Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 3 > Pathological Mechanisms > Flashcards

Pathological Mechanisms Flashcards

1
Q

What are the divisions of the immune system?

A

Innate and adaptive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the innate immune system?

A

The non-specific defence mechanisms occurring immediately or within hours of the antigen appearing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does the innate immune system respond to?

A

Attacks are based on identification of general threats and cells respond through pre-existing mechanisms by recognising danger patterns with genetically determined receptors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is the adaptive immune system activated?

A

The innate immune system can activate the adaptive immune system if required. It’s activated by exposure to pathogens and creates a specific response to that pathogen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Which division of the immune system is faster?

A

The innate immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which division of the immune system up-regulates more cells?

A

Innate immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the divisions of the innate immune system?

A

soluble factors and cellular factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the soluble factors of the innate immune system with location and function?

A

Antibacterial factors - Lysozyme: found at mucosal surfaces and breaks down Gram +ve cell wall - Lactoferrin: mucosal surfaces, chelates iron in GI-respiratory tract to inhibit bacterial growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the cellular factors of the innate immune system?

A

Phagocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is complement and what substances are involved?

A

Complement: A general immune response marking pathogens for destruction and punctures the cell membrane of the pathogen. Consists of inactivate proteins that circulate the blood and initiate the complement cascade when activated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How are proteins activated in complement?

A

Classical pathway - antigen:Ab complexes MB-lectin pathway - Lectin binding to pathogen surfaces Alternative pathway - pathogen surfaces These all result in complement activation and require an antigen to signal a threat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is opsonisation?

A

Process in which pathogens are identified by their antigens and marked for phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What occurs due to complement activation?

A
  • Chemotaxis (Recruitment of inflammatory cells) - Opsonisation of pathogens - Phagocytosis (Killing of pathogens)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is chemotaxis?

A

Recruitment of inflammatory cells and the movement of macrophages and neutrophils via cytokines and chemokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the role of C3 in complement?

A

As complement is activated, Complement 3 (C3) binds to the pathogen surface causing inflammation and formation of complement proteins which leads to opsonisation and phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the cells in the innate immune system?

A

Macrophages, neutrophils, eosinophils, basophils/mast cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What’s the precursor to macrophages?

A

Monocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Where are macrophages found?

A

In the tissue Kupffer cells: liver Microglia: CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the functions of macrophages?

A
  • Constantly sample surrounding area to identify pathogens through Pattern Recognition Receptors (on surface on intracellularly) - Antigen presentation: processes engulfed particles, travel to draining lymph nodes to present antigen to T Cells in MHC II (CD4) - Phagocytosis: direct clearance of pathogens/harmless debris - Cytokine production: e.g. TNF-a to signal other cells e.g. neutrophils to area
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What would render the innate immune system not enough to fight infection?

A
  • Highly pathogenic bacteria (adapted to overcome body systems) - Structure failure (something causing it to not work properly e.g. gallstone) Usually a bit of both
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What cells have the most rapid response to infection?

A

Neutrophils (can see rapid spike of neutrophils in blood at beginning of an infection)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What cells make up a majority of WBCs?

A

Neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the functions of neutrophils?

A
  • Degranulation: split to release products - Chemotaxis: migrate toward bacteria, chemokines and danger signals (e.g. complement proteins) - Phagocytosis: ingest and destroy pathogens using proteases, ROS, lysosymes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Describe the lifespan of neutrophils

A

Neutrophils are produced and die quickly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What happens when neutrophils die?

A

See characteristic pus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the functions of eosinphils?

A
  • Chemotaxis - Degranulation: release toxic substances onto the surface of parasites - Cytokine production: produced in large amounts and this drives inflammation (IL-1, -2, -4, -8 and TNF-a)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What cells drive inflammation?

A

Eosinophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the pathological role of eosinophils?

A

Allergy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Where are basophils/mast cells found?

A

Basophils: blood Mast cells: mucosal membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the functions of basophils/mast cells?

A
  • Degranulation: release of pre-formed granules containing cytokines and mediators e.g. Histamine (Wheel and Flare) - Cytokine release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the role of Histamine?

A

Dilates vessels to increase blood flow and cell migration to the area of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the precursor of dendritic cells?

A

Monocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Please draw the tree diagram for WBC

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Please draw the tree diagram for the precursors from stem cell to mature cell

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are dendritic cells?

A

They are antigen presenting cells

They sample the environment and undergo a conformational change in shape when activated by a foreign substancre from sampling to presenting mode.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the functions of dendritic cells?

A
  • Antigen presentation to CD4 T Cells and can initiate an adaptive immune response
  • Migration
  • Phagocytosis (not specialised for this but can do it)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Where do dendritic cells go when activated?

A

Draining lymph nodes to present antigen to CD4 T cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the roles of adaptive immunity?

A
  1. Provides specific antibodies to the innate immune system to enchance pathogen clearance
  2. Provides cytokines to the innate immune system to upregulate activity
  3. Finishes the job of clearing pathogens
  4. Develops memory to prevent futher infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the divisions of the adaptive immune system?

A

Humoral and cellular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the humoral division of the adaptive immune system?

A

Consists of B cells (aka plasma cells) which express antibodies (aka immunoglobulins) on their surface.

When B cells are activated from the naive form, they undergo clonal expansion and differentiation. Antibodies are then secreted in response to extracellular pathogens.

The end of the antibody that binds to receptors on phagocytes changes with antigen binding and activates complement (Classical pathway)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the role of antibodies (immunoglobulins)?

A
  • Opsonise for phagocytosis
  • Activate complement cascade for lysis
  • Neautralise toxins and pathogen binding sites
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

List the antibody isotypes and their main role.

A
  • IgM: main antibody of the primary immune response (i.e. when first in contact with antigen)
  • IgG: main antibody of secondary immune response (memory responses) and mother-to-baby immunity
  • IgA: neutralises action of pathogens by blocking the binding of pathogens. Present in secretions and lines epithelial surfaces
  • IgE: coats mast cells and has a role in allergy. Has a high affinity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the chacteristics of IgM and IgG?

A

IgM: low affinity (not very specific) and many binding sites

IgG: higher affinity and crosses the placenta (mother-to-child immunity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What cells are involved in the cellular component of adaptive immunity and what are their roles?

A

CD4+ T Cells (T Helper Cells): direct B cells and CD8 T cells to pathogens, and release cytokines

CD8+ T Cells (Cytotoxic T Cells): targets intracellular pathogens e.g. viruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Where are B cells formed and where do they mature?

A

Formation: bone marrow

Maturation: bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Where do naive B-cells circulate?

A

Lymphatic system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How are B-cells activated?

A

Naive B cells circulate in the lymphatic system and are activated through presence of a pathogen and co-stimulus from T-Helper cells to cause clonal expansion and differentiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is involved for optimal B cell response?

A

Requires T-cell help for clonal expansion of specific B-cells and subsequent differentiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are on the surface of B cells?

A

antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What can B-cells differentiate into and what are their role?

A
  • Antibody-secreting plasma cells: high quantities of antibody secretion
  • Isotype switching from IgM to IgG immunoglobulin: smaller numbers but very specific (specific response to a pathogen)
  • Memory B-Cells: high affinity Ig expressiong B-cells produced
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are primary and secondary responses to infection?

