid retention
- b. Maximum cardiac output is Limited - ie exercise tolerance is reduced
- d. Renin level Remains elevated
- e. Fluid retention plays a major role in attempting to maintain CO by increasing preload and volume status
- A 50 year old man with an acute myocardial infarction has a BP 130/80. He can maintain his BP because of:
- a. An absolute increase in cardiac output.
- b. Increased systolic filling pressure
- c. Increased right atrial pressure
- d. Increased water absorption
- e. Decreased sympathetic outflow
a. An absolute increase in cardiac output.
as per Nick, and I agree: Seems to conflict with other answers and the textbook with regards to compensation in heart failure. Implies a reduction in TPR
Would expect an increased HR or sympathetic response -> increased contractility to maintain BP in the face of reduced cardiac ability
- in left heart failure
- a. failure is typically secondary to right heart failure
- b. ascites is a predominant feature
- c. right heart failure is rarely, if ever, associated with left heart failure
- d. renal congestion and acute tubular necrosis are less common.
- e. pulmonary congestion and oedema are rare
d. renal congestion and acute tubular necrosis are less common.
More common in Right HF as raised venous pressures -> organ congestion -> reduce renal perfusion pressure
- congestive cardiac failure is characterized by all of the following EXCEPT:
- a. perivascular and interstitial transudate
- b. Kerley A lines on chest Xray. Kerley B
- c. Activation of renin-angiotentin-aldosterone system
- d. Haemosiderin-containing macrophages in the alveoli
- e. Progressive oedematous widening of alveolar septa
b. Kerley B lines on chest Xray.
The histological appearance of contraction bands in association with MI indicate
- Previous old MIs
- Early aneurysmal formation
- Compensatory responses to decreased myocardial contractility
- Right ventricular infarct
- Recent reperfusion injury
Recent reperfusion injury
Occurs because contraction of salvedged but injured cells causes calcium leak, causing infarcted cells to contract
After occlusion of a coronary artery
- The ischaemia is most pronounced in the epicardial region.
- Loss of contractility occurs only when ultra structural changes in the myocyte are present.
- Reperfusion of the ischaemic area can result in new cellular damage, due to the generation of oxygen free radicals
- Q waves on an ECG are diagnostic of transmural infarction.
- None of the above
Reperfusion of the ischaemic area can result in new cellular damage, due to the generation of oxygen free radicals
- The ischaemia is most pronounced in the Subendocardial region
- Loss of contractility occurs within 2 minutes, whereas ultrastructural (electron micro changes) take approx. 30min
- Q waves on an ECG can be due to transmural infarction, or can be physiological or due to HOCM
Regarding acute MI all of the following are true except
- Irreversible cell injury occurs after 3-4 hours.
- HRT is protective against MI
- Isolated right ventricular infarction is uncommon
- The macroscopic changes of MI are visible at 18 hours post infarct
- Coagulative necrosis will be observed at 6 hours post infarct
Irreversible cell injury occurs after 30 mins
In MI the microvascular changes start
- Immediately
- In 30-40 minutes
- In more than 1 hour
- In 6-12 hours
- More than 12 hours
In more than 1 hour
regarding acute MI
- the majority of cases are uncomplicated
- approximately 1/3 of complicated cases progress to cardiogenic shock
- 75% of complicated cases involve arrhythmia
- >50% of complicated cases have further thromboembolic events in the recovery period
- LVF and pulmonary oedema are uncommon complications
75% of complicated cases involve arrhythmia
- the majority of cases (75%) are complicated
- approximately 10% of complicated cases progress to cardiogenic shock
- ??% of complicated cases have further thromboembolic events in the recovery period
- LVF and pulmonary oedema are common complications
With regard to acute MI (2 CORRECT)
- Gross necrotic changes are visible within 2-3 hours.
- Irreversible cell injury occurs in less than 10 minutes.
- Fibrotic scarring is completed in 2 weeks.
- Death occurs in 20% cases within 2 hours
- It is most commonly caused by occlusion of the left circumflex coronary artery.
- Time onset between onset of ischaemia and irreversible injury is 1-2 hours.
