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M101 > W7/8 Cardiovascular system > Flashcards

W7/8 Cardiovascular system Flashcards

Inc lectures - Blood pressure and CVS continuum

1
Q

What are the 3 components of the CVS?

A

Blood, Vessels, Heart

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2
Q

What does the blood transport? (5)

A
  • O2, CO2 and other gases movement
  • Nutrients
  • Electrolytes
  • Metabolic waste
  • Hormones, Cytokines
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3
Q

What is the function of the blood in protection?

A
  • Immune response (Antibodies, complement proteins, WBC)
  • Blood loss-Clotting (platelets)
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4
Q

What are the functions of the blood relating to Regulation?

A
  • Body temp
  • pH
  • Circulatory body fluid volume/concentration (osmosis)
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5
Q

Characteristics of blood:
Type of fluid tissue?
Colours?
Blood volume?

A

A liquid connective tissue (only fluid tissue in human body)
A sticky viscous opaque fluid
Scarlet red: High oxygen (in artery)
Dark Red: Low oxygen (in vein)
Blood volume: 1.2 to 1.5 gallons: 8-10% of body weight
Male: 5-6 L and Female 4.5 L

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6
Q

What is the blood made up of? (%)

A

55% Plasma
1% Buffy coat (platelets, leukocytes)
44% Solids (RBC- Erythrocytes)

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7
Q

What is the blood plasma made of? (5)

A

90% water
10% soluble components

Plasma proteins- Albumin, globulin, fibrinogen
- Nutrients- Glucose, Amino acids, Cholesterol
- Gases- O2, CO2, traces (little bit <1%)
- Electrolytes- Sodium, Potassium, Chlorides & others
- Metabolic wastes- Urea

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8
Q

Haematopoiesis definition

A

Haem- Relating to blood
Poiesis- Formation of/Production of
(Formation of blood)

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9
Q

What are the functions of Haematopoietic stem cells/ Haemocytoblast?
What determines the type of cell formed?
What do the produced cells enter through?

A
  • Formation of RBC, WBC and Platelets
  • Hormonal/Growth factors determine the type of cells
  • Produced cells enter through blood sinusoids
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10
Q

Definitions
Leucopoiesis
Erythropoiesis:
Thrombopoiesis:

A

Formation of WBC

Production of Red blood
cells/erythrocytes

Production of platelets/ Thrombocytes

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11
Q

What is the difference between Granulocytes and Agranulocytes?

A

Obvious granules (light microscope)
No obvious granules (light microscope)

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12
Q

What are the 3 types of granulocytes?
What type of cells are they?

A

Neutrophils
Eosinophils
Basophils

These are all polymorphonuclear cells

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13
Q

Give a description of a Neutrophil:
-What do they act against?

A

Type of granulocyte;
-Major Abundant/Common type
-Larger cells
-3-4 segments/lobes of nucleus
-Smaller granules

Bacterial Infection

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14
Q

Describe the appearance of Eosinophils:

What do they fight against?

A

-Larger granules
-2 lobes of nucleus with thick strand of chromatin

Parasitic Infection

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15
Q

Describe the appearance of Basophils:
-nucleus shape
-what they respond to

A

Huge granules
Horseshoe shaped nucleus
2 big lobes joined together
Migrate into the tissue, Mast cells
Histamine- Proinflammatory

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16
Q

What are Polymorphonuclear cells? (literally)

The type of immune cell that has what..?

A

A type of immune cell that has granules (small particles) with enzymes that are released during infections, allergic reactions, and asthma. Neutrophils, eosinophils, and basophils are polymorphonuclear leukocytes.

Under a light microscope- Granules are seen so called granulocytes

More than one, Many different structure of cells/ morphology, relating mostly to the nucleus

e.g. Neutrophils- 3/4 lobes nucleus with thin chromatin strands

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17
Q

What are the 3 types of Agranulocytes?

A

Monocytes
Thrombocytes
Lymphocytes

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18
Q

-Describe the appearance of Thrombocytes: (platelets)
-Function?