A

Primary response: occurs when an antigen comes into contact with the immune system for the first time

Secondary response: occurs when the 2nd/3rd/4th/etc. time the body is exposed to the same antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Compare primary and secondary immune responses

A

P: 5-10 day lag, S: 1-3 day lag

P: Smaller peak response, S: Larger peak response (i.e. more antibodies produced)

Antibody isotype - P: IgM>IgG, S: IgG

Antibody affinity - P: lower average affinity, more variable, S: higher average affinity (affinity maturation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Why does the secondary immune response quicker to reach peak antibody levels?

A
  • Memory B and T cells are already at higher frequency
  • Memory lymphocytes have a lower threshold for activation (specific to particular pathogen)
  • Pre-formed antigen specific IgA prevents antigen binding
  • Pre-formed IgG rapidly opsonises pathogen for phagocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Where do T cells form and mature?

A

Formation: bone marrow

Maturation: Thymus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is a T-cell receptor (TCR)?

A

Receptor found on T-cell surface that only recognises an antigen when presented in a MHC molecule i.e. only recognises pathogen once it’s been broken down into short peptide lengths

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What are expressed on the surface of T cells?

A

T-cell receptors and either CD4 receptors (on helper cells) or CD8 receptors (on killer cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What do T-helper cells secrete?

A

Interleukins (a group of cytokines) to regular immune responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What can T cells differentiate into?

A

T-regulatory cells - these regulate function of other immune cells, especially T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are the different types of T cells?

A

CD4 T-Helper Cells

CD8 T-Killer Cells

T-Regulatory Cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are the different types of MHC (Major Histocompatability Complex)?

A

MHC Class I: presents intracellular antigens and found on all cells. Present to CD8 T Cells

MHC Class II: presents extra-cellular antigens and found on APCs. Present to CD4 T Cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are the primary and secondary organs of the adaptive immune system?

A

Primary: thymus and bone marrow

Secondary: lymph nodes, spleen, MALT (GI tract), BALT (bronachia tree, Bronchus Associated Lymphoid Tissue)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Draw the anatomy of a lymph node

A
  • Kidney bean shape
  • <5mm long

deep cortex: T lymphocytes

outer cortex: B lymphocytes

medullary cords: B-lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is the function of lymph nodes?

A

Act as a filter for lymph - bacteria will travel through lymphatic vessels to the first regional lymph node which will filter any bacteria

Mechanical filtration: protein-rich lymph travels through afferent lymphatics into the subscapular space. Here, flow changes from high to low pressure and fast to slow. Lymph either comes around edges of capsule into medullary sinuses or takes a short cut through cortical sinuses. Any bactria will settle in the lymph node.

Biological Filtration: fixed, stellate macrophages clean the lymph nodes. Macrophages held by long processes forming loose lattice network. Lymphocytes are also found in lymph and lymphoid tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is the histological evidence that a lymph node is engaged in an immune response?

A
  • Lymphoid nodules (antibody response) are seen in the lower cortex
  • Larger lymphocytes are dividing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What are lymphoid nodules?

A

They represent antibody reponse and are found in lymphoid organs (mostly lymph nodes and spleen)

I.e. sign of infection

  • An antigen will causes response in B-cells: the antigen will bind to the Ab, activating B-cells to divide and form cluster
  • A lymphoid nodule starts with stimulation of one B-lymphocyte
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What do lymphoid nodules consist of?

A

Within the nodule there are medium and large lymphocytes and lymphoblasts (immature cells)

Around one pole of the nodule (mantle zone/corona): made of small lymphocytes, this faces the lumen

The rest of nodule - germinal centre: made of medium/large lymphocytes that are dividing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is the spleen made up of (histology)?

A

Red pulp: connective tissue that filters the blood of antigens and defective or worn-out RBCs

White pulp: peri-arterial lymphoid sheath containing a central arteriole. T lymphocytes surround arteriole and B cells make up rest of white pulp. White pulp = where lymphoid nodules would appear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What is the thymus?

A

It’s a primary lymphoid organ and programmes T-cells.

It itself doesn’t engage in immune response therefore will never see lymphoid nodules in the thymus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What happens the tymus in adults?

A

It involudes (shrinks due to age) and is replaced by fat as no longer needed to programme T-cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

How do the lymphoid organs prevent autoimmunity?

A

If either the B- or T-cell receptor binds strongly to self-antigens in bone marrow or thymus respectively, the cell will die by apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are the hypersenitivity classes?

A

Type : Description : Principle Cause

Type I : Immediate, atopic : IgE mediated

Type II : cytotoxic, antibody dependant : IgM or IgG bould to cell/matrix antigen

Type III : immune complex : IgM or IgG bound to soluble antigen

Type IV : cell mediated : T cells (CD4 and CD8)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Which hypersensitivity class has the most immediate response?

A

Type I Hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What can be said about all hypersensitivity classes?

A

They are all adaptive immune responses i.e. sensitisatio of the immune system must occur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Describe the response in a Type I hypersensitivity reaction?

A
  • Immediate (sec-min): if no reaction within 24hrs its not hypersensitivity
  • -* Severity increases with repeated exposure (1st time - small rash/itch)
  • Predominantly mediated by mast cells bound to IgE
  • Mast cells degratulate to release mediators that damage the parasite and the skin*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What cells are involved in Type I hypersensitivity?

A

Mast cells bound to IgE

They degranulate to release mediators that damage both the parasite and the skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Give 2 examples of Type I hypersensitivity

A

Hayfever, asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is the pathway for Type I Hypersensitivity?

A
  1. Sensitisation - immune system responds to substance to produce antibodies
  2. Identified by mast cells which are then primed with IgE
  3. Re-exposure
  4. Antigen bings to IgE-associated mast cells
  5. Mast cells degranulate (releasing pro-inflammatory cytokines, prostaglandins, chemokines, toxins, Histamine)
  6. Pro-inflammatory process stimulates and amplifies future responses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What occurs during Type I Hypersensitivity (effects on the body)?

A

Early (minutes):

  • Due to histamine (increases vascular permeability) and prostaglandin (smooth muscle contraction) release
  • Prostaglandins affect airflow, but this improves quickly

Late (hours/days):

  • Due to T-cell recruitment and other immune cells
  • Sustained smooth muscle contraction and tissue remodelling
  • Persistent airway effects which could lead to anaphylaxis (allergic reaction)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is anaphylaxis and what happens during it?

A

A severe, systemic type I hypersensitivity

  • Widespread mast cell degranulation due to systemic exposure to antigen e.g. penicillin
  • Increased vascular permeability (Histamine) could cause soft tissue swelling, threatening the airway, and loss of circulatory volume causing shock
  • Can be fatal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is Type II Hypersensitivity and what causes it?

A

Caused by binding of antibodies directed against self

  • Antibody binds to boundary between demis and epidermis
  • Common cause of autoimmune diseases
  • Blistering type rash
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What is the pathway for Type II Hypersensitivity?

A
  1. Sensitisation
  2. Opsonisation (Ab bind to cells)
  3. Cytotoxicity - complement activation, inflammation and tissue destruction as a result of antibody binding (classical pathway)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What causes Type III Hypersensitisation?

