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Cardiovascular Flashcards

1
Q

What is haemopoiesis?

A

Production of blood cells and platelets
Continues throughout life

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2
Q

Where does haemopoiesis take place at different ages of the foetus?

A

0-2 months: yolk sac
2-7 months: liver, spleen
5-9 months: bone marrow

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3
Q

Where does haemopoiesis take place in infants?

A

Bone marrow

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4
Q

Where does haemopoiesis take place in adults?

A

Vertebrae, ribs, sternum, skull, sacrum and pelvis, proximal ends of femur

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5
Q

Stages of haemopoiesis to form erythrocyte

A

Haemocytoblast
Common myeloid progenitor
Proerythroblast
Erythroblast
Reticulocyte (nucleus extracted)
RBC

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6
Q

Stages of haemopoiesis to form basophils, eosinophils and neutrophils

A

Haemocytoblast
Common myeloid progenitor
Myeloblast
Myelocyte
Baso-, eosino-, neutro-

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7
Q

Stages of haemopoiesis to form macrophages

A

Haemocytoblast
Common myeloid progenitor
Monoblast
Monocyte
Macrophage

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8
Q

Stages of haemopoiesis to form lymphocytes

A

Haemocytoblast
Common lymphoid progenitor cell
Lymphocyte (goes on to B and plasma, T)

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9
Q

Stages of haemopoiesis to form platelets

A

Haemocytoblast
Common myeloid progenitor
Megakaryocyte
Platelets (thrombocytes)

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10
Q

Describe RBCs

A

Diameter: 6-8μm
Lifespan in blood: 120 days
Flexible biconcave disc
Carries O2 or CO2
Males conc of 4.5-6.5x10^12/L
Females 3.9-5.6x10^12/L

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11
Q

What is the structure of haemoglobin?

A

4 polypeptide chains- 2 alpha 2 beta all with their own haem group
Hb A main type in blood, Hb F and Hb A2 also exist in small quantities

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12
Q

What is anaemia?

A

Reduction in the haemoglobin concentration of the blood
Less than 135g/L in adult males
Less than 115g/L in adult females

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13
Q

What is acute chest syndrome?

A

Complication of sickle cell
Acute lung injury, distinct from pneumonia
Chest pain, fever, dyspnoea

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14
Q

Describe white blood cells

A

4-11x10^9/L in blood
Diameter: 7-30μm
Lifespan: hours-years
Non-specific and specific immunity

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15
Q

Describe neutrophils

A

Diameter: 12-15μm
Lifespan: 6-10hrs
No.: 1.8-7.5x10^9/L
Function: protection from bacteria and fungi

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16
Q

Describe monocytes

A

Diameter: 12-20μm
Lifespan: 20-40hrs
No. : 0.2-0.8x10^9/L
Protection from bacteria and fungi

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17
Q

Describe eosionophils

A

Diameter: 12-15μm
Lifespan in blood: Days
No.: 0.04-0.44x10^9/L
Protection against parasites

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18
Q

Describe basophils

A

Diameter: 12-15μm
Lifespan in blood: Days
No.: 0.01-0.1x10^9/L

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19
Q

Describe lymphocytes

A

Diameter at rest: 7-9μm
Diameter active: 12-20μm
Lifespan in blood: weeks-years
No.: 1.5-3.5x10^9/L
B cells: immunoglobulin synthesis
T cells: protection against viruses, immune functions

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20
Q

Which white blood cells are responsible for innate immunity?

A

Neutrophils
Eosinophils
Basophils
Mast cells
Macrophages

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21
Q

Which white blood cells are responsible for adaptive immunity?

A

CD4 T helpers
CD8 T cells
B cells

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22
Q

Describe the maturation process of B cells

A

1.Bone marrow stem cell
2.Bone marrow
3.Mature B lymphocytes
4.Blood

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23
Q

Describe the maturation process of T cells

A
  1. Bone marrow
  2. Thymus
  3. Mature T lymphocytes
  4. Blood, lymph
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24
Q

List some WBC abnormalities

A

neutropenia
eosinopenia
myeloid malignancies
lymphoma
basophilia
monocytopenia

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25
Q

What is GVHD?

A

Graft-vs-host disease
Donor derived immune cells, particularly T, reacting against recipient tissues

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26
Q

What is CAR-T?

A

Chimeric antigen receptors cell therapy
Used for relapsed/refractory B cell malignancies
Involves collecting and using patient’s immune cells to treat their own condition

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27
Q

Describe platelets

A

Diameter: 0.5-3μm
Lifespan in blood: 10 days
No.:140-400x10^9/L
Function: haemostasis, clotting

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28
Q

What do platelets contain?

A

Plasma membrane
Cytoskeleton
Dense tubular system
Electron dense granule
alpha-granule
Lysosome
Mitochondria
Glycogen
Peroxisome

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29
Q

In platelets, what does the electron dense granule secrete?

A

ADP, Ca2+, Serotonin

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30
Q

In platelets, what does the alpha-granule secrete?

A

Fibrinogen, factor V, VWF, fibronectin, PF 4, PDGF

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31
Q

What are the major platelet functions?

A

Adhesion
Aggregation
Release reactions and amplification

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32
Q

How are platelets produced?

