Brainscape's Knowledge GenomeTM

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


See full index

Phase 3 > General Pathological Mechanisms > Flashcards

General Pathological Mechanisms Flashcards

1
Q

Describe the types of necrosis

A

Coagulative: Firm, tissue outline retained (Haemorrhagic - due to blockage of venous drainage or Gangrenous - larger area especially lower leg)

Colliquitive: Tissue becomes liquid and its structure is lost (e.g. infective abscess or cerebral infarct)

Caseous: Combination of coagulative and colliquitive, appearing cheese-like (caseous), classical for granulomatous inflammation, especially TB

Fat: Due to action of lipases on fatty tissue

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

Describe Carcinoma in Situ

A

Full thickness epithelial dysplasia extending from the basement membrane to the surface of the epithelium

Applicable only to epithelial neoplasms, if the entire lesion is no more advanced than CIS then the risk of metastasis is zero

This is because there are no blood vessels or lymphatics within the epithelium above the basement membrane

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

Define chronic inflammation and describe the circumstances in which it arises

A

‘a physiological response characterised by infiltrates of lymphocytes, plasma cells and macrophages that persists and lacks resolution when the inflamed tissue is unable to overcome the effects of the injurious agent’

Many factors are important, including site affected, type of wound, presence of infection and type of organism involved, presence of indigestible material, treatment given and background disease

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

Describe methods to establish a neoplastic diagnosis

A
  • History & Clinical Examination
  • Imaging – X-Ray, US, CT, MRI
  • Tumour Markers Laboratory Analysis – CEA, AFP, Ca125
  • Cytology – Pap Smear, FNA, Flow Cytometry
  • Biopsy – Histopathology, ICC
  • Molecular – Gene Detection
  • Bloods - As Appropriate
  • Scopes - ENT, Bronchoscopy, Gastroscopy, Colonoscopy, Cystoscopy, Colposcopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the histological changes seen in necrosis

A

Cell swelling, vacuolation and disruption of membranes of cells and its organelles including mitochondria, lysosomes and ER

Release of cell contents (cell lysis) including enzymes causes adjacent damage and acute inflammation

DNA disruption and hydrolysis

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

Describe the possible sequelae of acute inflammation

A
  • Resolution (complete restoration of tissue to normal)
    • If minimal tissue damage
    • If occurs in tissue with regenerative capacity i.e. skin
    • If cause is rapidly removed or destroyed
    • If there is good vascular drainage
  • Healing by fibrosis
    • After substantial tissue damage
    • Tissue incapable of regeneration
    • Abundant fibrin exudate
  • Progression to chronic inflammation
    • Persistent stimulus
    • Tissue destruction leading to ongoing inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the two types of Post-Mortem Examination

A
  • Hospital ‘Consented’ PM
    • Usually at the request of clinicians to answer question about the patient’s pathology or treatment
    • Requires specific consent of the family
    • Few cases per year (40-50 in Glasgow)
  • Medico-Legal PM
    • At the instruction of the Procurator Fiscal (Scotland) or Coroner (England and Wales)
    • Does not require consent of the family
    • Constitute the vast majority of PMs performed in the UK (110,000 per year in England and Wales, 6500 in Scotland)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the various stages of cutaneous wound healing

A
  • Haemostasis
    • Aggregation of platelets, vasoconstriction and inflammatory factor release
  • Inflammation
    • Increased vascular permeability allows migration of inflammatory cells
  • Tissue Proliferation
    • Re-Epithelialisation by keratinocytes moving into the wound
    • Neovascularisation by proliferation of collagen-producing fibroblasts to support new blood capillaries
  • Tissue Remodelling
    • Cross-linking of collagen into thick bundles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Define apoptosis

A

Genetically programmed (physiological) or activated cell death (pathological) requiring energy and distinct pathways

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

Describe the principles of tumour grading and staging and their clinical relevance

A

As tumours become more poorly differentiated, the higher the grade

Therefore, a poorly differentiated tumour is a high-grade malignancy and a well-differentiated tumour is a low-grade malignancy

Tumour stage is based on its size, extent of invasion into the surrounding tissue, spread to regional lymph nodes and presence or absence of lymph nodes

Grading and staging are of prognostic importance and can help determine treatment options

