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FRCEM Primary > Pathology > Flashcards

Pathology Flashcards

1
Q

Inflammatory Response - normal phases (6)

A 
Vascular
Exudative
Resolution
Supparation
Organisation
Chronic inflammation
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2
Q

What is the vascular phase of inflammation and how long does it last

A

Lasts 15 mins to several hours. Up to 10 fold increase in blood flow increases the hydrostatic pressure and causes a transudate (low protein). Plasma protein leaks into the tissues due to the decreased intravascular oncotic pressure.

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3
Q

What causes the increased vascular permeability of the vascular phase of inflammation?

A

Contraction of endothelial cells

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4
Q

What are the three phases of the exudative phase?

A

Margination
Adhesion
Emigration

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5
Q

Inflammation, exudative phase, what is margination

A

The loss of intravascular fluid due to a breach from injury causes increased plasma viscosity, so flow slows at the injury site allowing neutrophils to flow closer to the epithelium

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6
Q

Inflammation, exudative phase, what is adhesion and what impairs it

A

Neutrophils adhere to the endothelial surface by increased expression of leukocyte adhesion molecule and increased expression of epithelial surface adhesion molecule

Impaired by diabetes, corticosteriod use, acute alcohol intoxication, inherited adhesion deficiencies

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7
Q

Inflammation, exudative phase, what is emigration

A

Migration of neutrophils through the basement membrane by active amoeboid movement

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8
Q

Inflammation, what is resolution

A

Back to normal state with regeneration of damaged tissue

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9
Q

Inflammation, what is supparation

A

A persistent causative agent that leads to pus formation and becomes walled off by a pyogenic membrane that is inaccessible to the body’s defences.

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10
Q

Inflammation, what is fibrosis

A

Where a large area of tissue is destroyed or unable to regenerate. The scar tissue is mainly collagen, inflexible and may impair function

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11
Q

Inflammation, what is chronic inflammation

A

A persistent causative agent that lasts months to years. There is tissue destruction and cellular exudate changes. It is mainly dominated by macrophage, lymphocyte and plasma cells, and their toxins damage host tissue

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12
Q

In the later stage of inflammation, what is chemotaxis

A

Neutrophils are attracted towards complement, IL8, leukotriene B4 and bacterial products

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13
Q

What is opsonisation

A

This prepares a particle for phagocytosis by coating it in Ig or complement, thus marking it for destruction

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14
Q

How do bacteria activate the complement pathway?

A

Bacterial polysaccharides activate the alternative complement pathway and generate C3b.
Antibodies bind bacterial antigens and activate the classical complement pathway and generate C3b

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15
Q

What happens at the phagocytosis phase

A

Neutrophils send out pseudopodia around the opsonised particles which fuse, containing the particle in a phagosome bound by a cell membrane. Lysosomes bind with the phagosome forming a phagolysosome to begin intracellular killing

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16
Q

Explain oxygen dependent intracellular killing

A

Neutrophils produce hydrogen peroxidase which reacts with myeloperoxidase to produce microbicidal agents. Oxygen is reduced by NADPH oxidase to produce free radicals.

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17
Q

What does oxygen independent intracellular killing use?

A

Lysozymes, lactoferrin, acid hydrolase and defensins

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18
Q

What happens in chronic granulomatous disease?

A

NADPH is deficient causing recurrent bacterial infections

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19
Q

What happens in myeloperoxidase deficiency

A

Frequent candidal infections

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20
Q

Chemical mediators - histamine

A

From mast cells, basophils and platelets. Stimulated by C3a, C5a, IgE, lysosomal proteins and physical injury

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21
Q

Chemical mediators - serotonin

A

from platelets - causes vasodilation, increases vascular permeability and promotes chemotaxis

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22
Q

Chemical mediators - lysosomal compounds

A

from neutrophils - causes vasodilation, increases vascular permeability and promotes chemotaxis

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23
Q

Chemical mediators - Prostaglandins

A

From arachadonic acid
Thromboxane A2 - from platelets, causes vasoconstriction and platelet aggregation
Prostacyclin - from endothelium, inhibits platelet aggregation
Prostaglandin - causes pain

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24
Q

Chemical mediators - Cytokines

A

From arachadonic acid
IL1 +TNF - causes fever, increases adhesion molecules and activates neutrophils
IL8 - chemotactic

