Brainscape's Knowledge GenomeTM

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


See full index

BMS3052 > Cardiovascular Disease > Flashcards

Cardiovascular Disease Flashcards

1
Q

Define

Ischaemic Stroke

A

Stroke caused by occlusion of a blood vessel by thrombus

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

Define

Cerebral ischaemia

A

a flow of blood to the brain that is insufficient to meet its metabolic demands, leading to loss of function and cell death

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

Define

Thrombus

A

a blood clot formed in situ within the vascular system of the body and impeding blood flow

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

Define

Embolic ischaemic stroke

A

Stroke cause by embolism in body that travels to the brain

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

Define

Thrombotic ischaemic stroke

A

Stroke caused by a thrombus growing and eventually blocking a blood vessel

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

Define

Haemorrhagic stroke

A

Stroke caused by the rupture of a blood vessel

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

Define

Subarachnoid haemorrhagic stroke

A

Stroke caused by bleeding in the space around the brain

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

Define

Intracerebral haemorrhagic stroke

A

Stroke caused by bleeding in the brain tissue itself

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

Define

Tissue plasminogen activator (tPA)/clot buster

A

a protein involved in the breakdown of blood clots

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Define

Mechanical thrombectomy

A

the interventional procedure of removing a blood clot (thrombus) from a blood vessel

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

Define

Reperfusion

A

the action of restoring the flow of blood to an organ or tissue, typically after a heart attack or stroke.

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

Define

Cortical infarct

A

a small localized area of dead tissue involving the cortical gray matter resulting from failure of blood supply

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

Define

Bregma position

A

the anatomical point on the skull at which the coronal suture is intersected perpendicularly by the sagittal suture

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

Define

Excitotoxicity

A

the pathological process by which neurons are damaged and killed by the overactivations of receptors for the excitatory neurotransmitter glutamate, such as the NMDA receptor and AMPA receptor

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

Define

Amnion Epithelial Cells (hAEC)

A

a subset of placental-derived stem cells that display plasticity and immunomodulation, and possess advantages over the other populations of stem cell-like cells in the placental tissues

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

Define

Stem cell-derived exosomes

A

nano-sized vesicle secreted from cells that contains any of various biomolecules, such as proteins or nucleic acids

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

Definition

Stroke caused by occlusion of a blood vessel by thrombus

A

Ischaemic Stroke

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

Definition

a flow of blood to the brain that is insufficient to meet its metabolic demands, leading to loss of function and cell death

A

Cerebral ischaemia

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

Definition

a blood clot formed in situ within the vascular system of the body and impeding blood flow

A

Thrombus

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

Definition

Stroke cause by embolism in body that travels to the brain

A

Embolic ischaemic stroke

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

Definition

Stroke caused by a thrombus growing and eventually blocking a blood vessel

A

Thrombotic ischaemic stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Definition

Stroke caused by the rupture of a blood vessel

A

Haemorrhagic stroke

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

Definition

Stroke caused by bleeding in the space around the brain

A

Subarachnoid haemorrhagic stroke

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

Definition

Stroke caused by bleeding in the brain tissue itself

A

Intracerebral haemorrhagic stroke

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

Definition

a protein involved in the breakdown of blood clots

A

Tissue plasminogen activator (tPA)/clot buster

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

Definition

the interventional procedure of removing a blood clot (thrombus) from a blood vessel

A

Mechanical thrombectomy

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

Definition

the action of restoring the flow of blood to an organ or tissue, typically after a heart attack or stroke.

A

Reperfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Definition

a small localized area of dead tissue involving the cortical gray matter resulting from failure of blood supply

A

Cortical infarct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Definition

the anatomical point on the skull at which the coronal suture is intersected perpendicularly by the sagittal suture

A

Bregma position

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

Definition

the pathological process by which neurons are damaged and killed by the overactivations of receptors for the excitatory neurotransmitter glutamate, such as the NMDA receptor and AMPA receptor

A

Excitotoxicity

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

Definition

a subset of placental-derived stem cells that display plasticity and immunomodulation, and possess advantages over the other populations of stem cell-like cells in the placental tissues

A

Amnion Epithelial Cells (hAEC)

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

Definition

nano-sized vesicle secreted from cells that contains any of various biomolecules, such as proteins or nucleic acids

A

Stem cell-derived exosomes

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

Approximately how many strokes occur in Australia per year?

A

~60,000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

True or False:

Stroke is Australia’s fifth leading cause of death

A

False

Stroke is Australia’s third leading cause of death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What age bracket do 50% of strokes occur in?

A

45-75 years old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Are men or women more likely to die after a stroke?

A

Women are morelikely to die after a stroke than men

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

True or False:

More women die from stroke than from breast cancer

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Do men or women suffer more strokes?

A

Men

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

True or False:

Stroke is considered a cardiovascular disease

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

True or False:

Stroke is the worst disease in Australia in terms of suffering and cost

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What proportion of people who suffer a stroke die, become dependent and recover?

A

Death: 1/3

Dependency: 1/3

Recovery: 1/3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What percentage of stroke sufferers experience a recurrent stroke?

A

10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Lack of what molecules/nutrients cause neuronal cell death during a stroke?

A

Oxygen

Glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Which important molecule is strangely not stored in the brain?

A

Glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the two main types of stroke?

A

Ischaemic stroke

Haemorrhagic stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are the two types of Ischaemic stroke?

A

Embolic

Thrombotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the two types of haemorrhagic stroke?

A

Subarachnoid

Intracerebral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is the most common major type of stroke?

A

Ischaemic (~85%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the five biggest risk factors for ischaemic stroke?

A

Hypertension

Atrial fibrilation

Smoking

Diabetes

Age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

True or False:

Hypertension is more likely to cause a heart attack than a stroke

A

False

Hypertension is more likely to cause a stroke than a heart attack

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Why is time so critical in treating stroke?

A

Approximately 2 million neurons die every minute that a person is suffering a stroke and the average person will suffer a stroke for several hours resulting in significant neurological damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is the current treatment plan for Ischaemic stroke?

A
  1. Diagnose stroke type (MRI, CT scan)
  2. If stroke is ischaemic and occured under 4.5 hours ago, clot buster enzyme (tPA) will be injected (only 2-8% of patients satisfy this)
  3. High blood pressure treated
  4. Anticoagulants, antiplatelet drugs to thin the blood - if ischaemic)
  5. Osmotic agents (and elevate head) - if haemorrhagic
  6. Physiotherapy, speech therapy - ASAP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the only therapy currently available for stroke?

A

Clot buster enzyme (tPA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Why is it important to treat high blood pressure after a stroke has occurred?

A

To prevent subsequent strokes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

After 4.5 hours, what drugs are used to prevent further damage in ischaemic and haemorrhagic stroke?

A

Ischaemic - Anticoagulants and antiplatelt drugs to thin the blood

Haemorrhagic - Osmostic agents (& elevation of head)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

When is clot buster (tPA) given to a patient?

A

When a CT scan indicates an ischaemic stroke and it is within 4.5 hours of onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Why isn’t clot buster (tPA) given to patients after 4.5 hours of stroke onset?

A

Increased risk of haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Why are people who have a stroke overnight often ineligible for tPA?

A

We often cannot be sure that the stroke begun within 4.5 hours prior to hospital presentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What percentage of people who receive tPA benefit?

A

30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is the name of the procedure that involves physically removing a clot?

A

Mechanical thrombectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Mechanical thrombectomy is only performed in patients with occlusion of which vessels?

A

Large cerebral artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

When can a mechanical thrombectomy be performed?

A

Within 24 hours of stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Will patients eligible for tPA receive the tPA or mechanical thrombectomy first?

A

tPA first (unless contraindicated)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Why is mechanical thrombectomy only performed in patients with occlusion of large cerebral artery?

A

The stent can’t get into small vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

How can hypothermia be used to manage stroke?

A

Hypothermia slows cellular processes, decreasing neuronal death and the size of the infarct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Why have patients own bone marrow stem cells shown more promise than neural stem cells in overcoming stroke damage?

A

Using the patients own stem cells ensures that the cells won’t be targetted by the host immune system. The bone marrow stem cells adminstered via IV release a cocktail of chemicals into the blood which trigger growth and repair of neurons in the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What are the drawbacks of using stem cell therapy to treat stroke damage?

A

It takes a long time to prepare and administer stem cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Stroke causes most neurons to die via which process? Why don’t we focus on this process in research?

A

Most cells die due to excitotoxicity that occurs in the first few hours. However, since most patients don’t present to the hospital until hours after onset so most current research focuses on the subsequent neuroinflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Approximately what percentage of neurons die due to neuroinflammation?

A

30-40%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is the main mechanism by which hAECs may improve stroke outcome?

A

Immunomodulatory properties since this process occurs in the first few days following stroke

  • Decreasing immune cells infiltrating the brain
  • Decreasing cerebral infarct damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are the potential consequneces of hAEC IV administration?

A

Stem cells can clump during IV administration and get stuck in lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

How do we overcome the limitations of hAEC IV administration?

A

Isolated stem cell-derived exosomes which contain the cocktail of repair chemicals which are able to pass through the lungs and blood-brain barrier without issue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Why are stem cell-derived exosomes more promising for improving stroke outcomes than regular stem cells?

A
  • They are able to pass through lungs and BBB
  • Can inject higher dose
  • Ready to inject within minutes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Define

Abdominal aortic aneurysm

A

an enlarged area in the lower part of the major vessel that supplies blood to the body (aorta)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Define

Aneurysm

A

an excessive localized swelling of the wall of an artery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Define

Apo B-100

A

a protein that plays a role in moving cholesterol around your body. It is a form of low density lipoprotein (LDL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Define

Apo-A-I

A

a structural and functional protein that constitutes approximately 70% of the protein in high density lipoprotein (HDL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Define

Apoprotein

A

a protein which together with a prosthetic group forms a particular biochemical molecule such as a hormone or enzyme.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Define

Astrocytosis

A

an abnormal increase in the number of astrocytes due to the destruction of nearby neurons from central nervous system (CNS) trauma, infection, ischemia, stroke, autoimmune responses or neurodegenerative disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Define

Atherosclerosis

A

a disease of the arteries characterized by the deposition of fatty material on their inner walls.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Define

Autologous blood injection model

A

involves drawing a small volume of venous blood from the patient and re-injecting this in and around the tendon origin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Define

Axonal sprouting

A

a process where fine nerve processes – sprouts – grow out from the intact axons to reinnervate denervated muscle fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Define

C-reactive protein (CRP)

A

a protein made by your liver. It’s sent into your bloodstream in response to inflammation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Define

Cerebral aneurysm

A

a bulging, weakened area in the wall of an artery in the brain, resulting in an abnormal widening, ballooning, or bleb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Define

Cholesterol

A

a compound of the sterol type found in most body tissues. This molecule and its derivatives are important constituents of cell membranes and precursors of other steroid compounds, but a high proportion in the blood of low-density lipoprotein (which transports cholesterol to the tissues) is associated with an increased risk of coronary heart disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Define

Chylomicrons

A

a droplet of fat present in the blood or lymph after absorption from the small intestine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Define

Congenital aneurysm

A

a weakness in the blood vessel wall that is present from birth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Define

Dissecting aneurysm

A

An aneurysm in which the wall of an artery rips longitudinally. This occurs because bleeding into the weakened wall splits the wall.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Define

Endothelin

A

peptides with receptors and effects in many body organs. They constricts blood vessels and raises blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Define

Endovascular coiling

A

a minimally invasive technique where a catheter is passed through the groin up into the artery containing the aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Define

Familial hypercholesterolaemia

A

a common life-threatening genetic condition that causes high cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Define

Foam cells

A

a type of macrophage that localize to fatty deposits on blood vessel walls, where they ingest low-density lipoproteins and become laden with lipids, giving them a foamy appearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Define

Fusiform aneurysm

A

a type of aneurysm that bulges or balloons out on all sides of the blood vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Define

Giant aneurysm

A

aneurysms greater than 25 mm in diameter14 and represent 5% of all intracranial aneurysms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Define

High density lipoproteins (HDL)

A

lipoprotein of blood plasma that is composed of a high proportion of protein with little triglyceride and cholesterol and that is correlated with reduced risk of atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Define

Hyperlipidaemia

A

the presence of excess fat or lipids in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Define

Ischemic penumbra

A

tissue surrounding an ischemic event that is ischemic but still viable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Define

LDL receptor

A

a mosaic protein of 839 amino acids that mediates the endocytosis of cholesterol-rich LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Define

Lipoproteins

A

any of a group of soluble proteins that combine with and transport fat or other lipids in the blood plasma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Define

Low density lipoproteins (LDL)

A

a lipoprotein of blood plasma that is composed of a moderate proportion of protein with little triglyceride and a high proportion of cholesterol and that is associated with increased probability of developing atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Define

Lp(a)

A

a low-density lipoprotein variant containing a protein called apolipoprotein(a).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Define

Mannitol

A

an osmotic agent used to lower intracranial pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Define

PCSK9 inhibitors

A

a new class of drugs that lower LDL, or “bad,” cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Define

Photothrombotic stroke

A

aims to induce an ischemic damage within a given cortical area by means of photo-activation of a previously injected light-sensitive dye. Following illumination, the dye is activated and produces singlet oxygen that damages components of endothelial cell membranes, with subsequent platelet aggregation and thrombi formation, which eventually determines the interruption of local blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Define

Plasminogen

A

the zymogen of plasmin, the major enzyme that degrades fibrin clots

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Define

Reverse cholesterol transport

A

a multi-step process resulting in the net movement of cholesterol from peripheral tissues back to the liver first via entering the lymphatic system, then the bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Define

Saccular aneurysm

A

the most common type of brain aneurysm. They have a “neck” that connects the aneurysm to its main (“parent”) artery and a larger, rounded area called the dome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Define

Statins

A

a class of lipid-lowering medications that reduce illness and mortality in those who are at high risk of cardiovascular disease. They are the most common cholesterol-lowering drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Define

Subarachnoid hemorrhage

A

bleeding within the subarachnoid space, which is the area between the brain and the tissues that cover the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Define

Surgical clipping

A

to isolate an aneurysm from the normal circulation without blocking off any small perforating arteries nearby

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Define

Thoracic aortic aneurysm

A

an aortic aneurysm that presents primarily in the thorax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Define

Venous thrombosis

A

a blood clot that starts in a vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Define

Very low density lipoproteins (VLDL)

A

cholesterol that is produced in the liver and released into the bloodstream to supply body tissues with a type of fat (triglycerides)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Definition

an enlarged area in the lower part of the major vessel that supplies blood to the body (aorta)

A

Abdominal aortic aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Definition

an excessive localized swelling of the wall of an artery.

A

Aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Definition

a protein that plays a role in moving cholesterol around your body. It is a form of low density lipoprotein (LDL)

A

Apo B-100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Definition

a structural and functional protein that constitutes approximately 70% of the protein in high density lipoprotein (HDL)

A

Apo-A-I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Definition

a protein which together with a prosthetic group forms a particular biochemical molecule such as a hormone or enzyme.

A

Apoprotein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Definition

an abnormal increase in the number of astrocytes due to the destruction of nearby neurons from central nervous system (CNS) trauma, infection, ischemia, stroke, autoimmune responses or neurodegenerative disease

A

Astrocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Definition

a disease of the arteries characterized by the deposition of fatty material on their inner walls.

A

Atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Definition

involves drawing a small volume of venous blood from the patient and re-injecting this in and around the tendon origin

A

Autologous blood injection model

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Definition

a process where fine nerve processes – sprouts – grow out from the intact axons to reinnervate denervated muscle fibers

A

Axonal sprouting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Definition

a protein made by your liver. It’s sent into your bloodstream in response to inflammation.

A

C-reactive protein (CRP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Definition

a bulging, weakened area in the wall of an artery in the brain, resulting in an abnormal widening, ballooning, or bleb

A

Cerebral aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Definition

a compound of the sterol type found in most body tissues. This molecule and its derivatives are important constituents of cell membranes and precursors of other steroid compounds, but a high proportion in the blood of low-density lipoprotein (which transports cholesterol to the tissues) is associated with an increased risk of coronary heart disease.

A

Cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Definition

a droplet of fat present in the blood or lymph after absorption from the small intestine.

A

Chylomicrons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Definition

a weakness in the blood vessel wall that is present from birth

A

Congenital aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Definition

An aneurysm in which the wall of an artery rips longitudinally. This occurs because bleeding into the weakened wall splits the wall.

A

Dissecting aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Definition

peptides with receptors and effects in many body organs. They constricts blood vessels and raises blood pressure

A

Endothelin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Definition

a minimally invasive technique where a catheter is passed through the groin up into the artery containing the aneurysm

A

Endovascular coiling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Definition

a common life-threatening genetic condition that causes high cholesterol

A

Familial hypercholesterolaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Definition

a type of macrophage that localize to fatty deposits on blood vessel walls, where they ingest low-density lipoproteins and become laden with lipids, giving them a foamy appearance

A

Foam cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Definition

a type of aneurysm that bulges or balloons out on all sides of the blood vessel

A

Fusiform aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Definition

aneurysms greater than 25 mm in diameter14 and represent 5% of all intracranial aneurysms

A

Giant aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Definition

lipoprotein of blood plasma that is composed of a high proportion of protein with little triglyceride and cholesterol and that is correlated with reduced risk of atherosclerosis

A

High density lipoproteins (HDL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Definition

the presence of excess fat or lipids in the blood

A

Hyperlipidaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Definition

tissue surrounding an ischemic event that is ischemic but still viable

A

Ischemic penumbra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

Definition

a mosaic protein of 839 amino acids that mediates the endocytosis of cholesterol-rich LDL

A

LDL receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

Definition

any of a group of soluble proteins that combine with and transport fat or other lipids in the blood plasma.

A

Lipoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

Definition

a lipoprotein of blood plasma that is composed of a moderate proportion of protein with little triglyceride and a high proportion of cholesterol and that is associated with increased probability of developing atherosclerosis

A

Low density lipoproteins (LDL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

Definition

a low-density lipoprotein variant containing a protein called apolipoprotein(a).

A

Lp(a)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

Definition

an osmotic agent used to lower intracranial pressure

A

Mannitol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

Definition

a new class of drugs that lower LDL, or “bad,” cholesterol

A

PCSK9 inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

Definition

aims to induce an ischemic damage within a given cortical area by means of photo-activation of a previously injected light-sensitive dye. Following illumination, the dye is activated and produces singlet oxygen that damages components of endothelial cell membranes, with subsequent platelet aggregation and thrombi formation, which eventually determines the interruption of local blood flow

A

Photothrombotic stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

Definition

the zymogen of plasmin, the major enzyme that degrades fibrin clots

A

Plasminogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

Definition

a multi-step process resulting in the net movement of cholesterol from peripheral tissues back to the liver first via entering the lymphatic system, then the bloodstream

A

Reverse cholesterol transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

Definition

the most common type of brain aneurysm. They have a “neck” that connects the aneurysm to its main (“parent”) artery and a larger, rounded area called the dome

A

Saccular aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

Definition

a class of lipid-lowering medications that reduce illness and mortality in those who are at high risk of cardiovascular disease. They are the most common cholesterol-lowering drugs

A

Statins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

Definition

bleeding within the subarachnoid space, which is the area between the brain and the tissues that cover the brain

A

Subarachnoid hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

Definition

to isolate an aneurysm from the normal circulation without blocking off any small perforating arteries nearby

A

Surgical clipping

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

Definition

an aortic aneurysm that presents primarily in the thorax

A

Thoracic aortic aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

Definition

a blood clot that starts in a vein

A

Venous thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

Definition

cholesterol that is produced in the liver and released into the bloodstream to supply body tissues with a type of fat (triglycerides)

A

Very low density lipoproteins (VLDL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

What are the most common areas for an aneurysm to form?

A

Along the aorta and in the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

What causes an aneurysm?

A
  • a weakness in the blood vessel wall that is present from birth (congenital aneurysm)
  • High blood pressure (hypertension) - weakening of blood vessels
  • Previous aneurysm: increased likelihood to have another.
  • Race: African Americans are more likely than Caucasians to have a subarachnoid hemorrhage.
  • Fatty plaques (atherosclerosis) resulting in a weakness of the blood vessel wall
  • Inherited diseases that may result in weaker than normal blood vessel walls
  • Gender. Women are more likely to develop a brain aneurysm or to suffer a subarachnoid hemorrhage.
  • Trauma, such as a crush injury to the chest
  • The sexually transmitted infection (STI) syphilis, if untreated, targeting the aorta and weakening its walls
  • Polycystic kidney disease increasing the risk of cerebral aneurysm
  • Very occasionally, an infection targeting and weakening a section of blood vessel.
  • The cause sometimes remains unknown.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

What is the current theory on why women are more likely to develop a brain aneurysm?

A

Oestrogen is protective in the cardiovascular system so when women have a dramatic drop in oestrogen following menopause they are at higher risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

What are the three main types (location) of aneurysms?

A

Cerebral aneurysm

Thoracic aortic aneurysm

Abdomincal aortic aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

What are the symptoms of an unruptured cerebral aneurysm?

A

An unruptured cerebral aneurysm may have no symptoms related to it at all and may be discovered incidentally.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

What are the symptoms of an ruptured cerebral aneurysm?

A

Symptoms of a ruptured cerebral aneurysm include severe headache with rapid onset, neck pain and stiffness, increasing drowsiness, paralysis, seizures, impaired speech and visual problems.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

What is the most common type of cerebral aneurysm?

A

Saccular (80-90%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

What is the fatality and disability rate of rupture cerebral aneurysms?

A

Ruptured brain aneurysms are fatal in about 40% of cases. Of those who survive, about 66% suffer some permanent neurological deficit.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

What age range are brain aneurysms most prevalent?

A

35-60

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

What are the four main types (shape) of aneurysms?

A

Saccular

Fusiform

Giant

Dissencting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

What type is this aneurysm?

A

Saccular aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

What type is this aneurysm?

A

Fusiform aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

What percentage of aneurysms do not rupture during the course of a person’s lifespan?

A

50-80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

What is the most damaging type of aneurysm?

A

Dissecting aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

How does a dissecting aneurysm occur?

A
  • The wall of an artery rips (dissects) longitudinally
  • Occurs because bleeding into the weakened wall splits the wall.
  • Creates a false lumen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

The prevalence of AA sharply increases with increasing _____

A

The prevalence of AA sharply increases with increasing age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

What is the mortality rate of an aortic aneurysm rupture?

A

~80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

Surgical repair of ruptured AA has a mortality of around ___%.

A

Surgical repair of ruptured AA has a mortality of around 50%.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

What things should be considered when deciding whether or not to treat an unruptured aneurysm?

A
  • Risk of Hemorrhage—Is it probable or not that the aneurysm will rupture?
  • Size and Location
  • Age and Health of Patient
  • Family History—Is there a family history? Have any of those aneurysms ruptured?
  • Surgical Risks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

What are the two types of surgical treatments of unruptured aneurysms?

A

Surgical clipping

Endovascular coiling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

What drug is used as an osmotic agent following haemorragic stroke?

A

Mannitol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

What is Mannitol used for strokes?

A

Used to reduce edema, intracranial pressure following haemorrhagic stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

How does Mannitol reduce intracranial pressure?

A
  • Used to raise the serum osmolarity
  • Plasma osmotic pressure is increased relative to cerebrospinal fluid.
  • Causes an increase in osmotic pressure in the serum and water follows from tissue into blood.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

What are the adverse effects of Mannitol?

A
  • About 10% of patients will develop edema
  • Can be very dangerous depending on site in brain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

Why do 10% of patients given Mannitol develop edema, the very condition Mannitol is used to treat?

A

If the vessels or BBB are leaky, the Mannitol will get into the brain tissue causing fluid to follow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

Why is one animal model for stroke not enough?

A

Mimicking all aspects of human stroke in one animal model is not feasible because stroke in humans is a heterogeneous disorder with a complex pathophysiology.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

Which animal models are used for ischaemic stroke?

A

Middle cerebral artery occlusion

Photothrombotic stroke

Endothelin-1 stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

Which animal models are used for haemorragic stroke?

A

Autologous blood injection

Endovascular puncture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

What are the pros and cons of middle cerebral artery occlusion as an animal model?

A

Pros:

  • Mimics human stroke ie MCAO
  • Reperfusion and duration is controlled
  • Blood flow is measured
  • Most common mode

Cons:

  • Variable infarct damage
  • Invasive surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

What are the pros and cons of photothrombotic stroke?

A

Pros:

  • Induces a thrombus
  • Minimal surgical intervention
  • Highly reproducible infarct damage

Cons:

  • Little or no ischemic penumbra (unlike humans)
  • Unable to measure blood flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

How does the middle cerebral artery occlusion animal model work?

A

A silicone-coated filament is inserted into the external carotid artery and pushed up into the brain until the laser doppler probe indicates a drop in blood flow meaning the filament is blocking the middle cerebral artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

How does a photothrombotic stroke work?

A

A photosensitive dye is administered to the animal. The skin covering the skull is removed and a bright light is positioned over the skull. The light and dye cause free radical formation which damages endothelial cells leading to platelet aggregation and subsequent clots

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

What are the pros and cons of the endothelin model?

A

Pros:

  • Conscious model of stroke
  • Reproducible infarct damage
  • Low mortality

Cons:

  • Induces astrocytosis and facilitates axonal sprouting
  • Unable to measure blood flow changes
  • Lacks BBB breakdown
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

What are the pros and cons of the autologous blood injection model?

A

Pros:

  • Blood is injected into the striatum to establish a haemtoma
  • Widely used model
  • Good reproducibility and relevant to ICH patients

Cons:

  • Does not simulate blood vessel rupture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

What are the pros and cons of the endovascular puncture model?

A

Pros:

  • Closely mimics SAH in the clinic
  • Blood flow can be measured

Cons:

  • Invasive surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

How does the endovascular puncture model work?

A

Similar to the middle cerebral artery occlusion model except the filament punctures the blood vessel causing a bleed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
Q

How is fat transported around the cardiovascular system?

A

As a lipoprotein

Lipid (hydrophobic core) and apoprotein (hydrophillic coat)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

What are the four main types (in decreasing size) of lipoprotein?

A

Chylomicrons

VLDL

LDL

HDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
193
Q

What ligand does VLDL and LDL have that allows LDL reuptake?

A

Apo B-100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
194
Q

True or False:

Due to size VLDL, but not LDL, can easily penetrate the vascular endothelium

A

False

Due to size LDL, but not VLDL, can easily penetrate the vascular endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
195
Q

Which molecule is Lp(a) similar to and competes with?

A

Plasminogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
196
Q

What is the exogenous pathway of lipoprotein transport in the blood?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
197
Q

What is the endogenous pathway of lipoprotein transport?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
198
Q

Which cells synthesise LDL receptors?

A

Liver and vascular smooth muscle cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
199
Q

How does the immune system impact atherosclerosis?

A

Vascular inflammation drive atherosclerosis

  1. Vascular cholesterol uptake by LDL receptors
    • Excess LDL infiltrates artery
    • Oxidised LDL induces adhesion molecule expression on endothelium
    • Oxidised LDL phagocytosed by macrophages (now called foam cells)
  2. Monocyte recruitment into arterial wall
    • Adhesion molecules facilitate entry
    • Differentiate into macrophages
    • Macrophages release mediators creating inflammatory milieu
  3. Inflamm/immune cell surveillance
    • T cells infiltrate….
    • Activated T cells produce Th1cytokines e.g. IFNγ, IL-1β, IL-6, TNF
    • Amplification of vascular inflammation
    • T regs oppose, release IL-10, TGF-β
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
200
Q

What is the main vascular and circuating inflammatory biomarkers of atherosclerosis?

A

C-reactive protein (CRP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
201
Q

Why is CRP a good biomarker for atherosclerosis?

A
  • Acute phase protein synthesised in liver
  • Stimulated by IL-6 from inflamm cells
  • Binds to surface of dying cells; promotes phagocytosis
  • Predictive of inflammation/CVD
  • Informs on statin therapy
202
Q

Describe the steps from a healthy epithelium to a ruptured fibrous cap seen in atherosclerosis

A
203
Q

What make up fatty streaks?

A

Oxidised LDL taken up by macrophages, known as foam cells

204
Q

Why do fibrous caps form?

A

Formation of fibrous cap trying to stabilise underlying lipid core

205
Q

How does inflammatory signalling affect the collagen cap?

A

↓ collagen synthesis (T cell driven)

↑ degradation due to MMP released from macrophages

↑ tissue factor released from macrophages (thrombosis potential)

206
Q

What are the chronic drug treatments for atherosclerosis?

A

Reduce lipid/plaque/inflamm burden

  • Lipid-lowering drugs e.g. Statins, new drugs
  • Anti-platelets
  • Anti-coagulants (not covered here- phew!)
207
Q

What happens to cholesterol hepatic synthesis and LDL-R transcription as intracellulat cholesterol levels increase?

A

They both decrease

208
Q

How are hyperlipidaemias treated?

A
  • consider CV status and risk factors
  • secondary to other disease?
    • treat disease first- eg diabetes, hypertension
  • dietary / lifestyle modification BEFORE any drug treatment

Rationale:

  • reduce progression of atherosclerosis and improve survival in patients with established CV disease
  • reduce premature cardiac morbidity and mortality in people at high risk of CV disease
209
Q

What are the two major drug types for treating hypercholesterolemia?

A

Statins

PCSK9 inhibitors

210
Q

Which enzyme do statins target?

A

HMG-CoA reductase

Resposible for the rate limiting step in cholesterol synthesis where HMG-CoA is converted to cholesterol

211
Q

What is the mode of action of statins?

A
  • block cholesterol synthesis in liver (competitive enzyme inhibitor)
  • reduces endogenous cholesterol in hepatocytes which promotes increased expression of LDL receptors on hepatocytes (i.e. disrupt feedback regulation)
  • Leads to increased LDL plasma clearance
  • Many effects unrelated to ↓LDL such as improved endothelial function, plaque stabilisation
  • Lipoprotein profile: ↓↓LDL, ↓TG, HDL
212
Q

What are the clinical uses of statins?

A
  • primary prevention cardiovascular disease (high risk with elevated cholesterol)
  • High risk CHD (with/without elevated chol)
  • secondary prevention of myocardial infarction & stroke (symptomatic)
213
Q

What are the potential side-effects of statins?

A

GI disturbance

diabetes risk

Memory loss (reversible)

214
Q

What can CRP levels tell us about a patients response to statins?

A

Patients who have low CRP levels after statin therapy have better clinical outcomes

215
Q

What is PCSK9?

A

circulating serine protease (enzyme) that binds to LDL rec; facilitates lysosomal degradation → LDL rec recycling to cell surface

reduces LDL clearance; elevating circulating LDL

216
Q

What molecules are used to inhibit PCSK9?

A

Antibodies

217
Q

How do statins upregulate LDL receptors and LDL clearance?

A

By inhibiting HMG-CoA reductase and decreasing intracellular cholesterol

218
Q

Without ________ attached, the LDL receptor is recycled to the cell surface, and can continue to clear LDL particles

A

Without PCSK9 attached, the LDL receptor is recycled to the cell surface, and can continue to clear LDL particles

219
Q

How does PCSK9 prevent recycling of LDL receptors?

A

PCSK9 ‘tags’ LDL receptor, resulting in its degradation in the lysosome

220
Q

What are the downsides of PCSK9 inhibitors?

A

Can’t be administered orally (injections only)

Expensive

221
Q

Define

Allocative efficiency

A

an output level where the Price equals the Marginal Cost (MC) of production. Concerned with efficient distribution of available resources and potential opportunity costs.

222
Q

Define

Technical efficiency

A

the effectiveness with which a given set of inputs is used to produce an output. Looks at efficient management of single condition and considers cost-effectiveness

223
Q

Define

Cost-benefit analysis

A

a systematic approach to estimating the strengths and weaknesses of alternatives used to determine options which provide the best approach to achieving benefits while preserving savings. Does not consider the potential health benefits

224
Q

Define

Cost-effectiveness analysis

A

a form of analysis that compares the relative costs and outcomes (effects) of different courses of action.

225
Q

Define

Cost-utility analysis

A

a form of analysis used to guide procurement decisions. Net costs/net change in QALYs

226
Q

Define

Quality-Adjusted Life Year (QALY)

A

a generic measure of disease burden, including both the quality and the quantity of life lived

227
Q

Define

Dominated intervention

A

When a new intervention is both clinically inferior and increases costs

228
Q

Define

Dominant intervention

A

When a new intervention is both clinically superior and cost saving

229
Q

Define

Angina

A

chest pain or discomfort caused when your heart muscle doesn’t get enough oxygen-rich blood

230
Q

Define

Coronary heart disease (CHD)

A

occurs when a coronary artery clogs and narrows because of a buildup of plaque overtime

231
Q

Define

Acute coronary syndrome (ACS)

A

a term used to describe a range of conditions associated with sudden, reduced blood flow to the heart

232
Q

Define

Acute mycardial infarction (AMI)

A

the medical name for a heart attack.

233
Q

Define

Troponin

A

a group of proteins found in skeletal and heart (cardiac) muscle fibers that regulate muscular contraction. Acts as a biomarker to help detect heart injury

234
Q

Define

Stable angina

A

when a person has brief episodes of pain, squeezing, pressure, or tightness in the chest

235
Q

Define

Heart failure

A

occurs when your heart muscle doesn’t pump blood as well as it should. Certain conditions, such as narrowed arteries in your heart (coronary artery disease) or high blood pressure, gradually leave your heart too weak or stiff to fill and pump efficiently

236
Q

Define

ST-elevation myocardial infarction (STEMI)

A

a very serious type of heart attack during which one of the heart’s major arteries (one of the arteries that supplies oxygen and nutrient-rich blood to the heart muscle) is blocked

237
Q

Define

Non-ST-elevation myocardial infarction (NSTEMI)

A

A type of heart attack that is less damaging than its counterpart involving no elevation of the ST segment

238
Q

Define

Myoglobin

A

an iron- and oxygen-binding protein found in the skeletal muscle tissue of vertebrates in general and in almost all mammals

239
Q

Define

Creatine kinase (CK)

A

an enzyme found in the heart, brain, skeletal muscle, and other tissues. Increased amounts of this molecule are released into the blood when there is muscle damage

240
Q

Define

Natriuretic peptides

A

a peptide that induces natriuresis, which is the excretion of sodium by the kidneys

241
Q

Define

Atrial natriuretic peptides (ANP)

A

a natriuretic peptide hormone secreted from the cardiac atria that in humans is encoded by the NPPA gene. The main function of this molecule is causing a reduction in expanded extracellular fluid (ECF) volume by increasing renal sodium excretion

242
Q

Define

Brain natriuretic peptides (BNP)

A

a hormonse secreted by cardiomyocytes in the heart ventricles in response to stretching caused by increased ventricular blood volume. It is released from the ventricle of patients with heart failure.

243
Q

Define

Nitric oxide (NO)

A

a mediator of vasodilation in blood vessels

244
Q

Define

Dyspnea

A

the medical term for shortness of breath

245
Q

Define

HFrEF

A

The heart muscle does not contract effectively, and therefore less oxygen-rich blood is pumped out to the body

246
Q

Define

HFpEF

A

a clinical syndrome in which patients have clinical features of heart failure in the presence of normal or near-normal left ventricular ejection fraction, usually defined as ejection fraction at 50% or above

247
Q

Definition

an output level where the Price equals the Marginal Cost (MC) of production. Concerned with efficient distribution of available resources and potential opportunity costs.

A

Allocative efficiency

248
Q

Definition

the effectiveness with which a given set of inputs is used to produce an output. Looks at efficient management of single condition and considers cost-effectiveness

A

Technical efficiency

249
Q

Definition

a systematic approach to estimating the strengths and weaknesses of alternatives used to determine options which provide the best approach to achieving benefits while preserving savings. Does not consider the potential health benefits

A

Cost-benefit analysis

250
Q

Definition

a form of analysis that compares the relative costs and outcomes (effects) of different courses of action.

A

Cost-effectiveness analysis

251
Q

Definition

a form of analysis used to guide procurement decisions. Net costs/net change in QALYs

A

Cost-utility analysis

252
Q

Definition

a generic measure of disease burden, including both the quality and the quantity of life lived

A

Quality-Adjusted Life Year (QALY)

253
Q

Definition

When a new intervention is both clinically inferior and increases costs

A

Dominated intervention

254
Q

Definition

When a new intervention is both clinically superior and cost saving

A

Dominant intervention

255
Q

Definition

chest pain or discomfort caused when your heart muscle doesn’t get enough oxygen-rich blood

A

Angina

256
Q

Definition

occurs when a coronary artery clogs and narrows because of a buildup of plaque overtime

A

Coronary heart disease (CHD)

257
Q

Definition

a term used to describe a range of conditions associated with sudden, reduced blood flow to the heart

A

Acute coronary syndrome (ACS)

258
Q

Definition

the medical name for a heart attack.

A

Acute mycardial infarction (AMI)

259
Q

Definition

a group of proteins found in skeletal and heart (cardiac) muscle fibers that regulate muscular contraction. Acts as a biomarker to help detect heart injury

A

Troponin

260
Q

Definition

when a person has brief episodes of pain, squeezing, pressure, or tightness in the chest

A

Stable angina

261
Q

Definition

occurs when your heart muscle doesn’t pump blood as well as it should. Certain conditions, such as narrowed arteries in your heart (coronary artery disease) or high blood pressure, gradually leave your heart too weak or stiff to fill and pump efficiently

A

Heart failure

262
Q

Definition

a very serious type of heart attack during which one of the heart’s major arteries (one of the arteries that supplies oxygen and nutrient-rich blood to the heart muscle) is blocked

A

ST-elevation myocardial infarction (STEMI)

263
Q

Definition

A type of heart attack that is less damaging than its counterpart involving no elevation of the ST segment

A

Non-ST-elevation myocardial infarction (NSTEMI)

264
Q

Definition

an iron- and oxygen-binding protein found in the skeletal muscle tissue of vertebrates in general and in almost all mammals

A

Myoglobin

265
Q

Definition

an enzyme found in the heart, brain, skeletal muscle, and other tissues. Increased amounts of this molecule are released into the blood when there is muscle damage

A

Creatine kinase (CK)

266
Q

Definition

a peptide that induces natriuresis, which is the excretion of sodium by the kidneys

A

Natriuretic peptides

267
Q

Definition

a natriuretic peptide hormone secreted from the cardiac atria that in humans is encoded by the NPPA gene. The main function of this molecule is causing a reduction in expanded extracellular fluid (ECF) volume by increasing renal sodium excretion

A

Atrial natriuretic peptides (ANP)

268
Q

Definition

a hormonse secreted by cardiomyocytes in the heart ventricles in response to stretching caused by increased ventricular blood volume. It is released from the ventricle of patients with heart failure.

A

Brain natriuretic peptides (BNP)

269
Q

Definition

a mediator of vasodilation in blood vessels

A

Nitric oxide (NO)

270
Q

Definition

the medical term for shortness of breath

A

Dyspnea

271
Q

Definition

The heart muscle does not contract effectively, and therefore less oxygen-rich blood is pumped out to the body

A

HFrEF

272
Q

Definition

a clinical syndrome in which patients have clinical features of heart failure in the presence of normal or near-normal left ventricular ejection fraction, usually defined as ejection fraction at 50% or above

A

HFpEF

273
Q

Who is the main funding contributer to Australian Healthcare?

A

Australian Federal Government (41%)

State and Territory Governments (27%)

Private (32%)

274
Q

What are the key challenges of the Australian healthcare system?

A
  • expense and affordability
  • rising costs, driven by both volume (ageing population) and expensive technology
  • goals:
    • safety, quality and efficiency
    • patient-centred healthcare
    • value-based healthcare
275
Q

What are the two types of efficieny in healthcare?

A

Allocative

Technical

276
Q

What are the three types of health economic analyses?

A

Cost-benefit

Cost-effectiveness

Cost-utility

277
Q

Which type of health economic analysis doesn’t consider health benefits?

A

Cost-benefit

278
Q

If a disease has a utility weight of 0.8 and a person has lived with the disease for 2 years. What is the equivalent of how many years lived without disease?

A

1.6 years

279
Q

What is the incremental cost-effectiveness ratio?

A

A line that divides the top right quadrant (net positive costs and net health gain) into two halfs. The line represents the points that $50,000 are spent per QALY. Beneath the line the benefits are worth the cost but above they are not

280
Q

What type of interventions may be considered “dominated”?

A

Medications prescribed to incorrect patients

281
Q

What type of interventions may be considered “dominant”?

A

Surgery

Vaccination

282
Q

What are some acute examples of coronary heart disease?

A

Acute coronary syndrome

  • Angina
  • Acute myocardial infarction (AMI; heart attack)
283
Q

What are some chronic examples of coronary heart disease?

A

Stable angina

Heart failure

284
Q

Which layer of the heart tissue is vulnerable ischaemia?

A

Sub-endocardial zone

285
Q

Which stage of a heart beat do coronary arteries fill?

A

Diastole

286
Q

Where does the sub-endocardial zone receive blood from?

A

Balance of supply from coronary arteries and diffusion from left ventricle

287
Q

What is the order of the acute coronary syndrome continuum?

A

Normal

Angina

ACS

NSTEMI

STEMI

288
Q

What are the two groups that Acute coronary syndrome is split into based on ECG results?

A
  1. Patients with acute chest pain and persistent (>20 min) ST-segment elevations (STEMI)
  2. Patients with acute chest pain but no persistent ST-segment elevation (NSTEMI)
289
Q

What does a STEMI ECG look like?

A
290
Q

What is the difference between NSTEMI and STEMI in terms of vessel occlusion and thickness of infarct?

A

NSTEMI: Partial vessel occlusion and partial thickness infarct

STEMI: Complete vessel occlusion and full thickness infarct

291
Q

Which biomarker is the best for indicating AMIs?

A

Cardiac toponin

292
Q

Why isn’t myoglobin used as a cardiac biomarker?

A

It is detected in the blood after AMI and skeletal muscle injury

i.e. it is not selective

293
Q

Where is creatine kinase found and why can it be used as a cardiac biomarker?

A

It is found in the heart and skeletal muscle. It can be used as a cardiac biomarker because the MB isoform is relatively heart-specific

294
Q

When does troponin start to increase after AMI and how long is it abnormal for?

A

Detected 4-10 hours after AMI, peak at 12-48 hours, abnormal for 4-10 days

295
Q

Which biomarkers are released from dying muscle?

A

Creatine kinase-MB

c-troponin

296
Q

What causes the release of natriuretic peptides?

A

Atrial distension (ANP) and left ventricle stretch/stress (BNP)

297
Q

BNP and N-terminal breakdown product (NT-proBNP) are biomarkers for what condition?

A

Heart failure

298
Q

What are the causes of AMIs?

A
  • Coronary artery occlusion- plaque build up +/- rupture
  • Aortic valve problems
  • Coronary artery aneurysms
  • Electrical failure (arrhythmias)
  • Illicit drugs (cocaine, amphetamine…)
  • Anticancer drugs etc
  • Increased risk, e.g. hypertension, diabetes
299
Q

Which part of the heart does the infarct usually occur during a heart attack?

A

Usually left ventricle - thicker muscle

300
Q

How is heart tissue repaired following a heart attack?

A

Reorganisation (replacement by fivrous tissue) - minimal regeneretive capacity for cardiomyocytes

301
Q

Why is there a potential for cardiac rupture in the week following a AMI?

A

The structure of the heart is weakened

302
Q

What are the symptoms of angina?

A

Pain, severe, crushing, sub-sternal, may radiate

With/without shortness of breath; lasts a few minutes

Females often present differently: nausea, vomiting, back/jaw pain

303
Q

What causes angina?

A

Coronary artery disease, coronary vasospasm

i.e. imbalance: myocardial O2 demand >> O2 supply

304
Q

When is urgent medical attention required for angina?

A
  • worsening angina (unstable angina)
  • chest pain lasting more than a few minutes
305
Q

What are the three types of angina?

A

Chronic, stable

Unstable

Variant (vasospastic)

306
Q

What causes chronic, stable angina?

A

In people with high levels of atherosclerosis, caused by ‘demand’, e.g. exercise, stress-test etc.

307
Q

What causes unstable angina?

A

In people with some atherosclerosis, unpredictable, may involve thrombi formation

308
Q

What causes variant angina?

A

In people without atherosclerosis, spasm of coronary artery

309
Q

Which factors increase the risk and precipitate angina?

A

Risk factors: hypertension, cholesterol, smoking etc.

Precipitation factors: exertion, cold, stress, large meals etc.

310
Q

How do you treat angina?

A
  • Modification of risk factors: smoking, obesity, hypertension, hyperlipidemia, diabetes
  • Surgical: angioplasty/stents/CABG Pharmacological: tPA (all immediate action)
  • Drug treatments (chronic) (for relatively stable forms of angina)
311
Q

What drugs are used to treat angina? What are their mechanisms?

A
  • nitro-vasodilators
  • β1 -adrenoceptor antagonists
  • Ca2+ channel antagonists

Mechanisms

  • Increased coronary perfusion to increase oxygen supply
  • Decrased metabolic demand
  • Combination of both
312
Q

What is the role of nitric oxide (NO) in the cardiovascular system?

A

Antithrombotic

Vasodilator

313
Q

What is the mechanism of nitrates in treating angina?

A
  • Venous dilatation reduces venous pressure and pre-load, with consequent fall in cardiac oxygen consumption
  • Arteriolar dilatation reduces peripheral resistance and after-load with consequent fall in cardiac oxygen consumption
  • Coronary dilatation- e.g. variant angina
  • No effect of NO in cardiac/sk muscle
314
Q

In what forms can nitrates be administered for angina?

A

Fast-acting sublingual tablet prior to exertion

Chronic patch for stable angina

315
Q

What are the limitations of using nitrates to treat angina?

A
  • Decreased blood pressure is associated with a reflex tachycardia
  • Tendency to increase cardiac oxygen consumption
316
Q

Why must nitrate patches only be used for short periods of time?

A

To prevent tolerance

317
Q

Where are majority of nitrates metabolised?

A

In the liver (>90%)

318
Q

What are the adverse effects of nitrates?

A
  • Hypotension (fainting): should not be combined with Viagra or similar drugs
  • Tachycardia
  • Headache
  • Flushing
319
Q

Right heart failure causes back pressure to which part of the circulation?

A

Systemic

320
Q

Left heart failure causes back pressure to which part of the circulation?

A

Pulmonary

321
Q

What can cause heart failure?

A

Hypertension

Heart conditions

  • valves
  • ischaemia
  • arrythmia
  • cardiomyopathy
  • CHD, atherosclerosis

Lung conditions

  • pulmonary hypertension

Other co-morbidities

  • renal failure
  • diabetes
322
Q

What are the two types of chronic heart failure?

A

HFrEF: HF with reduced ejection fraction

HFpEF: HF with preserved ejection fraction

323
Q

Which type of chronic heart failure involves systolic dysfunction?

A

HFrEF

324
Q

Which type of chronic heart failure involves diastolic dysfunction?

A

HFpEF

325
Q

In which populations is the prevalence of HFpEF particularly increasing?

A

Older population

Females

Diabetics

326
Q

What are the features of HFpEF? What does the heart look like?

A

Preserved cardiac ouput (contraction)

Relaxation (diastole) impaied

Decreased cardiac output with exercise

Often caused by hypertension

327
Q

What are the features of HFrEF? What does the heart look like?

A

Depressed cardiac output (ejection fraction)

Change in geometry (dilation)

Often caused by heart attacks that result in global remodelling

328
Q

How does the cardiovascular system compensate for decreased cardiac output?

A
329
Q

What does the compensatory mechanisms for decreased CO do to cardiac state over time?

A

Worsened cardiac state (positive feedback)

330
Q

Define

ACE

A

a central component of the renin–angiotensin system (RAS), which controls blood pressure by regulating the volume of fluids in the body. It converts the hormone angiotensin I to the active vasoconstrictor angiotensin II

331
Q

Define

ACE inhibitors

A

a class of medication used primarily for the treatment of high blood pressure and heart failure. They work by causing relaxation of blood vessels as well as a decrease in blood volume, which leads to lower blood pressure and decreased oxygen demand from the heart

332
Q

Define

ACE2

A

an enzyme attached to the cell membranes of cells in the lungs, arteries, heart, kidney, and intestines. It lowers blood pressure by catalysing the hydrolysis of angiotensin II into angiotensin

333
Q

Define

Aldosterone

A

the main mineralocorticoid hormone, is a steroid hormone produced by the zona glomerulosa of the adrenal cortex in the adrenal gland. It is essential for sodium conservation in the kidney, salivary glands, sweat glands and colon

334
Q

Define

Aldosterone receptor antagonist

A

a diuretic drug which antagonizes the action of aldosterone at mineralocorticoid receptors. This group of drugs is often used as adjunctive therapy, in combination with other drugs, for the management of chronic heart failure

335
Q

Define

Alpha receptor

A

any of a group of receptors that are present on cell surfaces of some effector organs and tissues innervated by the sympathetic nervous system and that mediate certain physiological responses (such as vasoconstriction, relaxation of intestinal muscle, and contraction of most smooth muscle) when bound by specific adrenergic agents

336
Q

Define

Angiogram

A

the radiographic visualization of the blood vessels after injection of a radiopaque substance

337
Q

Define

Angiotensin

A

a peptide hormone that causes vasoconstriction and an increase in blood pressure. It is part of the renin–angiotensin system, which regulates blood pressure. It also stimulates the release of aldosterone from the adrenal cortex to promote sodium retention by the kidneys

338
Q

Define

Angiotensin I

A

formed by the action of renin on angiotensinogen and acts as the precursor to Ang II

339
Q

Define

Angiotensin II

A

acts on the CNS to increase vasopressin production, and also acts on venous and arterial smooth muscle to cause vasoconstriction. It also increases aldosterone secretion; it therefore acts as an endocrine, autocrine/paracrine, and intracrine hormone

340
Q

Define

Angiotensin receptor blockers

A

are a group of pharmaceuticals that bind to and inhibit the angiotensin II receptor type 1 (AT1) and thereby block the arteriolar contraction and sodium retention effects of renin–angiotensin system

341
Q

Define

Angiotensinogen

A

an α-2-globulin synthesized in the liver and is a precursor for angiotensin, but has also been indicated as having many other roles not related to angiotensin peptides

342
Q

Define

Arteriole tone

A

the degree of constriction experienced by a blood vessel relative to its maximally dilated state

343
Q

Define

Beta blockers

A

any of a class of drugs (such as propranolol) that decrease the rate and force of heart contractions and lower high blood pressure by blocking the activity of beta-receptors

344
Q

Define

Beta receptor

A

any of a group of receptors that are present on cell surfaces of some effector organs and tissues innervated by the sympathetic nervous system and that mediate certain physiological responses (such as vasodilation, relaxation of bronchial and uterine smooth muscle, and increased heart rate) when bound by specific adrenergic agents

345
Q

Define

Bradykinin

A

a kinin that is formed locally in injured tissue, acts in vasodilation of small arterioles, is considered to play a part in inflammatory processes, and is composed of a chain of nine amino acid residues

346
Q

Define

Calcium channel blockers

A

any of a class of drugs (such as verapamil) that prevent or slow the influx of calcium ions into smooth muscle cells and are used especially to treat some forms of angina pectoris and some cardiac arrhythmias

347
Q

Define

Chronic obstructive pulmonary disease (COPD)

A

pulmonary disease (such as emphysema or chronic bronchitis) that is characterized by chronic typically irreversible airway obstruction resulting in a slowed rate of exhalation

348
Q

Define

Diuretics

A

tending to increase the excretion of urine

349
Q

Define

Echocardiogram

A

the use of ultrasound to examine the structure and functioning of the heart for abnormalities and disease

350
Q

Define

Electrocardiogram

A

an instrument for recording the changes of electrical potential occurring during the heartbeat used especially in diagnosing abnormalities of heart action

351
Q

Define

Hypertension

A

high blood pressure

352
Q

Define

Inotropic agents

A

drugs that act by increasing or decreasing the force of muscular contractions

353
Q

Define

Loop diuretic

A

a diuretic that inhibits reabsorption in the ascending limb of the loop of Henle causing greatly increased excretion of sodium chloride in the urine and to a lesser extent of potassium

354
Q

Define

Polycythemia

A

a condition marked by an abnormal increase in the number of circulating red blood cells

355
Q

Define

Pulmonary hypertension

A

a type of high blood pressure that affects the arteries in your lungs and the right side of your heart

356
Q

Define

Pulmonary thromboendarterectomy

A

surgical excision of a thrombus and the adjacent arterial lining

357
Q

Define

Renin

A

a proteolytic enzyme of the kidney that plays a major role in the release of angiotensin

358
Q

Define

Thiazide diuretic

A

a type of diuretic (a drug that increases urine flow). They act directly on the kidneys and promote diuresis (urine flow) by inhibiting the sodium/chloride cotransporter located in the distal convoluted tubule of a nephron (the functional unit of a kidney).

359
Q

Define

Type 1 pulmonary hypertension

A

the type of pulmonary hypertension that is associated with the narrowing of the small blood vessels in the lungs. It also is called pulmonary arterial hypertension (PAH) and includes cases where the underlying cause of the narrowing is not known (idiopathic pulmonary hypertension).

360
Q

Define

Type 2 pulmonary hypertension

A

pulmonary hypertension caused by left heart disease. Long-term problems with the left side of the heart can lead to changes in the pulmonary arteries and cause pulmonary hypertension.

361
Q

Define

Type 3 pulmonary hypertension

A

includes pulmonary hypertension resulting from lung diseases or shortage of oxygen in the body (hypoxia)

362
Q

Define

Type 4 pulmonary hypertension

A

pulmonary hypertension caused by blood clots obstructing the pulmonary arteries. This also can be referred to as chronic thromboembolic pulmonary hypertension (CTEPH).

363
Q

Define

Type 5 pulmonary hypertension

A

the type of pulmonary hypertension that includes other less-common causes that do not fit into any of the other four groups

364
Q

Define

Vasoconstriction

A

narrowing of the lumen of blood vessels

365
Q

Define

Vasodilation

A

widening of the lumen of blood vessels

366
Q

Define

Vasopressin

A

a polypeptide hormone secreted by the posterior lobe of the pituitary gland or obtained synthetically that increases blood pressure and decreases urine flow

367
Q

Definition

a central component of the renin–angiotensin system (RAS), which controls blood pressure by regulating the volume of fluids in the body. It converts the hormone angiotensin I to the active vasoconstrictor angiotensin II

A

ACE

368
Q

Definition

a class of medication used primarily for the treatment of high blood pressure and heart failure. They work by causing relaxation of blood vessels as well as a decrease in blood volume, which leads to lower blood pressure and decreased oxygen demand from the heart

A

ACE inhibitors

369
Q

Definition

an enzyme attached to the cell membranes of cells in the lungs, arteries, heart, kidney, and intestines. It lowers blood pressure by catalysing the hydrolysis of angiotensin II into angiotensin

A

ACE2

370
Q

Definition

the main mineralocorticoid hormone, is a steroid hormone produced by the zona glomerulosa of the adrenal cortex in the adrenal gland. It is essential for sodium conservation in the kidney, salivary glands, sweat glands and colon

A

Aldosterone

371
Q

Definition

a diuretic drug which antagonizes the action of aldosterone at mineralocorticoid receptors. This group of drugs is often used as adjunctive therapy, in combination with other drugs, for the management of chronic heart failure

A

Aldosterone receptor antagonist

372
Q

Definition

any of a group of receptors that are present on cell surfaces of some effector organs and tissues innervated by the sympathetic nervous system and that mediate certain physiological responses (such as vasoconstriction, relaxation of intestinal muscle, and contraction of most smooth muscle) when bound by specific adrenergic agents

A

Alpha receptor

373
Q

Definition

the radiographic visualization of the blood vessels after injection of a radiopaque substance

A

Angiogram

374
Q

Definition

a peptide hormone that causes vasoconstriction and an increase in blood pressure. It is part of the renin–angiotensin system, which regulates blood pressure. It also stimulates the release of aldosterone from the adrenal cortex to promote sodium retention by the kidneys

A

Angiotensin

375
Q

Definition

formed by the action of renin on angiotensinogen and acts as the precursor to Ang II

A

Angiotensin I

376
Q

Definition

acts on the CNS to increase vasopressin production, and also acts on venous and arterial smooth muscle to cause vasoconstriction. It also increases aldosterone secretion; it therefore acts as an endocrine, autocrine/paracrine, and intracrine hormone

A

Angiotensin II

377
Q

Definition

are a group of pharmaceuticals that bind to and inhibit the angiotensin II receptor type 1 (AT1) and thereby block the arteriolar contraction and sodium retention effects of renin–angiotensin system

A

Angiotensin receptor blockers

378
Q

Definition

an α-2-globulin synthesized in the liver and is a precursor for angiotensin, but has also been indicated as having many other roles not related to angiotensin peptides

A

Angiotensinogen

379
Q

Definition

the degree of constriction experienced by a blood vessel relative to its maximally dilated state

A

Arteriole tone

380
Q

Definition

any of a class of drugs (such as propranolol) that decrease the rate and force of heart contractions and lower high blood pressure by blocking the activity of beta-receptors

A

Beta blockers

381
Q

Definition

any of a group of receptors that are present on cell surfaces of some effector organs and tissues innervated by the sympathetic nervous system and that mediate certain physiological responses (such as vasodilation, relaxation of bronchial and uterine smooth muscle, and increased heart rate) when bound by specific adrenergic agents

A

Beta receptor

382
Q

Definition

a kinin that is formed locally in injured tissue, acts in vasodilation of small arterioles, is considered to play a part in inflammatory processes, and is composed of a chain of nine amino acid residues

A

Bradykinin

383
Q

Definition

any of a class of drugs (such as verapamil) that prevent or slow the influx of calcium ions into smooth muscle cells and are used especially to treat some forms of angina pectoris and some cardiac arrhythmias

A

Calcium channel blockers

384
Q

Definition

pulmonary disease (such as emphysema or chronic bronchitis) that is characterized by chronic typically irreversible airway obstruction resulting in a slowed rate of exhalation

A

Chronic obstructive pulmonary disease (COPD)

385
Q

Definition

tending to increase the excretion of urine

A

Diuretics

386
Q

Definition

the use of ultrasound to examine the structure and functioning of the heart for abnormalities and disease

A

Echocardiogram

387
Q

Definition

an instrument for recording the changes of electrical potential occurring during the heartbeat used especially in diagnosing abnormalities of heart action

A

Electrocardiogram

388
Q

Definition

high blood pressure

A

Hypertension

389
Q

Definition

drugs that act by increasing or decreasing the force of muscular contractions

A

Inotropic agents

390
Q

Definition

a diuretic that inhibits reabsorption in the ascending limb of the loop of Henle causing greatly increased excretion of sodium chloride in the urine and to a lesser extent of potassium

A

Loop diuretic

391
Q

Definition

a condition marked by an abnormal increase in the number of circulating red blood cells

A

Polycythemia

392
Q

Definition

a type of high blood pressure that affects the arteries in your lungs and the right side of your heart

A

Pulmonary hypertension

393
Q

Definition

surgical excision of a thrombus and the adjacent arterial lining

A

Pulmonary thromboendarterectomy

394
Q

Definition

a proteolytic enzyme of the kidney that plays a major role in the release of angiotensin

A

Renin

395
Q

Definition

a type of diuretic (a drug that increases urine flow). They act directly on the kidneys and promote diuresis (urine flow) by inhibiting the sodium/chloride cotransporter located in the distal convoluted tubule of a nephron (the functional unit of a kidney).

A

Thiazide diuretic

396
Q

Definition

the type of pulmonary hypertension that is associated with the narrowing of the small blood vessels in the lungs. It also is called pulmonary arterial hypertension (PAH) and includes cases where the underlying cause of the narrowing is not known (idiopathic pulmonary hypertension).

A

Type 1 pulmonary hypertension

397
Q

Definition

pulmonary hypertension caused by left heart disease. Long-term problems with the left side of the heart can lead to changes in the pulmonary arteries and cause pulmonary hypertension.

A

Type 2 pulmonary hypertension

398
Q

Definition

includes pulmonary hypertension resulting from lung diseases or shortage of oxygen in the body (hypoxia)

A

Type 3 pulmonary hypertension

399
Q

Definition

pulmonary hypertension caused by blood clots obstructing the pulmonary arteries. This also can be referred to as chronic thromboembolic pulmonary hypertension (CTEPH).

A

Type 4 pulmonary hypertension

400
Q

Definition

the type of pulmonary hypertension that includes other less-common causes that do not fit into any of the other four groups

A

Type 5 pulmonary hypertension

401
Q

Definition

narrowing of the lumen of blood vessels

A

Vasoconstriction

402
Q

Definition

widening of the lumen of blood vessels

A

Vasodilation

403
Q

Definition

a polypeptide hormone secreted by the posterior lobe of the pituitary gland or obtained synthetically that increases blood pressure and decreases urine flow

A

Vasopressin

404
Q

What is the difference between primary and secondary hypertension?