- Arrhythmia occurs in 60-70% of patients
- The majority of transmural infarcts affect the left ventricle
- Overall mortality in the 1st year is 20%
The majority of transmural infarcts affect the left ventricle
- Gross necrotic changes are visible at 4 hours
- Irreversible cell injury occurs in 30 minutes
- Fibrotic scarring is completed in 8 weeks
- Death occurs in 20% cases within 2 hours
- cannot find answer in R&C, but given mortality at 1 year is 30%, this is likely wrong
- It is most commonly caused by occlusion of the LAD
- Time onset between onset of ischaemia and irreversible injury is 30 mins
- Arrhythmia occurs in many patients (as per R&C)
- Overall mortality in the 1st year is 30%
The most common complication of acute MI is
- Sudden cardiac death
- Congestive heart failure
- Valvular dysfunction due to papillary muscle rupture
- Ventricular aneurysm
- Arrhythmia
Congestive heart failure
R&C doesnt give numbers, but CHF is ‘usually some degree of LV failure with hypotension, pulmonary congestion, and interstitial pulmonary infiltrates which can progress to pulmonary oedema…’
Arrhythmia is ‘many patients have myocardial irritability…’
Make of those statements what you will
With respect to acute MI
- Caused by embolisation of atherosclerotic thrombus in 90%
- Transmural infarctions have the same prognosis as subendocardial infarctions
- Are complicated by arrhythmia in 50%
- Thrombolysis reestablishes patency in 95% cases
- Is found to be the cause of 25% or less of sudden cardiac death
Caused by embolisation of atherosclerotic thrombus in 90%
R&C states that coronary thrombosis is responsible for 90% of cases.
Does not mention prognosis of different patterns of injury, nor give specific numbers for complications or therapy outcomes.
following MI
- ATP is down to 50% at 10 minutes
- Irreversible cell injury occurs within 5 minutes
- ATP depletion begins at 2 minutes
- Microvascular injury occurs within 30 mins
- Wavy fibres are present within 20 minutes
ATP is down to 50% at 10 minutes
- Irreversible cell injury occurs within 30 minutes
- ATP depletion begins within seconds
- Microvascular injury occurs after 1 hour
- Wavy fibres are present at 0.5-4 hours
- Myocardial infarction
- a. Is characterized by necrosis beginning approximately 30 minutes after coronary occlusion.
- b. Most often involves occlusion of the left circumflex coronary artery.
- c. Are apparent macroscopically at around one hour after coronary occlusion
- d. Typically results in liquefactive necrosis.
- e. Is subendocardial if only two thirds of the ventricular wall is involved
a. Is characterized by necrosis beginning approximately 30 minutes after coronary occlusion.
- b. Most often involves occlusion of the LAD then RCA then LCA
- c. Are apparent macroscopically at around 4 hour after coronary occlusion
- d. Typically results in Coagulative necrosis
- e. Is subendocardial if only one thirds of the ventricular wall is involved
- regarding the changes to myocardium after MI
- a. pallor at 24 hours.
- b. wavy fibres are found centrally
- c. decreased contractility after 5 minutes. Within 2 minutes
- d. liquefactive necrosis is typical. Coagulative
- e. sarcoplasm is resorbed by leukocytes
a. pallor at 24 hours.
As per Nick, however R&C states 12-24 hours dark mottling, and 1-3 days development of a yellow-tan infarct centre (no mention of pallor)
All other answers seem to be wrong
- b. wavy fibres are found peripoherally
- c. decreased contractility Within 2 minutes
- d. coagulative necrosis is typical
- e. sarcoplasm is resorbed by macrophages
- With regard to MI
- a. Gross necrotic changes are present within 3-5 hours
- b. Irreversible cell injury occurs in less than 10 minutes
- c. Fibrotic scarring is completed in less than 2 weeks
- d. Death occurs in 20% of cases in less than 2 hours
- e. Is most commonly caused by occlusion of the left circumflex coronary artery
a. Gross necrotic changes are present within 3-5 hours
R&C states a time of 4-12 for dark mottling, but 2-3 hours it is possible to tell on autopsy
d. Death occurs in 20% of cases in less than 2 hours (Nicks answer)
Mortality at 1 year is 30%, and many acute deaths are due to arrhythmia, cardiogenic shock, or ventricular wall rupture, which could cause death out to a few days. I think it is likely much lower than 20% but the number is not in the textbook.
- b. Irreversible cell injury occurs in 20-40 minutes
- c. Fibrotic scarring is completed in 8 weeks
- e. Is most commonly caused by occlusion of the LAD > RCA > LCx
- A young man presents with central chest pain presumed to be associated with vasoconstriction. The most likely cause of the pain is local
- a. Hypoxia
- b. Decreased ATP
- c. Increased CO2
- d. Catecholamines acting on alpha 1 receptors
- e. Acetylcholine stimulation
d. Catecholamines acting on alpha 1 receptors
Confusing question - do they want the physiology of the pain receptors causing the pain, or the underlying pathology causing the vasoconstriction?
The textbook has no clear answers. The above would cause vasoconstriction, but it is likely that CO2 or hypoxia is the direct cause of the associated pain.
- Regarding myocardial infarction:
- a. The size of the infarct is independent of collateral circulation.
- b. Is mainly precipitated by vasospasm.
