Ph1124 > Unit 2 > Flashcards

Unit 2 Flashcards

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1
Q

What is blood pressure a measure of

A

Korotkoff sounds
Blood flow generated by turbulent flow

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2
Q

What is turbulent flow

A

When the blood velocity is too high for the diameter

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3
Q

How do u find the systolic and diastolic pressures

A

1st sound = systolic pressure
When sound stops = diastolic pressure

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4
Q

Mean arterial pressure equation

A

1/3( systolic - diastolic) + diastolic

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5
Q

Physical factors effecting mean atrial pressure

A

Cardiac output
Total peripheral resistance = resistance of flow ( how narrow blood vessels are )
Central venous pressure = pressure in veins

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6
Q

Which factor effects the mean arterial pressure most

A

The total peripheral resistance ( resistance of flow )

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7
Q

What system is responsible for,s for immediate control of blood pressure

A

Autonomous nervous system
- receptors in the heart, blood vessels and muscles detect change and feedback a signal to the brain, which sends out a signal to change blood pressure

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8
Q

Where are arterial barroreceptors found

A

In the aortic arch and carotid sinus

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9
Q

What do arterial barroceptors do

A

Response to stretch which increases firing of action potential, pressure sensitive

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10
Q

What are chemo sensors

A

Response to ischaemic metabolites
Mediate pain associated with angina
Produce sympathetic activation and rise blood pressure

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11
Q

What are myelinated veno atrial mechanoreceptors

A

Sense central blood volume / filling pressure
Increase in volume = increase in firing rate

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12
Q

What are 3 ways baroreceptors are sometimes bypassed

A
  1. Central resetting = when you exercise muscles send a signal to the brain to temporarily ignore high blood pressure, allowing blood pressure to rise and meet demands
  2. Peripheral resetting = if you have a high blood pressure for extended periods, they accept the high as a new baseline. Good as it can stay sensitive to small changes, bad as it loses track of what’s healthy
  3. Structural changes = over time high BP causes physical damage, there is a collagen buildup in the arteries and become stiff, increasing the intraluminal pressure causing less stretch
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13
Q

How is blood pressure controlled long term

A

Endocrine regulation of plasma by
1. Increases / decreases diuresis ( peeing)
2. Increased / decreased thirst
All based on the viscosity of the blood

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14
Q

When is ANP released

A

When there is too much stretch in the atria, increases renal salt and water excretion

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15
Q

Function of capillaries

A
  • delivery of nutrients and O2 into tissue
  • removal of waste products
  • regulation of water balance
  • flow through capillaries by dynamically controlled and linked to metabolic demand
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16
Q

Types of capillaries

A
  1. Continuous e.g. muscle, lungs
  2. Fenestrated e.g. renal glomerulus
  3. Discontinuous e.g. spleen, liver
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17
Q

What varies of the capillary bed

A

The density
Subcutaneous tissue = low
Cardiac = high

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18
Q

How does diffusion occur across the capillary wall

A

Water flows down a pressure gradient
Hydrostatic pressure = pushes water out of the capillaries into surrounding tissue
Oncotic pressure = pulls water from the tissue into the capillaries

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19
Q

What are the determinants of diffusion rate

A
  1. Concentration gradient
  2. Surface area
  3. Distance
  4. Permeability
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20
Q

What does starlings principle of fluid exchange

A

Movement of water is governed by this principle
Depends on the hydrostatic and oncotic pressure

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21
Q

What number resembles hydrostatic pressure is equal to oncotic pressure

A

0
If oncotic pressure exceeds hydrostatic pressure ( move towards arterial end) then there is a net loss of fluid from tissue into the capillary

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22
Q

What is net delivery

A

Hydrostatic pressure exceeds oncotic and fluid goes into the tissue

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23
Q

What is the functions of the lymphatic system

A

Fluid balance
Nutrition
Defence

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24
Q

What is oedema caused by

A

Fluid exceeds the ability of the lymphatic system to clear it away
Caused by long hall flights, malnutrition and lymphatic insufficiency

