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MCD > Histopathology > Flashcards

Histopathology Flashcards

1
Q

What are the most commonly run chemical pathology tests?

A
  • Electrolytes (esp. Na + K)
  • Urea & Creatinine
  • Calcium & Phosphate
  • Liver Function (LFTs = liver enzyme measurements)
  • Hormone Assays
  • Glucose
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2
Q

Anticoagulants are added to samples - what is the purpose of the following:

(a) EDTA
(b) Fluoride Oxalate

A

(a) EDTA = potassium = maintains cells
(b) Fluoride Oxalate = poison

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3
Q

What 5 qualities should all diagnostic tests have?

A
  • Specificity
  • Sensitivity
  • Rapid
  • Non-invasive
  • Cost effective
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4
Q

What can virological tests detect?

A
  • Inefctious virus
  • Viral protein componenets (i.e. antigens)
  • Viral genetic components
  • Host response
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5
Q

List some of the potential sample sites for virological sampling

A
  • Throat swap, NPA, broncheolar lavage etc. = resp. viruses
  • Stool = GI viruses
  • Urine = UT viruses
  • CSF = viruses capable of crossing BBB (eg: herpes)
  • Blood = serology (i.e. antibody detection)
  • Saliva = serology
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6
Q

Briefly outline what the following techniques are used for (in reference to diagnostic virology)

  • EM
  • Immunofluorescence
  • Serology
  • Quantification Assays
A
  • EM
    • Visualisation of viral structures
  • Immunofluorescence
    • Detection of viral antigens
  • Serology
    • Detection of antibodies
  • Quantification Assays
    • Measuring viral load
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7
Q

With regards to diagnostic microbiology, what is the optimal time for the collection of specimen?

A

In the acute phase of illness

Before antimicrobials have been started

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8
Q

Give an example of a sterile and non-sterile culture site for diagnostic microbiology

A

Sterile = blood or CSF

Non-sterile = skin or throat swab

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9
Q

Briefly outline what the following techniques are used for (in reference to diagnostic microbiology)

  • Microscopy
  • Serology
  • PCR
A
  • Microscopy
    • Gram-staining, identification of bacteria
  • Serology
    • Monitor Ab response, identification of bacteria
  • PCR
    • Used to detect MRSA
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10
Q

Define the role of a cytopathologist

A

Cytopathologists make diagnoses on cells

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11
Q

Define the role of a histopathologist

A

Histopathologists make diagnoses based on tissue

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12
Q

List some of the uses of clinical immunology

A
  • Immunodeficiency
  • Malignancy
  • Auto-immunity
  • Inflammation
  • Tissue typing
  • Histopathology
  • Diagnostics
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13
Q

Define inflammation

A

Inflammation is a provoke response to tissue injury

  • It is a complex reaction of vascularised connective tissue to injury
  • It is non-specific
  • Aim = destory, dilute or “ward off” injurous angents
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14
Q

Briefly outline the main difference between acute and chronic inflammation

A

Acute = short duration, rapid response, usually physiological

Chromic = long duration, slow response (often follwos acute inflammation), usually pathological

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15
Q

What are the 5 clinical signs of acute inflammation?

A
  • Rubour - redness
  • Tumour - swelling
  • Calor - heat
  • Dolor - pain
  • Functio laesa - loss of function
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16
Q

What are some potential causes of acute inflammation?

A
  • Physical agents (eg: trauma)
  • Chemical agents (eg: poisons)
  • Bacterial agents
  • Immunological reactions
  • Hypoxia
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17
Q

What are the effects of acute inflammation?

A
  • Fever
    • Increased pulse + BP
    • Increased temperature + chills
    • Anorexia
  • Leukocytosis
  • Protein production (liver)
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18
Q

What are the outcomes of acute inflammation?

A
  • Complete resolution
  • Healing with scar formation
  • Chronic inflammation
  • Abcess formation
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19
Q

What three processes are invovled in acute inflammation?

A
  1. Vascular Changes
  2. Cellular Changes
  3. Chemical Mediators
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20
Q

Outline the three major vascular changes that occur with acute inflammation

A
  1. Changes in vascular calibre
    • ​Brief vasoconstriction (minimise spread)
    • Prolonged vasodilation (increase blood flow to combat invaders)
    • Physical = rubor + calor
  2. Changes in vascular permeability
    • ​Increased permeability (plasma proteins + WBCs)
  3. Changes in blood flow
    • ​Increased blood flow (accomodates emigraton of WBCs)
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21
Q

What is the difference between (a) exudate and (b) transudate?

A

Exudate

  • Inflammatory extra-vascular fluid
  • Protein rich
  • Result of inflammation

Transudate

  • Ultra-filtrate of blood
  • Low [protein]
  • Result of hydrostatic or osmotic imbalance
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22
Q

Extravasation of luekocytes (i.e. cellular events) is a co-ordinated event in acute inflammation - what steps are involved?

