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Block 2 AR > Blood > Flashcards

Blood Flashcards

1
Q

Which oxygen molecule binds to haemoglobin the easiest?

A

4th and last one, as quaternary structure changes as each molecule of oxygen is added and makes it progressively easier for more molecules to bind

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2
Q

Which factors can cause a rightward shift of the oxygen dissociation curve and therefore haemoglobin has a lower affinity for oxygen?

A 
CADET!
CO2
Acid
2-3-DPG
Exercise
Temperature
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3
Q

What is the Bohr effect?

A

In acidic conditions, oxygen dissociation curve shifts right and so Hb ha a reduced affinity for oxygen

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4
Q

What is the Haldane effect?

A

Increasing oxygen binding to Hb decreases affinity for CO2 and H+ ions by modifying quaternary structure

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5
Q

What is inflammation?

A

Protective mechanism
Rid body of cause of injury
Remove debris and tissue damage secondary to injury

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6
Q

What can cause excessive inflammation?

A

Inappropriately triggered eg rheumatoid arthritis

Poorly controlled eg abscess - leakage of enzymes from cells

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7
Q

What can cause inadequate inflammation?

A

Immunodeficiency eg AIDS/HIV

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8
Q

What are the beneficial effects of inflammation?

A 
dilution of toxins 
entry of antibodies 
fibrin formation to initialise repair
nutrients and oxygen 
deliver neutrophils 
stimulation of the immune response 
entry of drugs
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9
Q

What problems can inflammation cause?

A 
destruction of normal tissue
swelling 
blockage of tubes 
loss of fluid 
pain 
inappropriate inflammation
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10
Q

What 6 things can cause inflammation?

A 
Microbes
Foreign bodies
Dead cells
Allergens
Physical trauma and damage 
Chemical injury
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11
Q

What are the 3 phases of acute inflammation in first 48 hours?

A

Oedema
Neutrophils
Monocytes/macrophages

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12
Q

What are the 3 hallmark features of chronic inflammation?

A

Ongoing inflammation
Ongoing tissue destruction
Ongoing tissue repair

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13
Q

What are the 5 cardinal signs of acute inflammation?

A 
Rubor - red
Tumor - swelling
Calor - heat 
Dolor - pain
Functio laesa - loss of function
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14
Q

How does a tissue injury lead to oedema?

A

Increased blood flow to area due to opening of capillary beds
Dilation of blood vessels so decreased velocity of flow
Increased leakiness of microvasculature due to squamous endothelium retraction
Plasma proteins and leukocytes infiltrate area

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15
Q

What happens to lymphatics during inflammation?

A

Increase drainage of excess fluid

Proliferate

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16
Q

Which leukocytes are recruited in acute inflammation?

A

Neutrophils

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17
Q

What are the 3 phases of cellular changes that occur in acute inflammation?

A

Recruitment - delivery and extravasation of leukocytes
Accumulation
Activation - recognition of microbes and necrotic tissue, removal of stimulus

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18
Q

Which part of acute inflammatory response can lead to tissue injury?

A

Activation of leukocytes

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19
Q

What are the 4 stages of recruitment and migration of neutrophils?

A

Margination
Adhesion
Emigration
Chemotaxis

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20
Q

What is margination?

A

Dilation of vessels - turbulent flow allows WBC to come into contact with endothelium
Stagnation in the microcirculation displaces cells from the central axial
flow
Rolling occurs in unaffected area due to low affinity receptors

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21
Q

What is adhesion?

A

In areas of injury, endothelial cells possess high affinity receptors (integrins) and so neutrophils adhere to these receptors. Chemokines at injury site activate integrins

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22
Q

What happens in the process of emigration of neutrophils?

A

Neutrophils secrete enzymes to digest the basement membrane which allows them to invade the tissue

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23
Q

What is chemotaxis?

A

Chemokines induce movement of neutrophils. Area of high concentration of chemokines is where most damage is so neutrophils move down concentration gradient

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24
Q

How do neutrophils recognise dead tissue or foreign material?

A

Directly via mannose receptors

Indirectly via opsonins & Fc and C3b receptors

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25
Q

What is opsonisation?

A

Marking a foreign body for destruction by phagocytosis

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26
Q

How does neutrophilic phagocytosis occur?

A

Recognition and attachment
Engulfment
Phagosome fuses with lysosome
Oxygen dependent (free radicals) or independent (enzymes) system degrades microbes

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27
Q

Which microbe can survive neutrophil phagocytosis?

A

Mycobacterium tuberculosis

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28
Q

What part of chronic inflammation can cause scarring?

A

Fibrous repair

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29
Q

What changes occur that lead from acute to chronic inflammation?

A 
Angiogenesis 
Mononuclear cell infiltrate
Fibrosis (scar)
Progressive tissue injury
Collagen deposition 
Loss of function
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30
Q

What are the 4 morphological patterns of inflammation?