A

In the bone marrow by fragmentation of the cytoplasm of megakaryocytes

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33
Q

Describe platelet activation

A
  1. Break in endothelial lining
  2. Platelets activated and change shape, increases SA, spiculated and pseudopodia
  3. Activate GPIIB/IIIA into form to bind to fibrinogen, leading to cross linking

Number of GbIIb/IIIa receptors increased, affinity for fibrinogen increase

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34
Q

Describe platelet adhesion

A

Platelets adhere to exposed connective tissue
Collagen receptors bind to subendothelial collagen exposed
GbIIb/IIIa binds to VWF (attached to collagen)
Soluble agonists released and activate platelets

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35
Q

What happens when ADP activates P2Y1 (purinergic receptor)?

A
  • ADP binds to and activates P2Y1 receptor
  • Phospholipase C pathway activated: calcium released
  • Protein kinase C pathway activated
  • Initiation of platelet aggregation and shape change
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36
Q

Role of GPVI (glycoprotein 6) in platelet activation

A

-Binds to collagen in the vessel wall and activates platelets
-Lead to platelets releasing thromboxane A2, amplification

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37
Q

Role of cyclooxygenase 1 (platelets)

A
  • COX-1 converts arachidonic acid into prostaglandin H2
  • COX-1 mediates GI mucosal integrity
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38
Q

Pathway from arachidonic acid to vasoconstriction in platelets

A
  • Arachidonic Acid converted by COX1 to Prostaglandin H2
  • Prostaglandin H2 forms thromboxane A2
  • Thromboxane A2 leads to platelet aggregation and vasoconstriction
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39
Q

Role of cyclooxygenase 2 (endothelial cells)

A
  • Arachidonic acid converted by COX 2 to prostaglandin H2
  • COX 2 mediates inflammation
  • Involved in prostacyclin production to inhibit platelet aggregation and affect renal function
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40
Q

Pathway from arachidonic acid to inhibiting platelet aggregation (in endothelial cells)

A
  • Arachidonic acid converted by COX 1/2 to prostaglandin H2
  • Prostaglandin H2 converted to prostacyclin
  • Prostacyclin inhibits platelet aggregation and vasoconstriction (opposite to thromboxane a2)
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41
Q

What effect does aspirin have?

A

Low dose inhibits COX 1
High dose inhibits both COX 1 and 2

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42
Q

What are the purinergic receptors in platelets?

A

P2Y receptors
They are G protein coupled
Receptor on outer surface of membrane
Inner surface side linked to G protein
P2Y1 linked to Gq, P2Y12 linked to Gi

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43
Q

What happens when ADP binds to P2Y12?

A
  • ADP binds to and activates P2Y12
  • Gi activates PI3 kinase pathway
  • Gi inhibits adenylate cyclase
  • Amplifies platelet activation, aggregation and granule release
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44
Q

Describe process of ADP-induced platelet aggregation

A
  1. ADP binds to P2Y1, initiating platelet activation
  2. GPIIb/IIIa activation, binding of fibrinogen and crosslinking of platelets
  3. ADP also binds to P2Y12, amplification pathway
  4. Dense granules release ADP which causes further activation
  5. Activation of GPIIb/IIIa also amplifies response (outside-in signalling)
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45
Q

How does thrombin activate platelets?

A

Thrombin generated through coagulation cascade
Activates PAR-1 (and other receptors)
Leads to aggregation response and release of ADP from dense granules

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46
Q

Describe platelet procoagulant activity

A

Aminophospholipids on inner surface of platelet membrane
1. Platelet activation causes release of Ca2+ from intracellular stores
2. Calcium increase inhibits translocase and activates scramblase
3. Scramblase flips aminophospholipids to outer surface
4. Aminophospholipids allow assembly of coagulation cascade proteins
5. Prothrombin to thrombin

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47
Q

Describe the platelet-fibrin clot

A

Fibrin strands form mesh
Platelets and red blood cells in mesh

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48
Q

What is the fibrinolytic system?

A

Breaks down fibrin clots
- Endothelium releases tissue plasminogen activator
- tPA converts plasminogen into plasmin
- plasmin breaks down fibrin into fibrin degradation products
- plasminogen activator inhibitor-1 (PAI-1) regulates tPA
- antiplasmin inhibits plasmin so we don’t all bleed to death

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49
Q

How can platelets drive inflammatory response?

A

P-selectin of platelet outer surface binds to PSGL-1 on leukocytes
Increases inflammatory response

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50
Q

What are some anti-thrombotic drugs?

A

Aspirin
Heparins
Clopidogrel
Cangrelor

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51
Q

What is the platelet type of bleeding?

A

thromobocytopenia, thrombocytopathy
- petechial rash
- WF disease
- skin or mucosal bleeding, early post-procedural
- medication, liver disease, renal failure

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52
Q

What is the haemophilia type of bleeding?

A

factor deficiency
- late post-procedural bleeding
- large suffusions, haematomas

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53
Q

How would thrombocytopenia be classified?

A
  • Reduced production: congenital or acquired, reduced megakaryocytes
  • Increased destruction: increased megakaryocytes, immune, microangiopathic, consumptive
  • altered redistribution
  • pseudothrombocytopenia
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54
Q

Describe normal haemostasis

A
  • Normal platelet count and function
  • coagulation cascade with normal pro/anticoagulants
  • termination
  • fibrinolysis, normal pro/antifibrinolytic
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55
Q

What is haemostasis like in liver cirrhosis?

