Essentials Of Clinical Medicine 2

Front 1

What is pathology?

Back 1

The branch of medicine concerned with the cause, origin and nature of disease, including the changes occurring as a result of the disease

Front 2

List 4 roles of the histopathologist

Back 2

1. Specimen preparation
2. Biopsy reporting and 'surgicals'
3. Cytology
4. Autopsies

Front 3

List 3 types of pathologist

Back 3

Could be:
microbiologist
histopathologist
virologist
immunologist
haematologist
chemical pathologist
e.t.c.

Front 4

List 5 causes of cell injury

Back 4

1. Hypoxia
2. Chemical
3. Physical
4. Infection
5. Immune
May also be radiation caused by free radicals

Front 5

What is the difference between lethal and sub-lethal injury and how would you tell the difference between the two?

Back 5

Sublethal injury is reversible and lethal injury is not.

Sublethal injury may display:
• Generalized swelling
• Clumping of nuclear chromatin
• Blebs
• Autophagy by lysosomes
• ER and mitochondrial swelling with small densities
• Dispersion of ribosomes
• Aggregation of intramembranous particles

Lethal injury may display:
• Defects in the cell membrane
• Lysis of the ER
• Mitochondrial swelling with large densities
• Rupture of lysosomes and autolysis
• Myelin figures
• Nuclear pyknosis (irreversible condensation of chromatin = misshapen nucleus) or karyorrhexis (fragmentation of nucleus) or karyolysis (dissolution of chromatin = swollen nucleus)

Front 6

What are the 4 general pathogeneses of cell injury?

Back 6

1. Mitochondrial damage = reduced ATP synthesis
2. Loss of calcium homeostasis
3. Disrupted membrane permeability
4. Free radicals

Front 7

What is necrosis? List 3 of it patterns

Back 7

Deaths of groups of contiguous cells in a tissue or organ
May be:
1. Coagulative - can tell what the cell originally was but now only a 'ghost' = most often found in organ tissue
2. Liquefactive - all tissue becomes mushy (often in the brain after an infarct)
3. Caseous - 'cheese-like' (often found following TB)

Front 8

Define apoptosis

Back 8

Programmed single-cell suicide where the cell expends energy in order to die

Front 9

What are the major differences between necrotic and apoptotic cells (3)?

Back 9

1. Necrosis has swelling and rupture of the mitochondria and lysis of the plasma membrane spilling cell contents; apoptosis has no lysis but blebs plasma and nuclear membranes and still shoes cytoplasm shrinkage with the membrane intact.
2. Necrosis chromatin clumps together; apoptosis DNA clumps into 200bp fragments
3. Necrosis triggers inflammatory response; apoptosis has no such response as cell contents are in membrane-bounded bodies

Front 10

Name 3 factors that may influence the evolution of acute inflammation into chronic inflammation

Back 10

1. Nature of the pathogenic mechanism
2. Persistence of the injurious agent
3. Presence of certain cell types

Front 11

What are the 4 cardinal signs of acute inflammation?

Back 11

1. Rubor (redness)
2. Calor (heat)
3. Tumor (swelling)
4. Dolor (pain)

Also loss of function

Front 12

Describe the process of acute inflammation in terms of vascular and cellular events

Back 12

Immune response causes:
1. Haemodynamic changes - vasodilation of arterioles = increase blood flow (hyperaemia) to local areas so increased heat and redness
2. Alterations in the permeability of vessels - causes leakage of plasma proteins (e.g albumin, fibrinogen and antibodies) and fluid from vessels into tissues. May be caused by direct injury to vessels or venule endothelial cell contraction caused by activated contractile proteins
= oedema manifested as swelling due to accumulation of excess extravascular fluid (known as exudate as high protein concentration)
3. Leukocytes are recruited, activated and migrate to area via a series of chemical secondary messengers and complement - accumulation of polymorphic granulocytic neutrophils which phagocytose damaged tissue and foreign material either via enzymes in the ECF of oxidative-burst prothesis

Also may cause fever due to endogenous pyrogens, lymphoid hyperplasia, malaise, nausea, anorexia and acute phase response

Front 13

What are the main differences between acute and chronic inflammation (3)?

Back 13

1. Acute is often tissue's 1st response to trauma; chronic is a long-standing response
2. Acute uses polynucleated cells e.g. neutrophils; chronic uses mononucleated cells e.g. lymphocytes
3. Acute inflammation may heal fully; chronic inflammation will never fully resolve and often causes scarring and dysfunction (e.g. intestinal stenosis (narrowing) in Crohn's)

BUT note that chronic inflammation may occur de novo (e.g. due to autoimmune disease) or alongside acute inflammation (e.g. in severe persistant inflammation)

Front 14

List 4 causes of chronic inflammation with examples

Back 14

1. Persistant infection e.g. TB, viral hepatitis
2. Prolonged exposure to toxins e.g. silica
3. Autoimmune disease e.g. coeliac's, primary biliary cirrhosis
4. Non-resolving acute inflammation e.g. bed sores

Front 15

Give 3 patterns of chronic inflammation and give an example of what may cause it

Back 15

1. Lymphocytic e.g. hepatitis, auto-immune thyroid disease
2. Granulomatous e.g TB, Crohn's
3. Mixed acute and chronic inflammation e.g. ulcerative colitis, chronic active gastritis

Front 16

What is a granuloma?

Back 16

A collection of activated macrophages characteristic of diseases such as TB and Crohn's disease

Front 17

List 4 types of cells involved in chronic inflammation

Back 17

1. Macrophages (most important - destroys and repairs tissues)
2. Lymphocytes (T cells release cytokines and B cells release antibodies)
3. Plasma cells
4. Eosinophils

Front 18

Give 4 causes of granuloma formation

Back 18

Granulomas are collections of macrophages, often making giant cells
Caused by:
1. Response to chronic (persistent) low-grade antigen stimulation
2. Delayed hypersensitivity reaction
3. Foreign material
4. Insoluble antigens

Front 19

What are the 3 main roles of macrophages?

Back 19

1. Phagocytosis
2. Cytokine production
3. Tissue repair

Front 20

What is granulation tissue?

Back 20

Key tissue involved in the healing process = specialist organ of repair
Forms on the surface of the wounds etc
Mixture of blood vessels, ECM, inflammatory cells (macrophages, myofibroblasts etc) and rich in growth factors, antibodies and fluid

Front 21

What is the difference between regeneration and repair in healing?

Back 21

Regeneration = replacement of functional differentiated cells
Repair = production of a collagen fibrous scar (usually in areas that can't replace tissues easily e.g. the heart)

Front 22

What are the 3 main processes involved in wound healing?

Back 22

1. Cellular migration
2. ECM re-organisation and remodelling
3. Cell proliferation

Front 23

List some local and general factors that may effect wound healing

Back 23

Local:
• Site
• Size
• Tissue type
• Apposition, fixation
• Infection
• Blood supply
• Foreign material
• Radiation, damage
General:
• Age
• Chronic disease
• Drugs (steroids)
• Cardiovascular status
• Dietary and vitamin status (e.g. Vit C deficiencies in Scuvy)

Front 24

What is the complement system and what principle is it based on?

Back 24

• Complement is a biochemical cascade that helps clear pathogens from an organism
• Based on a cascade of mediator formation to activate it
• Causes inflammation

Front 25

What is metaplasia and give an example of when it occurs

Back 25

A change in tissue type where mature cells/tissues changes into a completely different type, usually due to abnormal signalling
Fertile ground for dysplasia and malignancy
E.g. the epithelium of the oesophagus will change from squamous to become glandular like the stomach in Barrett's CLO (acid reflux)

Front 26

What is a tumour?

Back 26

A swelling

Front 27

What is a neoplasm?

Back 27

Abnormal growth of cells that persists even after the initiating stimulus is removed = cell growth has escaped from its normal regulatory mechanism
Can be benign or malignant

Front 28

What is hyperplasia?

Back 28

An increase in cell number

Front 29

What is hypertrophy?

Back 29

An increase in cell size

Front 30

What is atrophy?

Back 30

Decreased in cell/organ size

Front 31

What is the difference between regeneration and repair in healing?