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

Describe the role of neutrophil polymorphs in inflammation

A

Opsonise and phagocytose

Intra-cellular killing of micro-organisms (both oxygen dependent and independent)

Release lysosomal products, propagating the response

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

Describe differences between benign and malignant neoplasms

A
  • Benign Neoplasm
    • A neoplasm that grows without invading adjacent tissue or spreading to distant sites
    • Usually well-circumscribed due to lack of invasion of surrounding tissues
  • Malignant Neoplasm
    • A neoplasm that invades the surrounding normal tissue
    • Can spread to distant sites (metastasise)
    • Usually is not well circumscribed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the features of irreversible cell injury

A

Permanent

Cell death (usually necrosis) follows

Features include:

ATP Depletion

Calcium Influx

DNA Damage

Accumulation of Oxygen Free Radicals

Extensive Physical Damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Define congenital anomaly and developmental anomaly

A

Congenital anomalies are ones that exist at or before birth, regardless of the cause and may be either functional/metabolic or structural

Developmental anomaly is a deformity, absence or excess body parts/tissues which occur when normal growth is disturbed

Developmental Anomaly = Structural Congenital Anomaly

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

Describe the role of complement in inflammation

A

Activated by the classical pathway (Ag/Ab complexes), alternative pathway (bacterial products), products of dying cells in tissue necrosis, components of kinin, coagulation or fibrinolytic systems

C3a/C5a - Chemotactic for neutrophils, increases vascular permeability and releases histamine from mast cells

C5-C9 - Cytolytic Activity

C2a/C3b/C4b - Opsonisation of Bacteria

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

Define neoplasm

A

‘an abnormal tissue mass the growth of which is excessive (i.e. not an adaption to physiological demands) and uncoordinated compared to adjacent normal tissue that persists even after cessation of the stimuli that caused it’

i.e. Uncontrolled or Irreversible

Can be Benign or Malignant

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

Describe the effects of the mechanical tissue injury, diverticula

A

Circumscribed pouch/sac caused by herniation of the lining mucosa of an organ through defect in muscular coat

  • Diverticular Disease
    • Effects include inflammation, bleeding, perforation and fistulation
    • When there is chronic inflammation and healing, there will be fibrosis which in turn will cause hypertrophy of the muscle which can lead to stenosis and large bowel obstruction
  • Meckel’s Diverticulum
    • Congenital
    • Two inches long, blind-ending duct that is a remnant of the yolk sac at the terminal ileum
    • Contains all layers of the intestine and often has ectopic pancreatic/gastric tissue within
    • Complications include inflammation, bleeding, perforation, obstruction, intussusception and pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Define atrophy, describe important physiological and pathological factors and describe stimuli responsible

A

‘shrinkage in the size/number of the cells by the loss of cell substance resulting from decreased protein synthesis and increased protein degradation’

Causes include; Loss of Innervation, Diminished Blood Supply, Inadequate Nutrition, Decreased Workload, Loss of ENdocrine Stimulation, Aging (Senile Atrophy)

e.g. Post-Menopausal Uterus Atrophy, Cortical Atrophy in Dementia

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

Describe Type IV Hypersensitivity

A

T-Cell Mediated Response

Delayed-type hypersensitivity, presents several days after exposure

Mediated by action of lymphocytes infiltrating the area

e.g. Contact Dermatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the role of mast cells in inflammation

A

Reside in tissues

Contain histamine and heparin in preformed granules

Stimulated to release contents by injury, complement and IgE

Play an important role in allergy/anaphylaxis

Also make eicosanoids to propagate immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe how various chemical mediators affect the inflammatory response

A

Histamine - Vasodilation, Increased Vascular Permeability, Endothelial Activation

Serotonin - Vasodilation, Increased Vascular Permeability

Prostaglandins - Vasodilation, Pain, Fever

Leukotrienes - Increased Vascular Permeability, Chemotaxis, Leucocyte Adhesion

NO - Killing of Microbes, Vascular Smooth Muscle Relaxation

!L-1/TNF/IL-6 - Endothelial Activation, Fever, Pain, Shock

Chemokines - Chemotaxis, Leucocyte Activation

22
Q

Describe Type II Hypersensitivity

A

Cytotoxic, Antibody Dependent

IgM/IgG Bound to Cell /Matrix Antigen

Caused by binding of antibodies directed against human cells (usually IgG)

