Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ESA 2: Cardiovascular > Cardiovascular: Session 5 > Flashcards

Cardiovascular: Session 5 Flashcards

1
Q

How is blood pressure regulated short term?

A

Baroreceptor reflex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where can the baroreceptors be found?

A

Carotid sinus and Aortic Arch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the mechanism of action for baroreceptors?

A

They are sensitive to stretch. Increased arterial pressure cause the receptors to stretch more and there is feedback to the cardiovascular centre of medulla. This has a negative effect on the sympathetic system and causes bradycardia and vasodilation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Why doesn’t the baroreceptor reflex have any effect on sustained increase in blood pressure?

A

Baroreceptor reflex resets after 15 mins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How is blood pressure controlled long term?

A

Neurohumoral responses.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What ion does the neurohumoural control target and what does this result in?

A

Sodium ions. This results in control of extracellular fluid volume.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What component of the blood does the controlling sodium levels in the body control?

A

The plasma volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where is renin released from?

A

Kidneys (granular cells of the afferent arteriole of juxtaglomerular apparatus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What causes increased Renin release?

A
  • Reduced perfusion pressure in the kidney causes release of Renin
  • Sympathetic stimulation of juxtaglomerular apparatus increases release of renin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does Renin do?

A

Renin catalyses the breakdown of Angiotensin to Angiotensin 1.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does ACE do?

A

Converts Angiotensin 1 to Angiotensin 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which receptors does Angiotensin 2 bind to?

A

The are two types of Ang II receptors. AT1 and AT2. The main is via AT1 receptors which is a G-protein coupled receptor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the function of the Angiotensin 2 on arterioles?

A

Vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the function of the Angiotensin 2 on kidney?

A

Stimulates Na+ reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the function of the Angiotensin 2 on Sympathetic Nervous System?

A

Increased release of noradrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the function of the Angiotensin 2 on Adrenal Cortex?

A

Stimulates release of aldosterone from adrenal cortex.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the function of Angiotensin 2 on Hypothalamus ?

A

Increases thirst sensation (stimulate ADH release).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is a side effect of ACE inhibitors?

A

They act on ACE inhibitors to block the conversion of Angiotensin 1 to Angiotensin 2. It also causes accumulation of bradykinin which is thought to cause a dry cough.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the effect of high levels of sympathetic stimulation on renal blood flow?

A

There is a reduction in renal blood flow. Vasoconstriction of arterioles and decrease in GFR so a decrease in sodium excretion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the effect of sympathetic stimulation on JG cells?

A

Stimulates renin release.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the role of the Antidiuretic hormone?

A
  • To form concentrated urine by retaining water by retaining sodium.
  • To also stimulate Na+ reabsorption
  • Causes Vasoconstriction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What stimulates the release of ADH?

A

An increase in plasma osmolarity or severe hypovolaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Name an example of diuretic used to reduce circulating volume.

A
  • Thiazide diuretics (preffered)

- Aldosterone antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Where is Atrial Natriuretic peptide synthesised?

A

They are synthesised and stored in the atrial myocytes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are ANP released in response to?

A

Released in response to stretch. High pressure causes it to be released and low pressure causes the release to be inhibited

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the effect of reduced effective circulating volume on release of ANP?

A

The release of ANP is inhibited to support the Blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the actions of ANP?

A
  • Causes vasodilation of the afferent arteriole
  • Increased blood flow increases GFR
  • Inbits Na+ reabsorption along the nephron
  • Causes loss of sodium into the urine (acts in the opposite direction to other neurohumeral regulators).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the actions of prostaglandins?

A
  • Act as vasodilators
  • Locally acting prostaglandins (mainly PGE2) enhance the glomerular filtration and reduce Na+ reabsorption
  • Acts as a buffer to excessive vasoconstriction produced by the SNS and RAA system.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Where is dopamine formed?

A

It is formed in the kidneys from circulating L-DOPA.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the actions of Dopamine?

A
  • Causes vasodilation

- Reduce reabsorption of NaCl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Where are dopamine receptors present?

A

Dopamine receptors are present on renal blood vessels and cell of PCT & TAL.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is stage 1 hypertension?

A
  • Greater or equal to 140/90 mmhg in clinic

- Average Greater or equal to 135/85 mmhg at home

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is stage 2 hypertension?

A
  • Greater or equal to 160/100 mmhg in clinic

- Average greater or equal to 150/95 mmhg at home

34
Q

What is severe hypertension?

A

-Greater or equal to 180 systolic or 110 diastolic in the clinic

35
Q

What some factors leading to primary hypertension?

A
  • Genetic factors when high BP tends to run in the families

- Environmental factors

36
Q

What is important to treat in secondary hypertension?

A

The primary cause.

37
Q

How does renovascular disease lead to secondary hypertension?