- c. Irreversible tissue damage appears within 30 minutes.
- d. Acute cellular swelling is due to ATP depletion.
- e. Occlusion of right coronary artery is responsible for most infarcts in the anterior wall of the left ventricle.
d. Acute cellular swelling is due to ATP depletion.
Due to intracellular accumulation of Na/H20
- a. The size of the infarct is dependent of collateral circulation.
- b. Is mainly precipitated by Rupture of atherosclerotic plaque
- c. Irreversible tissue damage appears within 30 minutes.
- Nick says 4 hours, R&C states that irreversible cellular damage starts within 30 minutes. d) above is correct as per the cell and tissue teaching.
- e. Occlusion of LAD is responsible for most infarcts in the anterior wall of the left ventricle.
- Myocardial infarction:
- a. Is usually a consequence of coronary vessel occlusion by embolus
- b. Is characterized morphologically by liquefactive necrosis
- c. Is most commonly complicated by ventricular rupture
- d. Can be either transmural or subendocardial
- e. Is apparent on light microscopy within minutes
Initial answer was d. Can be either transmural or subendocardial but on further review, could be a), although my notes state that it is usually acute thrombosis, not embolus.
- '’Usually a result of acute thrombosis over an atherosclerotic plaque’*
- Note that my notes state that there are 3 patterns of injury: transmural, subendocardial, or multifocal microinfarction due to small emboli, vasculitis etc*
- The histological appearance of contraction bands in association with acute myocardial infarction indicate:
- a. Previous old myocardial infarction
- b. Early aneurismal formation
- c. Compensatory responses to decreased myocardial contractility
- d. A right ventricular infarct
- e. Recent reperfusion therapy
e. Recent reperfusion therapy
- After occlusion of a coronary artery
- a. The ischaemia is most pronounced in the epicardial region.
- b. Loss of contractility only occurs when ultrastructural changes in the myocyte are present.
- c. Reperfusion of the ischaemic area can result in new cellular damage, due to the generation of oxygen free radicals
- d. Q waves on the ECG are diagnostic of transmural infarction.
- e. None of the above are true
c. Reperfusion of the ischaemic area can result in new cellular damage, due to the generation of oxygen free radicals
- a. The ischaemia is most pronounced in the Subendocardial (furthest away)
- b. Loss of contractility occurs before ultrastructural changes in the myocyte are present (<2min vs within 30min)
- d. Q waves on the ECG are not always diagnostic of transmural infarction. Only pathological Q-waves (eg physiological Q-waves in the high lateral leads)
- Post myocardial infarction
- a. ATP is down to 50% at 10 minutes
- b. Irreversible cell injury occurs within 5 minutes
- c. ATP depletion begins at 2 minutes
- d. Microvascular injury occurs within 30 minutes
- e. Wavy fibres are seen within 20 minutes
a. ATP is down to 50% at 10 minutes
- b. Irreversible cell injury occurs within 2 minutes
- c. ATP depletion begins within seconds
- d. Microvascular injury occurs >60minutes
- e. Wavy fibres are seen within 0.5-4 hours
- What is the most common histological change seen in myocardial infarction less than 24 hours duration?
- a. Pallor and oedema
- b. Haemorrhage
- c. Hyperaemic border
- d. Liquefactive necrosis
a. Pallor and oedema
R&C never seem to mention pallor - within 24 hours you see dark mottling grossly, and coagulative necrosis, oedema, and haemorrhage on light microscopy.
I would hazard a guess at b) haemorrhage, but the answer is not clear in the text.
- With regard to acute coronary occlusion
- a. Collaterals do not flow for 4-6 hours
- b. Striking loss of contractility within 60 seconds.
- c. 50% recanalise spontaneously
- d. ischaemia occurs after 60 minutes.
- a. Collaterals do not flow for 4-6 hours
- ???
- b. Striking loss of contractility within 2 mins
- c. 50% recanalise spontaneously
- 10% do not have significant atherosclerotic disease on angio, and are presumbed to be vasospastic, embolic, or intrinsic disease (eg vasculitis, sickle cell etc)
- d. ischaemia (irreversible cell injury) occurs after 30 mins
- Acute severe MI causes:
- a. Pulmonary oedema
- b. Thoracic pressure
- c. Increased right atrial pressure
- d. Decreased arterial pressure
Shit question. Nick says:
a. Pulmonary oedema
But pulmonary oedema is likely to also cause increased right atrial pressure due to LVF -> RV backlog
Cardiogenic shock also possible -> reduced arterial pressure
- Coronary thrombus
- a. If asymptomatic, carries a low risk.