A
  • Margination
    • WBCs come out of central axial column to the periphery
    • WBCs align along the endothelial surface
  • Adhesion
    • ​Activation of endothelial cells upreguates adhesion proteins
    • Adhesion proteins enable WBCs to leave the vessel lumen
  • Rolling​
  • Diapediesis
    • Leukocytes pierce the basement membrane and degrade it
  • Chemotaxis
    • ​Locomotion oriented along a chemical gradient
    • Assisted by chemo-attractants
  • Phagocytosis
    • ​Recongition + Attachment
    • Engulfment
    • Killing + Degradation
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23
Q

What 4 families of adhesion proteins are involved in acute inflammation?

A
  • Selectins
  • Immunoglobulins
  • Integrins
  • Mucin-like glycoproteins
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24
Q

Outline the role of cytokines during the acute inflammatory process

A

Adhesin proteins are partially under the control of cytokines - they help to increase their affinity for endothelial binding sites, enabling stable binding between the endothelium and the WBCs (via the adhesin proteins)

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25
Q

What is the difference between a plasma-derived and cell-derived chemical mediator of acute inflammation?

A

Plasma-derived = synthesised in pre-cursor form, must be activate, short-lived

Cell-derived = synthesised de novo in active form, short-lived

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26
Q

Name and describe the two major vasoactive amines

A

Histamine

  • Cell-derived
  • Widely distributed
  • Released in response to trauma and immune reactions
  • Causes dilation of aterioles

Serotonin

  • Cell-derived
  • Present in platelets
  • Simiar action to histamine
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27
Q

How is acute inflammation terminated?

A

Eradication of offending agent leads to the discontinuation of the inflammatory response

The process is aided by the short-lived nature of cells and chemicals invovled in inflammation

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28
Q

Define Chronic Inflammation

A

Chronic inflammation = prolonged inflammation in which active inflammation, tissue destruction + attempts at repair are occuring simultaneous

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29
Q

Describe the two scenarios which can potentially result in chronic inflammation

A
  1. Following acute inflammation
  2. Low-grade, long-standing inflammatory resposne
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30
Q

List some of the potential causes of chronic inflammation

A
  • Persistent infection (eg: TB)
  • Prolonged exposure to toxins
  • Autoimmunity
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31
Q

Name three histological features of chronic inflammation

A
  • Infiltration by mononuclear cells (i.e. macrophages, lymphocytes, plasma cells)
  • Tissue destruction
  • Attempts at healing (i.e. connective tissue laying and fibrosis)
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32
Q

Name the 4 cell types invovled in chronic inflammation

A
  • Macrophages
  • Lymphocytes
  • Eosinophils
  • Mast Cells
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33
Q

Outline the role of macrophages in chronic inflammation

A
  • Macrophages are the major cell type invovled
  • There is macrophage accumulation in chronic inflammation
    • Recruitment from blood via adhesion molecules
    • Immobilisation of cells at inflammatory site (controlled by cytokines)
    • Stimulation of cellular influx (macrophages attract cytokines etc.)
  • This becomes unregulated in chronic inflammation leading to tissue damage
34
Q

Define: granuloma

A

A granuloma is a focus of chronic inflammation consisting of an aggregate of macropahges which have been transformed into epitheloid cells surrounded by mononuclear leukocytes

35
Q

Define: epitheloid cell

A

An epitheloid cell is a macrophage with an elongated appearance - they arise due to a pattern of chronic inflammation

36
Q

Name and describe the three types of granuloma

A
  • Foreign body granuloma - incite by relatively inert foreign bodies (eg: form around ruptured implants)
  • Immune granuloma - caused by insoluble particles capable of inducing a cell-mediated immune respons (eg: TB)
  • Unknown aetiology - eg: sarcoidosis
37
Q

What is a casseating granuloma

A

A casseating (cheese-like) granuloma is typical of TB where the immun granuloma has started to necrose

38
Q

What are the two types of cell injury?

A

Lethal = leads to cell death via necrosis or apoptosis

Non-lethal = degenerative changes that can be regenerated

39
Q

Define degeneration

A

Degeneration = alteration or loss of struction and function in cells following injury or ageing

There are two types - pigmentation and non-pigmentation

40
Q

What are the two major types of degenerative joint/bone disease?

A

Osteoarthritis & Rheumatoid arthritis - these are examples of non-pigment related degeneration.

They are assoiated with loss of function and pain due to the degeneration of structures

41
Q

Give some examples of neurodegnerative diseases

A

Dementia & Parkinsons - these are both characterised by progressive, loss of function changes (i.e. neurodegenerative changes)

42
Q

What are amyloids?

