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.
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
- 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
- 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