A

Immune complexes bound to soluble antigens

  • Aggregations of antibodies with many binding sites for binding to antigens
  • Soluble antigens have more than one binding site
  • Aggregates form in small blood vessels causing problems: direct occlusion, complement activation, privascular inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Examples of Type III Hypersensitisation

A

Autoimmune disease and drug allergies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is Type IV Hypersensitivity?

A

Delayed type hypersensitivity

  • Presents days after exposure
  • Mediated by lymphocytes infiltrating the area
  • T-cells cause inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What is autoimmune disease?

A

A harmful inflammatory response directed against self-tissue by the adaptive immune response

  • Can be organ specific or systemic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What’s an example of an organ specific autoimmune disease?

A

Type I Diabetes

  • Selective, atuoimmune destruction of pancreatic B-cells in Islets of Langerhans
  • Mix of Type II and Type IV
  • Causes insulin deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What is an example of a systemic hypersensitivity reaction?

A

Rheumatoid Arthritis

  • Chronic, auto-inflammatory condition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What are the characteristics (/symptoms/signs) of rheumatoid arthritis?

A
  • Thickened and inflamed synovial membrane (synovium) damages cartilage leading to loss of joint function
  • Weight loss and anaemia
  • Systemic inflammation problems: pulmonary nodules and fibrosis, pericarditis and vulvular inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What is the pathophysiology of rheumatoid arthritis?

A
  • IgM and IgA directed against IgG, forming large immune complexes
  • These are found in high concentrations in synovial fluid, also found in other tissues
  • Inflammation leads to enzyme release
  • Amplification of inflammatory cascade and further chemoattraction of inflam cells into synovium (macrophages/neutrophils/lymphocytes)
  • Osteoclast activation causing joint destruction
  • FIbrobalst activation and synovial hyperplasia
  • Systemic inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What is the treatment for rheumatoid arthritis?

A

Biologic therapy

  • Block soluble cytokines to reduce activation of macrophages, neutrophils and lymphocytes into synovium
  • Infliximab is a monoclonal antibody and anti-TNF agent, which acts to reduce inflammation
  • Benefits: reduces joint swelling and pain, reduces systemic inflammation and delays appearance of bony deformities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What’s the pathogenesis for RA?

A

Mix of genetic predisposition and environmental factors

Genetic: recognising self-antigens as foreign. Example genes involved - MHC I & II, cytokines

Environmental: persistence of inflammatory response to develop chronic disease. Examples - infection (molecular mimicry), geographical (Vit. D deficiency), modifiable personal RFs (smoking)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What is a cell?

A

The smallest structural and functional unit of an organism, typically miscroscopic and consists of cytoplasm and a nucleus enclosed in a membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is a tissue?

A

A group of cells that have a similar structure and act together to perform a specific function

Broad tissue types: epithelial, connective tissue, neuro-glial, haemato-lymphoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What is an organ?

A

A self-contained group of different tissues that performs a specific function in the body e.g. heart, liver

95
Q

What is an organ system?

A

A group of organs working together to perform one or more functions

E.g. gastro-intestinal, cardiovascular, skin, respiratory, GU, neurological

96
Q

Define disease

A

An abnormality of cell/tissue structure and/or function

97
Q

How can we view pathology?

A

General: disease causes and processes i.e. what’s happening to individual cells e.g. inflammation, necrosis

Systemic: general processes occuring in each system e.g. cardiovascular

98
Q

What are the levels of magnification?

A
  1. Gross (naked eye)
  2. Light microscopy
  3. Electron microscopy
  4. Molecular cell biology
99
Q

What is homeostasis?

A

The tendancy towards a relatively stable equilibruim between interdependant elements

100
Q

What environmental factors could change a cell’s structure and function?

A

External: Internal:

  • Physical factors - More/Less functional demand
  • Chemical factors -Hormones/Metabolic
  • Infection - Immune response etc.
  • Nutrition
  • Cells can usually easily adjust to mild changes*
101
Q

What can cause a cell to undergo adaptions?

A

Increased stress

Cells can easily adjust to mild environmental changes, but if stress overcomes homeostasis then cells undergo further adaption esp. changes in cell growth (atrophy, hyperplasia etc.)

102
Q

Generally, what causes cell injury?

A

Prolonged, severe or a specific type of stress, or sensitive cells

103
Q

WHen does an environmental change become a cell stress then cell injruy?

A

Stress factors: type/intensity of change

Cell factors: sensitivity of cell (e.g. lack of protective factors)

104
Q

What do you need to comment on when looking at pathology specimems?

A
  • Size, shape, colour, texture
  • Consider the tissues present whether normal or abnormal
  • What is the organ/tissue?
  • Is it normal or abnormal?
105
Q

Define atrophy, hypertrophy, hyperplasia, metaplasia and dysplasia

A

Atrophy: Cells decrease in size

Hypertrophy: Cells increase in size

Hyperplasia: Increase in the number of normal cells

Metaplasia: the exchange of epithelium for another type of epithelium

Dysplasia: A condition marked by abnormal cells that can lead to enlarged tissue or pre-cancerous cells

106
Q

What are some of the causes of cell injury with examples?

A
  • congenital
  • physical agents e.g. mechanical trauma, temperature extremes
  • Chemicals/drugs e.g. penicillin, chemotherapy
  • Infection
  • Hypoxia e.g. respiratory failure
  • Ischaemia
  • Immunological reactions e.g. anaphylaxis (T1), autoimmune reactions (T2/T3)
  • Nutritional imbalance
  • Endocrine/Metabolic
  • Genetic disease e.g. abnormalities in gene number or structure
107
Q

What is the definition of hypoxia and how does it affect cells?

A

Def: deficiency of oxygen

  • Disrupts oxidative respiratory processes in mitochondria so decreases ATP
108
Q

What is the definition of ischaemia and how does it affect cells?

A

Def: reduction of blood supply to a tissue

  • Caused by blockage of arterial supply or venous drainage e.g. atherosclerosis
  • Leads to depletion of oxygen (as with hypoxia) and nutrients
  • More severe and rapid than hypoxia
109
Q

What’s the difference between reversible and irreversible cell injury?

A

Reversible: temporary changes due to stress in the environment and cells return to normal once stimulus is removed

Irreversible: permanent damage and necrosis usually follows

There is a continuum between the two i.e. a threshold which depends on type, duration and severity of injury

110
Q

What is the pathogenesis of cell injury?

A

Damage to many structures in cell

  • Mitochondrial damage: disrupted aerobic respiration (ATP synthesis)
  • Cell membrane: disrupts ion concentrations, esp. causes inc. in Ca ions
  • Cytoplasm/Ribosomes: disrupts enzyme and structural protein synthesis and architecture
  • Nucleus: disrupts DNA maintenance and causes DNA damage

Oxidative Stress

  • Caused by ROS which are formed by absorption of radiation, toxic chemicals, hypoxia (ROS normally formed in small amounts due to respiration but this is much larger quantities)
  • Lack of antioxidants due to poor nutrition makes damage from ROS more likely
  • Damage can be more severe due to different types of injury
111
Q

What features in a cell particularly depict reversible cell damage?