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25
Q

Complement C5a

A

Chemotactic

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26
Q

Complement C3b, C4b, C2a

A

Oponin

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27
Q

Complement C3a, C5a

A

Stimulates histamine release

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28
Q

Complement C5b-C9

A

Membrane attack complex

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29
Q

The Kinin cascade

A

Activated by factor XII and leads to formation of bradykinin which causes vasodilation, increased vascular permeability, bronchoconstriction and pain

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30
Q

Beneficial local effects of inflammation (6)

A

Permits entry of antibodies leading to the breakdown of microorganisms, increased delivery of nutrients and oxygen, dilution of toxins and stimulation of the immune system

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31
Q

Harmful local effects of inflammation (2)

A

Damage to normal tissue

Swelling (epiglottitis, compartment syndrome)

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32
Q

Systemic effects of inflammation (5)

A

Malaise, anorexia, nausea, pyrexia, raised ESR

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33
Q

Causes of leukocytosis - neutrophilia

A

Pyogenic infection

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34
Q

Causes of leukocytosis - eosinophilia

A

Allergy and parasites

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35
Q

Causes of leukocytosis - lymphocytosis

A

Chronic infection and viral

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36
Q

Causes of leukocytosis - monocytosis

A

mononucleosis, some bacterial (TB, Typhoid)

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37
Q

Causes of abnormal inflammation (9)

A

Genetic malformation, cancer, atherosclerosis, allergy, asthma, autoimmune, chronic inflammation, vasculitis, transplant rejection

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38
Q

What is CRP

A

An acute phase reactant hat rises dramatically with inflammation in response to increased Il6 released by macrophages. Rises more in bacterial infections than viral. It is synthesised and secreted by the liver. It binds phosphocholine opsonizing damaged or foreign cells for phagocytosis

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39
Q

What is Rheumatoid Factor

A

An autoantibody against the Fc portion of IgG. High levels indicate rheumatoid arthritis and Sjogren’s syndrome. The sigher the level the higher the risk of a more destructive arthropathy.

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40
Q

What is ANF

A

Antinuclear factor or antinuclear antibodies are autoantibodies against the cell nucleus, present in various disorders

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41
Q

Specific subtype of ANF found in SLE

A

All ANF

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42
Q

Specific subtype of ANF found in systemic sclerosis

A

All ANF, Scl-70

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43
Q

Specific subtype of ANF Limited scleroderma

A

All ANF, anti-centromere

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44
Q

Specific subtype of ANF Sjogren’s syndrome

A

All ANF, anti-RO, Anti-La

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45
Q

3 layers of the normal immune response

A

Physical, innate, adaptive

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46
Q

Physical immune barriers (5)

A 
Coughing and sneezing
Tears and urine to flush away
Skin and mucus
Commensal flora outcompete
Gastric acid neutralises most bacteria
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47
Q

What is the innate immune response

A

Non-specific. Initiated when microbes are identified from components common to large groups of microbes and when injured cells signal

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48
Q

What are the four main functions of the immune system?

A

Recruit immune cells to the site
Activate the complement cascade
Identify and remove foreign substances
Activate the adaptive response by antigen presentation

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49
Q

First innate immune response is

A

Inflammation

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50
Q

Second innate immune response is

A

Cellular response - white cells (neutrophils, eosinophils, basophils and natural killer cells) identify and eliminate pathogens

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51
Q

Third innate immune response

A

Complement cascade

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52
Q

When is the adaptive immune response initiated?

A

When the innate response presents enough antigen

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53
Q

What is the function of the adaptive immune response

A

Recognises non-self
Generate specifically tailored immune responses to the particular pathogen
Develop a memory to remember the pathogen and allow easier elimination of subsequent infections

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54
Q

What are the main cellular components of the adaptive immune response

A

T and B lymphocytes

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55
Q

Explain the adaptive immune response: Antigens are presented to…

A

Naïve T lymphocytes which activate to become either cytotoxic CD4 cells or helper CD4 cells.
Cytotoxic T lymphocytes undergo rapid clonal expansion and travel in search of the antigen. Cells with the antigen are punctured and lysed by cytotoxins.

56
Q

Activation of the T lymphocyte requires either

A

a strong signal or a prompt from a CD4 helper cell

57
Q

What happens after the infection resolves

A

Some T cells remain to form immune memory, ready to be quickly activated if the same pathogen returns.

58
Q

What do CD4 helper cells do?

A

Manage the immune response and activation leads to the release of assorted cytokines

59
Q

What do B cells do?