A
  1. Occlusion of the renal artery causes a fall in perfusion pressure in that kidney
  2. Decreased perfusion pressure leads to increased renin production
  3. Activation of the RAAS system
  4. Vasoconstriction and Na+ retention at other kidneys
38
Q

How does renal parenchymal disease lead to secondary hypertension?

A
  1. Earlier stage may be a loss of vasodilator substances

2. In later stage Na+ and water retention due to inadequate glomerular filtration

39
Q

What are some adrenal causes of secondary hypertension?

A
  • Conn’s syndrome - Aldosterone secreting adenoma
  • Cushing’s syndrome - excess secretion of glucocorticoid cortisol. At high concentration acts of aldosterone receptors leading sodium and water retention
  • Tumour of the adrenal medulla - Secretion of catecholamines
40
Q

What are the symptoms of Hypertension?

A

Hypertension is asymptomatic.

41
Q

What are the effects of hypertension?

A

It can have damaging effects on heart and vasculature. the potentially leads to heart failure, MI, stroke, renal failure and retinopathy.

42
Q

What are treatments targeting renin-angiotensin-aldosterone system?

A
  • Prevent production of Ang II from Ang I using ACE inhibitors
  • Ang II receptors antagonists
43
Q

What are the effects of vasodilators in treating hypertension?

A
  • L-type Ca channel blockers to reduce Ca2+ entry too vascular smooth muscle class and relaxation of vascular smooth muscle
  • Could use A1 receptor blockers to reduce sympathetic tone but can cause postural hypertension
44
Q

What are the effects of diuretics in treating hypertension?

A
  • Inhibit Na/Cl co-transporter on apical membrane of cells in distal tubule.
  • Thiazide directs reduce circulating volume
  • Aldosterone antagonists will also lower BP
45
Q

What are the effects of Beta blockers in treating hypertension?

A

-Blocking B1 receptors in the heart will reduce effects of sympathetic output. This reduces heart rate and contractility.

46
Q

When are beta blockers used?

A

It would only be used if there are other indications such as previous myocardial infarction.

47
Q

What are the equations for calculating the mean arterial Blood pressure?

A

Mean arterial BP = CO X TPR
Mean arterial BP = SV X HR X TPR
Mean arterial BP = Diastolic pressure + 1/3 pulse pressure

48
Q

Describe Haemodynamic shock

A

Acute condition of inadequate blood flow throughout the body
A catastrophic fall in arterial blood pressure lead to circulatory shock
Shock can be due to fall in CO or fall in TPR beyond capacity of the heart to cope

49
Q

What are the types of shock associated with Fall in cardiac output?

A
  • Cardiogenic shock (pump failure) : Ventricle cannot empty properly
  • Mechanical shock (obstructive) : Ventricles cannot fill properly
  • Hypovolaemic shock : Reduced blood volume leads to poor venous return
50
Q

What is cardiogenic shock and what are the causes?

A
  • Acute failure of the heart to maintain cardiac output - pump failure.

Potential Causes:

  • Following myocardial Infarction leading to damage to left ventricle
  • Due to serious arrhythmias
  • Acute worsening of heart failure
51
Q

What happen to arterial blood pressure and central venous pressure in cardiogenic shock?

A
  • Dramatic drop in arterial BP

- Central venous pressure may be normal or raised

52
Q

Which tissues are poorly perfused in cardiogenic shock and what is the result?

A
  • Coronary artery may be poorly perfused which exacerbates the problem
  • Kidneys may be poorly perfused and this leads to reduced urine production - Oliguria
53
Q

What is Cardiac Arrest?

A

Unresponsiveness due to associated lack of pulse. the heart has stopped or has ceased to pump effectively.

54
Q

What are some causes of Cardiac arrest?

A
  • Asystole (loss of electrical and mechanical activity)
  • Pulseless electrical activity
  • Ventricular fibrillation (following MI or electrolyte imbalance or some arrhythmias)
55
Q

How do you respond to a cardiac arrest?

A
  • Basic life support
  • Advanced life support such as defibrillation where electric current is delivered to the heart. it depolarises all the cells and put them all in refractory period enabling coordinated electrical activity to begin
  • Adrenaline enhances myocardial function and increases peripheral resistance
56
Q

What type of shock is cardiac tamponade?

A

Mechanical shock

57
Q

What is cardiac tamponade?

A
  • Cardiac tamponade is compression of the heart leading to a fall in arterial blood pressure (haemodynamic compromise) and high venous pressure. This is due to blood or fluid build up in pericardial space.
  • There is restricted filling of the heart so limits end diastolic volume. it also affect the left and right sides of heart
  • There is still electrical activity so heart attempts to beat
58
Q

What is pulmonary embolism?

A

Embolus occludes a large pulmonary artery

59
Q

What are the effects of a pulmonary embolism?