A

Amyloids are proteinaceous substances deposited in tissues that can cause amyloidosis (i.e. degeneration within the depostied structure)

43
Q

List the (a) normal, (b) exogenous and (c) endogenous pigments involved in degeneration

A

(a) Normal

  • Melanin
  • Bilirubin

(b) Exogenous

  • Carbon
  • Tattoo

(c) Endogenous

  • Lipofuscin
  • Haemosiderin
  • Melanin
44
Q

Define: steatosis

A

Steatosis = abnormal accumulation of triglycerides within cells - it is an early indication of sress and injury

45
Q

Define the following:

(a) Tissue Repair
(b) Regeneration
(c) Healing

A

(a) Tissue Repair = replacement of lost/damaged tissue by regeneration and/or healing
(b) Regeneration = growth of cells and tissue to replace lost structures
(c) Healing = tissue response leading to the formation of scar tissue and/or fibrosis

46
Q

Compare and contrast healing and regeneration

A

Healing

  • Tissue response to injury
  • Occurs in tissues unable to regenerate
  • Involves repair and scarring

Regeneration

  • Tissue response to lost structures
  • Involves growth of cells
47
Q

What is the difference between “true” and “functional” regeneration?

A

Treu Regeneration = occurs in labile tissues (eg: stem cells)

Functional Regeneration = occurs in stable/quiescent tissues (i.e. compensatory growth)

48
Q

What pre-requisit is required for regeneration to take place?

A

Regeneration requires an intact connective tissue scaffold

49
Q

Outline the process of true regeneration

A
  • Regeneration involves the stimulation of division + migration of cells which induce replication
  • Replication of cells restores function of damaged cells
  • There can be de-differentiation of adult cells and secondary development to facilitate this
50
Q

Outline the process of functional regeneration

A

Regeneration involves stimulation of the cell cycle to cause replication (this restores function)

51
Q

What determines whether or not a tissue can be regenerated?

A

Its proliferative activity

52
Q

Describe a labile tissue

A
  • Continuously dividing cells
  • Consist of lossely aggregated cells - these are highly susceptible to sublethal injury but readily regnerate
  • Includes = skin, mucosa etc.
53
Q

Describe a quiescent tissue

A
  • Stable tissue
  • Tissues have a complex structure of cells with high longevity
  • Growth is a compensatory mechanism if any cells are damaged
  • Includes = liver, kidney and pacreatic cells
54
Q

What two factors help to stimulate cell replication (for regenerative purposes)?

A

Growth Factors

  • Natrually occuring proteins capable of stimulating cell growth, proliferation + differentiation
  • Function as ligands to stimulate secondary signalling pathways

ECM

  • ECM surrounds cells
  • Acts as a signal transducer
55
Q

Define Scarring

A

Scarring = the healing of permentant tissues which are inacapable of regenerating - tissue will no longer function as before but is not in a damaged state

56
Q

Describe a permenant tissue

A
  • These are non-dividing tissues
  • They are highly complex and cannot undergo any post-natal divisions
  • Includes = cardiac cells and neurons
57
Q

Define the following growth disorders:

(a) Hyperplasia
(b) Hypertrophy
(c) Metaplasia
(d) Dysplasia

A
  • ​Hyperplasia = increase in cell number without structural change
  • Hypertrophy = increase in cell size within an organ
  • Metaplasia = change from one cell to to another
  • Dysplasia = disordered cell growth with loss of uniformity
58
Q

What is a neoplasm

A

A neoplasm = abnormal and autonomous cell growth

  • Growth exceeds surrounding tissues
  • Growth is uncoordinated
  • Can either be benign or malingnant
  • aka - tumour
59
Q

What are the 4 main causes of epithelial dysplasia?

A
  • Infection
  • Inflammation
  • Environmental, physical & chemical factors
  • Genetics
60
Q

What are the implications of dysplasia

A
  • Irreversible changes to the cell
  • Cancer (some changes are carcinogenic)
61
Q

Name some common sites of dysplasia

A

**Squamous Cells **

  • Cervix
  • Oesophagus
  • Skin
  • Lungs

**Glandular Cells **

  • Cervix
  • Uterus
  • Bowel/colon
  • Breast
  • Liver
62
Q

Outline the microscopic features of dysplasia

A
  • Atypia (loss of normal cellular appearance)
  • Cytomegaly
  • Anarchy (loss of cellular polarity)
  • Nuclear atypia
  • Nucleomegaly
  • Loss of maturation
63
Q

Outline the pathogenesis of dysplasia

A
  • Recovery and regeneration over time leds to changes in cell morphology
  • Dysplasia is a type of cellular adaptation
    • Begins with hyperplasia
    • Then carcinoma in situ
    • Finally, invasive cancer
64
Q

Outline the adenoma-carcinoma sequence

A
  • Cancers develop from multiple sequential mutations in a step-wise manner
  • Adenoma-carcinoma sequence is in colon cancers
    • The colon can undergo 4 mutations before carcinoma sets in
    • Normal –> Adenoma –> Dysplasia –> Carcinoma
65
Q

What are normal physiological levels of calcium?