- b. Increased tissue plasminogen activator inhibitor causes extension of thrombus
- c. Vessels mostly occluded to decrease blood velocity
- d. Is at increased risk of because of mechanical stressors
- e. 50-75% occlusion is likely to cause infarction.
b. Increased tissue plasminogen activator inhibitor causes extension of thrombus
tPA is used to resolve the thrombus and hence inhibtion is going to have a procoagulant effect
- a. If asymptomatic, carries a High risk
- c. Vessels mostly occluded to decrease blood velocity
- what does this even mean?
- d. Is at increased risk of because of mechanical stressors
- ?maybe. shite question and shite answers.
- e. ~90% occlusion is likely to cause infarction.
- Angina occurs at 70%
- The most common complication of acute myocardial infarction is
- a. Sudden cardiac death
- b. Congestive cardiac failure
- c. Valvular dysfunction due to papillary muscle rupture
- d. Ventricular aneurysm
- e. Arrythmia
b. Congestive cardiac failure
- Numbers/proportions not given in R&C, but it notes that ‘there is usually some degree of LV failure with hypotension, pulmonary vascular congestion, and interstitial pulmonary transudates, which can progress to pulmonary oedema’.*
- Cardiogenic shock occurs in 10-15% of patients and has a 70% mortality*
- Which of the possible complications of acute myocardial infarction would be expected to be most delayed in onset?
- Arrhythmia
- Myocardial rupture
- Congestive heart failure
- Mural thrombus
Mural thrombus
aneurysms are a late complication
Nick said rupture, but this occurs at day 2-4 usually
- Regarding myocardial infarcts
- Severe ischaemia causes immediate cell death
- All regions of the myocardium are equally ischaemic
- Reperfuison of the myocardium within 20min of the ischaemia onset may completely prevent necrosis
- A reperfused infarct is usually coagulative
Reperfusion of the myocardium within 20min of the ischaemia onset may completely prevent necrosis
Which of the following is false regarding heart murmurs
- Murmurs are caused by turbulent blood flow
- AS produces a systolic murmur loudest over the base of the heart
- MR produces a diastolic murmur loudest over the apex, with radiation to the axilla
- MR can produce a 3rd heart sound
- PS produces a systolic murmur loudest over the 2nd/3rd intercostals space left of parasternal
MR produces a systolic murmur loudest over the apex, with radiation to the axilla
- Infective endocarditis
- a. In the acute form, is most commonly caused by streptococci.
- b. Involves abnormal valves in most acute cases
- c. Is confirmed by positive blood cultures in less than 50% of cases.
- d. May cause splenic infarction
- e. May cause MacCallum’s plaques to form on affected valves
d. May cause splenic infarction
- a. In the acute form, is most commonly caused by Staph aureus
- b. Involves normal valves in most acute cases
- Subacute is most often abnormal or prosthetic valves
- c. Is confirmed by positive blood cultures in Approx 90% of cases
- e. May cause MacCallum’s plaques to form on affected valves
- Regarding acute endocarditis
- a. It has a mortality of <20%
- b. It is caused by virulent organisms
- c. 30% is caused by bacteria.
- c. Dilation of the left ventricle
b. It is caused by virulent organisms
90% cause by bacteria
- all of the following are features of rheumatic fever EXCEPT
- a. carditis
- b. subcutaneous nodules
- c. erythema nodosum.
- d. elevated antistreptolysin
c. erythema marginatum
Nodosum is much more common and seen in SLE and shit.
20.The most frequent of all valve abnormalities is
- Aortic stenosis
- Aortic regurgitation
- Mitral stenosis
- Mitral regurgitation
Aortic stenosis
- Which is not a major criteria for rheumatic fever
- Sydenham chorea
- Subcutaneous nodules
- Pancarditis
- Erythema multiforme.
Erythema Marginatum
Multiforme most commonly caused by HSV
- Mitral valve prolapse
- Is often an incidental finding in young males.
- Is associated with a mid diastolic click
- Is usually secondary to a hereditary connective tissue disorder ie Marfans
- Has a rare complication of causing infective endocarditis
Has a rare complication of causing infective endocarditis
Usually in young females
- Regarding Infective endocarditis which is the correct pairing
- Native but pre damaged ,otherwise normal valves: staph. Epidermidis.
- Prosthetic valves: staph aureus.
- Healthy valves: staph aureus
- Iv drug users haemophilus.
Healthy valves: staph aureus
Native damaged valves - strep viridans
Prosthetic - staph epidermidis
IVDU - staph aureus
- Acute rheumatic fever
- Histologically aschoff bodies are only found in the pericardium.
- Is due to an immune reaction against Group B streptococci
- Occurs around 7 days after the strep. Pharyngitis.