Back 31

Regeneration = replacement of functional differentiated cells
Repair = production of a collagen fibrous scar (usually in areas that can't replace tissues easily e.g. the heart)

Front 32

What are the 3 main processes involved in wound healing?

Back 32

1. Cellular migration
2. ECM re-organisation and remodelling
3. Cell proliferation

Front 33

List some local and general factors that may effect wound healing

Back 33

Local:
• Site
• Size
• Tissue type
• Apposition, fixation
• Infection
• Blood supply
• Foreign material
• Radiation, damage
General:
• Age
• Chronic disease
• Drugs (steroids)
• Cardiovascular status
• Dietary and vitamin status (e.g. Vit C deficiencies in Scuvy)

Front 34

What is the complement system and what principle is it based on?

Back 34

• Complement is a biochemical cascade that helps clear pathogens from an organism
• Based on a cascade of mediator formation to activate it
• Causes inflammation

Front 35

What is metaplasia and give an example of when it occurs

Back 35

A change in tissue type where mature cells/tissues changes into a completely different type, usually due to abnormal signalling
Fertile ground for dysplasia and malignancy
E.g. the epithelium of the oesophagus will change from squamous to become glandular like the stomach in Barrett's CLO (acid reflux)

Front 36

What is a tumour?

Back 36

A swelling

Front 37

What is a neoplasm?

Back 37

Abnormal growth of cells that persists even after the initiating stimulus is removed = cell growth has escaped from its normal regulatory mechanism
Can be benign or malignant

Front 38

What is hyperplasia?

Back 38

An increase in cell number

Front 39

What is hypertrophy?

Back 39

An increase in cell size

Front 40

What is atrophy?

Back 40

Decreased in cell/organ size

Front 41

What is dysplasia (4)? List sites where it often occurs

Back 41

Increased cell growth - often of atypical cells
Premalignant condition = preinvasive so found in mucosa but has not broken through the basal lamina
Can be caused by genetic abnormalities or altered differentiation
Can range from mild to severe - can classify according to this
Often occurs in the cervix, bladder, stomach/oesophagus, and polyps in the colon

Front 42

What are the differences between benign and malignant neoplasms (8)?

Back 42

Benign : Malignant
1. Cells grow as a compact mass (expansile, cohesive growth) and remain at the site of origin : Cell growth is uncontrolled and cells can spread to surrounding tissues and distant sites
2. Nuclear variation in size, chromasia and shape minimal : Nuclear variation in size, chromasia and shape minimal to marked
3. Low mitotic count, normal mitosis : Low to high mitotic count, abnormal mitosis
4. Retention of specialisation of function : Loss of specialisation
5. Structural differentiation retained : Structural differentiation shows wide range of changes
6. Variable growth rate, often low : Variable growth rate, sometimes high
7. Organised : Not organised
8. No metastases : Metastases

Front 43

What is metastasis?

Back 43

Ability of malignant cells to invade into lymphatics, blood vessels and cavities and to spread to distant (non-contiguous) sites

Front 44

How are benign and malignant epithelial and connective tissue tumours named?

Back 44

Epithelial:
Benign = adenoma, papilloma
Malignant = carcinoma

Connective tissues:
Benign = -oma e.g. lipoma
Malignant = sarcoma e.g. liposarcoma

Many others e.g. myeloma = malignant cells in bone marrow

Front 45

Name 5 causes of tumours

Back 45

1. Age
2. Geography and environment
3. Heredity
• Cancer syndromes
• Familial cancers
• DNA repair
4. Preneoplasmic disorders e.g. gastritis/ulcerative colitis
5. Carcinogenic agents
• Chemicals
• Microbes
• Radiation

Front 46

List the 7 essential alterations necessary for a benign tumour to become malignant

Back 46

1. Self-sufficiency in growth factors
2. Insensitive to negative growth signals
3. Defects in DNA repair
4. Avoid apoptosis
5. Limitless replicative potential
6. Angiogenesis
7. Invade and metastasize

Front 47

What is the difference between grading and staging cancer prognosis?

Back 47

Grade = how nasty it looks under a microscope
Stage = How far it has spread e.g. Duke's