Associated with Drug Associated Haemolysis more than allergy

Common cause of autoimmune disease

e.g. Autoimmune Haemolytic Anaemia

23
Q

Outline the nature, causes and effects of pathological calcification

A

Deposition of calcium salts

May be dystrophic (deposition in abnormal tissue with normal serum calcium) or metastatic (deposition in normal tissue with raised serum calcium, often in the connective tissue of blood vessels resulting in compromised tissue function)

Causes include increased levels of PTH due to a parathyroid tumour or kidney disease

24
Q

State some physiological and pathological aetiologies of apoptosis

A
  • Physiological:
    • Deletion of cell populations in embryogenesis
    • Cell deletion in proliferating populations (e.g. epithelium)
    • Deletion of inflammatory cells after an inflammatory response
    • Deletion of self-reactive lymphocytes in thymus
  • Pathological:
    • Viral Infection: Cytotoxic T-Lymphocytes
    • DNA Damage
    • Hypoxia/Ischaemia
25
Q

Describe the factors which may influence wound healing

A

Local - Type, size and location of wound, movement within wound, infection, presence of foreign/necrotic material, irradiation, poor blood supply

Systemic - Age, Nutrition (Vit C, Zinc), Systemic Disease (Renal Failure, Diabetes), Drugs (esp. Steroids), Smoking

26
Q

Describe congenital ectopias

A

An abnormal location or position of an organ or tissue, most often occurring congenitally but also as a result of injury

Ectopia Cordis: Displacement of heart outside the body

Ectopic Thyroid Tissue: Nodules of mature thyroid tissue located elsewhere in the neck

27
Q

Describe the role of vascular changes in inflammation

A
  1. Vasodilation
    1. Transient vasoconstriction then vasodilation
    2. Starts in the arterioles
    3. Increased blood flow
    4. Due to histamine and NO on vascular smooth muscle
  2. Increased Vascular Permeability
    1. Permits escape of protein-rich fluid exudate into extravascular tissue
    2. Contraction of endothelial cells increases inter-endothelial spaces
    3. Mediated by histamine, bradykinin and substance P
    4. Endothelial injury in severe injuries
    5. Injury can be caused by neutrophils
    6. Increased transcytosis
  3. Vascular Congestion/Stasis
    1. Slower flow and increased concentration
  4. Endothelial Activation
    1. By mediators produced during inflammation
    2. Increased levels of adhesion molecules
28
Q

Describe the features of reversible cell injury

A

Changes due to stress in the environment

Returns to normal once the stimulus is removed

Features include:

‘Cloudy Swelling’ - Osmotic disturbance due to loss of energy-dependent Na pump leads to Na influx and build up of intracellular metabolites

Cytoplasmic Blebs

Disrupted Microvilli

Swollen Mitochondria

‘Fatty Change’ - Accumulation of lipid vacuoles in cytoplasm caused by disruption of fatty acid metabolism, esp. in the liver

29
Q

Describe the main concepts of how infection may spread

A
  • Localised Infection
    • Remain at initial site
    • Spread to local lymph nodes via draining lymphatics
    • Five cardinal signs!
  • Systemic Infection
    • Haematogenous - i.e. spread through blood/lymph to cause SYSTEMIC INFLAMMATOrY RESPONSE
    • Can track through tissue to form abscess/infection elsewhere, e.g. psoas abscess
30
Q

Describe the effects of the mechanical tissue injury, intussusception

A

‘a process by which a section of intestine invaginates into the adjoining intestinal lumen’

Can result in small bowel obstruction, peritonitis or bowel perforation

31
Q

Define hyperplasia, describe important physiological and pathological factors and describe stimuli responsible

A

‘increase in the number of cells in an organ or tissue’

Adaptive response in cells capable of replication

Critical response of connective tissue cells in wound healing

Physiological - Hormonal (Normal Proliferative Endometrium) or Compensatory (Occurs when a portion of tissue is removed or diseased)

Pathological - Caused by excessive hormonal or growth factors stimulation (androgens; BPH or oestrogen; atypical endometrial hyperplasia)