A
  • Cloudy swelling due to loss of ATP-dep Na pump causing Na influx and osmotic disturbance
  • Cytoplasmic blebs (protrusions of the plasma membrane)
  • Disrupted microvilli

- Swollen mitochrondria and ER

- Fatty change due to accumulation of lipid vacuoles in the cytoplasm caused by disruption of FA metabolism

112
Q

Define necrosis and apoptosis

A

Necrosis

  • Unprogrammed cell death due to injury, disease or lack of blood supply

Apoptosis

  • Genetically programmed cell dealth occuring as a normal and controlled part of an organism’s growth or development
113
Q

Outline the differences between necrosis and apoptosis

A

Necrosis

  • Uncontrolled cell death
  • Due to external stimuli (injury/disease/lack of blood supply)
  • Always pathological
  • Cell contents released (cell lysus) causing acute inflammation

Apoptosis

  • Programmed and controlled cell death
  • Usually physiological (but can be pathological)
  • Cell contents aren’t released so no inflammation
  • Requires energy
  • Different morphology to necrosis
114
Q

What is the morphology necrosis?

A
  • Cell swelling
  • Vacuolation
  • Disruption of membranes inc. mitochondria and ER
  • Release of cell contents (cell lysis) inc. enzymes that cause adjacent damage and acute inflammation
  • DNA disruption
115
Q

Describe the morphology of nuclear changes seen in necrosis

A
  1. Nuclear fading: chromatin dissolution due to action of DNAases and RNAases
  2. Nuclear shrinkage: DNA condenses into a shrunken basophilic mass
  3. Nuclear fragmentation: nuclei membrane ruptures and nucleus undergoes fragmentation

These lead to nuclear dissolution

116
Q

Describe the types of necrosis

A

Coagulative: tissue death caused by infarction or ischaemia. Firm with tissue outline retained e.g. haemorrhagic is due to blockage of venous drainage

Colliquitive: tissue becomes a liquid mass and structure is lost e.g. infective abscess, cerebral infarct

Caseous: combination of coagulative and colliquative, appearing ‘cheese-like’ e.g. granulomatous inflammation (esp. TB)

Fat: due to action of lipases on fatty tissue

117
Q

How do you determine if a blockage is venous or arterial?

A

Arterial: causes lack of blood supply, (ischaemia - lack of oxygen and nutrients), will look white

Venous: lack of drainage, will look red and swolleb

118
Q

What are the effects of necrosis?

A
  • Functional: dependent on the tissue and area of tissue
  • Inflammation: stimulated by release of cell contents and causes damage. Inflammation will be acute with removal of stimulus followed by healing and repair, or chronic with persistence of stimulus
  • Necrosis ewill reduce function of the individual cells but also affect the body’s response to injury therefore the organ will fail to work
119
Q

What is the aetiology of apoptosis?

A

Physiological:

  • Embryogenesis
  • Hormone dependant involution (uterus, breast, ovary)
  • Cell deletion in proliferating cell populations to maintain cell number e.g. epithelium
  • Deletion of inflammatory cells after inflammatory response
  • Deletion of self-reactive lymphocytes in the thymus

Pathological:

  • Viral infection e.g. cytotoxic T cells
  • DNA damage
  • Hypoxia/Ischaemia
120
Q

What is the morphology of apoptosis?

A
  • Cell shrinkage
  • Chromatin condensation (unlike necrosis): packaging up nucleus
  • Membranes of cell and mitochrondria remain intact
  • Cytoplasmic blebs form and break off to form apoptotic bodies which are phagocytosed by macrophages
121
Q

What are the differences in morphology between apoptosis and necrosis

A

A: cell shrinkage, N: cell swelling (inc. cell volume)

A: plasma membrane blebs, N: loss of plasma membrane integrity

A: formation of apoptotic bodies, N: leakage of cellular contents

122
Q

What is amyloid?

A

Abnormally folded soluble protein fibrils into specific, abnormal, insoluble aggregates

  • Accumulation may be systemic/widespread or localised
  • Morphology resembles fibrosis but without prior inflammation
  • Stained with Congo Red (looks pink)
123
Q

Describe the pathogenesis of amyloid

A

It’s either:

  • Excessive production/accumulation of a normal protein, usually systemic deposition
  • Production/Accumulation of an abnormal protein, usually localised

Excessive production of normal protein: 2 types

  • AL amyloid: abnormal antibodies, immunoglobulin light chain. Produced in C-cell neoplasms e.g. mulitple myeloma
  • AA amyloid: serum amyloid associated protein (normal acute phase protein) produced in the liver. Produced in prolonged chronic inflammation e.g. rheumatoid arthritis

Many types of accumulation of abnormal proteins

  • E.g. Alzheimer’s disease
124
Q

What are the clinical effects of amyloid in the kidney, heart and brain?

A
  • Kidney: renal impairment or failure

Heart: heart failure

Brain: dementia

125
Q

What is the pathogenesis of pathological calcification?

A
  • Deposition of calcium salts

Can be:

  • Dystrophic: deposition of abnormal tissue with normal serum calcium

Metastatis: deposition of normal, living tissue with raised serum calcium (often in CT of blood vessels) and can compromise tissue function

126
Q

List the aetiology of raised calcium

A
  • Raised levels of parathyroid hormone (PTH): primary - parathyroid gland tumour, secondary - kidney disease
  • May be systemic effect with cancer
127
Q

What is the purpose of inflammatory processes?

A
  • To destroy/control the harmful stimulus
  • Initiate repair
  • Restore function
128
Q

Define acute inflammation

What general processes occur?

A

The immediate defence reaction of tissue to any injury, which may be caused by infection, chemicals or physical agents

  • Local blood vessels dilate, increasing local blood flow
  • WBCs enter tissue and begin to engulf bacteria/foreign particles
  • Macrophages remove and ocnsume dead cells, sometimes producing pus, enabling the healing process
129
Q

What are the clinical signs of inflammation (and what are they associated with)?

A
  • Redness: caused by hyperaemia
  • Swelling: caused by fluid exudate and hyperaemia
  • Heat: caused ny hyperaemia
  • Pain: caused by release of bradykinin and prostaglandins
  • Loss of function: caused by combination of the above
130
Q

List the steps involved in acute inflammation

A
  1. Vascular changes
  2. Exudate formation
  3. Cellular factors and release of mediators
  4. Removal of damaged tissue
  5. Repair and resolution or ongoing chronic inflammation
131
Q

What are the three main processes involved in acute inflammation

A
  1. Vascular dilatation
  2. Neutrophil activation
  3. Endothelial activation
132
Q

What causes vascular dilatation in acute inflammation?

What is the function of this process?

A

Caused by: histamine (released from mast cells) and prostaglandins

  • Arterioles dilate and increase blood flow to site
  • Rate of blood flow slows at site of injury helping with neutrophil activation
  • Allows fluid to pass into the tissue (forming an exudate) and causing swelling
133
Q

What causes neutrophil activation in acute inflammation?

What do activated neutrophils do / what is their role?

A

Caused by: leukotriene B4 and bacterial products

  • Activated neutrophils roll along endothelial cells, adhere to endothelial cells of blood vessels and pass between these cells into the ECM
  • Role: phagocytosis and bacteriocidal
134
Q

What causes endothelial activation in acute inflammation?

What is the role of this process?