- 1st attacks can occur in middle to late life
1st attacks can occur in middle to late life
Is due to an immune reaction against Group A streptococci
Histologically aschoff bodies are only found in the Endocardium and myocardium
Occurs 10-40 days after pharyngitis
- endocarditis in IV drug abusers typically
- a. involves the mitral valve.
- b. is caused by candida albicans.
- c. does not cause fever.
- d. has a better prognosis than other types of endocarditis.
- e. is caused by staph aureus
e. is caused by staph aureus
- a. involves the Tricuspid valve
- b. is caused by S aureus and skin flora
- c. does cause fever.
- d. has a worse prognosis than other types of endocarditis.
- The commonest cause of fungal endocarditis is
- a. Actinomycosis
- b. aspergillus
- d. candida
- e. blatomycosis
d. candida
- rheumatic carditis is associated with
- a. Curschmann spirals
- b. Ito cells
- c. Aschoff bodies
- d. Nutmeg cells
- e. Reed-Sternberg cells
c. Aschoff bodies
- The most likely organism responsible for prosthetic valve endocarditis is
- Staphylococci epidermis
- Staphylococcus aureus
- Streptococci viridans
- Haemophilus influenza
Staphylococci epidermis
- Staphylococcus aureus - native or IVDU
- Streptococci viridans - abnormal native valves
- Haemophilus influenza - ??
- in the developed world, the most common cause of myocarditis is
- a. SLE
- b. HIV
- c. Enteroviruses
- d. Chlamydiae
- e. Drug hypersensitivity
c. Enteroviruses
other causes include autoimmune disease
- Which of the following is NOT a change seen in the aging heart
- Decreased myocardial mass
- Increased left ventricular cavity size
- Decreased left atrial cavity size
- Dilatation ascending aorta with rightward shift
Decreased left atrial cavity size
Cavity size is increased
- In volume overload hypertrophy
- Is characterized by ventricular dilatation
- The wall thickness is the best way to measure hypertrophy in these patients
- The wall thickness is always reduced.
- None of the above are true
Is characterized by ventricular dilatation
Volume overload -> dilation
Pressure overload -> hypertrophy and diastolic dysfx
In volume overload, weighing the heart is the best way to measure hypertrophy
The wall thickness is Often increased, but can be reduced
- In left heart failure, which is an early and cardinal symptom?
- Weight gain
- Dyspnoea
- Fatigue
- Chest pain on exertion
Dyspnoea
- Regarding heart tumours
- Rhabdomyomas are the most frequent primary tumour of infants hearts and in the first year of life
- Fibromas are the most common primary tumour of the adult heart.
- 90% myxomas occur in the ventricles.
- Myxomas are rarely solitary.
Rhabdomyomas are the most frequent primary tumour of infants hearts and in the first year of life
- Myxomas are the most common primary tumour of the adult heart.
- 90% myxomas occur in the atria
- Myxomas are usually solitary.
- Hypertrophic cardiomyopathies
- Are associated with myocardial hyperplasia.
- Are associated with systolic dysfunction.
- Are a leading cause of LVH unexplained by other clinical/pathological cause
- The heart hypo-contracts
Are a leading cause of LVH unexplained by other clinical/pathological cause
Associated with hypertrophy and diastolic dysfunction (heart is too bulky to distend and fill with blood properly)
- The most common cause of pericarditis is
- a. SLE
- b. Drug hypersensitivity
- c. Trauma
- d. Post myocardial infarction
- e. Bacterial
- e. Aschoff bodies in the heart
d. Post myocardial infarction.
Viral infection is most common overall, post-MI (dresslers syndrome) is highest on that list though
- Regarding pericarditis
- a. Constrictive pericarditis only rarely follows suppurative pericarditis.
- b. Primary pericarditis is usually bacterial in origin
- c. Serous pericarditis may be due to uraemia
- d. Fibrinous pericarditis is due to Mycobacterium tuberculosis infection until proven otherwise.
- e. Haemorrhagic pericarditis is most commonly due to Klebsiella infection.
c. Serous pericarditis may be due to uraemia
Serous can have any cause but most often viral, rarely bacterial
- a. Constrictive pericarditis often follows suppurative pericarditis.
- b. Primary pericarditis is usually viral in origin.
- d. Caseous pericarditis is due to Mycobacterium tuberculosis infection until proven otherwise.
- e. Haemorrhagic pericarditis is most commonly due to Surgery, TB, cancer
- The most common form of congenital heart disease is
- a. Coarctation of the aorta
- b. Tetralogy of Fallot
- c. ASD
- d. PDA
- e. VSD
e. VSD
- Which is the most likely cause of cyanosis in early post natal life?