A

Serous - blister
Suppuration - large amount of pus, abscess
Fibrinous - large increase in vascular permeability allows fibrin to pass through. Fibrinous exudate deposited
Ulcers - exposure of lower layers of epithelium

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31
Q

What are the 8 cell derived mediators of inflammation?

A 
Vasoactive amines
Arachidonic acid metabolites
Platelet activating factor
Reactive oxygen species 
Nitric oxide 
Cytokines and chemokines
Lysosomal constituents 
Neuropeptides
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32
Q

What are prostaglandins, leukotrienes and lipoxins?

A

Arachidonic acid metabolites involved in inflammatory process

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33
Q

Which arachidonic acid metabolites cause vasodilation?

A

Prostaglandins

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34
Q

What do thromboxane A2 and leukotrienes C4, D4 and E4 do?

A

Cause vasoconstriction

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35
Q

Which cell derived mediators are important in anaphylaxis?

A

Vasoactive amines - histamine and serotonin

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36
Q

What feature of vasoactive amines makes them rapid acting?

A

Released from preformed vesicles

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37
Q

What do vasoactive amines do?

A

Cause dilation of arteries and arterioles

Increased permeability of venules

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38
Q

What does platelet activating factor do?

A

Platelet aggregation
Vasoconstriction
Bronchoconstriction
Increased AA production

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39
Q

What do reactive oxygen species do in inflammation?

A

Destruction of ingested particles
Increase chemokines, cytokines and adhesion molecules
Destruction of tissues

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40
Q

What effects does NO have on inflammation?

A

Control mechanism
Reduces adhesion of leukocytes and platelets
Vasodilation

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41
Q

What do chemokines do?

A

Promote inflammation and repair

Systemic manifestations - fever, decrease appetite, increase sleep

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42
Q

What is the membrane attack complex?

A

Complement system c5-9 punches hole in membrane so cell loses equilibrium control and is lysed

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43
Q

In what 3 ways can complement be activated?

A

Alternative pathway - opsonisation
Classical pathway - antibody
Lectin pathway - mannose binding

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44
Q

What does complement C3b do?

A

Deposited on microbe
Recognised by phagocyte receptor and phagocytosed
C3a fragment recruits and activates leukocytes

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45
Q

Why is factor XII important?

A 
Activates multiple systems which work together 
Clotting cascade
Complement cascade 
Kinin cascade
Fibrinolytic system
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46
Q

Describe the cycle of chronic inflammation

A

Recruitment of neutrophils and macrophages
IFN-y activate macrophages
Antigen presentation to T cells - cytokines
T cells release IFN-y
T cells are activated and release TNF, IL17 and chemokines
Further leukocytes are recruited

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47
Q

Macrophages are important in which parts of chronic inflammation?

A

Continuing inflammatory response

Starting process of repair

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48
Q

What cell mediators cause shock?

A

Massive quantities of TNF and IL1

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49
Q

When do we see chronic inflammation?

A

Persisting infection - h pylori gastric ulcer, viral hepatitis, TB
Chronic/autoimmune - bronchitis, crohns, rheumatoid
Foreign material - suture, silica
Inadequate immune response - HIV
Inadequate blood supply - leg ulcer, bed sore

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50
Q

Name a factor that favours continuing ulceration

A

Insufficient perfusion

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51
Q

When are eosinophils present?

A

Reactions mediated by IgE and parasitic infections

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52
Q

What are possible outcomes of chronic inflammation?

A 
Atrophy
Metaplasia
Repair
Scarring with dysfunction eg cirrhosis in viral hepatitis
Catastrophe eg perforated gastric ulcer
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53
Q

What is lymphoid hyperplasia?

A

Swollen lymph nodes

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54
Q

What can a C reactive protein (CRP) measurement be used for?

A

Measure levels of acute inflammation

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55
Q

Name 4 functions of the immune system

A

Infection and immunity
Inflammatory process
Removal of senescent cells
Defence against neoplasia

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56
Q

Give 3 types of immune disorder

A

Auto immune
Hypersensitivity
Immunodeficiency

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57
Q

What is serology?

A

Antibody detection after infection

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58
Q

What is a vaccine?

A

Prophylactic treatment against infection

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59
Q

What is an antigen?

A

Substance capable of inducing a specific immune response

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60
Q

Name 3 types of antigen

A

Microbes, neoplasms and foreign tissue

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61
Q

Give 3 examples of PAMPs (pathogen associated molecular patterns)

A

Bacterial lipopolysaccharide
Peptidoglycan
Flagellin

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62
Q

Antigens with PAMPs are most likely targeted by which mechanisms?

A

Innate

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63
Q

Which branch of the immune system provides the immediate response?

A

Innate

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64
Q

What advantages does the adaptive immune system provide?

A

Antigen presentation - specific
Clonal selection
Immunological memory

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65
Q

What parts make up the innate immune system?

A 
Epithelial barriers
Phagocytes
Dendritic cells - antigen presenting cells
Complement 
Natural killer cells
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66
Q

What parts make up the adaptive immune system?

A

B lymphocytes –> plasma cells, memory cells –> antibody production
T lymphocytes –> helper, memory, suppressor and cytotoxic

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67
Q

What are neutrophils?

A

Polymorhonuclear phagocytes

First line of defence of innate immune system

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68
Q

What are monocytes and macrophages?

A

Mononuclear phagocytes

Adaptive antigen presenting cells

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69
Q

What do basophils and mast cells do?

A

Inflammatory and hypersensitivity responses

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70
Q

What constitutes mucosa associated lymphoid tissue (MALT)?

A

Adenoids and tonsils

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71
Q

Where do T lymphocytes mature?

A

Thymus

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72
Q

Where does haematopoiesis and B cell maturation occur?

A

Bone marrow

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73
Q

What are a, B and y globulins?

A

Acute phase proteins
Innate humoral immunity
Eg complement (B), CRP, pro-calcitonin, mannose binding, antibodies (y)

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74
Q

What is the structure of an antibody?

A

Light chain - small
Heavy chain - big
Antigen binding site - variable
Y shaped

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75
Q

Which antibody is produced on first contact with antigen?

A

IgM

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76
Q

Which antibody does the major work and is present in later stages of infection?

A

IgG

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77
Q

What parts form physical barriers against infection?

A

Skin
Mucus
Respiratory cilia
Commensal organisms

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78
Q

Which parts form biochemical barriers against infection?

A

Sebaceous secretions in skin
Lysozyme in tears
Spermine in sperm
Gastric acidity

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79
Q

Which mucosal surfaces do most infections enter the body by?

A

Nasopharynx
Respiratory tract
Alimentary tract
Genito-urinary tract

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80
Q

What is a risk of intubation in an immuno compromised patient?

A

Ventilation associated pneumonia

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81
Q

What name is given to the process where microbes are recognised and engulfed which are then killed by the release of toxic chemicals into the enclosed vacuole?

A

Phagocytosis

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82
Q

What cell types are involved in phagocytosis?

A

Neutrophils

Macrophages and monocytes

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83
Q

What is neutropenia?

A

Abnormal low levels of neutrophils

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84
Q

Who might be susceptible to neutropenia?

A

Someone undergoing chemotherapy

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85
Q

What can a genetic inability to produce toxic chemicals within phagocytes cause?

A

Immunodeficiency - chronic granulomatous disease

Chadiak higashi syndrome

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86
Q

Describe the 7 stages of phagocytosis

A

Chemotaxis and adherence of microbe to phagocyte
Ingestion
Formation of phagosome
Fusion of phagosome with lysosome to form phagolysosome
Digestion by enzymes
Formation of residual body containing indigestible material
Discharge of waste material

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87
Q

What is an oxidative burst?

A

Rapid release of reactive oxygen species from phagocytes

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88
Q

What are natural killer cells?

A

Innate immune response

Lymphocytes that perform direct and antibody dependent cell toxicity

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89
Q

Which cells do not express MHC class 1?

A

Malignant or infected cells

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90
Q

What do natural killer cells detect, which activates them?

A

Lack of MHC class 1 at the cell surface

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91
Q

How do natural killer cells exert their cytotoxic effects?

A

Pore-forming molecules are inserted into target cell and cytotoxic chemicals are pumped in

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92
Q

In which diseases can NK cells be deficient?

A

Genetic diseases affecting T lymphocytes

X linked lymphoproliferative syndrome

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93
Q

What are acute phase proteins?

A

Innate humoral factors
Immediate and non specific cytotoxicity
C reactive protein, pro calcitonin, alkaline phosphatase, ferritin

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94
Q

What does CRP do?

A

Binds to surface molecules of bacteria and fungi
Inhibitory effects
Promotes complement binding

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95
Q

What are complement proteins and where are they made?

A

20 of them
B globulins
Produced by liver
Work in cascade

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96
Q

What 3 pathways can activate complement system?

A

Alternative - microbe activated
Classical - antibody activated
Lectin - mannose binding lectin activated

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97
Q

What does MHC stand for?

A

Major histocompatibility complex

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98
Q

Which cells express MHC class II?

A

Antigen presenting cells

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99
Q

Which cells will MHC class I be presented to?

A

Cytotoxic t lymphocytes

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100
Q

Which cells will MHC class II be presented to?

A

Helper T lymphocytes

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101
Q

What is important in organ transplantation?

A

MHC/HLA matching

102
Q

What are the 2 antigen presenting cells?

A

Macrophages

B lymphocytes

103
Q

What do T helper cells do?

A

Release cytokines to recruit more macrophages or antibody binding

104
Q

What do cytotoxic T cells that have detected an antigen do?

A

Replicate and differentiate

105
Q

Which cells are targeted by HIV?

A

CD4 - helper T cells

106
Q

What ensures a specific response and memory of the immune system?

A

Clonal selection and expansion

107
Q

What forms adaptive humoral immunity?

A

Antibodies

108
Q

Which cells produce antibodies?

A

Plasma cells - differentiated B lymphocytes

109
Q

What are 3 stimulating factors of the immune system?

A

Presence of antigen, helper T cells, cytokines

110
Q

What are 3 inhibiting factors of the immune system?

A

Removal of antigen, suppressor T cells, cytokine breakdown

111
Q

What improvements exist in the antibody response produced on second exposure to an antigen?

A

Less lag time
Larger peak response
Increase in IgG
Higher average affinity

112
Q

Where does the development of central T Cell tolerance occur?

A

Thymus

113
Q

Which cells produce interleukins?

A

MPS - macrophages and monocytes

Helper T cells

114
Q

What do interleukins cause?

A

Proliferation
Differentiation
Activation
Chemotaxis

115
Q

Which cells produce TNF?

A

MPS cells - macrophages and monocytes

116
Q

What effects can TNF have?

A

Fever, inflammation, enhanced immunity, septic shock, anorexia, cachexia (muscle wasting)

117
Q

Anti-TNF drugs are useful in treating autoimmune diseases, but what are their risks?

A

Cancer

Re activation of latent infections eg TB

118
Q

Which cells produce interferons?

A

Virus infected cells

T helper cells

119
Q

Which cells are activated by interferons?

A

NK cells and cytotoxic T cells

Macrophages and antigen presentation is upregulated

120
Q

Interferon preparations can be used as medicines, what are their side effects?

A

Flu like symptoms

121
Q

What does SIRS stand for?

A

Systemic inflammatory response syndrome

122
Q

What is an infection?

A

Invasion and multiplication of pathogenic microbes

123
Q

How is SIRS diagnosed?

A

> 1 of :
temperature 38°C
heart rate >90/min
respiratory rate >20/min or pCO2 12x10^9/dl or >10% immature WBCs

124
Q

Why will elderly people likely develop a different response pattern with SIRS/sepsis?

A

Elderly people dont have muscle mass to develop fever and so will drop their temperature when they’re septic

125
Q

What is sepsis?

A

Systemic inflammatory response to infection

SIRS + infection

126
Q

What is severe sepsis?

A

Sepsis + organ dysfunction

Includes septic shock

127
Q

What is septic shock?

A

Sepsis + hypotension (SBP <90mmHg) despite fluid

resuscitation + perfusion abnormalities eg. lactic acidosis, decreased urine output, decreased Glasgow coma scale score

128
Q

What can cause SIRS?

A

Pancreatitis
Burns
Trauma

129
Q

What is the main cause of sepsis?

A

Bacterial infection

130
Q

Give 6 infections which can potentially cause severe sepsis

A 
Meningitis
Pneumonia
Infective endocarditis
Bacterial gastroenteritis 
Pyelonephritis
Cellulitis
Osteomyelitis
Malaria
131
Q

What is the sepsis 6?

A

Within 1 hour of suspecting severe sepsis:

  1. Give high flow oxygen
  2. Take blood cultures
  3. Give empirical IV antibiotics
  4. Measure FBC and serum lactate
  5. Start IV fluid resuscitation
  6. Start urine output measurements
132
Q

What does plasma consist of?

A

Water
Organic compounds and electrolytes
Plasma proteins - albumin, globulins, fibrinogen

133
Q

What is haematopoiesis?

A

Production of mature blood cells - White, red, platelets

134
Q

Where does haematopoiesis occur?

A

Yolk sac
Liver and spleen
Red marrow

135
Q

What are the precursor cells of platelets?

A

Megakaryocytes

136
Q

Describe the cell lineage of T and B cells maturation

A

Pluripotent stem cells –> lymphoid multipotent progenitor cells –> t and b stem cells

137
Q

Describe the cell lineage of GEMM (granulocyte, erythrocyte, monocyte, megakaryocyte) cell maturation

A 
Pluripotent stem cells --> multipotent progenitor cells -->
Erythrocyte committed cells
Basophil committed cells
Megakaryocyte committed cells
Eosinophil committed cells 
Granulocyte/monocyte committed cells
138
Q

What is the process of production of non lymph blood cells called?

A

Myelopoiesis

139
Q

Which growth factors influence haematopoiesis?

A

Paracrine - G- CSF (colony stimulating factor)

Endocrine - EPO from kidney

140
Q

What three aspects of haematopoiesis are controllable?

A

Proliferation
Differentiation
Maturation

141
Q

What growth factor could be given to combat neutropenia?

A

Colony stimulating factor to stimulate cell division in bone marrow

142
Q

Why is the lifespan of erythrocytes important in monitoring diabetes?

A

Erythrocytes - 4 months

Glycosylated haemoglobin - HbA1c test shows glucose control over the lifespan of these cells. Prolonged time period

143
Q

Which blood cells have the shortest life span?

A

Basophils

144
Q

What is the process of erythropoiesis under control by at all stages?

A

Erythropoietin EPO

145
Q

What affect does EPO have on erythropoiesis?

A

Increases rate of mitosis

Decreases maturation time

146
Q

What 4 things does erythropoiesis require?

A

EPO
Iron
Folic acid
Vitamin B12

147
Q

How long do RBC precursors spend developing in the bone marrow?

A

7 days

148
Q

At what point during erythrocyte maturation do the cells stop undergoing mitosis?

A

Once they become late erythroblasts (orthochromatic)

149
Q

At which point during erythrocyte maturation is iron required?

A

Early on as it is required for Hb production

150
Q

What does maturation of erythrocytes involve?

A 
Decrease in cell size
Hb production
Loss of organelles
Acquisition of eosinophilic cytoplasm 
Extrusion of nucleus 
Acquisition of bi concave disc shape (cytoskeleton)
151
Q

What advantages does the biconcave shape of erythrocytes provide?

A

Large surface area
Minimise diffusion distance
Increase flexibility
Minimise tension with cell swelling

152
Q

What name is given to increased levels of erythropoiesis?

A

Polycythaemia

153
Q

What term describes an anaemia where the erythrocytes are pale?

A

Hypochromic anaemia

154
Q

What proteins form the RBC cytoskeleton?

A

Ankyrin, spectrin alpha and beta, actin

155
Q

What happens to RBC in which the cytoskeleton doesn’t form properly and the cells become spherocytes?

A

Splenic macrophages haemolyse them

156
Q

Give an example of a disease caused by miscoding of Hb

A

Sickle cell anaemia

157
Q

How is iron transported in the blood?

A

Bound to transferrin

158
Q

How does iron get from food to marrow?

A

Taken up from gut by heme transporter if heme iron
Taken up from gut by DMT1 if Fe2+
Can be stored as ferritin or transported into blood by ferroportin1
Travels in blood to the red marrow

159
Q

What is the normal range of iron levels?

A

35-90 mmol

160
Q

What are 3 causes of iron deficiency?

A

Increased demand
Inadequate absorption - Crohns, coeliac
Blood loss - external (internal bleeding, iron can be recycled)

161
Q

Describe how iron deficiency anaemia can develop

A 
Net loss of iron, exhaustion of store
Decreased serum iron
Compensatory increase in iron binding capacity 
Reduced transferrin saturation 
Reduced delivery to bone marrow
162
Q

What type of anaemia will vitamin B12 deficiency result in?

A

Macrocytic, normochromic anaemia

163
Q

What is required for vitamin B12 absorption?

A

Intrinsic factor

164
Q

Where is folic acid absorbed?

A

Duodenum and jejunum

165
Q

What is the main cause of vitamin B12 deficiency?

A

Malabsorption

166
Q

What can cause folic acid deficiency?

A

Reduced intake
Malabsorption
Drugs - alcohol, anticonvulsants
Increased demand - high cell turnover eg cancer

167
Q

What can cause marrow aplasia?

A

Environmental insult can cause stem cells to express new antigens or have reduced proliferative and differentiative capability
Chemotherapy
Autoimmune disorders

168
Q

What is aplastic anaemia?

A

Loss of trilineage haematopoiesis - pancytopaenia

Loss of ability of stem cells to generate mature blood cells

169
Q

What can cause leukopenia?

A

Suppression of haematopoietic stem cells
Suppression of committed granulocytic precursors
Ineffective haematopoiesis
Increased peripheral utilisation

170
Q

What can cause leukocytosis?

A

Increased production in marrow
Increased release from marrow stores
Decreased margination
Decreased extravasation into tissues

171
Q

What can cause increased production of leukocytes from the marrow?

A

Chronic infection or inflammation
Paraneoplastic - Hodgkin lymphoma
Myeloproliferative disorders - eg chronic myeloid leukemia

172
Q

What can cause Neutrophilic leukocytosis?

A

Acute bacterial infections

Sterile inflammation eg tissue necrosis from myocardial infarction, burns

173
Q

What can cause eosinophilic leukocytosis (eosinophilia)?

A

Allergic disorders - asthma, hay fever
Skin diseases - pemphigus, dermatitis herpetiformis
Parasitic infestations
Drug reactions
Malignancies - Hodgkin and some non-Hodgkin lymphomas
Collagen vascular disorders
Atheroembolic disease

174
Q

What can cause basophilic leukocytosis (basophilia)?

A

Rare, indicative of a myeloproliferative disease - chronic myeloid leukemia

175
Q

What can cause monocytosis?

A

Chronic infections - tuberculosis, bacterial endocarditis, rickettsiosis, and malaria
Collagen vascular diseases -systemic lupus erythematosus Inflammatory bowel diseases - ulcerative colitis

176
Q

What can cause lymphocytosis?

A

Accompanies monocytosis in many disorders associated with chronic immunological stimulation - tuberculosis, brucellosis
Viral infections - hepatitis A, cytomegalovirus, Epstein-Barr virus
Bordetella pertussis infection

177
Q

Which immune cells are likely involved in allergy, parasitic infections, infections by multicellular organisms?

A

Basophils and eosinophils

178
Q

How do dendritic cells work?

A

Engulf microbe then travel to lymph nodes where they present to cytotoxic T cells

179
Q

What is hypersensitivity?

A

Inappropriate and excessive immunological reaction to an antigen
Can be allergy and or anaphylaxis

180
Q

What is an allergen?

A

Antigen that induces a hypersensitivity reaction

181
Q

What is a type 1 hypersensitivity reaction?

A 
IgE and mast cell mediated 
Allergy
Asthma
Anaphylaxis 
Atopy
182
Q

What is a type 2 hypersensitivity reaction?

A 
Antibody dependent - IgM, IgG
Autoimmune haemolytic anaemia
Goodpastures syndrome
Myasthenia gravis
Graves' disease
183
Q

What is a type 3 hypersensitivity reaction?

A

Immune complex mediated
Serum sickness
Rheumatoid arthritis
Systemic lupus

184
Q

What is a type 4 hypersensitivity reaction?

A 
Delayed or cell mediated - t lymphocytes
Allergic contact dermatitis
Chronic transplant rejection
Multiple sclerosis
Tuberculin skin test
185
Q

What is atopy?

A

Pre disposition to allergy

Often familial or genetic

186
Q

Describe the process of a type 1 hypersensitivity reaction?

A

On first exposure to allergen, T helper cells are activated and via IL4, stimulate B cells to undergo class to produce IgE antibodies
IgE binds to mast cells to sensitise them
Second exposure to antibody, cross linking of IgE, activation of mast cell to release mediators - de granulation
Vaso active amines and lipid mediators cause immediate reaction - vasodilation, smooth muscle contraction, tissue damage
Late reaction caused by cytokines - inflammation, lymphocyte recruitment

187
Q

What symptoms may be seen in airway and eye mucous membrane from a type 1 hypersensitivity reaction?

A

Pruritus, sneezing, rhinorrhoea, lacrimation

188
Q

What reaction may be seen in the skin from type 1 and 4 hypersensitivity reactions?

A

Pruritus and urticaria - histamine reaction

189
Q

What reaction may be seen in oral and intestinal mucous membranes due to a type 1 hypersensitivity reaction?

A

Pruritus and angioedema

190
Q

What symptoms might be seen in anaphylaxis?

A 
Local swelling
Flushed
Faint
Dyspnoea
Peri oral paraesthesia 
Throat and chest tightness
Wheeze
Pale 
Sweaty 
Hypotensive collapse
Unconscious 
Death
191
Q

What blood measures can be taken to prove a type 1 hypersensitivity response?

A

Eosinophil count
Tryptase
IgE

192
Q

What is skin patch testing used for?

A

Allows identification of exact allergen causing a reaction

193
Q

What would a positive skin patch test show?

A

A lesion >3mm larger than the negative control

194
Q

How does de sensitisation therapy against allergens work?

A

Creates tolerance to allergen by exposure to gradually increasing doses delivered sublingually or sub cut
Small risk of anaphylaxis
Requires weekly/monthly treatment for 3 years

195
Q

What is the treatment strategy for anaphylaxis?

A 
ABC
Lie patient down
High flow oxygen
IV fluids
Adrenaline 500mcg IM (1:1000, 0.5ml of 1mg/mL)
IV chloamphenamine 
IV hydrocortisone
Nebulised salbutamol
Repeat Adrenaline after 5 mins if no improvement
196
Q

What layers make up a blood vessel wall?

A

Intima - endothelium, basement membrane, connective tissue, internal elastic lamina
Media - circumferentially arranged smooth muscle
Adventitia - connective tissue contains neurovascular supply

197
Q

What factors determine fluid transit across the capillary walls?

A

Plasma hydrostatic and oncotic pressure

Interstitial hydrostatic and oncotic pressure

198
Q

What 5 things can cause oedema?

A 
Increased hydrostatic pressure
Reduced plasma oncotic pressure
Lymphatic obstruction
Sodium retention 
Inflammation
199
Q

What disorders can result in oedema?

A 
Heart failure
Renal failure
Malnutrition
Decreased liver function
Nephrotic syndrome
200
Q

How does heart failure result in an increase in blood volume?

A

Decreased renal blood flow
Activation of RAAS
Na and water retention
Increased blood volume

201
Q

What factors affect the clinical consequence of oedema?

A

Volume
Site
Underlying cause
Risk of infection in involved tissues

202
Q

What causes nutmeg liver to be seen histologically?

A

Right sided heart failure

Central veins of liver have increased hydrostatic pressure, leads to cell death

203
Q

What is haemorrhage?

A

Extravasation of blood into extravascular space

204
Q

What are the 5 patterns of haemorrhage?

A 
Haematoma
Petechiae
Purpura 
Ecchymoses
Haemorrhage into body cavity
205
Q

What factors affect the significance of haemorrhage?

A

Volume of blood lost
Rate of blood lost
Medical fitness pre blood loss
Site of bleeding

206
Q

What is the pathological counterpart of haemostasis?

A

Thrombosis

207
Q

What are the 3 key components of haemostasis and thrombosis?

A

Vascular wall
Platelets
Coagulation cascade

208
Q

What is the sequence of normal haemostasis?

A

Endothelin release from damaged vessel causes vasoconstriction
Presence of collagen causes platelet adhesion as von willebrand factor binds to collagen
Platelets change shape and release granules including thromboxane A2 which recruits more platelets which aggregate to form platelet plug and ADP which activates a complex on platelets and allows them to bind fibrinogen
Tissue factor released from endothelium causes phospholipid expression on platelets which in turn leads to thrombin activation and fibrin polymerisation
Thrombomodulin and I-PA are released which start the anti-thrombotic events

209
Q

What factors normally contribute to making the endothelium anti - thrombotic?

A

Anti platelet - thrombin binding to receptor causes prostaglandin, NO and adenosine diphosphatase release from endothelium to inhibit platelet aggregation
Anti coagulant - thrombin binding to thrombomodulin causes activation of protein C which causes proteolysis of factor Va and VIIIa. Tissue factor pathway inhibition inactivates factor VIIa complexes. Anti thrombin III binds to heparin like molecule, this complex inactivates thrombin and factors Xa and IXa
Fibrinolysis - tPA from endothelium initiates fibrinolytic cascade

210
Q

What are the 2 key functions of platelets?

A

Form haemostatic plug

Provide surface for recruitment and concentration of coagulation factors

211
Q

How does aspirin prevent platelet aggregation?

A

COX inhibitor - inhibits synthesis of thromboxane A2 which normally stimulates recruitment of further platelets

212
Q

How does clopidogrel inhibit platelet aggregation?

A

Irreversibly inhibits P2Y12 receptor which is an ADP chemoreceptor on platelets
This means that new platelets cannot detect the aggregation signal (ADP) released from granules of the primary platelets

213
Q

How does Abciximab inhibit platelet aggregation?

A

Blocks GP IIb/IIIa receptor which prevents fibrinogen complexing and therefore no further platelets can aggregate

214
Q

What is the goal and end point of the coagulation cascade?

A

Produce thrombin and produce secondary haemostatic plug

215
Q

What extra factors do some steps of coagulation cascade require?

A

Ionised calcium

Phospholipid surfaces

216
Q

Describe some of the key steps of the coagulation cascade

A

Tissue factor released from damaged endothelium activates factor VII which in turn activates factor VIX. This activates factor Xa which activates thrombin from prothrombin
Thrombin activates fibrinogen to fibrin clot

217
Q

What factors does warfarin prevent activation of?

A

Prothrombin and factor VII by inhibition of vitamin K epoxide reductase

218
Q

How does heparin work?

A

Activates anti thrombin III which inactivates thrombin and clotting factors

219
Q

What is dabigatran?

A

Reversible inhibitor of thrombin

Effects measured by thrombin clotting time

220
Q

Why is heparin faster acting than warfarin?

A

Inactivates factors that are already present

Warfarin prevents formation of new factors but not the ones that are already there so they have to be used up first

221
Q

What are D Dimers?

A

Fibrin degradation products

Blood test to look at clot break down

222
Q

What is plasminogen?

A

Precursor to plasmin which degrades fibrin

223
Q

What is streptokinase?

A

Clot busting drug
Binds to plasminogen to make it functionally act like plasmin
Short half life
Degrades both fibrin and fibrinogen
Antigenic and can cause severe allergic reactions

224
Q

What are alteplase, reteplase and urokinase?

A

Recombinant tissue plasminogen activators

225
Q

Give an example of a bleeding disorder due to disorder of vessels

A

Hereditary haemorrhagic telangiectasia - leaky blood vessels

226
Q

Give an example of a bleeding disorder due to platelet disorder

A

Von willebrands disease

227
Q

Give an example of bleeding disorders caused by coagulation disorder

A

Haemophilia A (factor VIII) and B (factor IX, Christmas)

228
Q

What is Virchows triad?

A

Describes 3 main factors that predispose to thrombosis

Hypercoagulable state, circulatory stasis, endothelial injury

229
Q

What is heparin induced thrombocytopenia?

A

Development of low platelet count due to administration of heparin
Predispose to thrombus formation

230
Q

What is antiphospholipid syndrome?

A

Autoimmune disorder characterised by arterial and venous thrombosis
Hypercoagulability

231
Q

What is the fate of thrombi?

A

Propagation - move towards heart if in venous system
Embolisation - break off and move to distal site
Dissolution - fibrinolysis breaks down clot
Organisation - damaged tissue, scar, new blood vessels can form through clot

232
Q

What can be the clinical consequences of a thrombus?