A

Caused by: 5-HT, Histamine, bradykinin, leukotriene

Vascular endothelium activated to promote:

  • Increased cell adhesion molecules
  • Increased leakiness of endothelium
  • Allows plasma proteins to travel into tissue inc. Ig, complement and fibrinogen
135
Q

List 3 vascular changes that occur during acute inflammation

A

Vasodilatation

  • Starts in arterioles, increases blood flow
  • Due to histamine, no effect on vascular smooth muscle

Increased vascular permeability

  • Permits escape of protein rich exudate into extravascular tissue

Contraction of endothelial cells

Increased interendothelial spaces

Vascular congestion: slower flow, inc. concentration

Endothelial activation

  • Dye to mediators produced by inflammation
  • Inc. levels of adhesion molecules
136
Q

What cells are involved in acute inflammation?

A

Neutrophils

  • Opsonisation, phagocytosis, chemotaxis

Macrophages

  • Reside in tissues (in blood - monocytes)
  • Chemotaxis, phagocytosis, antigen presentation

Mast Cells

  • Reside in tissues
  • Histamine release (in granules): stimulated release contents by injury, complement or IgE

Lymphocytes

  • Antigen presentation, Ab production, cytokine produciton

Plasma cells

  • Ab production
137
Q

What cellular changes occur during acute inflammation?

A

Margination: the adhesion of WBCs to the walls of damaged blood vessels

Rolling

  • WBCs stick and detach from wall
  • Upregulated by interleukin-1 and TNF (macrophages)

Adhesion

  • Stimulated by IL-1 and TNF

Migration

  • Chemokines act of leucocytes to stimulate migration across the endothelium
138
Q

What chemical do macrophages release?

A

tumour necrosis factor (TNF-alpha)

139
Q

How are leucocytes activated?

A

Toll-like receptors (receptors for microbial products)

  • Stimulate microbe killing and cytokine production

GPCRs on neutrophils and macrophages

  • Induce migration of cells

Receptors for cytokines on surface of leucocytes

Leucocytes activated by

  • Classical pathway: ab-antigen complex
  • Alternate pathway: bacterial products
  • Products of dying cells in tissue necrosis

Complement

140
Q

How are the following complement substances involved in acute inflammation:

C3a

C5

C3b

A

C3a: recruitment of inflammatory cells

C5: formation of membrane attack complex (disrupts cell membranes)

C3b: opsonisation and phagocytosis

141
Q

What are the steps involved in phagocytosis?

A
  1. Opsonisation
  2. Engulfment
  3. Formation of phagosomes
  4. Fusion with lysosomes containing enzymes to form phagolysosomes
  5. Material destroyed and removed from cell by pinocytosis
142
Q

How does acute inflammation terminate?

A
  • Removal of stimulus
  • Neutrophils have a short-half life
  • Variation in cytokine stimuli
  • Neural impulses
  • Macrophages are activated to perform different functions
143
Q

List 3 beneficial and 2 detrimental effects of acute inflammation

A

Beneficial:

  • Dilution of toxins by oedematous fluid
  • Increased entry of Ab and drug transport
  • Fibrin traps micro-organisms
  • Delivery of nutrients
  • Stimulation of immune response

Detrimental:

  • Disgestion of normal tissue
  • Swelling eg. swollen epiglottis could block airways
144
Q

What are the 3 possible outcomes from acute inflammation and how would they arise?

A

Resolution: complete restoration of tissue to normal

  • If minimal tissue damage in tissue with regenerative capacity (eg. skin) and stimuli is rapidly removed

Healing by fibrosis

  • After sustained tissue damage and tissue is incapable of regeneration
  • Abundant fibrin exudate

Progression to chronic inflammation

  • Persistent stimulus
  • Tissue destruction leading to ongoing inflammation
145
Q

Define exudate

Define transudate

A

Exudate: An extracellular fluid with a high protein and cellular content

Transudate: An extracellular fluid with a low protein and cellular content

146
Q

List 3 types of exudate

A

Serous

Fibrinous

Suppurative (pus forming)

Haemorrhagic

Membranous

Necrotising (Gangrenous)

147
Q

What is the role of an exudate?

A
  • Delivery of nutrients, dilution of toxins, entry of Ab and stimultes the immune reponse
148
Q

List 3 ways in which infection can spread between people

A
  • Blood-borne
  • Natural barriers
  • Air borne
  • Immune factors
149
Q

How may infection spread within the host?

A

Localised infection

  • Remains at initial site, spreads to local lymph nodes via draining lymphatics
  • Five cardinal signs

Sytemic infection

  • Haematogenous ie. spread through blood/lymph to cause a systemic inflammatory response
150
Q

What controls the spread of infection within a host?

A
  • Virulence of an organism
  • Host condition ie. immunosuppression
  • Low protein levels
  • Poor vascular supply
  • Treatment
151
Q

What are the clinical features of systemic inflammatory response?

A

SIRS:

  • RR >20
  • HR >90
  • Temp: <36 or >38
  • WBC count <4 or >12
152
Q

The presence of what cell indicates acute inflammation?

A

Neutrophils (remain for 1-3 days post infection)

153
Q

Why is a post-mortem performed?

A

Medical questions

  • Confirm a diagnosis or its extent
  • Revealing a diagnosis or explain unexplainable findings
  • Investigating possible failings in surgery / other medical care

Medico-legal questions

  • suspicious death, death involving criminality, unexplained death, suicide, occupational related
154
Q

What are the differences between hospital consented post mortem and medico-legal post mortem?

A

Hospital consented PM:

  • At request of clinicians to get answers about treatment or pathology
  • Requires specific request form family
  • Few cases a year

Medico-legal PM:

  • At instruction of Procurator Fiscal (Scotland)
  • No consent required from family
  • Maj. of PMs
155
Q

What is involved in a post mortem?

A

Background check

  • Elicited from medical notes, inc. PMH, summary of clinical events and treatment

Autopsy

  • External and internal investigations

Further investigations

  • Histology, biochemistry, bacteriology etc.

At the end

  • All organs returned to body cavity

Death certificate

156
Q

What is involved in the external investigation during the autopsy in a PM?

A
  • Identification of deceased
  • Height, weight, BMI
  • Skin, hair , eye colour
  • General appearance, external disease eg. surgery, drainage, jaundice, clubbing, oedema
  • Medical treatment: scars, drains, IV lines
157
Q

What is involved in the internal investigation during autopsy in a post mortem?

A
  • Body cavities and systems: organs examinsed in turn
    1. Evisceration: specific incisions made
    2. Organ dissection
  • Macroscopic assessment and microscopic assesssment
158
Q

Define chronic inflammation

A

Persistent inflammation that lacks resolution when the inflamed tissue is unable to overcome the effects of the injurious agent

  • Persists for weeks, months, years
  • Characterised by infiltrates of lymphocytes, plasma cells and macrophages (longer 1/2 life than neutrophils)
159
Q

List 3 factors that contribute to developing chronic inflammation

A
  • Site affected ie. highly vascularised areas will heal quicker
  • Type of wound eg. depth, infection
  • Presence of infection and organism
  • Presence of indigestible material eg. if sutures are recognised as foreign
  • Treatment
  • Background disease
160
Q

What cells are involved in chronic inflammation?