A
  • primary haemostasis: low platelet count
  • coagulation cascade, low pro/anticoagulants and low fibrinogen
  • termination
  • fibrinolysis, low pro/antifibrinolytics
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56
Q

What is thrombocytosis?

A

High platelet count
Can be malignant or reactive (e.g. bleeding)

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57
Q

What is thrombocytopenia?

A

Typically a 10% fall in platelet count

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58
Q

What are some plasma derived products?

A

FFP
Albumin
Cryoprecipitate
Fibrinogen
Coagulation factors
IVIG

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59
Q

How do ABO antigens work?

A

A and B alleles catalyse addition of different carbohydrate residues to H
O allele is non-functional and doesn’t modify the H

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60
Q

Process of development of ABO antibodies in children

A

Infants less than 3 months produce little to no antibodies
First antibodies are 3 months
Maximal titre at age 5-10yrs
Titre decreases with age

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61
Q

What are the antigens and antibodies for group A?

A

Antibodies in plasma are anti-B
Antigens on RBC are A antigen

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62
Q

What are the antigens and antibodies on group B?

A

Antibodies in plasma: anti-A
Antigens on RBC: B

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63
Q

What are the antibodies and antigens of AB?

A

No antibodies in plasma
A and B antigens

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64
Q

What are the antibodies and antigens of Group O?

A

Antibodies in plasma: Anti-B and Anti-A
No antigens

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65
Q

Describe rhesus antigens

A

Over 45 different types
Genetic locus on chromosome 1
Highly immunogenic
Can cause haemolytic transfusion reactions and HDFN
Rh D main type

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66
Q

What is HDFN?

A

Haemolytic disease of the fetus and newborn
Occurs when Rh-negative mother pregnant with Rh-positive baby
Rh D+ blood from baby enters mothers bloodstream, cause production of antibodies in mother
Rh D+ antibodies attack the baby’s blood causing disease (often in 2nd child)

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67
Q

How does ABO typing work?

A

Forward: add reagent anti-A to patient spun down RBCs, add anti-B and anti-D to other tubes. RBCs will clump if antigen binds. E.g. add anti-A, clump, therefore has A antigen

Backwards: add RBCs with A/B antigen to patient’s plasma, line at top = positive result

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68
Q

What is the direct antiglobulin test?

A

Used for detecting antibody already on the red cell surface where sensitization has occured in vivo
Detects autoimmune or haemolytic disease

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69
Q

What is the indirect antiglobulin test?

A

Detect antibodies that have coated the red cells in vitro
Used as part of the routine antibody screening prior to transfusion and for detecting blood group antibodies in pregnant women

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70
Q

What is apheresis in blood donations?

A

Blood is removed and separated externally and then the components not needed are returned

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71
Q

How is fresh frozen plasma used?

A

From whole blood donations or apheresis
From male donors only
Indications of need: multiple clotting factor deficiencies and bleeding, single clotting factor deficiency where a concentrate isn’t available

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72
Q

How is cryoprecipitate used?

A

Thawing FFP and skimming off fibrinogen rich layer
Used in DIC with bleeding and massive transfusion, hypofibrinogenaemic

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73
Q

How is intravenous immunoglobulin used?

A

Normal IVIg: used in immune conditions
Specific IVIg: particular infections

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74
Q

How are factor concentrates used?

A

Single factor concentrates: Factor VIII for severe haemophilia A, fibrinogen concentrate
Prothrombin complex concentrate: multiple factors, rapid reversal of warfarin

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75
Q

What happens with serious ABO incompatibility

A

Rapid intravascular haemolysis
Cytokine release leading to acute renal failure and shock
Treatment: stop transfusion, fluid resuscitate
Blood goes back to lab to check why it happened

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76
Q

What is TRALI?

A

Transfusion-related lung injury
AB in donor blood reacting with recipient pulmonary endothelium/neutrophils
Plasma leaks into alveolar spaces

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77
Q

What is gastrulation?

A

Mass movement and invagination of the blastula to form 3 layers: ectoderm, mesoderm and endoderm

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78
Q

What comes from the ectoderm?

A

Skin
Nervous system
Neural crest (some contributes to the cardiovascular system)

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79
Q

What comes from the mesoderm?

A

All types of muscle
Most systems (most of cardiovascular system)
Kidneys
Blood
Bone

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80
Q

What comes from the endoderm?

A

GI tract (liver, pancreas, not smooth muscle)
Endocrine organs

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81
Q

When do the heart fields develop and what do they form?

A

Day 15
First HF: future left ventricle
Second HF: outflow tract, future right ventricle, atria

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82
Q

Describe the stages of heart development from day 15-50

A

Day 15: Heart fields
Day 21: Inflow tract into two future atria, single outflow tract, ventricle
Day 28: looped structure with ventricles and atria
Day 50: standard postnatal structure

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83
Q

What happens in formation of primitive heart tube?

A

day 19: 2 tubes
day 21: one single tube
contains bulbus cordis, ventricle, artium, right and left horns of sinus venosus

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84
Q

What happens during cardiac looping?