32
Q

Outline the nature, causes and effects of amyloid accumulation

A

Organisation of amyloid soluble protein fibrils into specific abnormal, insoluble aggregates

Can be due to multiple myeloma or chronic inflammation (e.g. RA)

Effects depend on site of deposition from renal impairment/failure, heart failure or dementia

33
Q

Describe Type I Hypersensitivity, including Anaphylaxis

A

Immediate, Atopic, IgE Mediated Response

Responsible for most allergies, including asthma, eczema and hayfever

Response to the challenge occurs immediately, tends to increase in severity with repeated exposure

Predominantly mediated by IgE bound to mast cells

Antigen binds to IgE associated with mast cell, causing degranulation and release of histamine, cytokines, prostaglandins and leukotrienes

Anaphylaxis is a life-threatening severe, systemic Type I Hypersensitivity as a result of systemic exposure to an antigen and vascular permeability is the immediate danger (soft tissue swelling threatens airway and loss of circulatory volume causes shock)

34
Q

Define hypertrophy, describe important physiological and pathological factors and describe stimuli responsible

A

‘increase in the size of cells and therefore an increase in the size of the organ/tissue’

Enlargement is due to an increased synthesis of structural proteins and organelles

Occurs when cells are incapable of dividing

Can be physiological (muscle hypertrophy) or pathological (LV hypertrophy)

Causes by increased functional demand and/or hormonal stimulation

35
Q

Describe the cellular changes in the vasculature associated with inflammation

A
  1. Margination
    1. WBCs become more peripheral due to stasis
  2. Rolling
    1. WBCs stick and detach from wall
    2. Mediated by Selectins
    3. Up-regulated by IL-1 and TNF (from Macrophages/PMNs)
  3. Adhesion
    1. Mediated by Integrins
    2. Stimulated by IL-1 and TNF
    3. Chemokines also facilitate binding (directly released at site of injury)
    4. Reorganisation of cytoskeleton
  4. Migration (Diapedesis)
    1. Chemokines act on leucocytes to stimulate migration across endothelium
36
Q

Define necrosis

A

Pathological, unprogrammed cell death following injury and which is uncontrolled and due to external stimuli

37
Q

Define dysplasia and describe its characteristic features

A

‘disordered growth in which cells fail to differentiate fully, but are contained by the basement membrane, i.e. non-invasive’

Cell nuclei become hyperchromic

Nuclear membranes become irregular

Nuclear to cytoplasmic ratio increases

Dysplasia may regress, persist or progress

38
Q

Describe the various stages of fracture healing

A
  1. Haematoma Formation
    1. Clotted blood forms around fracture site and area becomes inflamed as phagocytic cells remove debris
  2. Fibrocartilaginous Callus Formation
    1. Fibroblasts and chondroblasts from the periosteum arrive at the site to roughly lay down collagen and fibrocartilage (known as a fibrocartilaginous soft callus)
  3. Bony Callus Formation
    1. Pre-Osteoblasts differentiate to mature osteoblasts which lay down spongy bone
    2. Over time the fibrocartilage is replaced by spongy bone to form a bony (hard) callus
  4. Bone Remodelling
    1. Finally and remaining portions of dead bone are resorbed by osteoclasts
    2. The spongy bone around the periphery of the site is replaced with compact bone
39
Q

Describe healing by primary and secondary intention

A

Primary - Wound edges are close together with minimal tissue loss so can be held together with sutures, heal quickly with minimal scar formation

Secondary - Wound edges are separated with greater tissue loss, so healing occurs slowly with more scar tissue formation

40
Q

Describe inflammation

A

An acute or chronic physiological response to tissue injury with vascular and cellular components, terminating in resolution, repair or continuing inflammation