A

Plasma cells

  • Maj. Ab producing cells, derived from B cells
  • Eccentric nucleus (over to one side), paranuclear huff and clock faced nucleus (dots seen in the nucleus)

Lymphocytes

  • T Cells: procude cytokines to attract and activate macrophages (cell mediated immunity)
  • B Cells: antibody production

Macrophages

  • antigen-presenting cells
  • voluminous cytoplasm
161
Q

What is granulomatous inflammation?

What are the predominant cell types?

Give one example of a condition with granulomatous inflammation

A
  • Distinctive pattern of chronic inflammation reaction (subtype of chronic inflammation

Predominant cell types:

  • Activated macrophages with a modified appearance (epithelioid macrophages)
  • Giant cells formed from fused epithelioid macrophages

Example:

  • Tuberculosis (TB)
162
Q

List 3 causes of granulomatous inflammation

A
  • Infectious agents eg. tuberculosis leprosy
  • Foreign material eg talc
  • Sarcoidosis, Crohn’s disease
  • Response to tumour eg. Hodgkin’s lymphoma
163
Q

What cells are involved in granulomatous inflammation?

A

Epithelioid macrophages

  • Modified macrophages arranged in small clusteres
  • Secretory rather than phagocytosis role

Giant cells

Lymphocytes: CD8 and CD4

Formation of granulomas

  • A manifestation of T cell mediated immune response (delayed type hypersensitivity)
164
Q

How does chronic inflammation manifest and it’s pathology in rheumatoid arthritis?

What cells are involved?

A

RA: a chronic inflam disease

  • Affects skin, blood vessels, joints, muscles, heart, lungs

Pathology:

  • Proliferative synovitis
  • Destruction of articular cartilage

Cells:

  • Inflam infiltrate: lymphoctes, plasma cells, dendritic cells, macrophages
  • Increased vascularity due to vasodilation and angiogenesis
  • Fibrin aggregation
  • Pannus (granulation tissue) formation: leads to carilage and bone erosion
  • Neutrophils in synovial fluid
165
Q

What is the role of macrophages in atherosclerosis?

A

Endothelial injury due to stress/smoking etc.

  • Leads to inflammation and recruitment of macrophages
  • Macrophages that localise to fatty deposits: foam cells which can form a plaque leading to atherosclerosis
166
Q

List the 3 processes involved in wound healing

What happens during each stage?

A

Inflammation

  • Initial response to injury and removal of debris

Proliferation

  • Formation of granulation tissue

Maturation

  • Scar formation using granulation tissue
167
Q

What is granulation tissue?

A

Body’s reponse to a defect with small blood vessels forming at site of defect and merging to form vascular complexes to allow infiltration

  • Replaced with scar tissue over next 6-8 weeks
168
Q

What are the phases involved in healing?

A
  • Formation of blood clot
  • Formation of granulation tissue
  • Cell proliferation and collagen deposition
  • Scar formation
  • Wound contraction
  • Connective tissue remodelling
  • Recovery of tensile strength
169
Q

List 3 local and 3 systemic factors influencing wound healing

A

Local:

  • Type, size and location of wound
  • Movement within wound eg. if over a joint
  • Presence of infection
  • Presence of foreign material eg. glass
  • Poor blood supply

Systemic

  • Age
  • Nutrition eg. Vit C
  • Systemic disease eg. renal failure, diabetes
  • Drugs, esp. steroids
  • Smoking
170
Q

list the 3 stages involved in fracture healing

A

inflammation, repair remodelling

171
Q

What occurs during the inflammation stage of fracture healing?

A
  • Haematoma forms at the site of fracture
  • Prostaglandins recruit neutrophils, macrophages, lymphocytes and fibroblasts to area
  • Granulation tissue forms at haematoma and gradually replaces it
  • Ingrowth of vessels
  • Migration of mesenchymal cells: lay down collagen matrix
  • Nutrients and oxygen supposed by exposed bone and muscle
172
Q

What occurs during the repair phase of fracture healing?

A
  • Fibroblasts lay down stroma to support ingrowing vessels
  • Collagen matrix laid down (mesenchymal cells)
  • Osteoid secreted by osteoblasts and mineralised leading to soft callus formation
  • Callus ossifies after 4-6 weeks due formation of bridge of woven bone between fracture fragments
173
Q

What occurs during the remodelling phase of fracture healing?

A

Occurs slowly over months/years

  • Returns bone to original shape, structure and mechanical strenth
  • Facilitated by mechanical stress
174
Q

What is Virchow’s triad?

A
  • Describes the 3 broad cateogories of factors that are thought to contrinute to thrombosis
    1. Blood composition - hypercoaguable state
    2. Vessel wall - vascular wall injury
    3. Blood flow - circulatory stasis
175
Q

What are the three factors that are thought to contribute to thrombosis?

A

Virchow’s Triad:

  1. Blood composition - hypercoaguable state
  2. Vessel wall - vascular wall injury
  3. Blood flow - circulatory stasis
176
Q

Differentiate between arterial and venous thrombosis

A

Arterial:

  • ‘white thrombus’
  • many platelets and a small amount of fibrin: reflects high flow
  • If in leg: would look white as blockage to blood flow entering

Venous:

  • ‘red thrombus’
  • lots of fibrin with trapped red cells: reflects indolent flow
  • if in leg: would look red and swollen
177
Q

Define a deep vein thrombosis

A

A thrombus (blood clot) within a deep vein, usually in the thigh or leg

178
Q

List 4 risk factors of a DVT

A

Stasis: pregnancy, long-haul flights, obesity

Hypercoaguability: surgery, meds eg. birth control, oestrogen, thrombophilia, inflammatory conditions esp. cancer

Damage to the endothelial lining: surgery, varicose veins

179
Q

How may a deep vein thrombosis may occur in the leg?

A

The veins in the leg have to pump blood up to the heart against gravity and therefore have valves to prevent backflow of blood to the feet when pulsatile motion stops

  • DVT occurs when the valves aren’t working properly of a thrombosis forms to block the vein
180
Q

How would a DVT present?

A
  • Throbbing or cramping pain in one leg
  • swelling in one leg
  • warm skin around the painful area
  • red/darkened skin around the painful area
181
Q

How would a diagnosis of a deep vein thrombosis be confirmed or excluded?

A
  • Clinical presentation
  • Bloods: D-dimer (measure of dissolved thrombus)
  • image venous system of the leg: compression US (common) or venography (X-ray)
  • Wells Clinical Score: <2 means DVT is unlikely, >2 suggests it’s likely

Treat for DVT if:

  • +ve D-dimer
  • Wells Clinical score >2
182
Q

How is a DVT managed?

A

Aim: prevent the thrombus extending or embolising

  • Anticoagulation for 3-6 months: Heparin, warfarin, DOACs (usually rivaroxaban)
  • Remove RFs eg. OCP, lose weight etc.
  • Pain relief
  • Graduated elastic compression stocking (symptomatic relief)
183
Q

List 3 complications of a DVT

A
  • Painful swollen leg
  • Pulmonary embolism
  • Recurrent VTE (venous thromboembolism)
  • Venous insufficiency
  • Post-thrombotic syndrome (reduce risk by 50% with compression stockings)
184
Q

How can a pulmonary embolism present?