A

Cause obstruction to blood flow - oedema and congestion

Embolism and cause infarction in distal tissue

233
Q

What can be the clinical effects of an arterial thrombus?

A

Usually due to rupture of atheroma
Ischaemic necrosis (infarct) in tissue
Source of emboli
Can cause MI and stroke

234
Q

What are clinical consequences of a venous thrombosis?

A

Local effects of DVT

50% silent, swelling, pain, tenderness, discolouration, increased temperature

235
Q

What is disseminated intravascular coagulation?

A

Sudden or insidious onset of widespread fibrin thrombi in the microcirculation which can cause multi organ failure and consumptive coagulopathy and bleeding (clotting and bleeding at same time)
Risk of occurrence whenever there is widespread thrombin activation

236
Q

What can be the outcomes from a pulmonary thromboembolism?

A

Occlusion of medium or small pulmonary artery with or without infarct of lung
Massive embolism : saddle emboli which occludes main pulmonary arteries - sudden death
Multiple emboli may lead to pulmonary hypertension

237
Q

What are signs and symptoms of a PE?

A 
Chest pain
SOB
Collapse
Cough
Haemoptysis 
Tachycardia
Hypotension
Tachypnoea 
Elevated JVP
238
Q

What clinical consequences can an arterial thrombus cause?

A

Left side of heart eg ventricular thrombus in MI, atrial fibrillation, infected heart valve
Large artery, usually atheromatous - aneurysm of aorta
Effects include infarcts of organs e.g stroke, gangrene of limb

239
Q

What treatments are given for arterial thrombus?

A

Prophylaxis - aspirin, clopidogrel

Treatment - streptokinase, tPA

240
Q

When is the 1 occasion when a venous thrombus could enter the arterial circulation?

A

Via patent foramen ovale or septal defect

241
Q

Other than a thrombus, what things can cause emboli?

A 
Atheroma
Air
Amniotic fluid
Nitrogen 
Tumour cells
Fat
Foreign material
242
Q

What are the stages of athersclerotic plaque formation?

A

Fatty streak formation: Endothelial damage, Uptake of modified LDLs, Adhesion/infiltration of macrophages, foam cells when ingest LDL
Smooth muscle proliferation in intima, collagen deposition
Fibrous cap formation

243
Q

What modifiable factors can increase risk of formation of an atherosclerotic plaque?

A

Shear stress at artery branch points, increased in hypertension
Toxic damage by chemical exposure, eg cigarette smoke (oxidise LDL)
High lipid levels in FH, DM and high fat diets (glycate LDL)
Viral or bacterial infection

244
Q

What is claudication?

A

Reduced blood flow to the limb which causes cramp

245
Q

How can an atherosclerotic plaque lead to thrombus formation?

A

Collagen cap of plaque is fragile
Calcification of cap increases fragility further
Rupture of cap exposes blood to collagen which triggers thrombus formation

246
Q

What are some non modifiable risk factors for atherosclerotic plaque formation?

A

Age
Male, women after menopause
Family history of CHD or FH

247
Q

How do catecholamines cause vasoconstriction?

A

Bind to alpha receptors which are GPCRs bound to Gq
This activates phospholipase C which generates IP3 and DAG
This causes Ca release from stores which leads to opening of Ca activated Cl channels
Depolarisation causes voltage gated Ca channels to open
Ca binds to calmodulin which activates myosin light chain kinase
This phosphorylates myosin heads which form cross bridges and contraction occurs

248
Q

Which Ca channel blockers are cardio selective, vascular selective and intermediate?

A

Verapamil is cardio selective
Nifedipine is vascular selective
Diltiazem is intermediate

249
Q

How do catecholamines cause vasodilation?

A

Act on B receptors to activate Gs which causes increase in cAMP
This activates protein kinase A which activates Ca ATPase to pump Ca into sarcoplasmic reticulum, PKA phosphorylates K channels so causes hyperpolarisation, PKA phosphorylates myosin light chain kinase to inactivate it

250
Q

How does NO cause vasodilation? And where is it made?

A

Synthesised by endothelial cells by nitric oxide synthase, stimulated by increased Ca in endothelial cell (shear stress can cause this)
NO diffuses across membrane into tunica media to activate guanylate cyclase
This increases levels of cGMP which activates protein kinase G which stimulates Ca ATPase and K channels, and inactivates MLCK

251
Q

What is a Myogenic response?

A

An increase in arterial blood pressure will be compensated for locally by vasoconstriction of vascular beds to increase resistance and reduce blood flow in order to maintain a relatively constant perfusion to organs
Mechanosensitive ion channels detect stretch and depolarise so increasing Ca influx

252
Q

What is haemoglobin?

A

Binds oxygen at 4 sites to transport it around body
Tetrameric protein
2 alpha and 2 beta subunits
Each subunit has haem and globin groups

Block 2 AR (9 decks)

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