- Tetralogy of Fallot
- Transposition of the great arteries
- Truncus arteriosis
- Tricuspid atresia
Tetralogy of Fallot - ‘Most infants with TOF are cyanotic from birth or soon thereafter’
TOF is the most common of the list, though most will cause cyanosis shortly after birth
Tricuspid atresia - ‘cyansis is present virtually from birth’
TGA - does not specifically mention cyanosis, just that it can be incompatible with life.
- Beneficial effects of nitrates in treatment of angina include all of the following except:
- a. Decreased ventricular volume
- b. Decreased arterial pressure
- c. Decreased ejection time.
- d. Increased collateral flow
- e. Reflex increase in contractility
e. Reflex increase in contractility. Is a genuine effect but not beneficial
- a. Decreased ventricular volume - due to reduced pre-load and tachycardia
- b. Decreased arterial pressure - decreased arterial tone
- c. Decreased ejection time - baroreceptor reflex, unclear how this works exactly
- d. Increased collateral flow - due to dilation of vessels presumably.
- Glyceryl trinitrate
- a. Acts by effecting adenylyl cyclase.
- b. Acts by effecting nitric oxide
- c. Has high oral bioavailability.
- d. Has significant effects on cardiac muscle.
- e. Has no effect on pulmonary vascular pressure
b. Acts by effecting nitric oxide
- a. Acts by effecting guanylyl cyclase.
- c. Has low oral bioavailability - hence SL, transdermal, or IV admin.
- d. Has significant effects on vascular smooth muscle
- e. Reduces pulmonary vascular pressure - hence its utility in flash pulmonary oedema
- Verapamil
- a. Increases myocardial contractility.
- b. Is a positive inotrope
- c. Causes skeletal muscle weakness.
- d. Blocks active and inactive Ca2+ channels
d. Blocks active and inactive Ca2+ channels
- a. Decreases myocardial contractility.
- b. Is a negative inotrope.
- c. Does not affect skeletal muscle
- GTN
- a. Works by NO
- b. Causes methaemoglobin.
a. Works by NO
- b. Causes methaemoglobin- Nitrites do, not nitrates (GTN does produce a minute amount of nitrite, but which is not sufficient to cause methaemoglobin)
- Regarding nitrates, they do not
- a. Increase collateral coronary blood flow
- b. Demonstrate tachyphylaxis/tolerance
- c. Demonstrate physical dependence
c. Demonstrate physical dependence
- Coronary artery dilation occurs with
- a. Adenosine
- b. High K+
- c. Propranolol.
- d. Enalapril
- e. None of the above
a. Adenosine
Beta-2-adrenoceptors cause vasodilation, hence betablockers like propranolol will cause constriction (or no effect)
- With regard to verapamil, which of the following is NOT true?
- a. It significantly increases serum digoxin levels via a pharmacokinetic interaction.
- b. Alpha blockade contributes to peripheral vasodilation.
- c. At therapeutic levels end systolic volume is decreased.
- d. Vasospastic angina is an indication for its use
- e. Combination with a beta blocker may cause atrioventricular block
c. At therapeutic levels end systolic volume is increased.
Higher EDV + lower contractility makes a higher ESV likely (though SV seems to be decreased based on a Google search.
- a. It significantly increases serum digoxin levels via a pharmacokinetic interaction. (↓ PGP)
- b. Alpha blockade contributes to peripheral vasodilation.
- d. Vasospastic angina is an indication for its use
- e. Combination with a beta blocker may cause atrioventricular block
- Nitrates, either directly or via reflexes, cause all of the following EXCEPT:
- a. Tachycardia.
- b. Decrease in contractility.
- c. Increase in venous capacitance
- d. Decrease in myocardial fibre tension
- e. Decrease in afterload
b. Increase in contractility.
Reflex increase in response to low BP
- a. Tachycardia -> Reflex to low BP
- c. Increase in venous capacitance - due to venous dilation
- d. Decrease in myocardial fibre tension - due to reduced preload and afterload
- e. Decrease in afterload - Arterial smooth muscle relaxation -> lower BP
- With regards to calcium channel blockers, which is NOT a characteristic feature?
- a. They have a high first pass effect
- b. They are highly plasma protein bound
- c. They are extensively metabolized
- d. They act primarily at T type voltage gated calcium channels.