41
Q

Describe the role of macrophages in inflammation

A

Macrophages - Tissue Resident, Monocyte - Circulating

Chemotaxis

Synthesise TNF, IL-1, IL-6

Phagocytosis

Antigen-presenting cells, link between innate and adaptive immune response

42
Q

Describe Type III Hypersensitivity

A

Immune Complex

IgM or IgG Bound to Soluble Antigen

Mediated by immune complexes bound to soluble antigen

Cause of autoimmune disease and drug allergy

Aggregates in small blood vessels causes direct occlusion, complement activation and perivascular inflammation

e.g. SLE or RA

43
Q

Describe different routes of tumour growth and spread

A
  • Local Invasion
  • Lymphatic Spread
    • Most common pathway for dissemination of carcinomas (although sarcomas can also use this route)
    • The pattern of lymph node involvement follows the natural routes of drainage
  • Haematogenous Spread
    • Typical of sarcomas
    • Arteries are more difficult for a tumour to penetrate than veins
    • With venous invasion, the blood-borne cells follow the venous flow draining the site of the tumour
    • Liver and lungs are frequently involved
  • Seeding of Body Cavities (Transcoelomic Spread)
    • Occurs when a malignant neoplasm penetrates into a natural ‘open field’ such as peritoneal cavity, pleural space, pericardial cavity, etc.
    • Most common examples include ovarian carcinoma and gastric carcinoma
44
Q

Describe granulomatous inflammation

A

A distinctive pattern of chronic inflammation with predominantly activated macrophages (with a modified epithelioid appearance) and giant cells (formed from fused epithelioid macrophages)

Epithelioid macrophages are arranged in small nodules or clusters and have a mainly secretory role rather than phagocytic and multinucleated giant cells form where material is difficult to digest

Granuloma formation is a manifestation of T-Cell mediated immune reaction (Delayed Type Hypersensitivity)

Associated with TB, Hodgkin Lymphoma, Sarcoidosis, Crohn’s Disease, Leprosy, Toxoplasmosis

45
Q

Define metaplasia, describe important physiological and pathological factors and describe stimuli responsible

A

‘reversible change from one fully differentiated cell type into another’

Adaptation so cells sensitive to a particular stress are replaced by other cells better able to withstand the adverse environment

Cigarette Smokers - 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

46
Q

Describe the various types of exudate

A

Exudate - Extracellular fluid with a high protein and cellular content

Transudate - Extracellular fluid with a low protein and cellular content

Serous - Usually a transudate found in pleural, pericardial and peritoneal spaces

Fibrinous Exudate - Fluid rich in fibrin, and exudate due to high protein content often on serosal surfaces such as the meninges

Suppurative Exudate - Pus-forming, and exudate rich in neutrophil polymorphs (abscess)

Pseudomembranous - Surface exudate on mucosal/epithelial sites

47
Q

Describe the effects of necrosis

A

Functional - Depends on the tissue/organ

Inflammation - Release of cell contents activates inflammation and causes damage (either acute with removal of stimulus and then healing and repair or chronic with persistence of stimulus and chronic inflammation)

48
Q

Describe Hamartoma

A

Malformation that may resemble a neoplasm that results from faulty growth in an organ

Composed of a mixture of mature tissue elements which would normally be found at that site which develop and grow at the same rate as the surrounding tissue

Chondroid Hamartoma - Benign lung lesion composed of epithelium, cartilage, fat and smooth muscle

49
Q

Describe the morphological features of apoptosis

A

Cell Shrinkage

Chromatin Condensation (Packaging up of nucleus, unlike in necrosis)

Membranes of Cell and Mitochondria Remain Intact

Cytoplasmic Blebs form and break off to form apoptotic bodies which are phagocytosed by macrophages

50
Q

Describe the process of a Post-Mortem Examination

A
  • External Examination
    • Identification of the deceased
    • Height/Weight/BMI
    • Skin/Hair/Eye Colour
    • Iatrogenic - Scars, Drains and IV Lines
    • Evidence of trauma
    • Jaundice, cyanosis, finger clubbing, oedema, lymphadenopathy
  • Evisceration
    • Single incision from sternal notch to symphysis pubis to remove thoracic, abdominal and pelvic organs
    • Second incision around posterior skull to reflect the scalp, remove the skull and remove the brain
  • Organ Dissection
    • Pathologist inspects each organ and carefully dissects (macroscopic assessment)
    • They may retain a small of tissue for microscopic assessment
  • Finally
    • Organs returned to patient’s body cavity
    • Death certificate issued
    • Report prepared and sent to PF or clinician
    • Body is reconstructed for viewing
    • Body released for burial/cremation

Phase 3 (14 decks)

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