A

Primary: Aetiology unknown, but risk factors include genetics, smoking, stress etc.

Secondary: High BP is a result of an abnormality/comorbidity or drug

405
Q

What are the symptoms of hypertension?

A

Often no symptoms (silent killer)

406
Q

What is hypertension a risk factor for?

A

Stroke

Heart failure

Coronary artery disease

407
Q

What can cause secondary hypertension?

A
  • Renal and renal vascular disease
  • Coarctation (narrowing) of aorta
  • Primary aldosteronism (Conn’s)
  • Glucocorticoid excess (Cushing’s)
  • Phaeochromocytoma (tumour releasing adrenaline/noradrenaline)
  • Drugs (cocaine, ketamine, nicotine, tricyclic antidepressants, SSRIs, steroids, NSAIDS, EPO, angiogenesis inhibitors….etc)
408
Q

Why is the pressure in the aorta and large arteries never below 70mmhg?

A

The aorta and large arteries are very elastic so pressure is maintained

409
Q

What is the usual cause of high bp in younger and older individuals?

A

Young: High cardiac output (high heart rate)

Old: High total peripheral resistance

410
Q

Most drugs that lower BP reduce what?

A

TPR

411
Q

What is the cut-off for clinical high blood pressure?

A

140/90

412
Q

What is the direct effects of long-term hypertension?

A
  • causes target organ damage; exacerbates tissue inflammation, oxid stress, hormones (Ang II)
    • blood vessels
    • organs- e.g. heart; kidney, eyes etc.
413
Q

What are the four classes of drugs used to treat hypertension? Which 3 are also used for heart failure?

A

ACE inhibitors & angiotensin antagonists

Beta blockers

Calcium channel blockers (NOT for HF)

Diuretics

414
Q

How is HF treated?

A
  • Lifestyle changes (weight, sodium, diet, exercise)
  • Decrease cardiac workload
    • Angiotensin inhibition
    • Diuretics
    • B blockers
  • Increase cardiac contractility
    • Positive inotropes (e.g. digoxin, dubutamine)
415
Q

What are the peripheral effects of angiotensin II?

A
  • vasoconstriction
  • aldosterone release (sodium reabsorption-kidney)
  • Increase NA release (sympathetic)
  • Fibrosis
  • Hypertrophy
  • oxidative stress
416
Q

What are the central effects of angiotensin II?

A
  • Increase BP
  • vasopressin release
  • drinking response
417
Q

What converts angiotensinogen into Ang I?

A

Renin

418
Q

What causes renin to be released?

A

Renal sympathetic nerve activity

Renal perfusion pressure

Glomerular filtration

B-agonist

419
Q

What natural molecule blocks the release of renin?

A

Atrial natriuretic peptide

420
Q

What enzyme converts Ang I into Ang II?

A

ACE

421
Q

Activation of AT1 (Ang II) receptors causes what?

A

Vasoconstriction

  • Direct
  • Via increased NA release from sympathetic nerves

Salt retention

  • Aldosterone secretion
  • Tubular Na+ reabsorption

Vascular growth

  • Hyperplasia
  • Hypertrophy
422
Q

What is the suffix and some examples of ACE inhibitors?

A

-“pril”

captopril

enalapril

perindopril

423
Q

What type of drug is captopril?

A

ACE inhibitor

424
Q

What type of drug is enalapril?

A

ACE inhibitor

425
Q

What type of drug is perindopril?

A

ACE inhibitor

426
Q

What affects to ACE inhibitors have?

A

Prevent angiotensin II formation and inhibit bradykinin breakdown (Decrease Ang II, Increase BK)

  • Decreases total peripheral resistance (vasodilator)
  • Increases sodium & water excretion
427
Q

What are the indications for ACE inhibitor use?

A

Hypertension, heart failure

Preserve renal function in diabetes (diabetic nephropathy)

428
Q

What are the adverse effects of ACE inhibitors?

A

Common:

  • cough (Increased BK in lungs), headache
  • Marked hypotension (start with low dose)
  • Hyperkalaemia (beware K+ supplements or K+ -sparing diuretics)

Infrequent:

  • Rash/itch, angioedema

Contraindications:

  • Renal failure if have bilateral renal artery stenosis
  • Avoid in pregnancy
429
Q

What two reactions does ACE facilitate?

A

Converting Ang I into Ang II

Breaking down bradykinin into inactive metabolites

430
Q

What is the prefix and some examples of angiotensin receptor (AT1) blockers?

A

-“sartan”

Iosartan

Irbesartan

Candesartan

431
Q

What effects for angiotensin receptor (AT1) blockers have?

A

inhibit angiotensin-induced vasoconstriction and aldosterone output (actually increase Ang II, unchanged BK- c.f. ACE inhibitors)

  • Decreases total peripheral resistance (vasodilator)
  • Increases sodium & water excretion
432
Q

What are the indications for AT1 blocker use?

A

Hypertension, heart failure, diabetic nephropathy

For patients intolerant to ACE inhibitors (e.g. cough)

433
Q

What are the adverse effects of AT1 blockers?

A

Same as ACE inhibitors:

Common:

cough (Increased BK in lungs), headache

Marked hypotension (start with low dose)

Hyperkalaemia (beware K+ supplements or K+ -sparing diuretics)

Infrequent:

Rash/itch, angioedema

Contraindications:

Renal failure if have bilateral renal artery stenosis

Avoid in pregnancy

434
Q

What reaction does ACE2 facilitate?

A

Ang II into Ang(1-7)

435
Q

What are the effects of Ang (1-7)?

A

Effects opposite Ang II (i.e. vasodilator, natriuretic)

Ang (1-7) may exert cardioprotective effects in its own right via another receptor; known as Mas receptor

436
Q

True or False:

ACE2 is not blocked by ACE inhibitors

A
437
Q

What receptor does SARS-Cov-2 bind to?

A

ACE2

438
Q

What effects do B-adrenoceptor antagonists have?

A
  • Decreased sympathetic drive to heart
    • ↓ CO ↓ HR ↓ TPR
  • Decrease sympathetic drive to kidneys
    • Inhibit renin release (↓ Ang II)
439
Q

What is the suffix and some examples of B blockers?

A

-“olol”

Propranolol (non-selective: B1 & B2)

Atenolol (B1 selective)

Metoprolol (B1 selective)

440
Q

What are B blockers used to treat?

A

Hypertension (not first line)

Angina

Post myocardial infarct

Arrythmias

Clinically stable heart failure

441
Q

Why are B blockers used in heart failure?

A

Chronic HF patients have massive sympathetic drive causing huge amounts of NA to be released. B-blockers reduce NA toxicity

442
Q

What B-blockers are used in chronic stable HF?

A

Carvediol

Nebivolol

443
Q

What are the long-term benefits and short-term risks of B-blockers in HF?

A

Long-term benefits:

  • Improved survival
  • Improved control of heart failure
  • Reduced need for hospitalisation
  • Improved quality of life
  • Improved left ventricular ejection fraction

Short-term risks:

  • Worsening heart failure
  • Bradyarrythmias
  • Prolonged intraventricular conduction
  • Hypotension
  • Worsening renal function
444
Q

What are the adverse side-effects of B-blockers?

A

Respiratory: bronchoconstriction (B2 effect)

Cardiovascular: decreased heart contractility, bradycardia, atrioventricular block, exercise intolerance, claudication, impotence, beware sudden withdrawal

Diabetes: exacerbate & mask hypoglycemia

445
Q

What are the effects of calcium antagonists?

A

Blockade of L-type (voltage operated) Ca2+ channels;

Reduces Ca2+ entry into vascular* / cardiac cells (not SkM)

Therefore, reduction in intracellular Ca2+

446
Q

Fill in this table and explain the red arrows

A

Calcium antagonists with low cardiac effects cause an increase in HR in response to the drop in BP. Drugs with stronger cardiac effects prevent this through direct action on the heart

447
Q

What are the indications for Ca channel blocker use?

A

Hypertension, angina, tachyarrhythmias (supraventricular)

448
Q

What are the contraindication for Ca channel blocker use?

A

Heart failure

verapamil or diltiazem when combined with β-blocker

449
Q

Why shouldn’t Ca channel blockers be used in patients with HF?

A

They reduce heart contraction

450
Q

What are the adverse effects of Ca blockers?

A

cardiac depression, bradycardia (contraindicated in heart failure)

flushing, edema, dizziness, headache

constipation, nausea

451
Q

What are the three classes of diuretic?

A

Loop diuretic

Thiazide diuretic

Aldosterone receptor antagonists

452
Q

Which class of diuretic has the greatest efficacy?

A

Loop diuretic

453
Q

What do loop diuretics do?

A
  • Act at thick ascending limb of L of H to block Na+ /K+2Clsymporter
  • Ceiling effect: block 15-25% filtered sodium reabsorption - class with greatest diuretic efficacy
454
Q

What do Thiazide diuretics do?

A
  • Act at distal conv tubules to block Na+ /Cl- symporter
  • Modest increase in sodium excretion (5-10%)
455
Q

When are loop diretics used?

A

Mild to moderate hypertension

456
Q

When are Thiazide diuretics used?

A

oedema due to:

  • congestive heart failure (+/- hypertension)
  • +/- pulmonary congestion
  • renal; liver disease
457
Q

What are the adverse effects of loop/thazide diuretics?

A
  • Electrolyte imbalance:
    • Hypokalaemia (drug interactions)
  • Hyperuricaemia (gout)
  • hypercholesteraemia
  • hyperglycaemia - diabetogenic effect
458
Q

Which type of diuretic does not decrease K levels?

A

Aldosterone receptor antagonists

459
Q

Where do aldosterone receptor antagonists act?

A

Distal tubule/collecting ducts

460
Q

What actions does aldosterone receptor antagonists have?

A
  • inhibits mineralocorticoid (aldosterone) receptor (kidney)
  • Heart: inhibits aldosterone-induced fibrosis (improves HF)
461
Q

What are the clinical uses of spironolactone (aldosterone receptor antagonist)?

A
  • used in combination with thiazide or loop diuretics to produce (weak) diuresis without hypokalaemia
  • used particularly in conditions associated with hyperaldosteronism
  • resurgence of interest in CHF (improves survival)
  • resistant hypertension? (add-on therapy)
462
Q

What is a possible adverse effect of aldosterone receptor antagonists?

A

Hyperkalaemia

463
Q

Why do aldosterone receptor antagonists lead to hyperkaelemia?