- e. They bind more effectively to channels in depolarized membranes
d. They act primarily at L type voltage gated calcium channels
Not T-type
- Regarding calcium channel blockers:
- a. Verapamil blocks only activated calcium channels
- b. They act from the inner side of the membrane
- c. The degree of block is unaffected by plasma concentration of calcium
- d. They predominantly affect the T-type calcium channels in cardiac muscle
- e. They do not affect AV nodal conduction velocity
b. They act from the inner side of the membrane*
(alpha 1 subunit spans the membrane as the inner pore, but I cannot find exactly where it is blocked - most pictures show the block occuring from the outside to the channel so this answer could be wrong)
- a. Verapamil blocks both inactivated and activated calcium channels
- **c. The degree of block is reduced by increased plasma concentration of calcium (competitive block - I assume at a guess as this answer is wrong apparently)
- d. They predominantly affect the L-type calcium channels in cardiac muscle
- e. They definitely do affect AV nodal conduction velocity
- Verapamil
- a. Binds more effectively to calcium channels in depolarized membranes
- b. Increases the contractility of the heart
- c. Decreases the calcium available in skeletal muscle causing weakness
- d. Lessens ankle oedema in congestive cardiac failure.
- e. Is a weak alpha adrenergic agonist.
a. Binds more effectively to calcium channels in depolarized membranes
- b. Decreases the contractility of the heart
- c. Does not affect skeletal muscles
- d. Increases ankle oedema in congestive cardiac failure.
- e. Is a weak alpha adrenergic antagonist.
- This fact comes up a reasonably often, but I cannot find specifics of it except a paper from 1982 on rat myocardium - please update if you have more information
- Verapamil
- a. Is a positive inotrope. Negative
- c. inhibits activated and inactivated sodium channels
- d. is a dihydropyridine
c. inhibits activated and inactivated sodium channels
- a. Is a negative inotrope.
- d. is a phenylalkylanine - dihydropyridines are felodipine, amlodipine, nifedipine (the peripheral ones)
- The calcium channel blocker with the most rapid onset of action when given orally is
- a. Diltiazem
- b. Nifedipine
- c. Verapamil
- d. Felodipine
- e. nicardipine
b. Nifedipine
Given as answer, but nicardipine has a shorter half-life (onsets not given for all)
- a. Diltiazem - T1/2 - 5 hours, onset >30min oral (<3min IV)
- b. Nifedipine - T 1/2 - 4 hours (IV onset <1min)
- c. Verapamil - - T1/2 - 5 hours, onset >30min oral (<3min IV)
- d. Felodipine - T 1/2 - 11-16 hours
- e. nicardipine - T1/2 - 2-4 hours
- Methyldopa
- Lowers the heart rate and cardiac output more than clonidine does
- Causes reduction in renal vascular resistance
- Has minimal CNS side effects
- Has 80% bioavailability
- Usual therapeutic dose is about 1–2mg/day
Causes reduction in renal vascular resistance
Despite not causing a decrease in TPR (does not affect peripheral alpha-receptors, just central ones)
Maintains CV reflexes
Clonidine lowers HR and CO more than Methyldopa
Therapeutic dose is 1-2 grams/day
Bioavailability 25%
Has CNS effects as it works there - primarily sedation
- Propranolol
- Is a B1 specific blocker
- Causes prominent postural hypotension
- Inhibits the stimulation of renin production by catecholamines
- Has a half life of 12 hours
- Has no effect on plasma lipids
Inhibits the stimulation of renin production by catecholamines
Same as all beta-blockers
- Is a non-selective blocker
- Causes minimal postural hypotension
- Has a half life of 12 hours
- Has no effect on plasma lipids
- Hydralazine
- Dilates veins but not arterioles
- Is contraindicated in the treatment of preeclampsia
- Can cause an SLE type syndrome in up to 10 – 20% of patients
- Causes orthostatic hypotension in many cases
- e. Is extremely useful as a single agent in treatment of hypertension
The ACE inhibitors
- Inhibit peptidyldipeptidase thus preventing the inactivation of bradykinin
- Captopril is a prodrug
- Are to be used with caution in patients with IHD as reflex sympathetic activation occurs secondary to the hypotensive effects of the ACE inhibitors
- Have no role in treating the normotensive diabetic patients
- Are useful antihypertensive agents in late pregnancy
Captopril is a prodrug
- Inhibit angiotensin-converting enzyme thus preventing the inactivation of bradykinin
- Are to be used with caution in patients with IHD as reflex sympathetic activation occurs secondary to the hypotensive effects of the ACE inhibitors
- Have no role in treating the normotensive diabetic patients
- Are useful antihypertensive agents in late pregnancy
The following drugs when combined with ACE inhibitors may produce troublesome problems EXCEPT
- a. Diclofenac
- b. Potassium supplements
- c. Spironolactone
- d. Lithium
- e. Theophylline