A

-Fragments/Platelets
-Contains no nucleus
-Contains mitochondria (require ATP)

-They help form blood clots to slow or stop bleeding and to help wounds heal

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19
Q

Describe the appearance of Monocytes:

A

Type of Agranulocyte:
-Horse shoe lobed nucleus
-Migrate into tissue,
-Differentiate into Macrophages
-Phagocytosis- Bacteria
-Dendritic cells

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20
Q

What are the types of lymphocytes? (4)

A
  1. B- Lymphocytes (Plasma cells or Natural killer)
  2. T helper
  3. T Suppressor
    - All produce antibodies to fight viral infection
  4. T-Cytoxic
    - Cancer cells

B cells require T helper cells to signal

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21
Q

What does HIV target?

-If HIV isn’t treated, it can lead to AIDS

A

HIV targets T-helper cells

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22
Q

What are the terms for:
-Low WBC Count:
-High WBC Count:

A

Penia- Deficiency/not enough

Philia- Surplus/ excess cytosis: increase

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23
Q

What could occur from a low WBC count? (3)

A

Leucopenia- low wbc count
- risk of infection
- sepsis and lethal

Neutropenia -low neutrophils
-Risk of bacterial infections

Thrombocytopenia -low platelets
-the risk of blood loss
-an autoimmune condition in children

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24
Q

Differential white cell count examples

A

Leucocytosis : Sign of Infection
Neutrophilia?
(Neutrophil Leucocytosis)

  • Sign of bacterial Infection
    Eosinophilia?
  • Sign of parasitic Infection
    Lymphocytosis?
  • Sign of viral Infection
    Monocytosis?
    Sign of bacterial Infection in tissues, TB
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25
Q

Red blood cells features:

A

Biconcave- no nucleus and organelles
(Large surface area for exchange)
(Anaerobic ATP synthesis, don’t use O2)

97% of RBC is Haemoglobin – Gas Transport: Oxygen (Reversible binding)

Contain Spectrin, a plasma membrane protein-
(Flexibility of shape- to get through
smaller capillaries)

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26
Q

What is the structure of Haemoglobin?

A

Composed of 4 globins/polypeptides, 2 alpha and 2 beta.
Haem contains a central Iron. Each Fe2+ binds to one O2.
Each haemoglobin molecule can carry 4 O2 molecules

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27
Q

Oxyhaemoglobin meaning and colour:
Deoxyhaemoglobin meaning and colour

A

When Hb is binded to O2- Bright red
When Hb is not bonded to O2- Dark Red

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28
Q

Is haemophilia related to RBC?
If Hb has only one Fe2+ how does it bind to 4 O2?

A
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29
Q

Erythropoiesis definition:

A

Production and maturation of RBC- ~15 days

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30
Q

What is the regulation of Erythropoiesis:
What produces erythrocytes?

A
  • Hormonal (Negative Feedback Axis)
  • Kidney becomes hypoxic (renal arterial oxygen drops) triggering EPO release

Erythropoietin (released from kidney) stimulates Erythropoiesis.
It stimulates bone marrow to produce erythrocytes.

Erythrocytes increase O2 transport to the kidney and block EPO release

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31
Q

Hypoxia definition
Causes
Symptoms

A

Low oxygen levels in body tissues

Causes: Haemorrhage/Injury, Iron deficiency. High altitude or Lung disease (Pneumonia)

Symptoms: Confusion, restlessness, DIB, rapid HR, bluish skin
Can be life-threatening

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32
Q

What is the Oxygen sensor in the kidney called?

A

Hypoxia- inducible factor

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33
Q

Explain the regulation of Erythropoiesis:

A
  • Hormonal (Negative Feedback Axis)
  • Kidney becomes hypoxic (renal arterial oxygen drops) triggering EPO release
  • Erythropoietin (EPO) stimulate the red bone marrow to produce erythrocytes
  • Erythrocytes increases O2 transport to the kidney and block EPO release
    Testosterone enhances EPO production,
    (result in higher RBC in Males)
  • High EPO: Erythrocytes mature faster
  • Increase haematocrit, dehydration and blood
    viscosity (clotting, stroke, heart failure)
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34
Q

What is anaemia?

A

(Low haemoglobin) - A condition in which you lack enough healthy red blood cells to carry adequate oxygen to your body’s tissues.

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35
Q

What is Thalassemia?

A

-Globin chain in Hb is absent or malfunction
-RBC become thin, delicate and lack Hb
-Mild to Severe subtypes- Blood transfusions
-Predominantly in Mediterranean ethnics

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36
Q

What are two conditions that can result because of problems with red blood cells?

A

Thalassemia and Sickle cell anaemia

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37
Q

Sickle cell anaemia:

What is it?
Symptoms?

A

-Mutation in Hb: one amino acid is wrong in the globin B chain (6th AA- Glutamic
acid in normal RBC whereas 6th AA is Valine in sickle RBC)
-Sickle RBC is crescent-shaped
- O2 levels are low
- Crescent shape block flow in the blood vessels and leads to stroke and
other vascular diseases
-Very fatigue, lots of pain, challenged with work/exercise
-Predominantly in African ethnics

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38
Q

What is Polycythaemia?

A
  • Too many red blood cells in the blood
    Bone Marrow Cancer, People living in Highlands
    (low O2 in high altitude)
    Too thick too many cells increase the viscosity
  • Stroke
    -Coronary artery disease
    -Renal disease
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39
Q

What is haemostasis?

A

A physiological process to stop bleeding (clot)
(Blood coagulation)
Literally blood staying still

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40
Q

What are the Haemostasis steps? (3)
What type of feedback mechanism?

A
  1. VASCULAR SPASM - pain reflux, constriction of smooth muscle, triggers clotting chemicals/factors needed and directed to a site of injury.
  2. Platelet Activation- Plug
    Endothelial Damage
    Exposed Collagen

Platelets stick to exposed collagen- are activated
Platelets stimulate ADP,
Thromboxane (clotting factor) A2 and Serotonin
Von Willebrand Factor- Stabilises collagen-platelet adhesion

  1. Coagulation- Patch
    Clotting factors/procoagulants in Liver
    Vitamin K, the biosynthesis clotting factors
    Plasma proteins I to XIII

X-A, Prothrombin Activator converts into X Prothrombin then Thrombin then Fibrinogen (Insoluble) and Fibrin (soluble) and Fibrin (Mesh)

This is a positive feedback mechanism

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41
Q

What is thromboxane?

A

A clotting factor

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42
Q

What is Thrombosis?

A

Blood clotting (Thrombus) in arteries, veins or capillaries

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43
Q

What is an Embolism?

A

Blockage in an artery, caused by a foreign body e.g. a blood clot (embolus)

Blood clot/endogenous materials
(Embolus) moving in the blood vessel and obstructing blood flow

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44
Q

Fate of clot and vessel healing:

What is the process?

What occurs in fibrinolysis?

A

Clot retraction concurrent with vessel repair:

  1. The actin and myosin in platelets contract and pull on fibrin strands
  2. Platelet-derived growth factor (PDGF)
    -Stimulate smooth muscle and fibroblast division
  3. Vascular endothelial growth factor (VEGF)
    -Rebuild endothelial lining by multiplying endothelial cells

Fibrinolysis
Plasminogen, =plasma protein trapped in clot is converted into Plasmin which digests Fibrin

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45
Q

Haemostasis disorders (3)

A

Thromboembolism
Unregulated Bleeding
Disseminated Intravascular Coagulation (DIC)

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46
Q

Blood groups

A

A- Antigen A and B
O group- No antigens (Universal donor)
A+
AB- Universal recipient as can recieve RBC from any blood type

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47
Q

Why are red blood cell counts higher in males?

A

Androgen levels such as Testosterone are higher (Which stimulates the release of EPO)

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48
Q

Which renal hormone triggers the red blood cells levels formation in bone marrow

A

Erythropoetin

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49
Q

What are the 3 types of circulation?

A

Pulmonary, Systemic, Coronary

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50
Q

What is the function of an Artery?
What is the structure of an artery?

A

Carries blood AWAY from the heart to the rest of the body

Consists of:
Lumen
Tunica Interna/Intima
Tunica Media
Tunica externa
NO valves

51
Q

Give a brief description of:
Tunica Interna/Intima
Tunica Media
Tunica externa

A

Tunica Interna/Intima- Flat layer, smooth squamous endothelium, smooth flow of blood.

Tunica externa- Thick layer w elastic tissues, stretch in and out. Handle the pressure (more in larger arteries)
Bright Red

52
Q

What is the function of a Vein?
What is the structure of a Vein?

A

Carries blood TOWARDS

Lumen- Slightly wider than artery
Externa Smooth muscle and Elastic fibres
Intima- Endothelial layer
No elastic adventia
Valves to prevent back flow/
Handle low pressure 8-10mmHg
Dark Red

53
Q

What are the 3 types of capillaries?

A

Continuous
Fenestrated
Sinusoids

54
Q

What is a Continuous capillary?

A

Found in Smooth and Skeletal muscle
Continuous arrangement
BBB- Very tight junction with an Intercellular cleft
(This restricts toxin exchanges)

55
Q

Where are fenestrated capillaries found?
They allow a higher permeability of what?

A

Found in Intestinal villi, kidney glomeruli & endocrine cells
Higher permeability of larger biomolecules

56
Q

What is a Sinusoid capillary?

A

Found in Red bone marrow and liver
Huge molecules perfusion
Blood cells, proteins and wastes

57
Q

What is the structure of a capillary?

A

Bundle of smooth muscles spread out pre-capillaries (provide elasticity)

Sphincters (pre-capillary) Vasotone-dilation- More blood into capillary (metabolic demand- Exercise)
apillary (200-400um in diameter)

Capillary walls are lined with endothelial cells
(5-10 um in diameter) for smooth flow

Various cell types around a blood vessel

Complex regulation
* Metabolic demand
* Hormonal
* Temperature and many others

58
Q

Heart (the life pump)

A

Size: ~ 14 cm long; 9 cm wide (fist of your hand)
Weight : 300-500 gms
Heartbeat: 70-100/min= 115000/day = ~3.5 billion in lifetime
Volume of blood pumped in a day = ~9000 L

59
Q

What is pericardium?
What is myocardium?
What is endocardium?

A

Pericardium Fibrous layer- Outermost layer
- provides elasticity and protects

Myocardium- Cardiac muscle (contract and relax)
Endocardium- Innermost layer

Septum- Divides heart
4 Pulmonary veins

60
Q

What can be a symptom of a congenital disease related to your Septum?

A

Poorly developed septum= Heart murmurs

61
Q

LubbDubb

A

Sound when atrioventricular and semilunar valves shut
S1= Lubb
S2= Dubb

62
Q

Where does the Brachial artery take blood to?

A

Brachial artery- Takes blood to hands
Cephalid vein- Drains blood into VC

Carotid artery- Takes blood to brain
Jugular vein- Drains blood into VC

Hepatic artery- Takes blood to liver
Hepatic vein- Drains blood

Femoral artery/Vein- Lower body/legs

63
Q

Why do we have a Hepatic portal vein?
(No direct drain from GI/Intestines into veins)

A

Toxins must be removed first
Processed by liver first

64
Q

Describe Venous return (flow of blood back to the heart’s right atrium) (3) (SAQ)

A
  1. Calf/skeletal muscle pump
    (coordinated contraction of muscle)
  2. Pulsatile arteries adjacent to vein complement the muscle pump/pressure and venous return
  3. Respiratory (Thoracic pump)
    - Interpleural pressure

Breath In (inspiration)
- Diaphragm compresses abdominal cavity
- Increase in pressure so pushes blood from abdomen cavity to thorax
- Reduced pressure in the thorax sucks blood from the abdominal cavity to the thorax
Breathing Out (expiration)
-

65
Q

Problems with Venous return can cause…

A

Pulmonary embolisms
Varicose Veins (chronic vein valve failure)

66
Q

What is coronary circulation?

A

Two tiny arteries leaving out the aorta
Profuse blood to myocardium
Handles high pressure (irrespective of heart contraction or relaxation)

67
Q

Describe the autoregulatory processes controlling the rate of oxygen exchange between the microcirculation and tissue (6)

A

Pre-Capillary Sphincters:
Less Oxygen (& metabolic) demand in tissues

Myogenic response

68
Q

What can occur due to problems with coronary circulation?

A

Blockage leads to the major cardiac problem- Heart attack
Coronary Thrombosis- Myocardial Infarction

69
Q

Capillary Perfusion: Microcirculation (Tissue fluid)

A
  • O2, CO2 and other gases movement
  • Nutrients
  • Electrolytes
  • Metabolic waste
  • Hormones, Cytokines

High hydrostatic pressure, low oncotic/osmotic pressure at arteriole end,
Low hydrostatic pressure at venue end
(Starling forces)

70
Q

Autoregulation of perfusion:
What are stimulated?

A

-CO2 , potassium (K+) or hydrogen (H+) ions (acidic pH)
-Lactic acid (by-products of cell metabolism)
-Histamine (Inflammation)
Body temp

1.Stimulate endothelial cells to release endothelin (peptides)
2.Platelet secretions and prostaglandins
3.Vasoconstriction of pre-capillary sphincters

71
Q

What is the myogenic response?

A

Reflex response of the afferent arterioles to changes in BP

Stretching of the smooth muscle in the walls of arterioles

Blood flow (High): Stretch
Blood flow (low): Constrict

Localised protective function to maintain the blood flow:

Ischemia (hypoxia) Vs Excessive perfusion
Stimulate endothelial cells to release NO
Vasodilation of precapillary

72
Q

What is systole and diastole? (Haemodynamic flow/Cardiac Cycle)

A

Systole- Heart contraction
Diastole- Heart relaxation

73
Q

Sino Atrial (SA) Node
(Pace maker)-

A

Specialised
electrically active
Myocardial tissue-Atria
Intrinsic/electrical unstable-
Physiological origin
of contraction
Spontaneous
depolarisation,
90-100 times/min
Generates electrical
activity-Impulse

74
Q

Where is the SAN and AVN?

A

SAN located in LHS of heart
AVN located in RHS of heart

75
Q

What is the AVN?

A

Specialised electrically active
Myocardial tissue- Atria-Ventricular mid line
Generates electrical activity-Impulse
Intrinsic/electrical unstable-
Spontaneous depolarisation,
Lower than SA (40-60 times/min)

76
Q

What is the Bundle of His? (AV bundle)

A

Collect and carry to higher and lower part of the ventricles (Apex); 20-40 times/min

77
Q

What are Purkinge Fibres?

A

Specialised myocardium for electrical
conduction (not contraction) towards
contractile myocytes (cardiac cells)

78
Q

What are the key properties of cardiac muscle?
(4)

A

1.Auto-rhythmicity
- Ability to initiate heartbeat (at a regular pace w/o external stimuli)

2.Excitability
- Ability to respond to stimuli, generate and process AP

3.Conductivity
- Ability to conduct&transmit impulse through cardiac tissue

4.Contractility
- Ability to contract in response to stimulation

79
Q

Briefly describe the structure of Cardiac muscle.

A

Striated type, branched muscle fibers (myofibrils) contains single nucleus, many mitochondria and T-tubules
* Connected by intercalated disks
Gap junctions- Depolarisation between cells
Desmosomes- Hold fibers together during contraction

80
Q

Describe excitation-contraction coupling in contractile myocytes:

A
  1. AP from adjacent cell excites myocytes and trigger membrane depolarisation in T-tubules
  2. Ca2+ enters the cells via voltage-gated channels and it enters the cells
  3. Ca2+ binds to Ryanodine receptor (RYR) and induce Ca2+ release from Sarcoplasmic Etc
  4. Ca2+ binds to troponin and triggers actino-myosin complex and contraction
  5. Ca2+ unbind from troponin and pumped back into SR
  6. Calcium unbinding cause relaxation and excess Ca2+ exchanged with Na+
  7. Na+ gradient is maintained by sodium-
    potassium- ATPase pump.
81
Q

What is the definition of myogenic?

A

Originating in muscle tissue (rather than from nerve impulses).

82
Q

What are the different Sinus Rhythms (ECG)?

A

P wave- Atrial contraction- a delay happens
Q R S- Ventricular systole
T- Ventricular relaxation/diastole

83
Q

How long does a cardiac cycle last?
What is a regular HR?

A

0.8 secs
70-100 BPM (75 BPM)

84
Q

How do you calculate BPM?

A

60/ Cardiac cycle length

85
Q

What is Sinus bradychardia?

A

HR <60BPM
Patient is usually asymptomatic and no treatment required.
Give advice re antihypertensives
(beta-blockers or calcium channel blockers)

86
Q

What is sinus tachycardia?

A

Rate is > 100bpm, but not usually > 130bpm
at rest
*Occurs normally in exercise / stress.
*Patient is usually asymptomatic.
*Hypovolaemia / underlying medical problems

87
Q

What is Sinus Arrhythmia?

A

Regularly irregular sinus rhythm

88
Q

What is Sinus Arrhythmia?

A

Regularly irregular sinus rhythm

89
Q

What is blood pressure by definition?

A
  • Pressure exerted on the walls blood vessel (largely referred to Arterial pressure)
  • Measured in mmHg
  • BP varies with age and pathological conditions Systolic BP: MAP during heart contraction
    Diastolic BP: MAP during heart relaxation
90
Q

What is Autoregulation?

A

Changes in blood flow detected by the local receptors during micro perfusion

91
Q

What are the terms for normal, high and low bp?

A

Normotension, Hypertension and Hypotension

92
Q

If the bp drops below 120/80mmHg it is considered..?

A

Low bp or hypotension

93
Q

What are baroreceptors?
Where are they located?

A

Pressure receptors
Carotid sinus and Aortic arch

94
Q

What is autoregulation?

A

Changes in blood flow detected by the local receptors during micro perfusion.

95
Q

What is neural regulation?

A

Short-term regulation of blood pressure, especially in responses to transient changes in arterial pressure, via baroreflex mechanisms

96
Q

What is included in hormonal regulation?

A
  • Renin-Angiotensin-Aldosterone
  • Anti-diuretic hormone (ADH; arginine vasopressin)
  • Atrial natriuretic hormone/peptide/factor
  • Erythropoietin
  • Adrenaline/Noradrenaline
97
Q

What happens in neural regulation when the bp is high?

A

Baroreceptors fire signals to the CVC in the brain This enhances the vagal activity which suppresses the heart rate.
The sympathetic cardiac activity decreases heart rate and decreases heart contraction
Due to both of these, cardiac output decreases.
Blood pressure falls and homeostasis restored.
CVC- Sympathetic vasomotor activity= vasodilation

98
Q

What happens in neural regulation when the bp is LOW? (hypotension)

A

The low arterial blood pressure is recognised by baroreceptors which slow down their firing rates to the cardiovascular centre
CVC increase signals sent down sympathetic cardiac activity and vagal activity decreases.
This increases heart contraction and also increases heart rate. This increases the cardiac output

The CVC also cause sympathetic vasomotor activity causes vasoconstriction

99
Q

What does Aldosterone do?

A

Sodium reabsorption
Osmotic pressure
Water reabsorption (water moves in direction of sodium)
Intravascular volume
Venous return
Cardia output

100
Q

What is Antidiuretic hormone (ADH or Vasopressin)?
What is the function of ADH?

ADH= dehydrated

A
  • ADH is secreted by the cells in the hypothalamus, transported to the posterior pituitary and stored until nervous stimuli
  • ADH signals kidneys to reabsorb more water
  • Prevent the loss of fluids in the urine
  • Increase overall fluid levels
  • ADH constricts peripheral vessels
  • Restore blood volume and pressure
101
Q

What is Hypovolemia?
What does it trigger?

A

Increase in tissue fluid osmolarity (loss of blood volume) trigger ADH release

102
Q

What is Atrial Natriuretic Hormone/peptide?
[ANH]
(opposite effect to ADH)

Atrial- Atria
Natri- Sodium

A
  • Secreted by cells in the atria of the heart (B-type ANH by ventricle)
  • Natriuretic hormones are antagonists to angiotensin ll
  • Prevent aldosterone release
  • Promotes loss of sodium and water from the kidneys
  • Suppress renin, aldosterone and ADH production and release
  • Promotes LOSS OF FLUID from the body
  • Blood volume and blood pressure drop
  • Restore blood volume
103
Q

How is Low blood pressure regulated by hormonal regulation?

A

Sensed by kidney. Renal hypoperfusion. Granular cells (juxtaglomerular) stimulate production of/ release of hormone Renin.

Liver synthesises Angiotensinogen. Converted into Angiotensin l and ll by ACE

Lungs- Angiotensin-converting enzyme (ACE) is created and secreted

(Angiotensin ll is a vasoconstrictor which is what we need to inc bp it also stimulates aldosterone release from the adrenal cortex)

104
Q

What is Angiotensin ll?

A

It is a peptide hormone and can act as a vasoconstrictor (constriction of vascular smooth muscle) causes arteries to constrict and inc blood pressure.Inc peripheral resistance.

It stimulates Aldosterone release from adrenal cortex

105
Q

What is Aldosterone?

A

The regulator of sodium and water homeostasis (in kidney)
Inc sodium reabsorption

106
Q

What is the RAAS?

A

Renin-Angiotensin-Aldosterone System

107
Q

How is high bp regulated by hormonal regulation (RAAS)?

A

Kidney senses high bp
Juxtaglomerular (Granular cells) stop Renin production
So no Angiotensin l and ll created so vasodilation occurs and peripheral resistance is reduced
No stimulus for adrenal cortex to stimulate aldosterone, so sodium is lost in urine and is excreted from kidney.

No sodium reabsorption, Less osmotic pressure, less water reabsorption, intravascular volume decreases, venous return decreases and cardiac output decreases.

108
Q

What is Starlings law?

A

Decreased venous return means decreased cardiac output.

109
Q

What do catecholamines do? What are some examples?

A

Adrenaline and Noradrenaline

Released by the adrenal medulla
Enhance and extend the body’s sympathetic
activity (“fight-or-flight” response)

Increases Heart rate
Force of contraction
Vasoconstriction (non essential organs)
Energy mobilisation to liver, muscle and heart

110
Q

What are other endocrine hormones that modulate BP?

A

Noradrenaline, adrenaline
Erythropoetin

111
Q

What is erythropoietin?

A

Blood flow and/or oxygen levels decrease (hypoxia)
EPO is released by the kidneys
EPO stimulates the production of erythrocytes by erythropoiesis within the bone marrow
Increases- blood viscosity, resistance and pressure

Decreases blood flow

112
Q

What is the cardiac output formula?

A

CO= SV x HR
Stroke volume X Heart Rate

113
Q

What is the blood pressure formula?

A

BP= CO x PR
Blood pressure= Cardiac output x Peripheral resistance

114
Q

What is Hypovolemia
Causes of hypovolemia?

A

Low blood volume

Haemorrhage
Dehydration
Diarrhoea
Burns
Diuretics

115
Q

What are risks of high blood pressure?
(8 conditions)

A

Heart disease
Heart attacks
Heart failure
Peripheral arterial disease
Strokes
Aortic aneurysms
Kidney disease
Vascular dementia

116
Q

What are diuretics?

A

Drugs that increase the excretion of urine.

117
Q

What can lead to decreased cardiac output? (5)

A

Valves disease
Ischemia
Myopathy
Pulmonary hypertension
Pericardial disease

118
Q

What can lead to decreased heart rate? (4)

A

Arrythmias
Sinus bradycardia
AV nodal block
Ventricular fibrillation

119
Q

What are the symptoms of hypotension?

A

*Light headedness or dizziness.
*feeling sick.
*blurred vision.
*generally feeling weak.
*confusion.
*fainting.

120
Q

What are the symptoms of hypertension? (8)

A

Severe headaches
Nosebleed
Fatigue or confusion
Vision problems
Chest pain
DIB
Irregular heartbeat
Blood in the urine

121
Q

What leads to an increase in Hypertension?

A

Sodium homeostasis:
-Renal disease
-Nephropathy
-Reduced nephron number
-GFR
(these inc stroke volume)

Hormonal imbalance:
Renin
Angiotensin II
Aldosterone
Erythropoietin
Adrenaline/Noradrenaline
(these all increase heart rate/bp)

Systemic vasoconstriction:
Stress
Autonomic dysfunction
(inc peripheral resistance)

Structural dysfunctions:
Obesity
Endothelial dysfunction
Altered cell membrane
Venous constriction
(inc peripheral resistance)

122
Q

What’s the difference between a thrombus and embolus? (thrombosis and embolism)

A

Thrombosis- Blood clotting (Thrombus) in arteries, veins or capillaries

Embolus- Blood clot/endogenous materials
(Embolus) moving in the blood vessel and
obstructing blood flow

123
Q

What type of regulation is the regulation of erythropoietin?
When there is hypoxia, what does the kidney release?
What causes hypoxia? (3)
How is erythropoietin regulated? (2)

A

Hormonal (negative feedback axis)
Erythropoietin
Causes: haemorrhage or injury,iron deficiency, high altitude or lung disease (pneumonia)

  1. EPO stimulates the red bone marrow to produce erythrocytes (vasoconstrictor)
  2. Erythrocytes increase of trans;let tkt the kidney and block EPO release

Inc: blood viscosity, resistance and pressure
Dec: Blood flow (slows it down so blood has more time to take oxygen from lungs)

M101 (41 decks)

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