A

Create antibodies - Y shaped proteins that identify and neutralise foreign material

60
Q

What are the 5 types of antibodies

A

IgA, IgD, IgE, IgG, IgM

61
Q

How are B cells activated

A

Antigen and signals from CD4 cells

62
Q

What do activated B cells do next?

A

Multiply and mature into plasma cells, which last 2-3 days and produce antibodies which bind antigens, opsonise and activate the complement cascade. 10% of plasma cells survive to form antigen specific immune memory cells to fight off repeated further infection.

63
Q

What is a type 1 hypersensitivity reaction

A

Allergic - includes atopy, anaphylaxis and asthma. Provoked by re-exposure to a specific antigen. IgE mediated - released from mast cells and basophils

64
Q

What is type 2 hypersensitivity reaction

A

Cytotoxic, antibody dependent reaction where antibodies bind antigens on ‘self’ and mark for destruction.
IgG and IgM mediated of autoimmune thrombocytopenic purpura and haemolytic disease of the newborn

65
Q

What is type 3 hypersensitivity reaction

A

Immune complex disease - small antibody-antigen immune complexes are not cleared by macrophages and are deposited in tissues causing disease. IgG or IgM mediated eg SLE, polyarteritis nodosum

66
Q

What is type 4 hypersentivity reaction

A

Delayed hypersensitivity - eg Type 1 DM, MS.

T cells mediated. T cells targeting specific ‘self’ cells proliferate and destroy on contact.

67
Q

What is Autoimmunity

A

Overactive immune response with a failure to distinguish self and non-self leading to immune attack of body tissues eg Autoimmune hepatitis, Goodpastures, MS, RA

68
Q

What is immunodeficiency

A

One or more components of the immune system are deficient or malfunctioning. It may be inherited or acquired.

69
Q

5 stages of wound healing

A 
Haemostasis
Inflammation
Reconstruction
Epithelialisation
Maturation
70
Q

Haemostasis stage of wound healing

A

Local vascular contraction, platelet plug formation and activation of the clotting cascade

71
Q

Inflammation stage of wound healing

A

Removes bacteria, foreign material and devitalised tissue to prepare the wound for healing. Prolongation of this stage causes increased macrophage activity and poor wound healing.

72
Q

Reconstruction stage of wound healing

A

Fibroblasts synthesise collagen and elastin and contract to bring the wound edges together. Macrophages release growth factor to stimulate new blood vessel formation

73
Q

Epithelialisation stage of wound healing

A

In wounds that are closed epithelial coverage develops in 24-48 hours, impaired by surface debris, eschar or devitalised tissue

74
Q

Maturation stage of wound healing

A

The amount of scar tissue formed depends upon the forces that act across a wound. Strength is gained as collagen matures and further modelling and maturation occurs over 2years.

75
Q

Wound healing specific tissues - skin

A

may need delayed closure.

76
Q

Wound healing specific tissues - tendon

A

Reconstruction lasts 6 weeks and full strength is never regained, It heals with fibrous scar tissue, Controlled movement while undergoing reconstruction aids healing

77
Q

Wound healing specific tissues - Peripheral nerves - levels of injury (3)

A

Neuropraxia
Axonotmesis
Neurotmesis

78
Q

What is neuropraxia

A

Mildest form of injury - block or reduction of conduction across a segment with conduction preserved above and below

79
Q

What is Axonotmesis

A

Middle severity - neural tube intact but axons disrupted - likely to recover

80
Q

What is Neurotmesis

A

Most severe - neural tube severed. Likely permanent without repair.

81
Q

3 phases of bone repair

A

Reactive
Reparative
Remodelling

82
Q

Reactive stage of bone repair

A

Incorporates haemostatic and inflammatory stages of normal wound healing

83
Q

Reparative stage of bone repair

A

Incorporates reconstruction and epithelialisation. There is callous formation and lamellar bone deposition. Periosteal cells proximal to the fracture and fibroblasts in the granulation tissue develop into chondroblasts and form hyaline cartilage. Periosteal cells distal to the fracture develop into osteoblasts and form woven bone. These tissues grow and unite to forma fracture callus. Osteoblasts then replace the fracture callus with lamellar bone

84
Q

Remodelling phase of bone healing

A

Lamellar bone is replaced with compact bone and is at 80% strength by 3 months. Full healing can take 18 months.

85
Q

Wound healing specific tissues - Myocardial plus complications

A

Injury usually comes from infarction where coronary arteries are blocked causing cell death which is irreparable. Collagen scar formation can lead to arrhythmias or rupture

86
Q

Wound healing specific tissues - brain

A

No reparative or regenerative function but sometimes other areas of the brain can take over function to compensate.

87
Q

How is anaemia classified and what are the three types

A

By red blood cells size
Macrocytic - larger
Normocytic - normal
Microcytic - smaller

88
Q

Causes of macrocytic anaemia (5)

A

Meagaloblastic anaemia - low B12 with or without concurrent low folate (either from poor intake or poor absorption)
Pernicious anaemia - poor absorption of B12 due to autoantibodies against intrinsic factor or the parietal cells that produce it
Gastric bypass surgery
Hypothyroidism
Methotrexate

89
Q

Causes of microcytic anaemia

A

Issues with haem synthesis - iron deficiency
Issues with globin synthesis - thalassaemia
Lead poisoning

90
Q

Causes of normocytic anaemia

A

Acute blood loss
Anaemia of chronic disease - cytokine action or iron metabolism
Aplastic anaemia
Haemolytic anaemia

91
Q

Investigations for anaemia

A

FBC, ESR, Ferritin, Serum iron, Transferrin, Serum B12 and folate. Occasionally a bone marrow biopsy is needed.

92
Q

What is leukaemia

A

Malignant disease or blood or bone marrow causing an increase in WBC. It presents as bruising, bleeding, petechial haemorrhage, frequent infections, anaemia, fever, chills, night sweats, splenomegaly, weight loss.

93
Q

Classification of leukaemia

A

Acute or chronic and then by cell line affected - lymphoblastic (lymphocytes - usually B cells) or myeloid (marrow cells that form RBC, eosinophils, basophils, neutrophils and platelets)

94
Q

What are acute leukaemias

A

Feature a rapid rise in immature cells. Crowding makes the bone marrow unable to produce healthy cells. Requires quick treatment to prevent malignant cells spilling into the blood stream. Most common form of childhood leukaemia

95
Q

What are chronic leukaemias

A

Feature an excessive build up of mature abnormal WBC that takes years or months to progress. More common in the elderly, but can be affect any age.

96
Q

Acute lymphoblastic leukaemia

A

Most common in young children but can affect adults over 65. Survival 85% in children, 50% in adults

97
Q

Chronic lymphoblastic leukaemia

A

Most common in adults over 55, almost never occurs in children. Incurable but chemo can control symptoms

98
Q

Acute myeloid leukaemia

A

More common in adults than children and men more than women. Survival 40% at 5 years

99
Q

Chronic myeloid leukaemia

A

Mainly adults but some children. 90% survival at 5 years.

100
Q

What is lymphoma

A

Lymphocyte cancers that present as a solid mass of lymphoid cells and are classified by cell type

101
Q

Types of lymphoma

A

Mature B cells - Burkitt’s lymphoma, follicular, Hodgkin’s

Mature T cells and NK cells - Aggressive NK cell lymphoma, anaplastic large cell lymphoma

102
Q

Signs and symptoms of lymphoma

A

Presents with night sweats, weight loss, lymph node enlargement and hepatosplenomegaly

103
Q

Investigations for lymphoma

A

Investigate with FBC, U&E, LFT, LDH, CXR, Staging CT and biopsy

104
Q

What is myeloma

A

An incurable cancer of plasma cells - the B cells which make antibodies. Signs and symptoms vary, depending on the proteins released by the malignant plasma cells

105
Q

Signs and symptoms of myeloma (5)

A 
Bone pain /fractures
Infections
Anaemia
Renal failure
Neurological symptoms
106
Q

Explain bone pain in myeloma

A

Plasma cells produce RANKL which binds osteoclasts and induces bone resorption. Bone lesions are lytic and cause hypercalcaemic

107
Q

Explain increased infection rate in myeloma

A

Decreased production and increased destruction of normal antibodies

108
Q

Explain renal failure in myeloma

A

Damage caused by hypercalcaemia and the deposition of light chains produced by the malignant plasma cell

109
Q

Explain neurological symptoms in myeloma

A

Weakness, confusion and fatigue due to hypercalcaemia. Spinal cord syndromes from pathological fractures

110
Q

Investigations for myeloma

A

FBC, U&E, Ca, Seruma nd Urine electrophoresis for paraproteins like Bence-Jones. Skeletal survey, bone marrow biopsy, Ig levels and B2 - microglobulin

111
Q

Treatment for myeloma

A

High dose chemo to induce remission. Younger patients may get a bone marrow transplant

112
Q

Low platelet count disorder - What is throbocytopenia

A

Causes low platelet count, eg ITP - autoantibodies against platelets

113
Q

Low platelet count disorder - What is Aplastic anaemia

A

Bon marrow failure secondary to autoimmune, toxins or infection. Causes pancytopenia as the bone marrow fails to make new cells

114
Q

Low platelet count disorder - What is Gaucher’s disease

A

A lysosomal storage disease where lipids accumulate in cells and tissues including the bone marrow, resulting in pancytopenia.