e. Theophylline
- a. Diclofenac - due to prostaglandin inhibition can cause impairment of bradykinin induced vasodilation
- b. Potassium supplements - can cause hyperkalaemia as ACEi inhibit aldosterone (which leads to potassium loss)
- c. Spironolactone - inhibits aldosterone, and so leads to potassium retention (risk of hyperkalaemia)
- d. Lithium - ACEi can increase serum levels of lithium
The nitrates
- a. Have an antianginal effect via vasodilation of arterioles only
- b. Serve to increase preload
- c. Have a direct effect on cardiac muscle to cause a decrease in anginal symptoms
- All have high oral bioavailability
- Are contraindicated in the presence of increased intracranial pressure
Are contraindicated in the presence of increased intracranial pressure
As they cause cerebral vasodilation (mechanism by which they cause headache)
Nitrates cause venous dilation primarily at low doses, which reduces preload and reduces cardiac work
They have low oral bioavailability (except ISMN), so are given IV, SL, or transdermal
- Regarding Calcium channel blockers
- Calcium channel blockers are not bound to plasma proteins
- Nifedipine has less vascular potency than verapamil
- Felodipine has been shown to inhibit insulin release in humans
- Diltiazem has a plasma half life of 3–4hours
- Verapamil has high affinity for cerebral blood vessels thus decreasing vasospasm post subarachnoid haemorrhage
Diltiazem has a plasma half life of 3–4hours
Hence TDS dosing of oral preparations
- Calcium channel blockers are mostly bound to plasma proteins
- Nifedipine has more vascular potency than verapamil
- Felodipine has been shown to inhibit insulin release in humans
- Seems unlikely
- Nimodipinel has high affinity for cerebral blood vessels thus decreasing vasospasm post subarachnoid haemorrhage
10.Which of the following calcium channel blockers is excreted predominantly in the faeces?
- a. Nifedipine
- b. Felodipine
- c. Diltiazem
- d. Nimodipine
- e. Verapamil
c. Diltiazem
11.Which of the following calcium channel blockers has the longest plasma half life?
- a. Felodipine
- b. Diltiazem
- c. Amlodipine
- d. Nimodipine
- e. Verapamil
c. Amlodipine
12.The following include major actions of digoxin on cardiac electrical functions EXCEPT
- a. Decreased PR interval on ECG
- Decreased conduction velocity at the AV node
- Increased automaticity of the atrial muscle
- Decreased effective refractory period in purkinje system/ventricles
- Bigeminy can be induced by digoxin
a. increased PR interval on ECG
due to the increased vagal tone at the AV node
- Increases inotropy through increased [Ca]i, and reduces HR by increasing vagal tone at SA and AV nodes
- Binds to K+ (extracellular site) of Na-K-ATPase, inhibiting its function
- Results in intracellular Na+ accumulation, and extra-cellular K+ accumulation
- The former triggers NCX (Na-Ca exchanger), thus bringing more calcium inside the cell
- Hence more Ca2+ is taken into the SR
- leading to greater Ca2+ release when the cell depolarises
- This is a direct determinant of ionotropic state
Electrical effects
- Initially, a transient prolongation of the AP
- Then the AP is shortened in the long-term, probably because intracellular calcium makes the membrane more permeable to potassium
- At higher doses, the RMP rises due to loss of Na-K-ATPase
- Additionally, delayed after depolarisations occur if calcium accumulates so much that NCX works in reverse and triggers a sodium influx
Autonomic effects
- Accentuates cholinergic transmission, hence slows SAN firing and AVN conductance can be used to treat SVTs
- ECG changes
- AV block or junctional rhythm; PVCs or bigeminy
13.Which of the following increases the risk of digoxin induced arrhythmias?
- a. Hyperkalaemia
- b. Hypercalcaemia
- c. Hypermagnesaemia
- d. Hyperuricaemia
- e. Hypernatraemia
b. Hypercalcaemia
Enhanced therapeutic effect - more Ca will come into the cells
Risk factors:
- For risk of ADRs: low potassium / magnesium, high calcium, renal impairment (less clearance)
- Amiodarone, verapamil, quinidine all increase plasma levels by displacing tissue binding sites and reducing renal excretion
- Digoxin
- Is poorly lipid soluble
- Is extensively metabolized
- Has a half life in the body of 40 hours
- Has minimal GI toxicity
- Is 80% bound to plasma proteins
Has a half life in the body of 40 hours
66% bioavailabilty and 66% excreted unchanged
15.Drugs which may increase digoxin effect include all of the following EXCEPT
- a. Amiodarone
- b. Diltiazem
- c. Frusemide
- d. Quinidine
- e. Antacids
e. Antacids
verapamil, amiodarone, spironolactone inhibit PGP and increase levels
PPI increase absorption and increase levels
Antacids reduce bioavailability
16.Which of the following drugs has the smallest volume of distribution?
- a. Chloroquine
- b. Verapamil
- c. Imipramine
- d. Warfarin
- e. Digoxin
d. Warfarin
99% protein bound
