Brainscape's Knowledge GenomeTM

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


See full index

PHASE ONE > Cardiovascular System > Flashcards

Cardiovascular System Flashcards

1
Q

What is haemopoiesis?

A

Formation of the blood cells

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

What is the lifespan of a red blood cell?

A

120 days

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

What is the lifespan of a platelet?

A

7-10 days

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

Where do the precursors of mature blood cells derive from?

A

Bone marrow.
In utero; yolk sac, liver and spleen, bone marrow

Children - all bones

Adults - axial skeleton

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

Haemopoietic stem cells

A

They are pluripotent, so they replicate and differentiate into red cells, white cells, platelets and marrow stroma.

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

Control of haemopoiesis

A

Replication and differentiation is stimulated by hormonal growth factors.
For red blood cells, the hormone is erythropoietin (EPO) which is used for renal failure therapy. White blood cells the hormone is Granulocyte-macrophage colony-stimulating factor (GM-CSF) used in chemotherapy. For platelets its thrombopoietin (TPO) drives production of platelets used in people who have low platelet count.

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

Histological features of red blood cells (erythrocytes)

A

Simple anucleate cells with no mitochondria
Biconcave
7.5micrometer diameter
Contain haemoglobin glycolysis enzymes

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

Haemoglobin

A

Carries oxygen from the lungs to the tissue. 4 globin chains each with its own haem group (O2 carrier)
Tetrametric protein with 2 alpha and 2 beta chains.
Allows O2 to reversibly combine with Fe2+ ions in an aqueous environment.

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

Method of looking at haemoglobin: High performance liquid chromatography (HPLC)

A

Separates haemoglobin on basis of electrical charge

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

Method of looking at looking at haemoglobin: Electrophoresis

A

Separates haemoglobin on basis of electrical charge

Acid and alkaline conditions

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

Abnormalities of haemoglobin

A

Sickle cell disease (heterozygous dominant)
Lack of the gene for alpha/beta thalaessemia - beta is more common since this is the chain that changes from the baby form of Hb.

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

What is the name for the condition where there is a deficiency of Hb?

A

Anaemia

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

For men and women respectively, what are low levels of Hb? Why do women have lower levels of haemoglobin?

A

Men - <130g/L
Women - <110g/L

Women have lower levels due to menstrual bleeding

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

What is acute blood loss?

A

Blood loss results in loss of red blood cells and plasma.

Initially the haemoglobin levels will be unchanged.

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

Whart is a result of production failure of RBC?

A 
Hypoplastic anaemia (not enough)
Dyshaemopoeitic anaemia (ineffective production)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why could there be increased removal of RBC?

A

Blood loss or haemolytic loss (breakdown of RBC). This can be due to intrinsic (within RBC) abnormalities or extrinsic (outside RBC) abnormalities.

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

Aplastic anaemia

A

Can be inherited or acquired for reasons such as idiopathic, chemical/drug, viral, radiation.

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

Dyshaemopoietic anaemia

A

Multiple mechanisms e.g. anaemia of chronic disease
Defective haemoglobin synthesis.
Defective DNA synthesis.

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

Haemolytic anaemia can be due to 2 reasons

A

Intrinsic RBC abnormalities

Extrinsic abnormalities

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

Haemolytic anaemia + intrinsic RBC abnormalities

A

It can be acquired such as with PNH (haemolysis - breaking apart of RBCs) or it can be for hereditary reasons such as membrane disorders, enzyme disorders, and haemoglobin disorders.

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

Haemolytic anaemia + extrinsic RBC abnormalities

A 
Antibody mediated (AIHA)
Mechanical trauma (DIC)
Infections (Malaria)
Chemicals (lead poisioning)
Sequestration (hypersplenism)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Iron deficency anaemia

A

This is the most common cause of anaemia caused by chronic bleeding in the gastrointestinal tract, poor diet, malabsorption, hook worm.
There is a reduction in mean amount of Hb in cell and cell volume.

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

Types of white blood cell

A 
Neutrophils
Monocytes
Lymphocytes
Basophils
Eosinophils

All cells except lymphocytes are termed phagocytes.

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

What is the most abundant WBC?

A

Neutrophils

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

What do neutrophils do?

A

They phagocytose bacteria and foreign material by releasing chemotaxins and cytokines important in the inflammatory response.

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

What is the inflammatory response?

A

Increased temperature
Increased blood flow
Local pain

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

What happens when there is a decreased number of neutrophils?

A

Recurrent bacterial infections

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

Monocytes

A

Macrophages which also phagocytose bacteria+foreign material. The majority transit through the blood to the tissues. They are dendritic cells which present antigens to the immune system.

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

How do neutrophils and monocytes differ?

A

Monocytes are present in tissues.

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

What do basophils become?

A

Basophils migrate to tissues becoming mast cells.

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

What are mast cells?

A

Mast cells are filled with histamine containing granules and express surface IgE. They have an important role in the immune and allergic response.

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

Eoisinophils

A

Rare

Special role in protection against parasites.

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

Where do B-lymphocytes mature?

A

Bone marrow of the rib

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

What percentage of lymphocytes in the blood do B-lymphocytes make up?

A

20%

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

Role of B-lymphocytea

A

Generate antibodies when stimulated by foreign antigens in the humoral immunity response.

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

Where do T-lymphocytes matures?

A

Thymus

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

What percentage of lymphocytes in the blood do T-lymphocytes make up?

A

80%

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

B-lymph have ??? receptors

T lymph have ??? receptors

A

B - IgE

T - TCR

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

Two types of T-lymph.?

A

Cytotoxic T-cells which target infected cells for death (cell mediated immunity).
T-helper cells stimulate the immune response of B-lymphocytes.

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

How does blood inside the vessels remain fluid?

A

Endothelial cells, anticoagulant pathway and fibrinolytic pathway actively keep it fluid. Platelets and proteins of the coagulation cascade circulate in an inactive state.

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

What is thrombosis?

A

When blood clots inside the vessel instead of outside the vessel as it should.

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

What do platelets contain?

A

Electron dense granules containing calcium, ADP/ATP and serotonin.

Alpha granules containing platelet derived growth factor (PDGF), fibrinogen, heparin antagonist (PF4) and VWF (von Willebrand Factor).

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

Platelets + primary haemostasis.

A

Platelets circulate in an inactive state. When there is damage to the blood vessel, they adhere to collagen via glycoprotein Ia on sub-endothelium.
Glycoprotein Ib and Glycoprotein IIIa bind von Willebrand Factor. Binding causes platelets to change shape and activate become elongated. Tethering of platelets causes them to activate further receptors on their surface which enables further crosslinking

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

Platelets + primary haemostasis.

A

Platelets circulate in an inactive state. When there is damage to the blood vessel, they adhere to collagen via glycoprotein Ia on sub-endothelium.
Glycoprotein Ib and Glycoprotein IIIa bind von Willebrand Factor. Binding causes platelets to change shape and activate become elongated. Tethering of platelets causes them to activate further receptors on their surface which enables further crosslinking with VWF and fibrinogen.
Activation releases contents and results in intracellular signalling causing platelets to release their stored granular contents. Aggregate to form a platelet thrombus (haemostatic plug). Lack of function leads to bleeding. Change in number leads to bleeding/thrombosis.

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

Platelet bleeding disorders: Bernard-Soulier syndrome

Cause and impacts?

A

Deficiency of GPIb receptor

Affects platelet adhesion

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

Platelet bleeding disorders: Glanzmann’s thrombasthenia

Cause and impacts?

A

Defect of GPIIb/IIIa receptor

Affects platelet cross-linking and aggregation.

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

Platelet bleeding disorders: Hemansky-Pudlak

Cause and impacts?

A

Defect in dense storage granules

Affects Platelet activation and aggregation

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

When is there a reduction in platelet number?

A

Thrombocytopenia
Increased bleeding
Spontaneous bleeding

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

When is there a increase in platelet number

A

Thrombocytosis
Arterial thrombosis
Venous thrombosis

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

Plasma

A

Clear, straw coloured liquid left after cellular component of blood is removed. It is 90% water but also has salts, glucose and proteins.

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

Proteins in plasma

A

Albumin
Carrier proteins
Coagulation proteins
Immunoglobulins

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

Where is albumin produced?

A

The liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the function of albumin?

A

To determine oncotic pressure of the blood and keep intravascular fluid in that space and keep the pressure within vessel.

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

What can a lack of albumin lead to?

A

Oedema

seen in liver disease; nephrotic syndrome

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

What produces immunoglobulins?

A

B-lymphocytes

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

What are immunoglobulins?

A

Antibodies

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

Different classes of immunoglobulins?

A 
IgG 
IgA
IgM
IgE
IgD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is the Coagulation Cascade?

A

Series of enzymes that circulate in an inactive state. They are sequentially activated in a ‘cascade sequence’ and convert soluble fibrinogen into insoluble fibrin polymer. This generates a stable clot.

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

What does inhibition of fibrin production lead to?

A

Bleeding

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

A sign of failure of coagulation proteins

A

Bleeding

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

A sign of overactive coagulation proteins

A

Thrombosis

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

What drugs affect platelet function? When are they used?

A

Aspirin
Clopidogrel
Used following a heart attack to reduce risk of further clots

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

Hemophilia A symptom

A

severe bleeding into muscles and joins

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

Why does Hemophilia A take place?

A

Deficiency of factor VIII, a blood clotting protein

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

How is Hemophilia A treated?

A

Recombinant factor VIII

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

Hemophilia A + genetics

A

X-linked condition

Alternate generations

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

Hemophilia B

A

Severe bleeding into muscles and joints

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

Why does Haemophilia B take place?

A

Deficiency of factor IX

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

How is Hemophilia B treated?

A

Recombinant factor IX

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

Von Willebrand Disease

A

Usually mild bleeding disorder which is often unrecognised due to a deficiency in VWF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Affect of aspirin and clopidogrel on bleeding?

A

Affect platelet function by reducing it

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

Affect of chemotherapy on bleeding?

A

Reduces platelet numbers

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

Which drugs affect coagulation cascade?

A

Heparin - a natural anti-coagulant produced by basophils and mast cells which inhibits platelet function while inactivating various coaguation factors such as factor IX
Warfarin
oral anticoagulants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Affect of steroids on bleeding?

A

Steroids affect tissues making them weaker causing bruising and bleeding

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

Liver disease + Blood

A

Coagulation factors such as factor VIII and factor IX are synthesised in the liver so LD is often associated with bruising and bleeding and prolonged prothrombin time.
May also result in low platelets.

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

Vitamin K + blood

A

Necessary for functional activity of coagulation factors II, VII, IX and X. Warfarin interferes with the vitamin K activation pathway.
Manifests as prolonged prothrombin

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

Disseminated intravascular coagulation

A

Breakdown of haemostatic balance.
Simultaneous bleeding and microvascular thrombosis which is life threatening.
Can cause sepsis

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

Transfusion reactions

A

If the patient is transfused with red blood cells that have antigens on their cell surface which the patient lacks on their own RBCs, the new RBCs are seen as foreign and they are haemolysed.

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

Blood group A alleles and plasma antibodies

A

AA or AO

Anti-B antibodies

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

Blood group B alleles and plasma antibodies

A

BB or BO

Anti-A antibodies

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

Blood group AB alleles and plasma antibodies

A

AB

No antibodies

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

Blood group O alleles and plasma antibodies

A

OO

Anti-A and Anti-B antibodies

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

Other blood group

A

Rhesus system (Rh)

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

5 most important antigens in the Rhesus system

A

D C c E e

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

Which is the most clinically significant antigen in the Rhesus system?

A

D
Responsible for the most clinical issues associated with the system
Can either be present Rh D+ or absent Rh D-

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

Anti-D and pregnancy

A

If women who are Rh D antingen negative (dd) have a baby inside which has Dd genotype, and D-antigen negative mother is exposed to D antigen from baby’s red blood cells, immunoglobins called IgG anti-D produced by the mother. As a result, baby causes transfusion reaction against mum. The IgG Anti-D can cross placenta and haemolyse the baby’s red cells.

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

What are packed red cells?

A

Packed = plasma depleted

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

When are platelets administered medically?

A

On oncology wards to patients who have bone marrow failure.

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

What is HAS?

A

Human albumin solution
Physiological plasma expender
Used to increased oncotic pressure (liver disease, nephrotic syndrome) keeping fluid within vessels.
Can reduce oedema.

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

What is gastrulation?

A

Mass movement and invagination of the blastula to form 3 layers:

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

What does the ectoderm eventually become?

A

Outside skin
Nervous system
Neural crest (which contributes to cardiac outflow and coronary arteries)

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

What does the mesoderm eventually become?

A

All types of muscle
Most systems
Kidneys
Blood

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

What does endoderm eventually become?

A 
Gastrointestinal tract (including liver and pancreas, but not smooth muscle) 
Endocrine organs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What does FHF stand for? What will it eventually become?

A

First heart field (future left ventricle)

The FHF generates a scaffold which is added by the second heart field and cardiac neural crest.

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

What does SHF stand for? What will it eventually become?

A

Second heart field (future outflow tract, future right ventricle, future atria)

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

During which days does the primitive heart tube form?

A

18-22

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

Why does the primitive heart tube begin to form?

A

Diffusion alone is no longer capable of sustaining the embryo

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

Where do progenitor heart cells originate from?

A

The epiblast

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

What happens on day 16?

A

Progenitor heart cells migrate through steak to the splanchic layer of lateral plate mesodemr. Cells specialise from lateral to medial to become different parts of the heart.

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

Where does the secondary heart field reside?

A

Splanchic mesoderm ventral to the pharynx. Cells extend laterally to form the left and right outflow.

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

What happens when the primary heart field cells are established?

A

They are induced by the pharyngeal endoderm to form cardiac myoblasts ad blood islands that develop into blood cells and vessels via vasculogenesis.

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

What happens from the blood islands

A

Blood islands unite into a horse-shoe endothelia lined tube surrounded by myoblasts. This is called the CARDIOGENIC region. The intraembryolic cavity (primitive body) surrounding it develops into the PERICARDIAL CAVITY.
The bilateral and parallel blood islands develop to form dorsal aorta (pair of longitudinal vessels).

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

What happens as the embryo folds head to toe and laterally (coupled with the rapid growth of the brain)

A

The heart and pericardial cavity move first to the cervical region and then to the thorax.

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

What happens to the developing heart tube after this

poles

A

The developing heart tube receives venous drainage as its caudal pole and begins to pump blood out of the first aortic arch into the dorsal aorta at its cranial pole. It bulges more into the pericardial cavity.

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

What happens on day 22?

A

The heart begins to beat

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

What happens on day 23?

A

Heart tube lengthenes and begins to bend

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

As looping of the heart tube begins, what begins to appear?

A

Primordial structures.
The atrial portion (paired suture outside the pericardial cavity) forms a common atrium and is incorporated into the pericardial cavity.
The atriventricular junction remains narrow and forms the atrioventricular canal which connects the common atrium and the early ventricle.

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

What does the ‘bulbis cordis’ develop into?

A

The trabeculated part of the right ventricle.

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

What does the conus cordis (the mid-portion of the bulbus cordis) develop into?

A

The outflow tracts of the ventricles

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

Before cardiac separation, what is there?

A

one common atrium and one common ventricle

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

Process of cardiac separation

A

The cardiac septum forms and the septum primum extends from the endocardial cushions into the atria from the atrioventricular canal. The ostium primum (the opening between the septum and endocardial cushions) closes as the endocardial cushions extend whilst perforations appear in the upper end of the septum primum forming the ostium secondum, eventually being closed by overlap by the septum secondum. Septum secondum extends to form the superior atrial wall, where the foramen ovale is found. At birth, as the lungs become functional the left atrial pressure exceeds that of the right forcing the septum primum against the septum secondum. This forms the fossa ovalis.

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

Which two kinds of arteries are there?

A

Elastic and Muscular

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

Function of elastic arteries

A

Increase efficiency

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

Function of muscular arteries

A

Control distribution

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

What are the arterioles?

A

Terminal branches of the arteries

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

Examples of elastic arteries

A 
Aorta
Brachiocephalic
Carotids
Subclavian 
Pulmonary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

What regulates blood flow in capillaries?

A

Precapillary sphincters

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

3 types of capillaries

A

Continuous
Fenestrated
Discontinuous

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

What drives embryonic vessel development

A

Angiogenic growth factors: (vascular endothelial growth factor, angiopoetin 1+2) which induce growth

Repulsive signals (plexin, semaphorin signalling, ephrin interactions) which prevent growth

Active signals - VEGF

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

How do you determine if a vessel is an artery or a vein? (receptor)

A

Ephrin-B2 receptor is only present on ARTERIES.

Ephrin-B4 receptor is only present on VEINS.

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

What do the first and second ‘aortic arches’ become?

A

They become minor head vessels.
The first aortic arch becomes a small part of maxillary.
The second aortic arch becomes artery to ear

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

What do the third aortic arches become?

A

Become common carotid arteries and proximal internal carotid arteries.
Distal internal carotids come from extension of dorsal aortae.

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

What happens to the right dorsal aorta and right 4th aortic arch?

A

The right dorsal aorta loosens connection with midline aorta and the 6th aortic arch, remaining connected to the right fourth arch. It acquires branch of 7th cervical intersegmental artery, which grows into the right upper limb. The right subclavian artery is diverted from the right fourth arch, right dorsal aorta and right 7th intersegmental artery.

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

Left dorsal aorta and Left 4th aortic arch

A

The left dorsal aorta continues into trunk as the descending aorta.
The left 7th cervical intersegmental artery grows into the left subclavian artery. The left subclavian artery is diverted from the left fourth arch, left dorsal aorta and left 7th intersegmental artery.

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

6th aortic arch

A

Right 6th arch may form part of the pulmonary trunk

Left arch forms ductus arteriosus - communication between pulmonary artery and the aorta.

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

Platelets and disease

A 
Thrombosis
Myocardial infarction 
Ischaemic Stroke
Critical leg ischaemia
Sudden death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What is atherogenesis?

A

formation of fatty deposits in arteries

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

What is atherothrombosis?

A

Blood clot within artery

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

What percentage narrowing ensures limited blood flow?

A

70%

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

What can atherothrombosis cause?

A

Angina

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

What can the inflammatory process driving the atherosclerosis lead to?

A

Thinning of capillary making it erode or rupture.

This leads to atherothrombosis since body wants to heal the rupture and form a thrombus.

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

What happens to a platelet when its activated?

A

Its shape changes. It changes from smooth discoid to spiculated (spikes/pointed) and pseudopodial.
The surface area increases
There is increased possibility of cell interactions because number of receptors increases.
There is increased affinity of receptor for fibrinogen (needed for platelet aggregation),

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

What receptors are on the surface of a platelet?

A

Glycoprotein IIb/IIa receptors

50,000-100,000 copies on resting platelet

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

Platelet action after atherosclerotic plaque rupture

A

Platelets adhere to damaged vessel wall. The collagen receptors bind to subendothelial collagen which is exposed. GPIIb/IIIa receptors on platelets bind to von Willebrand factor which is attached to collagen . The α2β1 receptor binds to collagen which slows the platelets down. Platelets come to a half and GPVI binds to collagen and activates platelets. Platelets release chemical which recruit other platelets and cause aggregation.

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

What is platelet adhesion?

A

A platelet spreading out on a collagen-coated surface

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

Platelet activation mechanisms

A

See M’s notes

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

COX-1 (Cyclooxygenase-1) enzyme

A

Mediates GI mucosal integrity

COX-1 –> Prostaglandin H2 –> Thromboxane A2

Thromboxane A2 released when platelet binds to collagen and mediates aggregation as well as stimulating contraction of the artery. Low doses of aspirin INHIBIT COX-1 pathway production of T-A2 which is good during/before heart attacks to prevent thrombus.

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

COX-2 (Cyclooxygenase-2) enzyme

A

Mediates inflammation

Mediates prostacyclin production, which inhibits platelet aggregation and affects renal function. keeps blood flowing.

COX-2/COX-1 => Prostaglandin H2 => Prostacyclin

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

Aspirin + COX

A

Low dose inhibits COX-1

High dose inhibits both COX-1 and COX-2.

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

What are the ADP receptors on platelets?

A

P2Y1

P2Y12

141
Q

P2Y1 receptor

A

Link to Gq protein activating phospholipase C, mobilising calcium and initiates platelet activation

142
Q

P2Y12 receptor

A

Linked to Gi protein which inhibits formation of cAMP, allowing for amplification of platelet activation.

143
Q

What do the P2Y1 and P2Y12 pathways lead to?

A

The production of dense granules which get shunted to the surface of activated platelets and released. One of the content of these granules is ADP, which further activates the pathways greating a positive feedback loop. When GPIIb/IIIa binds to fibrnogen this causes further amplification.

144
Q

What is an example of a receptor activated by Thrombin?

A

PAR-1

145
Q

Platelet procoagulant activity mediated by changes to the membrane lipid bilayer

A

1) Platelet activation causes a change in the lipid bilayer.
2) Activation of PAR-1 receptor due to thrombin causes the release of calcium ions from intracellular stores.
3) This inhibits translocase and scramblase enzymes, causing amino-phospholipids to flip and express themselves onto the outer platelet membrane.
4) This exposure allows prothrombinase to bind to the membrane and convert prothrombin into thrombin.

146
Q

What is the function of the fibrinolytic system?

A

Ensures a balance in the coagulation cycle

It is a system to break down the fibrinogen strands and dissolve the clot.

147
Q

Fibronlytic system

A

Healthy endothelial cells release tPa (tissue plasminogen activator) which converts plasminogen into plasmin.
Plasmin breaks down fibrin into fibrin degradation products, and dissolvs the clot.

148
Q

Inhibitors of the Fibronlytic system

A

PAI-1 blocks tPa

Antiplasmin blocks plasmin

149
Q

α granules

A
  • contribute to thrombotic response because they contain coagulation factors
  • drive inflammatory response due to their inflammatory mediators (wound healing)
  • contain P-selectin allowing platelets to bind to WBC
150
Q

Platelet summary

A

See M notes page 28-29

151
Q

Where can the apex beat be heard?

A

Left 5th intercostal space

Mid-clavicular line

152
Q

Which chambers of the heart is anterior?

A

Mainly right ventricle

153
Q

Which chambers of the heart are posterior?

A

Mainly left atrium and pulmonary veins

154
Q

2 layers of the pericardium

A

Visceral

Parietal

155
Q

What is a cardiac tamponade?

A

Restricts the rapid collection of pericardial fluid and impairs filling

156
Q

What does pleural reflection allow?

A

Drainage of pericardial fluid from the left of the xiphisternum

157
Q

What attaches papillary muscles of the ventricle to atriventricular valves?

A

chordae tendinae

158
Q

What is the function of the coronary sinus?

A

drains blood from the heart muscle into the right atrium

159
Q

What separates the smooth and trabeculated portions of the right atrium?

A

Crista terminalis

160
Q

What is the Fossa ovalis?

A

The remains of the foramen ovale which was patent in foetal life

161
Q

Where do coronary muscle cells cross link and join?

A

Intercalated discs

162
Q

From where do coronary arteries arise?

A

Aortic root sinuses

163
Q

How many main coronary arteries are there?

A

two - left and right

164
Q

What does the left main stem divide into?

A

Left anterior descending and circumflex branches

165
Q

Where does the left anterior descending branch?

A

The anterior interventricular groove

166
Q

What does the left anterior descending give off?

A

Septal and diagonal branches to the septum and left ventricular myocardium

167
Q

Where does the circumflex run?

A

Left atrioventricular groove

168
Q

What does the circumflex give off?

A

Obtuse marginal branches to the posterolateral left ventricular wall

169
Q

In 10% of people what does the circumflex provide?

A

Posterior descending artery

170
Q

Where does the right coronary artery run?

A

Right atrioventricular groove

171
Q

What does the RCA supply?

A

The sinus node
Atrioventricular node
Branches to the anterior right ventricle wall

172
Q

What does distal RCA branch into?

A

Posterolateral and posterior descending arteries

173
Q

Where does the posterior descending artery run?

A

Inferior septum

Left ventricle

174
Q

Components of the Heart Conduction system

A

SA node
AV node
Bundle of His
Purkinje Fibres

175
Q

What joins myocytes?

A

Intercalated discs (containing gap junctions and desmosomes)

176
Q

Properties of myocytes

A

Branched tubular cell (strirated)
High mitochondrial density
Contains sarcromeres/myofibrils

177
Q

Resting membrane potential of myocytes

A

Polarised
Negatively charged inside the cell (-90mV)
Unbalanced ion concentrations and active membrane pumps result in an external positive charge.

178
Q

What does the pump in myocyte membrane do?

A

Na/K pump
3Na+ ions are transferred outside the cell and 2K+ transferred inside the cell maintaining the cell polarisation.
(Calcium also moves out with sodium).

179
Q

What is the myocyte membrane permeable to?

A

Potassium ions.

The diffusion of potassium out of the cell allows negative polarisation inside the cell.

180
Q

Myocardial action potential

A

Spread from one cell to another through gap junctions (connexins) and this activates other myocytes.
AV node and Purkinje fibres have similar action potentials but at a slower rate, therefore usually stimulated by potentials spreading from the AV node.

181
Q

Summary of action potential process (6)

A 
Depolarisation
Repolarisation
Propagation
Excitation-contraction coupling
Automaticity related to pacemaker AP 
Refractory period
182
Q

Depolarisation

A

Rapid influx of sodium ions prolonged by influx of calcium ions

183
Q

Repolarisation

A

potassium diffuses out of membrane

184
Q

Propagation

A

Positive sodium ions depolarise adjacent cells and gap junctions

185
Q

Excitation-contraction coupling

A

Release of calcium from T-tubules and sarcoplasmic reticulum.

186
Q

Automacity related to pacemaker action potential

A

Slow sodium ion influx

187
Q

Refractory period

A

Fast sodium ion and slow calcium ion channels close.

188
Q

Phase numbers and their change in potential

A

0 = Rapid depolarisation (na+ inflow)

1 = Partial repolarisation
(K+ outflow/Na+ inflow stops)

2 = Plateau
(slow inflow of Ca2+)

3 = Repolarisation
(K+ outflow/inflow of Ca2+ stops)

4 = Resting potential
(K+ outflow only)

189
Q

Refractory period (two kinds)

A

ABSOLUTE refractory period = inactivation of the sodium channels which close and do not open.
RELATIVE refractory period = sodium channels start to activate gradually. If a lot of channels reactivate another action potential can be stimulated.

190
Q

Automaticity - pacemaker cells

A

Pacemaker cells have no true resting membrane potential and constantly drift towards the value of the action potential.

191
Q

2 kinds of autonomic control

A

Sympathetic stimulation

Parasympathetic stimulation

192
Q

What is sympathetic stimulation controlled by?

A

Adrenaline and noradrenaline and type 1 beta adrenoreceptors.
Increases adenyl cyclase => increases cAMP (Activating sodium and calcium channels and so allowing the the threshold to be reached sooner)

193
Q

What does increased sympathetic stimulation result in?

A

Increased heart rate
Increased force of contraction
Large increase in cardiac output by up to 200%

194
Q

What does decreased sympathetic stimulation result in?

A

Decrease in heart rate and decrease in cardiac output by 30%.
Blocking type 1 beta adrenareceptora (beta-blockers).

195
Q

What is parasympathetic stimulation controlled by?

A

Acetylcholine

M2 receptors - inhibit adenyl cyclase => reduced cAMP (less sodium and calcium ions, activation of potassium ions)

196
Q

What does increased parasympathetic stimulation result in?

A

Decreased heart rate
Decreased cardiac output ~50%
Decreased force of contraction

197
Q

What does decreased parasympathetic stimulation result in?

A

Increased heart rate

198
Q

Active Potential Propogation - why is it needed?

A

Effective cell-cell communication is critical for rapid, uniform conduction of cardiac action potentials because it allows the heart to contract co-ordinately.

199
Q

How does active propogation happen?

A

There is a free flow of positive sodium ions between cardiomyocytes through gap junctions within the intercalated discs. This then allows neighbouring cells to reach their threshold and activate their own voltage gated sodium channels. Cannot bounce backwards due to refractory period.

200
Q

Where is sinoatrial node located?

A

Posterior wall of Right Atrium

201
Q

Conduction pathway SAN

A

Wave front conducted through right atrium by backward bundles to the left atrium and down to the atrioventricular node.

202
Q

What does the SAN determine?

A

It is the primary pacemaker and normally determines the heart rate the heart beats.

203
Q

Resting membrane potential of SAN.

What is the AP driven by?

A

negative
-55mV to -60mV

AP driven by slow Ca2+ channels because of slow Na+ inflow

204
Q

Atrioventricular node

A

Transmits cardiac impulse between atria and ventricles.

Delays the impulse, allowing the atria to empty blood into ventricles.

205
Q

Adaptations of AV node for its function

A

Less gap junctions - sodium ions move less quickly

Smaller fibres than atrial fibres = longer transmission

206
Q

His-Purkinje System

A

Conduction down bundle of His to the left and right Purkinje fibres.

Spread from endocardium to pericardium.

207
Q

Speed of conduction in His-Purkinje system - and why? How is it adapted to suit this speed?

A

Rapid!
This allows coordinated ventricular contraction from apex base.
Very large fibres and high permeability at gap junction.

208
Q

Where in the heart can pacemaker cells be found?

A

SAN
AVN
HP system

209
Q

Hierarchy of pacemakers

A

A slower pacemaker is blocked by a faster one

210
Q

Myocardial Action Potential vs Skeletal Action potential

A

Key difference = the plateau phase.

Allows the heart to fill.

211
Q

Mycardial contraction vs skeletal contraction

A

M is 15x longer

212
Q

Excitation Contraction Coupling

purpose, which phase, what is it dependent on, what is the process

A

This stage is how an electrical impulse is translated into cardiac contraction. It’s dependent on calcium ions and happens during Phase 2 plateau.

Inward calcium current increases intracellular calcium concnetration, which activates receptors on sarcoplasmic reticulum leading to more release of calcium ions from the sarcoplasmic reticulum. Calcium ions bind to troponin C on actin filaments. This induces a conformational change exposing the actin-myosin binding site. Actin binds to myosin and cardiac contraction occurs.

213
Q

What does an ECG show?

A

Changes in voltage over time (not action potential)

214
Q

Baseline of ECG

A

Isoelectric point

= no net current flow in direction of lead

215
Q

Positive deflection (up) from baseline

A

Net current flow towards lead

216
Q

Negative deflection (down) from baseline

A

Net current flow away from lead

217
Q

1 big square ECG

A

5mmx5mm

218
Q

1 small square ECG

A

1mmx1mm

219
Q

Typical speed and voltage settings ECG

A 
Speed = 25mm/sec
Voltage = 10mm/mV
220
Q

Big/small squares (horizontal) and speed

A

5 big squares = 1 second
1 big square OR 5 small squares = 0.2 seconds
1 small square = 0.04 seconds

221
Q

Big/small squares (vertical) and voltage

A

2 big squares = 1mV

1 big square = 0.5mV

222
Q

What is an R-R interval

A

Time between beats/QRS complexes on ECG

223
Q

P wave

A

atrial depolarization

less than 3 small squares

224
Q

PR interval

A

Slow conduction between AV node and His-Purkinje system
3-5 small squares
120-200ms

225
Q

QRS complex

A

Ventricular depolarisation
up to 120 ms
3 small squares

226
Q

ST segment

A

The interval between depolarisation and repolarisation

227
Q

T wave

A

Ventricular repolarisation

228
Q

QT interval

A

Time of depolarisation and repolarisation

229
Q

What causes QT interval to vary

A

heart rate

faster heart rate = shorter QT

230
Q

Why can QT interval be prolonged? What are the values for prolonged QT in both men and women

A

Ischaemia, drugs, congenital issues
440 men
460 women

231
Q

How do you perform an ECG?

A

Electrodes are placed on the skin, 6 chest leads and 4 limb leads.

V1: 4th intercostal space right side septum
V2: 4th intercostal space left sternal edge
V4: 5th intercostal space on midclavicular line
V3: half way between LSE and MCL leads
V6: 5th intercostal space on midaxillary line
V5: halfway between MAL and MCL

232
Q

12 Lead ECG

A 
aVF => +- 90°
III => -60°, +120°
aVL => -30°, +150°
I => 0°, +180°
aVR => +30°, -150°
II => +60°, -120°
233
Q

Lateral Leads

A

I
avL
V5
V6

234
Q

Septal leads

A

V1

235
Q

Anterior leads

A

V2, V3, V4

236
Q

Inferior leads

A

II
III
avF

237
Q

What can be deduced about electrical impulses from viewing a single electrode?

A

Electrical impulse is only briefly in the direction of electrode before it changes direction.

238
Q

Wat can you say about electrical impulse for atria in comparison to ventricles

A

The impulse for the atria is smaller since atria are smaller and have less myocytes.

239
Q

Abnormalities in P wave - tall peaked P wave

A

right atrial enlargement

240
Q

Abnormalities in P wave - Bifid P wave

A

left atrial enlargement

241
Q

Abnormalities in P wave- inverted P waves

A

non sinus origin (junctional or ecptopic atrial)

242
Q

Abnormalities in QRS complex - broad complex

A

Ventricular origin (e.g. ventricular tachycardia)
Hyperkalemia (too much potassium)
Ventricular pacing
Left and right bundle branch block

243
Q

Abnormalities in QRS complex - high voltage

A

ventricular hypertrophy (thickening of wall)

244
Q

ST segment abnormalities: ST segment depression causes

A 
Digoxin toxicity 
Hypokalaemia
Ventricular hypertrophy
Myocardial infarction 
Pulmonary embolism 
Raised intracranial pressure
245
Q

Dextrocardia

A

Multiple -ve P waves
Low voltage V3-V6 with no progression
Can record right sided chest leads, which mirror the normal leads

246
Q

Main components of the myocardium

A

Contractile tissue
Connective tissue
Fibrous frame
Specialised conduction system

247
Q

What does myocardial metabolism rely on?

A

Relies on free fatty acids during aerobic metabolism (efficient energy production)

248
Q

Myocardial metabolism during hypoxia

A

During ypoxia, there is no FFA metabolism, thus anaerobic metabolism ensues. This relies on metabolising glucose anaerobically producing energy sufficient to maintain the survival or the affected muscle without contraction.

249
Q

Ultrastructure of the myocardial working cell: how are the contractile proteins arranged?

A

In a regular array of thick myosin and thin actin filaments (myofibrils)

250
Q

The sarcomere

A

The functional unit of the contracile apparatus. It is the region between a pair of Z-lines, containing two half I-bands and one A-band.

251
Q

The sarcoplasmic reticulum

A

A membrane network that surrounds the contractile proteins. It consists of the sarcotubular network at the centre of the sarcomere and the subsarcolemmal cisternae (T-tubules and sarcolemma) so that Ca2+ ions are always available.

252
Q

What lines the transverse tubule (T-tubule) system?

A

A membrane that is continuous with the sarcolemma, so that the lumen of the T-tubules carries the extracellular space towards the centre of the myocardial cell.

253
Q

Where is mitochondria found in myocardium

A

In between myofibrils.

254
Q

A-band

A

The region of the sarcomere occupied by the thick filaments (myosin)

255
Q

I-band

A

Occupied only by thin actin filaments that extend towards the centre of the sarcomere from the Z-lines. It also contains tropomyosin and troponins.

256
Q

What attaches atin filaments to the Z-lines?

A

Titin proteins, which provide elasticity.

257
Q

What happens when titin proteins are damaged?

A

Elongation of the muscle => heart failure.

258
Q

Summary of contraction mechanism

A
  • Depolarisation of the cell membrane.
  • Influx of Ca2+ inwards
  • Ca2+ binds to troponin.
  • Troponin changes shape and troponin-tropomyosin complex is lifted from the actin groove
  • The actin-myosin binding site is exposed
  • Actin moves closer to the centre of the sarcomere, allowing for myosin bridge to bind to actin and causes contraction
  • Sliding of actin over myosin by ATP hydrolysis through the action of ATPase in the head of the myosin molecule. These heads form the cross bridges that interact with actin, after linkage between calcium and troponin, and deactivation of tropomyosin and TnI (changed troponin).
259
Q

Repolarisation muscle

A

Cells spend energy to removed Ca2+ from troponin, allowing it to inhibit actin-myosin interaction. The bridges are separated and actin is moved back. Muscle relaxes.

260
Q

Myosin structure

A

2 heavy chains (responsible for the dual heads)
4 light chains
The heads are perpendicular on the thick filament at rest, and bend towards the centre of the sarcomere during contraction.
Alpha and beta myosin.

261
Q

Actin structure and properties

A

Globular protein
Double-stranded macromolecular helix (G) - creates a groove where the myosin acts which is covered by the troponin-tropomyosin complex.

262
Q

Tropomyosin structure and properties

A

Elongated molecule, made of two helical peptide chains.

It occupies each of the longitudinal grooves between the two actin strands.

263
Q

Troponin TnI

A

forms complex with tropomyosin to inhibit actin and myosin interaction

264
Q

Troponin TnT

A

binds troponin to tropomyosin

265
Q

Troponin TnC

A

high affinity calcium binding sites, signalling contraction

266
Q

Circulation in the heart

A

Superior + inferior Vena Cava bring deoxygenated blood to right atrium
 Blood moved across tricuspid valve to right ventricle
 Blood is squeezed out of right ventricle, through the pulmonary artery into the lungs across the pulmonary valve
 Oxygenated blood comes back to the heart through the 4 pulmonary veins into the left atrium
 Moved down into the left ventricle across the mitral valve
 Left ventricle squeezes blood out the aorta across the aortic valve into systematic circulation.

267
Q

Cardiac cycle overview of stages

A
  • Isovolumic contraction
  • Ejection
  • Isovolumic relaxation
  • Rapid inflow
  • Diastasis
  • Atrial systole
268
Q

ECG and cardiac cycle

A

P - atrium depolarised; occurs before atrial contraction
QRS - ventricle depolarisaed; occurs just as ventricles begin to contract
T - repolarisation

269
Q

First heart sound

A

Closure of the mitral valve at the end of diastole + beginning of isovolumetric contraction

270
Q

Second heart sound

A

Closure of the aortic valve at the end of ventricle emptying and beginning of isovolumetric relaxation

271
Q

Ventricular pressure + LV Conctraction

A

During isovolumetric contraction the volume of the ventricle does not change, both the valves are closed. The ventricle changes shape as it squeezes. This raises the pressure to open the aortic valve.

272
Q

How much blood remains in ventricle after it contracts?

A

30%

273
Q

Ventricular pressure during left ventricle relaxation

A

At the start of relaxation and reduced ejection the aortic valve shuts. The ventricle wall continues to relax and lose pressure with 1/3 of normal volume. Rapid LA filling causes blood to passively move into ventricles down pressure gradient when mitral valve opens. During diastasis the pressure in ventricles starts rising and pressure in atrium and ventricle are equal. There is no movement of blood. Atrial booster is contraction of atrium to squeeze in extra blood.

274
Q

What is a 4th heart sound indicative of?

A

Stiff atria/heart failure

275
Q

Ventricular contraction - systole

Steps

A

Wave of depolarisation arrives and opens the L-calcium tubule (on an ECG, this is the peak of R). Calcium ions arrive at the contractile proteins. Left ventricle pressure rises to above left atrial pressure. The mitral valve closes. Left ventricular pressure rises to above aortic pressure. Aortic valve opens and ejection starts.

276
Q

Ventricular relaxation - diastole

STEPS

A

LVp peaks then decreases. The influence of phosphorylated phospholambdan; cytosolic calcium is taken up into the sarcoplasmic reticulum. This creates a phase of reduced ejection. Aortic flow is maintained by aortic distensibility. Aortic pressure exceeds LVp, aortic valve closes.

277
Q

Ventricular filling - steps

A

LAp is greater than LVp, mitral valve opens, rapid filling starts. Ventricular suction may also contribute to E filling.
Diastisis - LVp = LAp. Filling temporarily stops. Filling is renewed when atrial booster raises LAp creating a pressure gradient.

278
Q

Preload

A

Load present before left ventricle contraction has started; amount of stress in ventricle.

279
Q

Afterload

A

Load after the ventricle contracts.

280
Q

Contractility (inotropic state)

A

The state of the heart which enables it to increase its contraction velocity, to achieve higher pressure, where contractility is increased.

281
Q

Elasitcity

A

the myocardial ability to recover its normal shape after removal of systolic stress.

282
Q

Compliance

A

compliance = how easily a chamber of the heart or the lumen of a blood vessel expands when it is filled with a volume of blood

the relationship between the change in stress and the resultant strain.

283
Q

Diastolic distensibility

A

The pressure required to fill the ventricle to the same diastolic volume.

284
Q

The pressure-volume loop

A

contractility in the end-systolic pressure volume relationship, while compliance is reflected at the end diastolic pressure volume relationship.

285
Q

Pulmonary and bronchial circulation

A

Dual blood supply
Pulmonary circulation from right ventricle
Bronchial circulation takes 2% of left ventricle output.

286
Q

Pulmonary vs Systemic arteries: vessel wall

A 
Pul. = thin 
System = thick
287
Q

Pulmonary vs Systemic arteries: muscularization

A 
Pulmonary = minor
Systematic = significant
288
Q

Pulmonary vs Systemic arteries: need for redistribution

A 
Pulmonary = not in normal state
Systematic = yes
289
Q

mPAP

A

mean pulmonary arterial pressure

290
Q

PAWP

A

pulmonary arterial wedge pressure (estimate of LA pressure)

291
Q

mPAP - PAWP = …

A

CO X Pulmonary vascular resistance

292
Q

What happens to mPAP and CO during exercise? Why is there a difference?

A

mPAP remains stable
CO increases signifiantly.
This occurs due to resistance falling by recruitment and distension of capillaries in response to increase pulmonary artery pressure.

293
Q

Hypoxaemia

A

low oxygen in blood

294
Q

Type 1 respiratory failure values of pO2 and pCO2

A

(O2) less than 8kPa

(CO2) less than 6kPa

295
Q

Type 2 respiratory failure values of pO2 and pCO2

A

pO2 less than 8kPa

CO2 more than 6kPa because with Type II there is a problem with removing CO2.

296
Q

Causes of hypoxaemia

A

Hypoventilation
Diffusion impairment across alveoli capillary membrane
Shunting (blood going through without ventilation)
Mismatch between ventilation and perfusion.

297
Q

Hypoventilation

A 
(occurs during type II RF) 
Failure to ventilate the alveoli. 
Leads to muscle weakness. 
Obesity. 
Loss of respiratory drive. 
Examples in motor neurone disease, kyphosis/scoliosis
298
Q

Diffusion impairment (hint: 3 types)

A
  1. Gaseous diffusion - pulmonary oedema (fluid build up in alveoli). Pulmonary fibrosis increases thickness of lungs.
  2. Blood diffusion - anaemia
  3. Membrane diffusion - interstitial fibrosis
299
Q

V/Q = 1

A

Optimal gas exchange, occuring when regions of lung are ventilated in proportion to their perfusion.

300
Q

V/Q mismatch cases

A

Pulmonary embolism
Asthma
Pneumonia
Pulmonary oedema

301
Q

V/Q > 1

A

(Dead space)
Ventilation in excess of perfusion.
However, pulmonary blood is passing ventilated alveoli and PaO2 is normal.

302
Q

V/Q 0-1

A

Perfusion in excess of ventilation.

increasing PAO2 will increase PaO2.

303
Q

V/Q = 0

A

shunt
Mixed venous blood entering the systemic circulation without being oxygenated vis passage through the lungs.
PaO2 falls.

304
Q

Physiological shunt

A

Bronchial arteries - blood not taking part on gas transfer

305
Q

Intracardiac shunt

A

Eisenmenger’s syndrome

Ventricular septum defect (VSD).

306
Q

Pulmonary shunt

A

Arterio-venous malformation (skipping the capillaries and so not oxygenating the blood).
Complete lobar collapse.

307
Q

Eisenmenger’s syndrome

A

Baby will not be born blue, as oxygenated bloood in the left ventricle moves to the right ventricle and out of the pulmonary artery. However excess volume under high pressure in the pulmonary artery damages it, creating narrowing, increasing resistance and pressure. Blood then goes from RV to LV, and patients present with cyanosis (blueish discolouration of skin). Rasping murmur will be heard. Another symptom of R/L shunt is clubbing of the nails, and polycythaemia (excess red cells with secondary erythrocytosis).

308
Q

Hypoxic Pulmonary vasoconstriction

A

Local action of hypoxia on pulmonary artery wall. Weak response as little muscle. Aims to improve V/Q matching.

309
Q

Diseases of the pulmonary circulation

A

Pulmonary embolism
Pulmonary hypertrophy
Pulmonary arteriovenous malformations

310
Q

Pulmonary embolism

A

A large thrombus = can block the lungs centrally.

A smaller clot is not as severe but causes infarction.

311
Q

How is a pulmonary embolism diagnosed?

A

CT scan
V/Q scan

Inhaling radioactive gas to see even ventilation.

312
Q

Virchow’s Triad

A

3 things that make you more likely to have bloodclots; risk increases with the more of these you have.

  1. Circulatory Stasis (blood not moving in the legs properly)
  2. Endothelial injury
  3. Hypercoagulable state (increased risk of bleeding thrombophilia (more likely to clot)).
313
Q

Pulmonary arterial hypertension progression

A

Normal pulmonary artery -> intermedia layer thickens.
The right ventricle increases in size
Left ventricle becomes smaller.
Increased pulmonary ventricular resistance.

314
Q

What does pulmonary arteriovenous malformation (shunt) cause

A

Hypoxaemia

315
Q

Blood pressure equation

A

BP = CO X Total peripheral resistance

316
Q

Pulse pressure equation

A

systolic - diastolic p

317
Q

Mean arterial pressure equation

A

Diastolic pressure + 1/3 pulse pressure

318
Q

Frank-Starling Mechanism.

A

Stroke volume increases as end-diastolic volume increases due to length-tension relationship of muscle. As the end-diastolic-volume increases, stretch increases and the force of contraction increases. Cardiac muscle at rest is not at is optiumum length.
↑VR = ↑EDV = ↑SV = ↑CO (even if HR constant)

319
Q

What factors effect blood volume

A

Renin-Angiotensin-Aldosterone system
ADH
Adrenals and kidneys

320
Q

How is blood pressure measured?

A

using a sphgmomanometer using bracial artery

321
Q

Control of pressure

A 
Autoregulation
Local mediators
Humoral factors
Baroreceptors
Central neural control
322
Q

Myogenic autoregulation - what is it and what does it regulate?

A

Stretching of the arteriole.

Regulates the constant flow despite perfusion pressure changes.

323
Q

Where is myogenic autoregulation excellent, moderate and poor?

A 
Excellent = renal/cerebral/coronary 
Moderate = skeletal muscle/splanchic
Poor = cutaneous (skin)
324
Q

Balancing intrinsic and extrinsic controls: brain &heart

A

Intrinsic control dominates to maintain bloodflow to vital organs

325
Q

Balancing intrinsic and extrinsic controls: skin

A

Blood flow is important in general vasoconstrictor response and also in responses to temperature (extrinsic) via hypothalamus.

326
Q

Balancing intrinsic and extrinsic controls: skeletal muscle

A

Dual effects: at rest, vasoconstrictor (Extrinsic) tone is dominant; upon exercise, intrinsic mechanisms predominate (Rapid release of blood into muscles)

327
Q

Local humoral factors (vasoconstrictors)

A

Endothelin- 1

Internal blood pressure (myogenic contraction).

328
Q

Local humoral factors (vasodilators)

A 
Hypoxia
Adenosine
Bradykinin
NO
Potassium ions
Carbon dioxide
[H+]
Tissue breakdown products
329
Q

What is the endothelium derived relaxing factor?

A

Nitric oxide, a potent vasodilator, which is produced by the endothelium.
L-Arginine is converted into NO by NO synthase.

330
Q

Prostacyclin

A

potent vasodilator

331
Q

Endothelin

A

potent vasoconstrictor

332
Q

Circulating (hormonal) factors - Vasoconstrictors

A

Epinephrine
Angiotensin II
Vasopressin

333
Q

Circulating (hormonal) factors - Vasodilators

A

Epinephrine

Atrial Natriuretic peptide (ANP)

334
Q

Baroreceptors

A

pressure receptors

335
Q

Primary baroreceptors

A

Arterial

=> carotid sinus and aortic arch

336
Q

Secondary baroreceptors

A

veins, myocardium, pulmonary vessels

337
Q

What is baroreceptor firing rate proportional to?

A

MAP and PP, integrated in the medulla

338
Q

How do arterial baroreceptors affect central control:

A

An increase in blood pressure leads to an increase in firing rate leading to an increase in parasympathetic nerve supply (?) and decrease in sympathetic nerve supply (?) leading to a decrease in cardiac outflow and total peripheral resistance and thus a decrease in blood pressure.

339
Q

Arterial baroreceptors

A

Key role in short-term regulation of BP; minute to minute control, response to exercise, haemorrhage.

340
Q

What happens if arterial pressure deviates from the norm?

A

If arterial pressure deviates from the norm for a few days the baroreceptors adapt or reset to new baselin pressure, for example in hypertension.

341
Q

Cardiopulmonary baroreceptors

A

Atria, ventricles, pulmonary artery

Stimulation leads to a decrease in vasoconstriction. Also leads to decrease in angiotensin, aldosterone and ADH/vasopressin, leading to fluid loss.

342
Q

Main neural influence on medulla

A 
Baroreceptors
Chemoreceptors
Hypothalamus
Cerebral cortex
Skin
Changes in blood [O2] and [CO2]
343
Q

Which higher centers do CV reflexes require

A

hypothalamus

pons

344
Q

Effect of stimulation of anterior hypothalamus on CVS

A

Decrease in blood pressure

Decrease in heart rate

345
Q

Effect of stimulation of posterolateral hypothalamus on CVS

A

Increase in BP and HR

346
Q

How can the cerebral cortex affect blood flow and pressure?

A

Stimulation of CC usually increases vasoconstriction, but emotion can increase vasdilation and depressor responses e.g. blushing or fainting. Effects mediated via medula, but some also directly.

347
Q

Central chemoreceptors

A

Chemosensitive regions in the medulla. An increase in PaCO2 leads to vasoconstriction, an increase in peripheral resistance and an increase in blood pressure.
A decrease in PaCO2 leads to a decrease in medullary tonic acitivty and a decrease in BP.

348
Q

Fainting (neuro-cardiogenic syncope) symptoms, physiology, signs and treatment

A

Nausea, air hunger, sweating, light headed.

Fall in HR and venous pooling

Collapse due to decrease in CO.

HR falls, CO falls, BP falls, perfusion to brain reduced.

Treatment = lay supine and elevate limbs to increase VR.

349
Q

Blood loss + homeostasis

A

Perfusion to brain must be maintained so local vasoconstriction. Cardiac output and blood pressure is maintained by increasing the heart rate.
Increase in sympathetic outflow.
Widespread cutaneous vasoconstriction (skin).
Eventually, the body goes into ‘shock’ i.e. BP down, pulse up, organ hypoperfusion and death.
Treatment: rapid volume replacement

PHASE ONE (19 decks)

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