115
Q

High platelet count disorder - What is thrombocytosis (primary and reactive)

A

Primary thrombocytosis isa myeloproliferative disorder causing increased risk of thrombosis and may progress to AML or myelofibrosis.
Reactive thrombocytosis can be due to inflammation, hyposplenia or asplenia

116
Q

Platelet dysfunction disorder - HELLP syndrome

A

A variant of pre-eclampsia

Haemolytic anaemia, Elevated Liver enzymes, Low Platelets.

117
Q

Platelet dysfunction disorder - Haemolytic Uraemic Syndrome

A

Toxins from enterohaemorrhagic E Coli cause haemolytic anaemia, acute renal failure and thrombocytopenia, mostly in children

118
Q

Platelet dysfunction disorder - Dengue

A

Viral haemorrhagic fever caused by flavivirus

119
Q

Platelet adhesion disorder - Von Willebrand disease (4 types)

A

Type 1 - heterozygous - decreased levels of vwf
Type 2 - qualitative defect
Type 3 - homozygous, most severe
Type 4 - platelet type - defect in the VWF receptor on the platelet

120
Q

Inherited coagulation disorders (2)

A

Von Willebrand Disease

Haemophilia - recessive X linked disorder affecting clotting factors

121
Q

Haemophilia A

A

Factor VIII deficiency, most common

122
Q

Haemophilia B

A

Factor IX Christmas disease

123
Q

Treatment of haemophilia

A

Infusions of the missing factor, but some people develop antibodies tot he replacement an therefore need larger amounts or nonhuman factor

124
Q

Causes of acquired coagulation disorders (4)

A

Toxins
Infections
Liver failure
DIC

125
Q

Toxins or drugs that cause acquired coagulation disorder

A

Rattlesnake and viper venom

Warfarin

126
Q

Actions of warfarin

A

Inhibits vitamin K dependent synthesis of clotting factors II, VII, IX, X, protein C, protein S and protein Z which regulate the clotting process

127
Q

Infections that cause acquired clotting disorder

A

Viral haemorrhagic fever - multifactorial aetiology - hepatic damage, consumptive coagulopathy, primary marrow dysfunction

128
Q

How does liver failure cause an acquired clotting disorder

A

decreased protein syntesis

129
Q

Acquired clotting disorders - DIC

A

A consumptive coagulopathy leading to depletion of platelets and clotting factors. Micro-emboli form in the vascular system, threatening end organ function.

130
Q

Causes of DIC

A 
Cancer (lung, pancreas, stomach)
Eclampsia
Amniotic fluid embolus
Massive trauma
Burns
Infection (Gram negative sepsis, strep pneumonia, malaria)
Snake/scorpion venom
131
Q

What is thrombophilia

A

An abnormality causing hypercoagulability - can be congenital or acquired

132
Q

Congenital causes of thrombophilia - Factor V Leiden

A

Factor V is a cofactor of Factor X that leads to activation of thrombin and is broken down by Protein C to limit clotting. Factor V Leiden is a form of factor V that cannot be broken down by Protein C.

133
Q

Congenital causes of thrombophilia - Protein C deficiency

A

Protein C is an anticoagulant that inhibits Factor V and Factor VIII

134
Q

Congenital causes of thrombophilia - Protein S deficiency

A

Protein S is a vitamin K dependent anticoagulant that acts as a cofactor to protein C

135
Q

Acquired causes of thrombophilia - antiphospholipid antibodies

A

Autoimmune issue. Has various forms that cause either up regulation of prothrombotic factors or inhibition of antithrombotic factors or a combination of the two.

136
Q

Signs and symptoms of thrombophilia

A

DVT, PE, clots in unusual places - venous sinus thrombosis, portal vein thrombosis, hepatic vein thrombosis, mesenteric vein thrombosis, renal vein thrombosis, recurrent miscarriage

FRCEM Primary (32 decks)

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