A

Aldosterone leads to production of Na/K channels that pump out K. If aldosterone is inhibited, these channels aren’t made and K is allowed to accumulate in the interstitium/blood

464
Q

What is normal mean pulmonary pressure and what is considered pulmonary hypertension?

A

Normal: ~14/15mmHg

Hypertension: >25mmHg (at rest)

465
Q

Why is the pulmonary arteries under significantly less pressure than other arteries?

A

The lungs are close to the heart so only need low pressure to get the blood there

Lung vessels are delicate

466
Q

What are the symptoms of pulmonary hypertension?

A
  • Shortness of breath
  • difficulty breathing with exer:on,
  • dizziness
  • rapid breathing, and
  • rapid heart rate
  • Edema or swelling
  • Chest pain
467
Q

What are the risk factors for pulmonary hypertension?

A

Family history

Obesity combined with obstructive sleep apnea

Gender (women)

Pregnancy

Altitude

Other diseases (e.g. lupus)

Drugs and toxins (meth)

468
Q

What is the cause of T1 pulmonary hypertension?

A

Idopathic

Inherited

Congenital heart disease

469
Q

What is the cause of T2 pulmonary hypertension?

A

Diseases that affect the left side of the heart

470
Q

What is the cause of T3 pulmonary hypertension?

A

Breathing conditions (e.g. COPD)

471
Q

What is the cause of T4 pulmonary hypertension?

A

Blood disorders

472
Q

How is pulmonary hypertension diagnosed?

A

ECG

Echocardiogram

Pulmonary function tests

Right heart catheterisation

Pulmonary angiogram

473
Q

What pharcomalogical agents are used to treat pulmonary hypertension?

A
  • Oxygen
  • Anticoagulants
  • Diuretics
  • Inotropic agents
  • Vasodilators
  • Endothelin-1 antagonists
  • Sildenafil (viagra)
474
Q

How does oxygen treat pulmonary hypertension?

A

replaces the low oxygen in your blood.

475
Q

How does anticoagulants treat pulmonary hypertension?

A

such as warfarin — decreases blood clot formation so blood flows more freely through blood vessels.

476
Q

How does diuretics treat pulmonary hypertension?

A

” [such as furosemide, spironolactone] — removes extra fluid from the tissues and bloodstream, which reduces swelling and makes breathing easier.

477
Q

How does inotropic agents treat pulmonary hypertension?

A

improves the heart’s pumping ability.

478
Q

How do vasodilators treat pulmonary hypertension?

A

lowers pulmonary blood pressure and may improve the pumping ability of the right side of the heart.

479
Q

How do endothelin-1 antagonists treat pulmonary hypertension?

A

helps block the action of endothelin, a substance that causes narrowing of lung blood vessels. These medications require monthly labwork to monitor liver function.

480
Q

How do sildenafil treat pulmonary hypertension?

A

relaxes pulmonary smooth muscle cells, which leads to dilation of the pulmonary arteries.

481
Q

What surgical therapies are used to treat pulmonary hypertension?

A

Pumonary thromboendarterectomy

Lung transplantation

482
Q

How is T1 pulmonary hypertension treated?

A

Medications (pills, inhalers and continuous infusions) developed specifically for the treatment of PAH to dilate, and reduce the inappropriate growth of cells in, the pulmonary arteries

483
Q

How is T2 pulmonary hypertension treated?

A

Therapies are focused on treating the underlying heart disease

484
Q

How is T3 pulmonary hypertension treated?

A

Therapies focused on treating the underlying lung disease

485
Q

How is T4 pulmonary hypertension treated?

A

Surgical removal of the clot, when possible, or oral medication if surgery is not possible or if PH remains after surgery

486
Q

How is T5 pulmonary hypertension treated?

A

Therapies are focused on treating the underlying disease

487
Q

Why does hypoxia cause constriction of the lung vessels?

A

The blood is diverted to the areas with good airflow by constricting the hypoxic vessels

488
Q

What does endothelin-1 do in the lung vessels?

A

Vasoconstricter

decreases luminal radius

489
Q

What happens to the smooth muscle surrounding lung vessels with chronic hypoxia?

A

Proliferation. SM layer thickens causing decreased luminal radius

490
Q

What contributes to the increased vascular resistance caused by chronic hypoxia?

A

Hypoxic vasoconstriction

Vascular remodelling

Polycythemia

491
Q

Activation of which pathway mediated Ca2+ sensitisation seen in pulmonary hypertension?

A

RhoA-Rho kinase (ROK) pathway

492
Q

Plaque rupture may cause thrombus formation due all of the following EXCEPT:

a) release of tissue factor
b) activation of platelets
c) production of tissue plasminogen activator
d) production of fibrin

A

Plaque rupture may cause thrombus formation due all of the following EXCEPT:

a) release of tissue factor
b) activation of platelets

c) production of tissue plasminogen activator

d) production of fibrin

493
Q

Used in the treatment of hypercholesterolaemia, statins act by:

a) increasing HMG-CoA reductase
b) decreasing endogenous cholesterol synthesis
c) reducing LDL plasma clearance
d) reducing plaque stabilisation

A

Used in the treatment of hypercholesterolaemia, statins act by:

a) increasing HMG-CoA reductase

b) decreasing endogenous cholesterol synthesis

c) reducing LDL plasma clearance
d) reducing plaque stabilisation

494
Q

Acute coronary syndrome may be diagnosed if a patient exhibits any of the following signs EXCEPT:

a) persistent ECG changes
b) elevated blood pressure
c) chest pressure at rest
d) pain without ST-segment elevation on ECG

A

Acute coronary syndrome may be diagnosed if a patient exhibits any of the following signs EXCEPT:

a) persistent ECG changes

b) elevated blood pressure

c) chest pressure at rest
d) pain without ST-segment elevation on ECG

495
Q

Hypertension and Heart failure may be managed with all of the following medications EXCEPT:

a) β1-adrenoceptor antagonists
b) AT1 receptor antagonists
c) calcium channel antagonists
d) loop diuretics

A

Hypertension and Heart failure may be managed with all of the following medications EXCEPT:

a) β1-adrenoceptor antagonists
b) AT1 receptor antagonists

c) calcium channel antagonists

d) loop diuretics

496
Q

The following drugs are matched with a major adverse effect EXCEPT:

a) captopril and angioedema
b) frusemide and hyperkalaemia
c) spironolactone and hyperkalaemia
d) losartan and hyperkalaemia

A

The following drugs are matched with a major adverse effect EXCEPT:

a) captopril and angioedema

b) frusemide and hyperkalaemia

c) spironolactone and hyperkalaemia
d) losartan and hyperkalaemia

497
Q

A 78-year-old female has been watching TV all afternoon by herself dozing in and out of sleep. Her daughter comes to visit and knocks on the door. The mother stands up to go and open the door and collapses. Her daughter uses a key to enter the house and finds her mother lying on the floor. The daughter calls 000 and the patient arrives at the hospital 1 hour later and has the following: slurred speech and right side hemiplegia. The first action should be to ………………. If it is an ischemic stroke in small cerebral artery, the second action should be to ………………

a) Perform a brain CT scan, administer tissue plasminogen activator
b) Perform a brain CT scan, give aspirin
c) Obtain a brain MRI, adminsiter mannitol
d) Obtain a brain MRI, remove the clot via mechanical thrombectomy

A

a) Perform a brain CT scan, administer tissue plasminogen activator

b) Perform a brain CT scan, give aspirin

c) Obtain a brain MRI, adminsiter mannitol
d) Obtain a brain MRI, remove the clot via mechanical thrombectomy

498
Q

Which of the following are the MOST LIKELY mechanisms by which administration of stem cell treatment 7 days (delayed) post-stroke may improve outcome?

a) Immunomodulatory properties, stimulate angiogenesis, and repair mechanisms
b) Neuronal differentiation, stimulate angiogenesis, and immunomodulatory properties
c) Stimulate angiogenesis, repair mechanisms, and neuronal differentiation
d) Repair mechanisms, immunomodulatory properties, and neuronal differentiation

A

Which of the following are the MOST LIKELY mechanisms by which administration of stem cell treatment 7 days (delayed) post-stroke may improve outcome?

a) Immunomodulatory properties, stimulate angiogenesis, and repair mechanisms
b) Neuronal differentiation, stimulate angiogenesis, and immunomodulatory properties

c) Stimulate angiogenesis, repair mechanisms, and neuronal differentiation

d) Repair mechanisms, immunomodulatory properties, and neuronal differentiation

499
Q

Which preclinical stroke model am I? I am the the most widely used model of stroke in rodents. I can accurately measure the level of cerebral ischaemia, but I do require invasive surgery. I am…?

a) Intraluminal suture middle cerebral artery occlusion model
b) Photothrombotic stroke model
c) Autologous blood injection model
d) Endothelin-1 middle cerebral artery occlusion

A

Which preclinical stroke model am I? I am the the most widely used model of stroke in rodents. I can accurately measure the level of cerebral ischaemia, but I do require invasive surgery. I am…?

a) Intraluminal suture middle cerebral artery occlusion model

b) Photothrombotic stroke model
c) Autologous blood injection model
d) Endothelin-1 middle cerebral artery occlusion

500
Q

An 89-year-old patient was diagnosed with having a saccular aneurysm on his middle cerebral artery with minor/moderate symptoms. An MRI indicated that the aneurysm had ruptured. Which of the following approaches would MOST LIKELY be the best treatment option?

a) Surgical clipping
b) Endovascular coiling
c) Open surgery
d) Mannitol

A

An 89-year-old patient was diagnosed with having a saccular aneurysm on his middle cerebral artery with minor/moderate symptoms. An MRI indicated that the aneurysm had ruptured. Which of the following approaches would MOST LIKELY be the best treatment option?

a) Surgical clipping

b) Endovascular coiling

c) Open surgery
d) Mannitol

501
Q

Richard is 65-years-old and has atherosclerosis, which is thought to have contributed to the development of an aortic aneurysm. What type of aortic aneurysm does Richard MOST LIKELY have?

a) Saccular
b) Fusiform
c) Dissecting
d) Giant saccular

A

Richard is 65-years-old and has atherosclerosis, which is thought to have contributed to the development of an aortic aneurysm. What type of aortic aneurysm does Richard MOST LIKELY have?

a) Saccular

b) Fusiform

c) Dissecting
d) Giant saccular

BMS3052 (26 decks)

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