A
  • Pulmonary artery pressure is high
  • Right ventricle cannot empty
  • Central venous pressure is high
  • Reduced return of blood to left heart
  • Limits filling of left heart
  • Left atrial pressure is low
  • Arterial blood pressure is low
  • Shock
  • Chest pain and dyspnoea
60
Q

How can an embolus reach the lungs?

A
  • Typically due to deep vein thrombosis
  • Portion of thumbs breaks off
  • Travels in venous system to right side of the heart
  • Pumped out via pulmonary artery to lungs
61
Q

What is hypovolaemic shock and the most common cause?

A
  • Reduced blood volume
  • Most common due to haemorrhage
  • <20% blood loss unlikely to cause shock
  • 20-30% blood loss shows some sign of shock response
  • 30-40% substantial decrease in mean aBP and serious shock response
  • Severity of shock is related to amount and speed of blood loss
62
Q

What are the effect of a haemorrhage?

A
  • Venous pressure falls
  • Cardiac output falls
  • Arterial pressure falls
  • Detected by baroreceptors
63
Q

What is the compensatory response in hypovolaemic shock?

A
  • Increased sympathetic stimulation
  • Tachycardia
  • Increased force of contraction
  • Peripheral vasoconstriction
  • Venoconstriction
64
Q

What is internal transfusion in relation to hypovolaemic shock?

A

The increased peripheral resistance reduces the capillary hydrostatic pressure. There is net movement of fluid into capillaries

65
Q

What are the signs of a patient with Hypovolaemic shock?

A

Patient has:

  • Tachycardia
  • Weak pulse
  • Pale skin
  • Cold, clammy extremities
66
Q

What else can result in Hypovolaemic shock?

A
  • Severe burns

- Severe diarrhoea or vomiting and loss of Na+

67
Q

What is Danger of Decompensation in hypovolaemic shock?

A

There is peripheral vasoconstriction so impairs tissue perfusion. Build-up of hypoxia so tissue damage so release of chemical mediators to vasodilate so peripheral resistance decreases so blood pressure falls dramatically and vital organs can no longer be perfused so multi system failure.

68
Q

How does the body attempt to restore blood volume n long term response?

A
  • Renin-angiotensin-aldosterone system

- Anti diuretic Hormone

69
Q

What is distirbutive shock?

A
  • Low resistance shock
  • Profound peripheral vasodilation so total peripheral resistance decreases. The blood volume is constant but volume of the circulation has increased.
70
Q

What are two types of distributive shock?

A
  • Anaphylactic shock

- Toxic shock

71
Q

What is sepsis?

A

A life threatening organ dysfunction due to dysregulated host response to infection

72
Q

What is septic shock?

A

Septic shock is persisting hypotension requiring treatment to maintain blood pressure despite fluid resuscitation.

73
Q

What does endotoxin release by circulating bacteria cause in Toxic (septic) shock?

A
  • PRofound inflammatory response
  • Causes profound vasodilation
  • Dramatic fall in TPR
  • Fall in arterial pressure
  • Impaired perfusion of vital organs
  • Capillaries also become leaky so reduced blood volume
  • Increased coagulation and localised hypo-perfusion
74
Q

What detects the decreased arterial pressure in septic shock and why doesn’t it get corrected?

A
  • The baroreceptors detect the deceased arterial pressure and there is increased sympathetic output
  • The vasoconstrictor effect is however overridden by mediators of vasodilation
  • The heart rate and stroke volume is increased (seagull sign)
75
Q

What are the symptoms of a patient sin septic shock?

A
  • Tachycardia
  • Warm, red extremities
  • At later stages of sepsis there is vasoconstriction so localised hypoperfusion
76
Q

What is anaphylactic shock?

A

-A severe allergic reaction involving release of histamine from mast cell.

77
Q

What are the signs of a patient in anaphylactic shock?

A

Patient will have

  • Difficulty breathing
  • Collapsed
  • Rapid heart rate
  • Red, warm extremities
78
Q

How is anaphylactic shock treated?

A

Adrenaline is given in order to cause vasoconstriction via the A1 adrenoreceptors.

79
Q

What is the action of aldosterone?

A
  • This Stimulates Na+ reabsorption at the kidney at principle cells of collecting ducts and therefore water reabsorption.
  • The apical Na+ channels and apical K+ channels activated.
  • Increased basolateral Na+ extrusion via sodium-potassium ATPase. Patients that have high aldosterone tend to have low K+.
80
Q

What occurs during an anaphylactic shock?

A
  • There is a powerful vasodilator effect leading to fall in total peripheral resistance.
  • This leads to dramatic drop in arterial pressure. At rest there is increased sympathetic response but the increase in cardiac output can’t overcome the vasodilation.
  • This leads to impaired perfusion of vital organs.
  • The mediators also cause bronconstriction and laryngeal oedema so difficulty breathing.

ESA 2: Cardiovascular (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions