Intro to Clinical Sciences Flashcards
Pathology:
Acute inflammation vs. Chronic inflammation
Cells involved?
Onset?
Duration?
Resolves?
Acute: Neutrophil inflammation
- Sudden onset
- Short duration
- Usually resolves
Chronic: Leukocyte inflammation
- Slow onset/follows acute
- Long duration
- May never resolve
Pathology:
Inflammatory cells
Mobile inflammatory cells? (3)
Other cells involved in inflammation? (2)
Neutrophils - pus cells (suppuration)
- short lived
- first on scene
- phagocytic, lysosomal granules, release cytokines/chemokines to attract inflammatory cells
Macrophages
- long lived
- phagocytic, antigen presenting cells
Lymphocytes
- long lived
- release cytokines/chemokines to attract inflammatory cells
- IMMUNOLOGICAL MEMORY
Endothelial cells
- become sticky (allow adhesion) in areas of inflammation
- become porous (allow cell migration)
- grow into areas of damage to form new vessels
- capillaries open (normally shut) in inflammation = redness
- oedema = oncotic pressure in tissues due to migration of plasma proteins
Fibroblasts
- Long lived
- Form collagen (scarring) in areas of chronic inflammation
Pathology:
Example of Acute and Chronic inflammation
Acute = Acute appendicitis
- Generalised pain around epigastric region then progresses to…
- Right lower quadrant/McBurney’s point sharp pain = inflammation reaches abdominal wall
Chronic = Tuberculosis
- Granulomas - mycobacteria
- No initial inflammation
- Fibrosis occurs
Pathology:
Treatment for Inflammation
NSAIDs: Ibuprofen, Aspirin (COX inhibitors)
Corticosteroids: Immune modulators
MOABs - targeted immune therapies
Pathology:
Resolution vs. Repair
Resolution:
- Initiating factor removed
- Tissue undamaged
- Regeneration
Repair:
- Initiating factor still present
- Tissue damage
- No regeneration
- Replacement by collagen (fibroblasts)
e. g. - Heart after MI
- Brain after cerebral infarction
- Spinal cord after trauma
Pathology:
Cells that regenerate?
Cells that cannot regenerate?
Cells that regenerate:
- Hepatocytes
- Pneumocytes
- All blood cells
- Gut epithelium
- Skin epithelium
- Osteocytes
Cells that cannot regenerate?
- Myocardial cells
- Neurones (CNS)
Pathology:
Define:
Thrombus
Thrombosis
Embolus
Embolism
Thrombus = blood clot within a vessel
Thrombosis:
Formation of a solid mass from blood constituents in an intact vessel in a living person
Causes laminar flow to be turbulent if larger enough can occlude
(Verkov’s Triangle)
Embolus = anything that causes embolism
Embolism:
Process of a solid mass (e.g. thrombus/air/fat) in the blood being carried in the circulation to a place it becomes stuck and occludes the vessel
e.g. a deep venous thrombosis of the leg veins which breaks off and embolises through the large veins and right side of the heart to the lungs
Pathology:
Define:
Ischemia
Infarction
Reperfusion injury
Ischemia = reduction in blood flow
Infarction = death of cells due to reduction in blood flow
Reperfusion injury = injury by superoxide radicals due to cellular response to elevated O2
Pathology:
Myocardial infarction is an example of…?
Which organs have dual blood/collateral supply?
Areas more susceptible to infarction?
End artery ischemia
Liver, Lungs, Brain - so infarctions are less likely to be fatal due to redundancy
Watershed ares - area boundary of adjacent arterial territories
Pathology:
Define.. Metaplasia Hyperplasia Dysplasia Neoplasia Atrophy Hypertrophy
Example for each?
Metaplasia – Transition from one cell type to another
e.g. metaplasia in bronchi of a smoker
Hyperplasia – increase in the number of cells within a tissue
e.g. Prostate gland – benign prostate hyperplasia
Dysplasia – Abnormal cell population
Neoplasia – Malignant new cells
Atrophy - Decrease in size of a tissue due to loss of number of cells
Hypertrophy - Increase in the size of a tissue caused by increase in size of constituent cells
e.g. Muscle atrophy/hypertrophy
Gastritis Common cause? Cell population? Cell type shift? Cancer risk?
Inflammation of the stomach
Helicobacter infection (Urea breath test, stain cells to diagnose)
Chronic or acute infection
Giant cells = lots of macrophages
Chronic gastritis increases risk of lymphoma
Atherosclerosis
Define
Where?
What’s in plaque?
Endothelial damage theory?
Build up of sclerotic plaque within arteries
Never within low pressure Common in high pressure
Early stage (reversible) - fatty streaks
Plaque = fibrous tissue, lipids, lymphocytes
Endothelial damage theory
- Free radicals, nicotine, carbon monoxide all damage (smoking) (vaping = fewer ROS but same nicotine)
- Hypertension = shearing forces on endothelial cells
- Poorly controlled diabetes = superoxide anions damage
- Hyperlipidaemia = direct damage to endothelial cells
- Pathogenesis
Recurrant endothelial cell injury
Pathology:
Define Apoptosis
Apoptotic detector protein?
Define Necrosis
Types of necrosis?
Apoptosis – programmed cell (singular) death due to apoptotic switch
e.g. DNA damage
P53 - gatekeeper of genome
Necrosis - traumatic cell death (multiple cells)
e.g. Frostbite, avascular necrosis
Types
Coagulative necrosis – thick and gooey
Liquefactive necrosis – (cerebral infarction)
Caseous necrosis – (Tuberculosis)
Pathology:
Define and give an example for:
genetic disease
congenital disease
acquired disease
Genetic disease - occurs primarily from a genetic abnormality
e.g. Sickle cell anaemia is caused by a point mutation in the β-globin chain of haemoglobin
Congenital disease - disease present at birth; can be genetic disease but also acquired
e.g. Rhesus haemolytic disease of the newborn
Acquired disease– disease occurs after birth; genetic and nongenetic environmental factors
e.g.
Pathology:
Give examples of pathology of ageing - Diagram!
Progeria = increased aging disease
- Cross-linking or mutations of DNA
- Telomere shortening: Hayflick limit
- Time-dependent activation of ageing/death genes
- Free radical accumulation
- Cross linking of proteins
- Loss of DNA repair mechanism
Pathology:
Common sites of carcinoma metastasis
Define adjuvant therapy
- Lymph nodes (drainage route)
- Bone, brain, liver (through the blood)
Adjuvant therapy = extra treatment given following surgical excision
e.g. radiotherapy to breast after lumpectomy
minimise the risk of micro metastases
Patholgy:
Define:
- Carcinogenesis
- Oncogenesis
- Benign/Malignant tumour
Carcinogenesis - The transformation of normal cells to neoplastic cells (cancer) through permanent genetic alterations or mutations - MULTISTEP
Oncogenesis – Formation of benign and malignant tumours (tumour = cancer in solid tissue)
Benign tumour – a growth that is not cancer and does not invade or destroy nearby tissue
Malignant tumour – a growth which is cancer and can invade and metastasise
Pathology:
Carcinogenesis is…?
Period exposure/cancer?
Classes of carcinogenesis
Multistep process Typically a latent interval between exposure and cancer Classes: - Chemical - Radiation (non and ionising) - Biologic (hormones, parasites, mycotoxins - Viral - Host
Pathology:
Define;
Carcinoma
Sarcoma
Neoplasm
Carcinoma – cancer of the epithelium
Sarcoma – malignancy of connective tissue
Neoplasm – lesion resulting from the autonomous or relatively autonomous abnormal growth of cells which persist after the initiating stimulus has been removed – new growth
Pathology:
Structure of a neoplasm?
Maximum size before it must recruit vasculature to grow?
- Neoplastic cells
o derived from nucleated cells – need DNA
o Synthetic activity is related to the parent cell (Thyroid cell still produces thyroxine)
o Growth pattern related to parent cell
o Monoclonal
Within Stroma
o Connective tissue framework (fibrin, collagen)
o Vasculature
o Neoplasm drives the formation of its stroma to nurture itself
2mm
Pathology:
Neoplasm behavioural classification
Histogenesis classification Papilloma? Adenoma? Carcinoma? Adenocarcinoma?
1) Benign - localised/non-invasive, slow growth, close resemblence to normal tissue
2) Borderline - defy binary like ovarian lesions
3) Malignant - invasive, metastasise, rapid growth, irregular border
The cell specific cell origin of a tumour
Neoplasm = …oma
Prefix depend on cell type
Papilloma
Benign neoplasm of squamous epithelium
Adenoma
Benign tumour of glandular or secretory epithelium
Carcinoma = Malignant tumour of epithelial cells
Prefix it with name of epithelial cell e.g. transitional cell carcinoma
Adenocarcinoma = carcinoma of glandular epithelium
Pathology:
In-situ neoplasia
What is invasion dependent on?
Define metastasis
In-situ neoplasia = epithelial neoplasms - no invasive carcinoma = no spread
Invasion = metastatic capaility
Invasion dependent on:
- decreased cellular adhesion
- increased cellular motility
- production of lytic enzymes degrade surrounding tissue
Metastasis is the process by which a malignant tumour spreads from its primary site to produce secondary tumours at distant sites
Pathology:
Routes of metastasis, via:
Blood vessels?
Lymphatics?
Due to surgery?
Blood vessels = Haematogenous
Lymphatics = Trans-coelomic
Surgery implantation = iatrogenic
Pathology:
Metastatic cascade (Diagram test) Haematogenous
Haematogenous metastasis:
1) Intravasation
2) Evasion of host immunity
3) Extravasion
4) Growth at metastatic site
5) Angiogenesis
Pathology:
Routes of metastasis
- Vein invasion
- From colon
Appearance of bone mets on X-ray?
Vein:
Vena cava - right side of the heart - Lung mets
Can reinvade (PV -> LA/LV -> Aorta) and spread all around the body
Colon:
Portal vein to liver = hepatic mets
“moth eaten bone”
Immunology:
Describe:
Innate immunity
Adaptive immunity
II – Instictive, non-specific, present from birth, barrier to antigen, Slow response, No memory
AI – Specific, acquired immunity, lymphocyte/antibody dependent, quick response
Immunology:
Describe separated blood:
Plasma
Buffy coat
Red layer
Plasma = straw coloured (90% water, electrolytes, proteins, lipids and sugars)
Buffy coat is Leukocytes (WBCs)
Haemtocrit: Erythrocytes (RBC) volume
Platelets
Immunology:
3 Polymorphonuclear leukocytes?
3 Mononuclear leukocytes?
Poly: Neutrophils, Eosinophils, Basophils
Mono: Monocytes (mature to macrophage in tissue), B-cells (mature to plasma cell), T-cells (CD4+, CD8+, Th17, T-regs
Immunology:
Humoral factors
Actions of complement (3) ?
Which complement carries out each function?
Direct lysis (MAC – membrane attack complex)
Chemotaxis - Attract leukocytes (C3a + C5a)
Opsonisation (C3b)