A

2.2-2.6 nM

66
Q

99% of the body’s calcium is within the bone, however, 1% is circulating - outline some of the key roles of circulating calcium

A

Normal nerve & muscle function

67
Q

Outline the role of PTH in the regulation of calcium

A
  • PTH = parathyroid hormone
  • Regulates calcium by negative feedback
    • Low calcium = high PTH
68
Q

In terms of calcium regulation - what does PTH cause?

A
  • Movement of calcium from the bone - increases free calcium levels in the blood
  • Activation of renal 1-a-hydroxylase - activates Vit. D to increase calcium absorption
  • Phosphate loss - increasing calcium absorption causes phosphate losses
69
Q

What are the major sources of Vit. D?

A
  • Vit. D3 = active vitamin, synthesised by the skin
  • Vit. D2 = active vitamin, found in plants
70
Q

Where is Vit. D processed?

A

Following ingestion (or absorption), Vit. D is hydroxylated by 25-hydroylase in the liver

(this is inactive, stored Vit. D)

71
Q

How is Vit. D activated?

A

Activation of 25-hyroxy-Vit. D (i.e. from liver) occurs in the kidneys via 1-a-hydroyxylase

This is under the control of PTH (and is rate-limiting)

72
Q

In reference to calcium, what is the role of Vit. D?

A

Vit. D controls the absorption of calcium from the small intestine (this is under the control of PTH)

73
Q

List some common conditions affecting calcium

A
  • Primary hyperparathyroidism
    • ​High Ca, High PTH, Low PO
  • Osteoporosis
    • ​Less bone, normal composistion
  • Osteomalacia
    • ​Same bone amount, abnormal composition
  • Vit. D deficiency
    • ​Paediatric = rickets
    • Causes secondary hyperparathyroidism
  • Paget’s disease (of the bone)
    • ​High alkaline phosphatase, normal Ca
  • **Cancer w/ bone mets. **
    • ​PTHRP release
    • Hypercalcaemia
74
Q

What is secondary hyperparathyroidism?

A

Low Vit. D = Low Ca = Secondary Hyperparathyroidism

  • Bones are continually releasing calcium stored due to low Vit. D = Low Ca
  • Bones become weaker
  • Rx = Vit. D + Ca
75
Q

Describe the clinical signs of low calcium levels

(hypocalcaemia = secondary hyperparathyroidism)

A
  • Tetany - intense muscle spasm (esp. in carpal mucles)
  • Alkalotic - presents as hyperventilation
  • Hypocalcaemic = calcium bound to albumin (can be tested via trousseau’s sign)
  • Trousseau’s Sign - arm spasms upon constriction
76
Q

Describe the biochemistry seen with hyperparathyroidism (secondary)

A

Secondary hyperparathyroidism = hypocalcaemia

  • Low Ca
  • Low PO
  • High PTH
  • High Alkaline phosphatase
77
Q

What are the two causes of hypercalcaemia

A

​Malignancy

  • Cancer w/ bone metastases

Primary Hyperparathyroidism

  • Benign tumour of PTH –> increases in PTH –> increases in Ca
78
Q

What is the clinical presentation of prmary hyperparathyroidism?

A
  • Bones - calcium out of bones = fractures
  • Stones - high circulating calcium = kidney stones
  • Moans - psychiatric symptoms
  • Groans - high calcium = constipation + abdo pain
79
Q

Briefly describe osteoporosis

A
  • Less bone, normal structure
  • One of the major metallic bone diseases
  • A type of degenerative bone disease
  • Commonly found in post-menopausal women (due to low oestrogen)
  • _Caused by hypocalcaemia _
  • Results in multiple pathological fractures and loss of bone mass
80
Q

Briefly describe osteomalacia

A
  • Same amount of bone, abnormal structure
  • One of the major metallic bone diseases
  • A type of degenerative bone disease
  • Caused by lack of Vit. D
  • Results in demineralisation of bone
  • Commonly found in:
    • Renal Px (no active Vit. D)
    • Rickets (lack of Vit. D)
    • Indian population (phytic acid = 24-hydroxy = inactivates Vit. D)
81
Q

Briefly describe Paget’s disease of the bone

A
  • Rare degenerative condition
  • Causes constant bone regeneration
    • Increased bone turnover but to high alkaline phosphatase
82
Q

What is PTHRP

A

PTHRP = parathyroid related protein

  • Physiological - expressed during pregnancy and lactation to release calcium enabling foetal bones to grow
  • Pathological - cancer causes bones to degenerate

MCD (13 decks)

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