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25
How thick are capillaries
One cell thick
26
What are the main functions of the blood
- transport oxygen from lungs to tissue - co2 from tissues to lungs - regulations of body temp
27
What is the composition of blood
Plasma Buffy coat = leukocytes and platelets Erythrocytes
28
When will leukocytes increase
When combating an infection
29
What do erythrocytes look like
Bi concave disk - max surface area to volume ratio Contains no nuceleus or cell organelles
30
What is the process of making new red blood cells called
Erythropoiesis
31
Describe the production of new red blood cells
1. Stem cells differentiate into proerthyroblasts 2. They then go through a series of stages where haemoglobin is made before the nucleus is ejected and a mature erythrocyte is released into circulation
32
What is the rate of generation of erythrocytes controlled by
The hormone erythropoietin Released in response to hypoxic conditions
33
How long are erythrocytes in circulation for
120 days
34
35
How are erythrocytes removed from circulation
Specialised cells in the wall of the blood vessels, reticulo endothelial cells, engulf it and break it down Main aim is to recycle iron
36
What occurs if same blood in blood transfusions aren’t used
Fatal haemolytic reactions Antigen antibody reactions
37
What is the universal donor blood
O
38
What is the universal recipient
AB
39
What is rhesus factor
Specific protein tag that lives on the surface of RBC, inherited by your parents. Determines whether blood is positive or negative
40
What are rhesus antibodies
Proteins that your immune system created if you are Rh negative and come into contact with Rh positive blood
41
Why is the D antibody most significant
Has a very strong immunogenic response in comparison to other antibodies Even a small amount of rh positive blood means immune system is highly likely to notice and react aggressively
42
What happenes when you have a Rh negative mother and Rh positive foetus
The maternal D antibodies cross the placenta and latch onto the baby’s Rh positive red blood cells, due to the mother coming in contact with the antigen The baby’s spleen idenfies them and destroys them This mean the babies loose red blood cells faster than they can make them
43
What is done to stop an erythroblastic baby from being produced
Give mum an I.V anti-d-y-globulin near time of delivery Preventing mother from producing antibodies against RhD positive baby’s blood
44
Haemostasis
Blood clots form to stop bleeding
45
What can inappropriate formation of blood clots lead to
Deep vein thrombosis, stroke or heart attack
46
haemolytic
Process that break downs clots
47
What does the endothelium do to inhibit haemostasis
Release different inhibitors that inhibit different parts of the haemostatic cascade Also acts as a barrier preventing blood from accessing underlying negatively charged matrix tissue (key initiator of the haemostatic cascade)
48
Primary stage of haemostasis
Initial response to vascular injury Localised vasoconstriction, platelet adhesion and platelet aggregation Ending with formation of a platelet plug
49
Platelet plug
Relatively weak structure but can be sufficient in allowing small injuries to heal
50
Secondary stage of haemostasis
Happens if more serious injury Continuation of process from primary haemostasis if required Ending with formation of fibrous clots - this is what’s seen on the skin
51
What do platelets (thrombocytes) look like and how do they survive
Small fragments of cytoplasm, no nucleus Survive 9-12 days Numbers need to be above 5million/ml to prevent haemorrhaging
52
How do platelets help in the formation of a platelet plug
Express proteins on the cell membrane that are necessary for adhesion to eachother
53
Mechanism of platelet aggregation
ADP released from platelet cytoplasm upon adherence induced exposure of fibrinogen receptors Fibrinogen binds to the exposed receptors Extracellular calcium dependent fibrinogen bridges link adjacent platelets
54
In a small injury what stops clotting factors driving process from plugs to fibrous clots
Anticoagulants
55
What is intrinsic activation of the clotting cascade
Activated by internal damage to blood vessels, slower than extrinsic
56
What is extrinsic activation of the clotting cascade
Initiated by damage to tissue cells in addition to vascular cells
57
What do both clotting cascades ends in
Activation of factor 10 In turn activation of thrombin which turns fibrinogen to fibrin (insoluble) which makes up clots
58
What removed the clot once blood vessel is repaired
The enzyme, plasmid removed the fibrin
59
What 2 cells make up the alveoli
1. AT1 cells = squamous epithelial cells ( 95% of Sa) 2. AT2 cells = responsible for generating for at1 cells and producing surfactant
60
What 2 categories does respiratory disease fall into
1. Restrictive = those that reduce lung capacity 2. Obstructive = increase the resistance of flow and effect airway
61
Pneumonthorax
Penetrating injury into the intrapleural space Atmospheric air enters the chest cavity causing lungs to collapse Lungs can’t inflate = no gas exchange
62
How to overcome surface tension of water
Rings of smooth muscle prevent airways from collapsing and sticking together Surfactants are also used , they are amphiphiles ( both hydrophobic and philic )
63
What do surfactants contain
1. Phospholipids 2. Proteins 3. Ions
64
Why do babies need the surfactants ?
Unable to overcome the surface tension of water that opens the bronchioles)
65
How is O2 transported
Not sufficiently soluble in water to supply body with needs. Has to bind to haemoglobin within red blood cells
66
What makes up a haemoglobin molecule
Contains a central core of iron encased in 4 polypeptide chains, each can bind to 1 oxygen molecule
67
What are the three ways CO2 is carried in the blood
1. Dissolved 2. Bound to amino acids 3. As bicarbonate ions = most
68
How is pH regulated
Bicarbonate system A shift of 0.5 low or 0.2 high can be life threatening, therefore controlled by the removal of CO2 via ventilation
69
What factors affect affinity for O2
- CO2 - pH - Temp
70
What is the Bohr shift
When your muscles are working hard, CO2 is produced. Carbonic acid - bicarbonate buffer is pushed to make more hydrogen ions. This change makes haemoglobin let go of oxygen more easily ( lowers affinity). Curve shifts or the right
71
What chemoreceptors respond to oxygen and carbon dioxide change
Central and peripheral chemo sensors
Ph1124
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