A
  • dyspnoea, chest pain, haemopytsis
  • collapse (massive PE)
  • death
  • recurrent VTE
  • chronic thromboembolic pulmonary hypertension
185
Q

Define atheroma

A

Degeneration of the walls of the arteries caused by accumulation of fatty deposits and scar tissue, leading to restriction of the circulation and a risk of thrombosis

186
Q

Define ischaemia

A

A restriction in blood supply to the tissues, causing a shortage of oxygen that’s needed for cellular metabolism

187
Q

Define infarction

A

Obstruciton of the blood supply to an organ or region of tissue, causing local death of tissue

188
Q

Define atherosclerosis

A

A specific form of arteriosclerosis in which an artery wall thickens as a result of the accumulation of fatty materials such as cholesterol and triglycerides

189
Q

List 3 risk factors for arteriosclerotic CV disease

A

Smoking

HTN

Hyperlipidaemia

Diabetes

Obesity

Family history

190
Q

List 3 complications following a myocardial infarction

A
  • Atrial fibrillation
  • death
  • pericarditis
  • myocardial rupture
  • mitral valve prolapse
  • heart failure
191
Q

List the lobes of the right and left lungs and their fissures

A

Right lung: upper, middle and lower lobes

  • Oblique fissure between upper and lower
  • Horizontal fissure between upper and middle lobes

Left lung: upper and lower lobes, separated by the oblique fissure

192
Q

Describe the positioning of the trachea and the clinical signficance

A

Trachea passes to the right of the aorta (so may be a little off centre)

  • branches at the carina into the right and left bronchi
  • right main bronchus is more vertically orientated than the left therefore aspiration occurs more commonly in the right
193
Q

What is beneath the right and left hemidiaphragms?

A

Left: stomach

Right: liver

194
Q

List the emergency and elective indications for a CXR

A

Emergency:

  • Acute respiratory symptoms
  • Chest pain
  • Septic screen
  • Acute abdomen
  • Post central line/chest drain insertion

Elective:

  • Persistent/Chronic resp. symptoms
  • Pre-op work-up
  • Metastatic screen
  • TB contacts
195
Q

How would you systemically work through a CXR?

A

Details: pt. name, previous CXRs

RIPE: Rotation, Inspiration, PA/AP, Exposure

  • *A**irways: tracheal deviation
  • *B**reathing
  • *C**ardiac: cardiac-thoracic angles
  • *D**iaphragm: visible? shape/size, what’s underneath them
  • *E**xtras eg. bones, soft tissue swelling
196
Q

Compare PA and AP projection for a CXR

A

PA Projection:

  • X-rays pass from posterior to anterior of patient
  • standard projection
  • can assess cardiothoracic ratio

AP Projection:

  • X-rays pass from anterior to posterior
  • usualy done on the ward or ICU (ie. unwell patients)
197
Q

What disiplines are involved in cellular pathology?

A

Cytopathology: study of cells

Histopathology: study of tissues

198
Q

List the three typical pathology specimen’s that are received in a lab

What are the purpose of these specimens?

A

Specimens:

  • Cytology samples eg. smears, aspirates (fine needle aspiration)
  • Small tissue biopsies eg. prostate chips, bladder chips, punch biopsies, skin biopsies
  • Larrger tissue resections

Purposes:

  • Diagnostic only

Diagnostic and/or treatment eg. removal of effusion, colectomy

199
Q

Define cytology and list an advantage and a disadvantage

A

Def: the study of cells (looking at cells in solution)

Advantages:

  • Can use cytology on fluids but can’t biopsy fluids
  • Less invasive, quicker and cheaper than tissue biopsies

Limitation:

  • No wider tissue architecture that you’d get with a biopsy
200
Q

Outline the two types of cytology samples

A

Exfoliative cytology

  • fluid cytology including effusions (cells fall off into the fluid)
  • scape, smear and brush cytology (inc. cervical)

Fine needle aspiration (FNA)

  • direct eg. sampling surface lumps
  • stick needly through skin to get a sample
  • under US guidance, same as direct plus endoscopic ultrasound eg. lymph nodes, pancreas
201
Q

List the four signs on cytology associated with malignancy

A
  • Quantity: uncontrolled neoplstic cell growth
  • Pleomorphism: state of having various forms
  • Hyperchromasia: replicating cells with lots of DNA
  • Increased nuclear:cytoplasm ratio
202
Q

Give an example of each type of sample that can be taken under histopathology

A

Small biopsies:

  • mucosal eg. colonic biopsy
  • needle core eg. liver biopsy
  • incisional eg. skin punch biopsy

Excision biopsy eg. suspected melanoma

Resections:

  • small eg. appendicectomy
  • large eg. pneumonectomy
203
Q

Define immunohistochemistry

A

The method of localising specific intra-cellular or surface antigen expression

eg. ER or PR on a breast lump - helpful for determining treatment

204
Q

Define developmental anomaly

List 3 causes of developmental anomalies

A

= Deformity, absence or excess body parts/tissues which occur when normal growth is disturbed

  • Any congenital defect that occurs when normal growth and differentiation of the foetus is disturbed

Causes:

  • genetic mutations
  • Chromosomal anomaly
  • Teratogens
  • Environmental factors eg. smoking, alcohol
205
Q

Define congenital anomaly

How is it classified?

A

Def: anomalies that exist at or before birth regardless of cause

Classification:

  • Structural ie. physical body deformity
  • Functional/Metabolic ie. how the body works

A developmental anomaly is a structural congenital anomaly

206
Q

What is a ventricular septal defect?

How does it present?

A
  • Its’s a congenital heart anomaly in which there is a hole in the septa separating the left and right ventricles

Presentation:

  • Dependent on size of the defect
  • Usually asymptomatic for first few days/weeks
  • Poor eating, failure to thrive
  • Tachypnoea and SOB
  • Fatigue
  • Acyanotic (left to right shunt) therefore no signs of cyanosis early on. However, uncorrected VSD can increase pulmonary resistance leading to the reversal of the shunt and corresponding cyanosis
207
Q

Outline the pathophysiology of a ventricular septal defect

A

Normal: deoxygenated blood RA - RL - pulmonary artery - lungs - LA - LV - aorta and body

  • The hole allows the flow of blood backward from the left to right ventricle as the pressure of the LV is greater than RV (left-to-right shunt therefore acyanotic)
  • Oxygenated blood mixed with deoxygenated blood
  • Causes backpressure on RV and inc. resistance on the pulmonary artery

If left untreated:

  • The pressure between LV and RV will equalise as pulmonary artery pressure inc. and deoxygenated blood will be able to move from RV to LV (reversed the shunt) and into the aortic system: cyanosis
208
Q

List 3 congenital anomalies

A

Ventricular septal defect

Spina bidifa

Hamartoma

Ectopia

209
Q

Define spina bifida

Outline the range of presentations

A

= congenital defect of the neural tube that involves an opening in the vertebral column due to failure of closure of a portion of the neural tube during embryological development

Presentation:

  • muscle weakness or paralysis
  • bowel and bladder problems
  • seizures
  • orthopaedic problems eg. deformed feet, uneven hips, scoliosis
  • hydrocephalus
210
Q

What is a hamartoma?

