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Body Systems Y1 > Body Systems L15 > Flashcards

Body Systems L15 Flashcards

1
Q

Name types of systemic & vascular disorders

A

Hypertension
Atherosclerosis
Thrombosis

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2
Q

Describe Hypertension

A

• Hypertension:
 Affects nearly one billion
 One of the main causes -> premature death.
 Nearly 8 million fatalities per year
 Types:
- Primary Hypertension
(Essential / Idiopathic)
 Unknown medical cause
 Links:
 Genetic predisposition
 Alcohol consumption
 Obesity
 Lack of excersise
 Diabetes
 Intrauterine environment
- Secondary Hypertension
 Known medical cause
1) Kidney Disease:
 Incr. Angiotensin II
» Vasoconstriction & expansion -> cellular fluid
2) General endocrine disorders
Eg. Diabetes, Cushing’s
3) Adrenal medulla disease (Phaeochroocytoma)
 Excessive adrenaline secretion
 Treatment:
- Inhibit angiotensin II production -> Angiotensin-Converting-Enzyme (ACE)
» Prevents renal absorption -> Na+/H2O
> Prevents incr. blood volume
- Ibhibition -> Angiotensin II induced vasoconstriction -> Angiotensin II receptor
blocker.
&raquo_space; Inhibitd membrane cardiac / vascular depolarizoation
> Decr. CO -> vasodilation.
- Calcium-channel blocker / thiazide diuretic
&raquo_space; Incr. loss -> Na+ & H2O
> Decreases fluid volume, venous return & cardiac output.
- Reduce TBR -> inhibition -> noradrenaline action.
- Alpha-adrenoreceptor Antagonists (alpha-Blockers)
 Reduce TBR -> inhibition -> noradrenaline action.
- Beta-adrenoreceptor Antagonists (beta-Blockers)
 Decr. CO2,
 Decr. central activity -> Symapthetic nervous system
 Decr. release -> Renin
-» Favourable secondary actions
 Risks:
- Atherosclerosis
- Stroke / Cerebrovascular Accident
- Heart Failure
- Renal Failure
- Aneurysms

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3
Q

What are the figures regarding those affected by hypertension

A

 Affects nearly one billion
 One of the main causes -> premature death.
 Nearly 8 million fatalities per year

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4
Q

Name the types of hypertension

A

Primary

Secondary

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5
Q

Describe primary hypertension & the main links associated with it

A 
-	Primary Hypertension
(Essential / Idiopathic) 
 Unknown medical cause
 Links:
	Genetic predisposition
	Alcohol consumption
	Obesity
	Lack of excersise
	Diabetes
	Intrauterine environment
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6
Q

Describe secondary Hypertension & the main known causes

A 
-	Secondary Hypertension
 Known medical cause
1)	Kidney Disease:
 Incr. Angiotensin II 
>> Vasoconstriction & expansion -> cellular fluid
2)	General endocrine disorders
Eg. Diabetes, Cushing’s
3)	Adrenal medulla disease (Phaeochroocytoma)
 Excessive adrenaline secretion

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7
Q

What are the types of secondary hypertension & what do they cause?

A

1) Kidney Disease:
 Incr. Angiotensin II
» Vasoconstriction & expansion -> cellular fluid
2) General endocrine disorders
Eg. Diabetes, Cushing’s
3) Adrenal medulla disease (Phaeochroocytoma)
 Excessive adrenaline secretion

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8
Q

What does kidney disease in relation to hypertension cause?

A

1) Kidney Disease:
 Incr. Angiotensin II
» Vasoconstriction & expansion -> cellular fluid

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9
Q

What does General endocrine disorders in relation to hypertension cause?

A

2) General endocrine disorders

Eg. Diabetes, Cushing’s

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10
Q

What does Adrenal medulla disease in relation to hypertension cause?

A

3) Adrenal medulla disease (Phaeochroocytoma)

 Excessive adrenaline secretion

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11
Q

Describe the treatment methods for Hypertension

A

 Treatment:
- Inhibit angiotensin II production -> Angiotensin-Converting-Enzyme (ACE)
» Prevents renal absorption -> Na+/H2O
> Prevents incr. blood volume
- Ibhibition -> Angiotensin II induced vasoconstriction -> Angiotensin II receptor
blocker.
&raquo_space; Inhibitd membrane cardiac / vascular depolarizoation
> Decr. CO -> vasodilation.
- Calcium-channel blocker / thiazide diuretic
&raquo_space; Incr. loss -> Na+ & H2O
> Decreases fluid volume, venous return & cardiac output.
- Reduce TBR -> inhibition -> noradrenaline action.
- Alpha-adrenoreceptor Antagonists (alpha-Blockers)
 Reduce TBR -> inhibition -> noradrenaline action.
- Beta-adrenoreceptor Antagonists (beta-Blockers)
 Decr. CO2,
 Decr. central activity -> Symapthetic nervous system
 Decr. release -> Renin
-» Favourable secondary actions

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12
Q

Outline the methods used to treat hypertensin

A
  • Inhibit angiotensin II production
  • Inhibit angiotensin II production
  • Calcium-channel blocker / thiazide diuretic
  • Reduce TBR -> inhibition -> noradrenaline action.
  • Alpha-adrenoreceptor Antagonists
    Beta-adrenoreceptor Antagonists
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13
Q

Describe how angiotensin II production is prevented in treatment of hypertension

A
  • Inhibit angiotensin II production -> Angiotensin-Converting-Enzyme (ACE)
    » Prevents renal absorption -> Na+/H2O
    > Prevents incr. blood volume
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14
Q

Describe how angiotensin II induced vasoconstriction is inhibited in treatment of hypertension

A

Ibhibition -> Angiotensin II induced vasoconstriction -> Angiotensin II receptor
blocker.
&raquo_space; Inhibitd membrane cardiac / vascular depolarizoation
> Decr. CO -> vasodilation.

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15
Q

Describe how - Calcium-channel blocker / thiazide diuretic is used in treatment of hypertension

A
  • Calcium-channel blocker / thiazide diuretic
    &raquo_space; Incr. loss -> Na+ & H2O
    > Decreases fluid volume, venous return & cardiac output.
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16
Q

Describe how Alpha-adrenoreceptor Antagonists are used in treatment of hypertension

A
  • Alpha-adrenoreceptor Antagonists (alpha-Blockers)

 Reduce TBR -> inhibition -> noradrenaline action.

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17
Q

Describe how Beta-adrenoreceptor Antagonists are used in treatment of hypertension

A
  • Beta-adrenoreceptor Antagonists (beta-Blockers)
     Decr. CO2,
     Decr. central activity -> Symapthetic nervous system
     Decr. release -> Renin
    -» Favourable secondary actions
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18
Q

Describe the risks associated with hypertension

A

 Risks:

  • Atherosclerosis
  • Stroke / Cerebrovascular Accident
  • Heart Failure
  • Renal Failure
  • Aneurysms
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19
Q

Describe Atherosclerosis

A

• Atherosclerosis:
 Narrowing of vessel lumen:
 Fibrous cap of dense extracellular matrix
Accumulation -> Plaque Formation:
 Lipids
 Macrophages
 Proinflammatory mediators
 White blood cells
 Endothelial cells
 Smooth muscle cells
&raquo_space; Arterial remodelling & neovessels occur -> compensatory enlargement
&raquo_space;Fragments of plaques can detach & lodge in small vessels
> Cause thrombosis
-» Restricts blood flow
> Lead to aneurysm formation & rupture

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20
Q

What is Atherosclerosis?

A

 Narrowing of vessel lumen:
 Fibrous cap of dense extracellular matrix
Accumulation -> Plaque Formation:

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21
Q

How is plaque formed in Atherosclerosis?

A 
Accumulation -> Plaque Formation:
	Lipids
	Macrophages
	Proinflammatory mediators
	White blood cells
	Endothelial cells 
	Smooth muscle cells
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22
Q

What does plaque formation cause in Atherosclerosis?

A

> > Arterial remodelling & neovessels occur -> compensatory enlargement
&raquo_space;Fragments of plaques can detach & lodge in small vessels
> Cause thrombosis
-» Restricts blood flow
> Lead to aneurysm formation & rupture

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23
Q

Describe thrombosis

A 
•	Thrombosis:
	Formation of blood clot in vein
-	Most common -> Deep Vein Thrombosis (DVP) -> legs
-	Pulmonary Embolism (PE) -> Lungs
            >> Swelling, Skin changes
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24
Q

What is thrombosis?

A

 Formation of blood clot in vein

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25
Q

Where is thrombosis commonly found?

A
  • Most common -> Deep Vein Thrombosis (DVP) -> legs

- Pulmonary Embolism (PE) -> Lungs

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26
Q

What does thrombosis cause?

A

> > Swelling, Skin changes

27
Q

Name major diseases of the heart

A
  • Ischaemic Heart Disease (Coranary Heart Disease -> CAD)
  • Valve defects:
  • Arrhythmias:
  • Chronic Heart Failure:
  • Aortic Disease:
28
Q

Describe • Ischaemic Heart Disease (Coranary Heart Disease -> CAD)

A

• Ischaemic Heart Disease (Coranary Heart Disease -> CAD)
 Leading cause of death -> Developed world
 30% Males
 23% Females
 Common cause:
 Atherosclerosis -> coronary artery
 Most frequent -> Left anterior interventricular artery
 Affects Left ventricle
 Occurs
 Insufficient Blood flow to myocardium
» Angina Pectoris (ischemia-induced pain)
-»Mediated by endogeneous vasodilators
» Results -> myocardial infarction
-» Death of heart muscle within 20 mins

29
Q

How much of the population does • Ischaemic Heart Disease (Coranary Heart Disease -> CAD) affect?

A

 Leading cause of death -> Developed world
 30% Males
 23% Females

30
Q

What are common causes of • Ischaemic Heart Disease (Coranary Heart Disease -> CAD)?

A

 Atherosclerosis -> coronary artery
 Most frequent -> Left anterior interventricular artery
 Occurs in Left ventricle
 Insufficient Blood flow to myocardium
» Angina Pectoris (ischemia-induced pain)
-»Mediated by endogeneous vasodilators
» Results -> myocardial infarction
-» Death of heart muscle within 20 mins

31
Q

Describe Valve defects of the heart

A 
•	Valve defects:
1.	Regurgitation 
	Inadequate closure 
>> Backflow of blood 
    > Causes Turbulence
->> Followed -> Decr. cardiac output
2.	Stenosis
	 Inadequate opening 
>> Obstructs blood flow
    > Causes thickening of valve, papillary muscle / chordae tendiane 
       (following disease)
Eg. Rheumatic fever -> mitral valve stenosis up to 20yrs after infection.
32
Q

What are the two types of valve defect of the heart?

A
  1. Regurgitation

2. Stenosis

33
Q

Describe regurgitation valve defects of the heart

A 
1.	Regurgitation 
	Inadequate closure 
>> Backflow of blood 
    > Causes Turbulence
->> Followed -> Decr. cardiac output
34
Q

Describe stenosis valve defects of the heart

A
  1. Stenosis
     Inadequate opening
    » Obstructs blood flow
    > Causes thickening of valve, papillary muscle / chordae tendiane
    (following disease)
    Eg. Rheumatic fever -> mitral valve stenosis up to 20yrs after infection.
35
Q

Describe arrhythmias

A

• Arrhythmias:
 Deviation of heart’s normal sinus (SAN) rhythm.
 Relatively rare
-> 1 in 5000-10000
 Found -> young individuals ; <25yrs
 Many arise
-> Defects in ion channels regulating ventricular action potentials
 Cause spontaneous multiple depolarizations
&raquo_space; Ventricular arrythmias
 Produce sustained abnormal rhythm
 Asymptomatic
 Palpitations
 Dizziness
 Syncope
 Heart Failure
 Sudden Death
1. Bradycarida:
 Slow Rhythm (<60bpm)
Causes:
 Slowed signal -> sinus bradycardia
 Pause / sinus arrest
 Blockage
&raquo_space; Due to SAN / conducting tissue damage
Treatment:
 Artificial pacemaker

  1. Tachycardia:
     Fast Rhythm (>100bpm)
     Sinus Tachycardia
     Innapropriate Sinus Tachycardia (IST)
    Invlolves:
    » Caffeine
    » Amphetamines
    » Overactive thyroid gland -> SNS
     Non-sinus Tachycardia
    -> Addition of abnormal inpulses -> normal cycle
    > Uncontrolled twitching / quivering -> muscle fibres (fibrils)
    > Blood not removed from heart -> ventricular fibrillation
    > Sudden cardiac death
    Caused by:
    » Automaticicity (enhanced pacemaker)
    » Triggered Beats (Early / delayed depolarization)
    » Re-entry Activity / Circus Activity (Conduction profile defects)
    » Conduction Block
    »Heart Damage
                       Pathology: 
>> Congenital Heart Disease
>> Elecrocution Accidents
>> Heart Injury 
>> Cardiomyopathies
>> Heart Surgery 
>> Ischamia
                    Ectopic
                    Action potential initiated in cardiac myocyte
                    > Can lead to (mainly harmless) single premature beat
                     SNS &amp; hypoxia incr, automaticity.
36
Q

Describe the characteristics of heart arrhythmias

A

• Arrhythmias:
 Deviation of heart’s normal sinus (SAN) rhythm.
 Relatively rare
-> 1 in 5000-10000
 Found -> young individuals ; <25yrs
 Many arise
-> Defects in ion channels regulating ventricular action potentials
 Cause spontaneous multiple depolarizations
&raquo_space; Ventricular arrythmias
 Produce sustained abnormal rhythm

37
Q

Describe some of the symptoms associated with arrhythmias

A 
	Asymptomatic 
	Palpitations
	Dizziness
	Syncope
	Heart Failure 
	Sudden Death
38
Q

Describe the general way in which most arrhythmias arise

A

 Many arise
-> Defects in ion channels regulating ventricular action potentials
 Cause spontaneous multiple depolarizations
&raquo_space; Ventricular arrythmias
 Produce sustained abnormal rhythm

39
Q

Describe bradycardia

A 
1.	Bradycarida:
	Slow Rhythm (<60bpm)
Causes:
 Slowed signal -> sinus bradycardia
 Pause / sinus arrest 
 Blockage 
      >> Due to SAN / conducting tissue damage
Treatment:
 Artificial pacemaker
40
Q

What is bradycardia?

A

Heart arrhythmia -> slow rhythm (<60bpm)

41
Q

What is tachycardia?

A

Heart arrhythmia -> Fast Rhythm (>100bpm)

42
Q

What are the causes of bradycardia?

A 
Causes:
 Slowed signal -> sinus bradycardia
 Pause / sinus arrest 
 Blockage 
      >> Due to SAN / conducting tissue damage
43
Q

How is bradycardia treated?

A

Treatment:

 Artificial pacemaker

44
Q

Name the types of tachycardia

A
  1. Sinus Tachycardia
     Innapropriate Sinus Tachycardia (IST)
  2. Non-sinus Tachycardia
45
Q

Describe Sinus Tachycardia & what it involves

A 
	Sinus Tachycardia
 Innapropriate Sinus Tachycardia (IST)
Invlolves:
>> Caffeine
>> Amphetamines
>> Overactive thyroid gland -> SNS
46
Q

Describe Non-sinus Tachycardia

A

 Non-sinus Tachycardia
-> Addition of abnormal inpulses -> normal cycle
> Uncontrolled twitching / quivering -> muscle fibres (fibrils)
> Blood not removed from heart -> ventricular fibrillation
> Sudden cardiac death
Caused by:
» Automaticicity (enhanced pacemaker)
» Triggered Beats (Early / delayed depolarization)
» Re-entry Activity / Circus Activity (Conduction profile defects)
» Conduction Block
»Heart Damage

                       Pathology: 
>> Congenital Heart Disease
>> Elecrocution Accidents
>> Heart Injury 
>> Cardiomyopathies
>> Heart Surgery 
>> Ischamia
                    Ectopic
                    Action potential initiated in cardiac myocyte
                    > Can lead to (mainly harmless) single premature beat
                     SNS &amp; hypoxia incr, automaticity.
47
Q

What are the characteristics of Non-sinus tachycardia?

A

 Non-sinus Tachycardia
-> Addition of abnormal inpulses -> normal cycle
> Uncontrolled twitching / quivering -> muscle fibres (fibrils)
> Blood not removed from heart -> ventricular fibrillation
> Sudden cardiac death

48
Q

What internal processes of the body is Non-sinus Tachycardia caused by?

A

Caused by:
» Automaticicity (enhanced pacemaker)
» Triggered Beats (Early / delayed depolarization)
» Re-entry Activity / Circus Activity (Conduction profile defects)
» Conduction Block
»Heart Damage

49
Q

What are pathological causes of arrhythmias

A 
Pathology: 
>> Congenital Heart Disease
>> Elecrocution Accidents
>> Heart Injury 
>> Cardiomyopathies
>> Heart Surgery 
>> Ischamia
50
Q

What does ectopic mean, and what can it cause?

A

 Ectopic
Action potential initiated in cardiac myocyte
> Can lead to (mainly harmless) single premature beat
SNS & hypoxia incr, automaticity.

51
Q

Describe Chronic Heart Failure

A

• Chronic Heart Failure:
 Inadequate cardiac output
-> Despite venous return
 Due to:
Decline in contractility
Inability to develop forceful contracture
 Diastole:
> Inability to fill
-> Stiff, thick chambers
 Systole:
> Inability to contract
-> Stretched, thin chambers
 Caused by:
> Muscle damage Eg. CAD
> Additional work of heart Eg. Hypertension
> Valve defects
 Causes:
> Breathlessness & fatigue
> Left Ventricular Failure:
-> Fluid accumulation -> lungs due to congestion of veins in lungs
> Right Ventricular Failure:
-> Fluid accumulation -> especially in tissues of legs & abdominal organs due
to incr. systemic capillary pressure.

52
Q

What is Chronic heart failure?

A

• Chronic Heart Failure:
 Inadequate cardiac output
-> Despite venous return

53
Q

What cardiac issues lead to chronic heart failure?

A

 Due to:
Decline in contractility
Inability to develop forceful contracture

54
Q

Describe diastole & systole of the heart during Chronic Heart Failure

A

 Diastole:
> Inability to fill
-> Stiff, thick chambers
 Insufficient blood causes overworking of heart
&raquo_space; Leads to stretching of heart muscle over time
Stretched thin chambers -> insufficient generation of force on contraction
 Systole:
> Inability to contract
-> Stretched, thin chambers

55
Q

What is chronic heart failure caused by?

A

 Caused by:
> Muscle damage Eg. CAD
> Additional work of heart Eg. Hypertension
> Valve defects

56
Q

What is caused as a result of chronic heart failure?

A

 Causes:
> Breathlessness & fatigue
> Left Ventricular Failure:
-> Fluid accumulation -> lungs due to congestion of veins in lungs
> Right Ventricular Failure:
-> Fluid accumulation -> especially in tissues of legs & abdominal organs due
to incr. systemic capillary pressure.

57
Q

Describe why left ventricular failure occurs

A

> Left Ventricular Failure:

-> Fluid accumulation -> lungs due to congestion of veins in lungs

58
Q

Describe why right ventricular failure occurs

A

> Right Ventricular Failure:
-> Fluid accumulation -> especially in tissues of legs & abdominal organs due
to incr. systemic capillary pressure.

59
Q

What does digitalis glycosides cause in relation to the heart?

A

• Digitalis Glycosides
> Incr. force of contraction
> Decreased vagal conduction

60
Q

Describe aortic disease

A

• Aortic Disease:
 Aortic aneurysm
 Weakening of aortal wall
» Bulges outwards

61
Q

How does a stroke occur?

A

• Stroke:

 Occurs as result of blockage -> blood supply to part of brain.

62
Q

Describe the cause of coronary heart disease?

A

• Coronary Heart Disease:
 Reduced flow / Blockage -> Oxygen rich blood to heart
» Atheroma (fatty material) accumulation -> coronary arteries

63
Q

What is a common symptom of peripheral arterial disease?

A

• Peripheral arterial disease:

 Common symptom -> leg pain while walking.

Body Systems Y1 (22 decks)

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