A

After formation of primitive tube
Sinus venosus moves to top
Primitive atria anterior to SV
Primitive ventricle moves to left
Bulbus cordis moves anteriorly down to right

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85
Q

What happens during cardiac septation?

A

After cardiac looping
Endocardial cushion grows from sides of AV canal to partition it into 2 separate openings
AV canal re-positioned to right side of heart

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86
Q

Why does the heart have a negative membrane potential (-90mV)?

A
  • the membrane is normally only permeable to K+
  • K+ diffuse out down gradient
  • Anions can’t follow, so remain in cell in excess
  • Negative potential
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87
Q

What are the concentrations of ions in the ECF?

A

Na+, 145 mmol/L
K+, 4 (more in ICF)
Ca2+, 2
Cl-, 120

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88
Q

What are the concentrations of ions in the ICF?

A

Na+, 14 mmol/L (more in ECF)
K+, 135
Ca2+, 0.0001 (more in ECF)
Cl-, 4 (more in ECF)

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89
Q

Describe the action potential process in myocyte membranes

A
  1. 3Na+ pumped out for every 2K+ pumped in (phase 4)
  2. Cell activated, voltage-gated channels open, Na+ in
  3. Potential changes from -90 to +20mV, depolarisation (phase 0)
  4. Small K+ movement out causes small repolarisation (phase 1)
  5. Calcium channels open and calcium enters cell, maintains depolarisation, plateau (phase 2)
  6. Outward movement of K+ repolarises cell and return to resting potential (phase 3)
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90
Q

How is the resting potential maintained?

A
  1. K+ move out of cell down gradient
  2. ECF more positive, ICF more negative
  3. Electrical gradient draws K+ back into cell
  4. Equilibrium and no net movement at -90mV
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91
Q

Describe the process of action potential propagation in cells

A
  1. local depolarization activates nearby Na+ channels to open, Na+ in
  2. influx of Na+ triggers nearby channels to open
  3. wave of depolarisation
  4. gap junctions allow cell to cell conduction and propagation across whole myocardium
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92
Q

What is excitation-contraction coupling?

A

Once heart is excited, simultaneous contraction of heart muscle
Calcium for contraction from action potential

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93
Q

Process of excitation-contraction coupling

A
  1. Calcium enters cell through surface ion channels
  2. 3Na leave cell, 1 Ca2+ moves in down gradient
  3. Calcium-induced calcium release from sarcoplasmic reticulum from activated ryanodine receptors
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94
Q

How does the troponin-tropomyosin-actin complex work?

A
  1. Calcium binds to troponin
  2. Conformational changes in tropomyosin reveals myosin binding sites
  3. Myosin head cross-links with actin
  4. Myosin head pivots causing muscle contraction
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95
Q

Why does cardiac muscle contraction last longer than skeletal?

A

Due to slow calcium changes
Decreased permeability to K+ after ap

96
Q

What are the phases of SAN action potential?

A
  • Phase 4: hyperpolarisation activated cyclic nucleotide gated channels activated and allow Na+ into cell for slow depolarisation to a threshold
  • Phase 0: -40mV, voltage gated Ca2+ channels open, influx of calcium to +ve membrane potential, at peak, channels close, K+ channels open
  • Phase 3: efflux of K+ out of cells, repolarisation
97
Q

Brief summary of SAN action potential

A

Phase 4: pacemaker potential
Phase 0: depolarisation
Phase 3: repolarisation
Phase 4: just before start of next one

98
Q

In SAN action potential, what is phase 4 affected by?

A

Autonomic tone
Hypoxia
Drugs
Electrolytes
Age

99
Q

How does sympathetic stimulation affect the heart?

A

Increases heart rate (up to 180-250bpm)
Increases force of contraction
Increases cardiac output (by up to 200%)

100
Q

How does parasympathetic stimulation affect the heart?

A

Decreases heart rate (temporary pause or as low as 30-40bpm)
Decreases force of contraction
Decreases cardiac output (by up to 50%)

101
Q

What controls sympathetic stimulation of the heart?

A

Adrenaline
Noradrenaline
Type 1 beta adrenoreceptors
Increase adenylyl cyclase —-> increase cyclic AMP

102
Q

What controls parasympathetic stimulation of the heart?

A

Acetylcholine
M2 receptors inhibit adenylyl cyclase, reducing cAMP

103
Q

What is the role of the AV node?

A
  • Transmits cardiac impulse between atria and ventricles
  • Delays impulse, allows atria to empty into ventricles, fewer gap junctions, AV fibres are smaller than atrial (all slows down)
  • Limits dangerous tachycardia
104
Q

What is the speed of atrial, ventricular and purkinje fibre conduction?

A

Artial and ventricular fibres: 0.3-0.5m/s
Purkinje: 4m/s (much faster)

105
Q

What is the role of the His-Purkinje system?

A
  • AV node to ventricles
  • Rapid conduction to allow coordinated ventricular conduction, through very large fibres and high permeability at gap junctions
106
Q

What is automaticity?

A

property of cardiac cells to generate spontaneous action potentials

107
Q

Brief summary of action potential phases

A

Phase 4: resting potential
Phase 0: depolarisation
Phase 1: small/initial repolarisation
Phase 2: plateau
Phase 3: repolarisation

108
Q

What is the refractory period and its purpose?

A

Heart can’t be stimulated when refractory, normally 0.25 seconds long (less for atria than ventricles), ion channels closed
- prevents excessively frequent contraction
- allows adequate time for heart to fill
In absolute refractory period, absolute no stimulation
Relative refractory period: strong stim cause ap

109
Q

What happens in long QT syndrome?

A
  • Abnormality of K+ channels (usually) causes loss of function
  • Slower efflux of K+, delayed repolarisation
  • risk of syncope or sudden cardiac death
110
Q

How does the ECG graph work (basic)?

A

Voltage against time
5 small squares = 0.2 secs = 1 big square
1 vertical big square = 0.5mV
Provides info on rate, rhythm, axis, conduction, myocardial health

111
Q

Equation to calculate rate from ECG

A

rate bpm= 300 divided by number of big squares between cardiac cycles

112
Q

What do the deflections on an ECG show?

A

Baseline, isoelectric point, no net current flow in direction of lead
Positive deflection (up, voltage increase): net current flow towards lead
Negative deflection (down): net current flow away from lead

113
Q

What do the waves on an ECG show?

A

P wave: atrial depolarisation and contraction
QRS complex: ventricular depolarisation
T wave: ventricular repolarisation

114
Q

What is the normal value for PR interval?

A

120-200ms
3-5 small squares on ECG

115
Q

What is the normal QRS width?

A

Less than 120ms
3 small squares on ECG

116
Q

What can cause a prolonged QRS complex?

A

Usually bundle branch block

117
Q

What is the normal value for the QT interval?

A

Men: 350-440ms
Women: 350-460ms

118
Q

Combinations of leads 1 and 2 on ECG that show deviation

A

Leads 1 & 2 positive = normal
Lead 1 positive, lead 2 negative = left axis deviation
Lead 1 negative, lead 2 positive = right axis deviation

119
Q

What are the different types of leads on ECG?

A

12 lead ECG with 10 electrodes
3 bipolar limb leads, 1,2,3,
3 unipolar limb leads, aVL, aVF, aVR
6 unipolar chest leads, V1-6

120
Q

What do the different ECG electrodes look at?

A

V1-2: Septal (LV), right coronary artery
V3-4: anterior LV, LAD
V5-6: lateral LV, left circumflex

121
Q

What are some of the elastic arteries and their purpose?

A

Major distribution vessels
Brachiocephalic, aorta, carotid, subclavian, pulmonary

122
Q

What are muscular arteries?

A

Main distributing branches
Small than elastic

123
Q

What regulates blood flow in capillaries?

A

Precapillary sphincters

124
Q

What are the 3 types of capillary + examples of where to find them?

A

Continuous
Fenestrated- kidney, small intestine, endocrine glands
Discontinuous- liver sinusoids

125
Q

Stages of the blood vessels forming

A

Day 17: formation of blood islands from the mesoderm, in yolk sac above embryonic disc
Day 18 + onwards: vasculogenesis commences and is added to by angiogenesis, other mesodermal cells recruited

126
Q

What drives embryonic vessel development?

A
  • Angiogenic growth factors: vascular endothelial growth factor, angiopoietin 1 and 2
  • Repulsive signals: plexin, semaphorin signalling, ephrin
  • Attractive signals: VEGF
127
Q

After day 29, what do the aortic arches go on to become?

A

1st arch: small part of maxillary artery
2nd arch: artery to stapedius
3rd arch: carotid arteries
4th arch: Right side loses aortic connection and goes to supply arm. Left side becomes part of aortic arch
6th arch: left becomes ductus arteriosus, right partly forms pulmonary trunk
note: no 5th arch, doesn’t exist

128
Q

How much of body weight comes from intracellular fluid?

129
Q

How much of body weight is in extracellular fluid and how does this divide?

A

20%
Splits into intravascular (plasma, 4%, circulates) and interstitial (between cells, 16%, surrounds cells doesn’t circulate)

130
Q

How much of body weight is from total body water?

131
Q

What is the role of ICF?

A

Stabilise cell
Maintain shape
Transport of nutrients

132
Q

What is osmotic pressure?

A

The pressure required to stop water from diffusing through a barrier by osmosis
Determined by solute concentration (water will try harder to diffuse into a high solute conc)

133
Q

What does a change in concentration of osmotic contents lead to?

A

Water moves from low osmolality to high osmolality
Results in isotonic solution

134
Q

What is osmolality?

A

The concentration of a solution expressed as the total number of solute particles per kg

135
Q

What is osmolarity?

A

Same as osmotic concentration
The concentration of a solution expressed as the total number of solute particles per litre

136
Q

What is in the ECF?

A

135mmol/L sodium, moved by active transport
chloride and bicarbonate
glucose and urea
proteins

137
Q

What is the predominant cation in ICF?

A

Potassium, 110mmol/L

138
Q

Where is water gained from?

A

Food
Drink
Metabolism

139
Q

How do you lose water?

A

Skin and expiration (insensible)
Urine
Faeces

140
Q

When would you give saline?

A

Blood loss if no blood available
Go into interstitial spaces

141
Q

When would you give 5% glucose solution?

A

Severe dehydration
Metabolised quickly and goes intracellularly

142
Q

Where does a colloid transfusion go?

A

Plasma volume

143
Q

Why don’t you give water intravenously?

A

Water would enter cells causing them to expand and burst

144
Q

What happens after water deprivation or dehydration?

A

Changes in ECF lead to rapid response
Water moves from ICF to ECF
Hypothalamus and thirst centre stimulated
ADH released from posterior pituitary

145
Q

What is the normal plasma osmolality?

A

275-295mmol/kg

146
Q

How does the renin-angiotensin-aldosterone system work?

A
  1. Kidney detects decrease in renal perfusion
  2. Juxtaglomerular apparatus releases renin
  3. Renin cleaves angiotensinogen into angiotensin 1
  4. Angiotensin 1 convert to Angiotensin 2 by ACE
  5. Adrenal gland detects Angiotensin 2 and secretes aldosterone
  6. Aldosterone acts on distal tubes of kidneys and changes reabsorption of potassium and sodium
147
Q

What are some causes of water depletion

A

Vomiting
Diarrhoea
Diuretics
Sweating
Reduced intake

148
Q

Signs of dehydration

A

Thirst
Dry mouth
Inelastic skin
Sunken eyes
Raised haematocrit
Weight loss
Confusion
Hypotension

149
Q

What happens in water excess?

A

ECF moves into ICF, cells swell
No stimulation of thirst
Inhibition of ADH
Increased urine volume
Risk of cerebral overhydration if acute excessive intake

150
Q

What is hyponatraemia

A

Blood sodium level below 135mmol/L
Extra water into cells, cells swell
Build up of fluid, in brain (cerebral oedema)

151
Q

What can cerebral overhydration cause?

A

Headache confusion
Convulsions
Cerebral oedema
Death

152
Q

How does water move in and out of vessels?

A

Water exits into interstitial at arterial end
Some goes into lymphatic
Reenters at venous end
Hydrostatic and oncotic pressure balance

153
Q

What is oedema?

A

Excess accumulation of fluid in the interstitial space
Disruption of the filtration and osmotic forces of circulating fluids

154
Q

What can cause oedema?

A

Obstruction of venous blood or lymphatic return
Inflammation
Loss of plasma protein, change in albumin concentration

155
Q

How does inflammatory oedema work?

A

Inflammation causes vasodilation and increases permeability
More water goes out than comes back in
Albumin leaves, so doesn’t help to draw water back in

156
Q

What is venous oedema?

A

Problem at the venous end
Caused by overweight or chronic heart failure, often seen in lower legs
More water coming out into interstitial at venous end, rather than going in

157
Q

What is lymphoedema?

A

Problem with the lymphatic system
Some water isn’t draining away, causes more pressure and water coming out at venous end

158
Q

What is hypoalbuminaemic oedema?

A

Plasma proteins no longer sustain osmotic pressure to counterbalance hydrostatic pressure
More water out as nothing to draw it back in

159
Q

What are pleural effusions?

A

Disruption of balance between hydrostatic and oncotic forces in the visceral and parietal pleural vessels
Different fluids enter the pleural cavity
Transudate (low protein content) pushed through capillary due to high cap pressure
Exudate (high protein content) leaks around cells of capillaries caused by inflammation

160
Q

How much fluid is normally in the pleural space?

A

10mL of fluid

161
Q

Difference between exudates and transudates

A

Exudates have high protein level, may contain cells, bacteria and enzymes
Transudates have low protein levels

162
Q

What is the normal range for sodium concentration?

A

135-145mmol/L

163
Q

What can cause hypernatraemia?

A

Water deficit (poor intake, diuresis, diabetes insipidus)
Sodium excess (mineralocorticoid excess, salt poisoning)

164
Q

What can cause hyponatraemia?

A

Sodium loss (diuretics, addison’s disease)
Excess water (IV fluids, SIADH)
Excess water and sodium (oedema)

165
Q

What is a myocyte?

A

muscle cell

166
Q

What happens to Ca2+ when a myocyte depolarises?

A

Ca2+ move into neighbouring cell and trigger more depolarisation

167
Q

What happens during myocyte depolarisation (calcium-induced calcium release)?

A
  • Ca2+ leave cell via gap junctions
  • If threshold reached, Na+ channels open and ions flow across cell membranes
  • Presence of T-tubules in neighbouring cells bring Ca2+ deep into cell
  • Ca2+ bind to ryanodine receptors on sarcoplasmic reticulum
  • More calcium released into cell
168
Q

What is the role of Ca2+ in heart contraction?

A

Help activate actin and myosin

169
Q

Describe the process of calcium excitation-contraction coupling

A
  • Troponin C is attached to tropomyosin which covers actin binding sites
  • Calcium ions bind to troponin C, causing tropomyosin to slide, exposing actin binding sites
  • Myosin heads bind to actin, forming a cross-bridge
  • Muscle contraction
  • Calcium eventually removed, returns to original shape
170
Q

What is the myosin ultrastructure?

A
  • 2 heavy chains, also 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 (row.)
  • alpha myosin and beta myosin
171
Q

What is actin?

A
  • Globular protein.
  • Double-stranded macromolecular helix (G).
    Both form the F actin.
172
Q

What are the 3 types of troponin and what do they do?

A

I: with tropomyosin inhibit actin and myosin interaction.
T: binds troponin complex to tropomyosin.
C: high affinity calcium binding sites, signalling contraction.

173
Q

What is the A band of a sarcomere?

A

Dark band: thick, high density, actin and myosin during contraction, mostly myosin when relaxed

174
Q

What does the I band look like in sarcomeres?

A

I band split in half
Striated muscle
Between two A bands
Light

175
Q

How is JVP related to right atrium?

A

No valves between jugular, SVC and R atrium
JVP follows right atrium pressure
Increase in right atrial pressure + increased JVP

176
Q

What causes the 4th heart sound (S4)?

A

Vibration of stiffened ventricular wall as blood pushed from atria to ventricles
E.g. in ventricular hypertrophy

177
Q

What is stroke volume?

A

Difference between end diastolic and end systolic volume
How much blood expelled from heart in each beat

178
Q

What is the eqtn for cardiac output?

A

Stroke volume x heart rate

179
Q

What can affect stroke volume?

A

central venous pressure (CVP) and Total Peripheral Resistance (TPR).

180
Q

What are the stages of the cardiac cycle?

A

Filling (diastole)
Isovolumetric contraction (ventricular systole)
Outflow phase (blood out)
Isovolumetric relaxation (ventricles relax)

181
Q

What is the average cardiac output for an adult?

A

5-8 litres blood in per minute

182
Q

What is preload?

A

the initial stretching of the cardiac myocytes prior to contraction

183
Q

What is afterload?

A

force or load against which the heart has to contract to eject the blood

184
Q

What is central venous presure?

A

blood pressure in the vena cava as it enters the right atrium
reflects the volume of blood returning to the heart and therefore the volume of blood the heart pumps back into the arteries

185
Q

What is total peripheral resistance?

A

the pressure in the arteries that blood must overcome as it passes through them, and thus dictates how easy it is for the heart to expel blood

aka afterload

186
Q

What happens in systolic heart failure?

A

heart has difficulty pumping blood out
weakened cardiac muscle cells contract less effectively, resulting in greatly reduced ejection fraction
frank-starling curve shifts downwards and to right
smaller SV

187
Q

What happens in diastolic heart failure?

A

heart has trouble filling
ventricles don’t fill normally as heart muscle doesn’t adequately relax between beats/ stiffens
ejection fracture normal, less blood than normal pumped out because ventricles are inadequately filled

188
Q

Describe cardiac cycle

A
  • Filling, ventricular diastole, AV open
  • SAN reaches threshold and fires, pressure rises, P wave, AV still open, excitation-contraction coupling
  • Ventricles full, EDV
  • Signal to AVN, atria contract, ventricles contract and pressure exceeds atria, AV valves shut, QRS complex
  • all valves closed and pressure rises
  • aortic valve opens and blood forced out
  • end systolic volume left in ventricles
  • ventricles repolarize, valves close, T wave
  • ventricle pressure falls below atrial and AV valves open
189
Q

What is the normal pressure in the left ventricle?

A

120 systolic
10 diastolic

190
Q

What is the normal left atrial pressure?

191
Q

What is normal right ventricle pressure?

A

25 systolic
4 diastolic

192
Q

What is normal right atrial pressure?

193
Q

What is normal pulmonary artery pressure?

A

25 systolic
10 diastolic

194
Q

What can reduce cardiac output?

A

decreased heart rate
decreased preload
decreased contractility
increased afterload

195
Q

What is the SAN?

A

cluster of pacemaker cells in R atrium
Establishes HR
Has natural automaticity

196
Q

What does the AVN do?

A

Above ventricular septum
Passes impulses from atria to ventricles
Slower than SAN
Has a 0.15 second delay

197
Q

What is the parasympathetic influence to heart?

A

Vagus synapses with postganglionic cells in SAN and AVN
When stimulated, ACh binds to M2 receptors and decreases HR

198
Q

What is the sympathetic influence on the heart?

A

Postganglionic fibres from cardaic plexus innervate SAN and AVN
Release noradrenaline which acts on B1 adrenoreceptors and increases HR

199
Q

Which out of sympathetic and para dominates at rest?

A

Parasympathetic
Resting HR of 60bpm

200
Q

What does starling law state?

A

the more the heart chambers fill, the stronger the ventricular contraction, and therefore the greater the stroke volume

under normal conditions, the heart pumps out of the right atrium all the blood returned to it without letting any back up in the veins

201
Q

What affect does the nervous system have on contractility?

A

sympathetic nervous system acts via B1 adrenoceptors and increases contractility (positive inotropic effect)
parasympathetic nervous system acts via muscarinic (M2) receptors and decreases contractility (negative inotropic effect)

202
Q

What is contracitility?

A

ability to increase its contraction velocity to achieve higher pressure independent of load.

203
Q

Equation for pulse pressure

A

Systolic - diastolic pressure

204
Q

Equation for mean arterial pressure

A

Diastolic pressure + 1/3 pulse pressure

205
Q

Equation for stroke volume

A

End diastolic vol - end systolic vol

206
Q

How can an occlusion of LAD lead to bundle branch block?

A

provides the major blood supply to the interventricular septum, and thus bundle branches of the conducting system.
Blockage can lead to impairment/ infarction of the conducting system.
Block of impulse conduction between the atria and the ventricles known as “right/left bundle branch block.”

207
Q

What does LAD supply?

A

the LAD artery and its branches supply:
- the anterior, lateral, and apical wall of the left ventricle
- most of the right and left bundle branches
- the anterior papillary muscle of the bicuspid valve
- provides collateral circulation to the anterior right ventricle, the posterior part of the interventricular septum, and posterior descending artery

208
Q

What is ohms law for blood flow?

A

Pressure gradient (change in) / resistance

Q= change in P / R

209
Q

What is poiseuilles law?

A

Flow directly proportional to radius^4

210
Q

What does Q stand for?

A

Blood flow

211
Q

What does V stand for?

A

Velocity of blood
V = distance/ time

212
Q

What causes the dicrotic notch in the cardiac cycle pressure graph?

A

Aortic valve closing, causing backflow of blood to bounce off

213
Q

What happens to the cardiac system when symp NS is activated?

A

Noradrenaline released and binds to B1-adrenergic receptors in heart
SAN fires more repidly
Heart beats faster

Calcium movements in contractile cells also enhanced

214
Q

What mediates parasympathetic cardiac responses?

215
Q

What does vagal tone of the heart mean?

A

Dominant influence is inhibitory as the heart is innervated by vagus
Without vagus input, heart would beat a lot fster

216
Q

What hormones have an effect on the heart?

A

Adrenaline
Noradrenaline
Thyroxine (increases metabolic rate and increases HR)

217
Q

Why would a transfusion reaction occur if a Rh- patient was given Rh+ twice?

A

Rh- people don’t have anti-Rh antibodies in the blood
If a person receives Rh+ blood, the immune system is sensitised and starts producing anti-Rh slowly after transfusion
If encountered again, anti-Rh attack

218
Q

What do auricles do?

A

Increase atrial volume

219
Q

Differences between skeletal and cardiac muscle

A

Skeletal: striated, long, cylindrical, multinucleate, abundant T tubules
Cardiac: striated, short, branched, 1-2 nuclei, gap junctions, less T tubules

220
Q

What is the general structure of arteries?

A

Lumen
Endothelium
Basement membrane
Intima
Internal elastic lamina
Media (sheets of elastin)
External elastic lamina
Adventitia

221
Q

What is the general structure of veins?

A

Lumen (wider than arteries)
Endothelium
Basement membrane
Intima
Internal elastic media
Media (thinner than arteries)
Adventitia

222
Q

What is the general structure of capillaries?

A

Lumen
Endothelium
Basement membrane (fenestrated capillaries have gaps)
Pericytes on outside

223
Q

Where are fenestrated capillaries found?

A

Areas of active filtration, absorption or endocrine secretion

224
Q

Where are continuous capillaries found?

A

Abudant in skin, muscles, lungs and CNS
Often have associated pericytes

225
Q

Where would you find elastic arteries and what are they?

A

Found near heart (aorta and branches)
Thick-walled, largest in diameter
Have elastin in all three tunica
They are pressure reservoirs

226
Q

Where and what are muscular arteries?

A

Distally from elastic, distribute blood to most organs/areas
Tunica media has more smooth muscle less elastin
More active in vasoconstriction and less capable of stretching

227
Q

What happens when arterioles change diameter?

A

Constrict: their tissues are largely bypassed
Dilate: blood flow increases dramatically

228
Q

What factors can affect blood pressure?

A

Blood viscosity
Cardiac output
Peripheral resistance

229
Q

What is the equation for mean arterial blood pressure from CO?

A

Cardiac output x total peripheral resistance

230
Q

What is the baroreceptor (short term) reflex from an increase bp?

A

Increase arterial BP detected by baroreceptors in carotid sinus/ aortic arch
Send rapid impulses to CV centre
Cardioinhibitory centre stimulated
Vasodilation and decreased CO decrease BP

231
Q

What is the baroreceptor reflex from a decrease in BP?

A

Decrease in BP detected by baroreceptors in carotid sinus and arch of aorta
Sympathetic response increases HR and contractility
BP raised

232
Q

What affect doe atrial natriuretic peptide (ANP) have on BP?

A

Causes kidneys to excrete more sodium and water, decreasing blood volume
Causes generalised vasodilation
Leads to reduction in blood pressure

233
Q

What hormones regulate BP?

A

Adrenaline
Noradrenaline
Angiotensin II
ANP
ADH (not usually important in short term, more in haemorrhage)

234
Q

What is the short term regulation of BP?

A

Hormones and baroreceptors

235
Q

What is the long term regulation of BP?

236
Q

How does RAAS work?

A

Arterial pressure drops
Renin facilitates conversion of angiotensinogen to angiotensin I
ACE converts into angiotensin II
Angiotensin II promotes release of aldosterone
Angiotensin II also vasocontricts and stimulates ADH release
Leads to increased water reabsorption and increased blood volume
Mean arterial pressure rises

237
Q

What does blood flow through the skin do?

A

Regulate body temp
Blood reservoir
Supplies nutrients to cells

Phase 1 (18 decks)

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