A

A benign, tumour-like growth consisting of a disorganised mixture of mature cells and tissues normally found in the area of the body that the growth occurs

  • Grows at the same rate as the surrounding tissue
211
Q

Define ectopia

A

An abnormal location or position of an organ or tissue, most often occuring congenitally but can occur as a result of injury

Eg. ectopic cordis: displacement of the heart outside of the body

Ectopic pregnancy: implantation occurring in the fallopian tube rather than the endometrium

212
Q

What are diverticulum?

Give 2 examples

A
  • Circumscribed sacs caused by herniation of the lining mucosa of an organ through a defect in the muscular coat

Examples:

  • Merkel’s diverticulum: terminal ileum
  • Sigmoid colon diverticula / Diverticular disease
213
Q

What is divericular disease?

Where does it usually occur?

Outline the complications of diverticular disease

A

= small diverticula form in the wall of the colon

  • Can form anywhere in the colon, but most commonly found in the sigmoid colon

Complications:

  • Inflammation, bleeding, perforation, fistulation
  • Chronic inflammation and healing lead to fibrosis and muscle hypertrophy. This may exacerbate the problem, leading to stenosis and eventually large bowel obstruction
  • Diverticular disease is not a problem until it becomes inflamed
214
Q

What is Merkel’s diverticulum?

What complications could it cause?

A

Diverticula in the terminal ileum

  • Congenital and a remnant of the umbilical cord
  • Contains all the layers of the intestine and often has ectopic tissue within it (pancreatic/gastric)

Complications:

  • inflammation, haemorrhage, perforation, fistulation, intussusception (telescoping of one part of the intestine into another and predisposes to perforation)
215
Q

Define haemostasis

How is this affected by injury?

A

Def: normal cells in a steady state

Injury can induce changes in haemostasis:

  • Injury can either be reversible or irreversible
  • Either leads to adaption or cell death
216
Q

How do cells adapt to stress?

A

Adaptions: reversible changes in the number/size/type of cells in repsonse to changes in the environment

Physiological: response of cells to nromal stimulation by hormones or endogenous chemical mediatiors

Pathological: responses to stress that allow cells to modulate their structure/function and avoid injury

217
Q

Define hypertrophy

Give an example of physiological and pathological hypertrophy

What causes hypertrophy?

A

Def: an increase in the size of cells and therefore an increase in the size of the organ

  • enlargement due to increased synthesis of structural proteins and organelles

Physiological: uterus during pregnancy, training muscles to get larger, cardiac hypertrophy in fit athelete

Pathological: left ventricular heart disease

Causes:

  • increased functional demand
  • hormonal stimulation
218
Q

Define atrophy

List 3 causes

A

Def: shrinkage in the size of the cell by the loss of cell substances

Causes:

  • loss of innervation eg. Palsy’s

diminished blood supply

  • inadequate nutrition
  • decreased workload
  • loss of endocrine stimulation eg. dementia
219
Q

Define metaplasia

A

Def: the reversible change from one fully differentiated cell type to another

  • occurs when cells sensitive to a particular stress are replaced by other cells better able to withstand the adverse environment
220
Q

Describe two examples of metaplasia

A

Cigarette smoke

  • normal ciliated columnar epithelial cells of the trachea and bronchi are replaced by stratified squamous epithelial cells

Chronic gastric reflux

  • normal stratified squamous epithelium of the lower oesophagus may undergo metaplasia to gastric columnar epithelium
  • Barrett’s oesophagus: condition in which the normal lining of the oesophagus changes to the lining of the stomach/intestine
221
Q

Define neoplasia

A

An abnormal tissue mass, the growth of which is excessive, ie. not an adaptation to physiological demands, and is unco-ordinated compared to adjacent normal tissue

  • persists after cessation of the causative stimuli
222
Q

What are the features of a benign neoplasm?

What is the suffix?

Give 3 examples

A

Feautures:

  • grows without invading adjacent tissue or spreading to distant sites
  • well-circumscribed due to lack of invasion of surrounding tissues

Suffix: -oma

Eg.

  • Chondroma (cartilage)
  • Osteoma (bone)
  • Lipoma (fat cells)
  • fibroma (CT)
  • adenoma (glandular origin)

Exceptions to the suffix: sarcoma, carcinoma, melanoma, lymphoma

223
Q

What are the features of a malignant neoplasm?

List the types of malignant neoplasm with it’s origin and an example

A

Features:

  • invades the surrounding normal tissue
  • can spread / metastasise
  • usually not well circumscribed

Types:

  • Sarcoma: mesenchymal origin eg. osteosarcoma
  • Carcinoma: epithelial origin eg. squamous cell carcinoma
  • Melanoma: melanocytic origin
  • Lymphoma: haematopoietic origin eg. Hodgkin’s and non-Hodgkin’s lymphoma
  • Germ cell tumours
224
Q

What do the following prefixes for well-known neoplasms

lipo-

osteo-

leio-

chondro-

fibro-

adeno-

angio-

phabdo-

A

Lipo: fat cells

Osteo: bone

Leio: smooth muscle

Chondro: cartilage

Fibro: CT

Adeno: glandular tissue

Angio: blood vessels

Phabdo: skeletal muscle

225
Q

How do you assess a mole for malignancy?

A

ABCD

Asymmetry

Border: regular

Colour: same colour or multiple colours within it

Diameter (<1cm)

226
Q

What does the level of differentiation of tumour cells mean?

How is it cateogorised?

What is the clinical importance?

A
  • Differentiation relates to the tissue type represented by the tumour and the extent to which the tumour cell resembles the original cell

Categorised: well-differentiated, moderately, poorly differentiated, undifferentiated

Importance:

  • can determine site of origin in metastatic disease
  • prognosis (well differentiated has the best prognosis)
  • helps determine treatment
227
Q

What does the grade and stage of a tumour mean?

A

Stage: describes the size of the tumour and how far it has metastasised

Grade: describes the appearance of the cancerous cells and the aggressiveness of the tumour

  • As a tumour becomes more poorly differentiated, the grade increases
228
Q

How is the stage of a tumour determined?

A

TNM system

Tumour: size, local invasion

Nodes: are lymph nodes involved and how many

Metastases: present or not

  • if mets are present, then it’s stage IV
229
Q

Define anaplasia

A

Lack of differentiation of a tumour ie. undifferentiated

230
Q

Define dysplasia

What cell changes are seen with dysplasia?

A
  • Disordered growth in which cells fail to differentiate fully, but are contained within the basement membrane

Cell changes:

  • cell nuclei become hyperchromatic
  • nuclear membranes become irregular
  • nuclear:cytoplasmic ratio increases
231
Q

What is carcinoma in-situ?

A
  • Full thickness epithelial dysplasia extending form the basement membrane to the surface of the epithelium
  • If the entire lesion is no more advanced than carcinoma-in situ, there is no risk of metastases
232
Q

Define metastasis

Outline the routes for metastases to occur

A

Def: implants of tumour discontinuous from the primary tumour

Spread to distant sites:

  1. Lymphatic spread
    - most common spread for carcinomas
    - pattern of LN involvement follows natural routes of drainage
  2. Haematogenous spread
    - Typical of sarcomas
    - with venous invasion, the blood-borne cells follow the venous flow
    - liver and lungs are frequently involved
  3. Transcoelomic spread
    - occurs when a malignant neoplasm penetrates into a natural ‘open field’ eg. peritoneal cavity
233
Q
A

Phase 3 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions