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Pathology Flashcards

1
Q

Steps of acute inflammation

A

Increased vessel calibre - inflammation cytokines (bradykinin, prostacyclin, NO) mediate vasodilation

  • Fluid exudate - vessels become leaky, fluid forced out of vessel
  • Cellular exudate - abundant in neutrophils
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2
Q

5 cardinal signs of acute inflammation

A
  • Rubor (redness due to dilation of small vessels)
  • Dolor (pain)
  • Calor (heat)
  • Tumor (swelling from oedema or a physical mass)
  • Loss of function
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3
Q

Causes of acute inflammation

A
  • Microbial infections
  • Hypersensitivity reactions
  • Physical agents
  • Chemicals
  • Bacterial toxins
  • Tissue necrosis
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3
Q

Outcomes of acute inflammation

A
  • Resolution - normal
  • Supporation - pus formation
  • Organisation - granulation tissue + fibrosis
  • Progression - excessive recurrent inflammation -> becomes chronic and fibrotic tissue
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3
Q

Neutrophil action at the site of inflammation

A
  • Phagocytosis
  • Phagolysosome + bacterial killing
  • Macrophages clear debris
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3
Q

Neutrophil action in acute inflammation

A

Margination - migrate to edge of blood vessel (plasmatic zone) due to increase in plasma viscocity and slow flow

  • Adhesion - selectins bind to neutrophil, cause rolling along the blood vessel margin
  • Emigration + diapedesis - movement out of blood vessel through or inbetween endothelium onto basal lamina and then vessel wall
  • Chemotaxis - site of inflammation
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3
Q

Chronic inflammation

A

Subsequent and prolonged response to tissue injury
- Lymphocytes, macrophages and plasma cells
- Longer onset, long lasting effects
- Autoimmune diseases

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3
Q

Macroscopic appearance of chronic inflammation

A
  • Chronic ulcer
  • Chronic abscess cavity
  • Granulomatous inflammation
  • Fibrosis
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3
Q

Causes of chronic inflammation

A
  • Resistance of infective agent
  • Endogenous + materials
  • Autoimmune conditions
  • Primary granulomatous diseases
  • Transplant rejection
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4
Q
A
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4
Q

Microscopic appearance of chronic inflammation

A
  • Lymphocytes, plasma cells and macrophages
  • Exudate is not a common feature
  • Evidence of continuing destruction
  • Possible tissue necrosis
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4
Q

Cellular cooperation in chronic inflammation

A

-B lymphocytes - transform into plasma cells and produce antibodies

  • T lymphocytes - responsible for cell-mediated immunity
  • Macrophages - respond to chemotactic stimuli, produce cytokines (interferon alpha and beta, IL1, IL6, IL8, TNF-alpha)
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4
Q

Types of granulomas

A
  • Central necrosis - TB (identified by Ziel-Neelsen stain)
  • No central necrosis - sarcoidosis, leprosy, vasculitis, Crohn’s disease
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4
Q

What are granulomas?

A
  • An aggregate of epithelioid histocytes (macrophages)
  • Granuloma + eosinophil -> parasite
  • Secrete ACE as a blood marker
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5
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A
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5
Q
A
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5
Q

Platelets

A
  • No nucleus, arise from megakaryocytes
  • Contain alpha granules (adhesion) and dense granules (aggregation)
  • Contain lysosomes
  • Activated, releasing their granules when they come into contact with collagen
  • Activation forms thrombus in intact vessels
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5
Q

What is thrombosis?

A

Solidification of blood constituents (mostly platelets) forming in vessels

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6
Q

Thrombosis formation (primary platelet plug)

A
  • Platelet aggregation, starts the coagulation cascade
  • Positive feedback loops
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6
Q

Causes of thrombosis (Virchow’s triangle, typically 2 out of these 3)

A
  • Endothelial injury (trauma, surgery, MI, smoking)
  • Hypercoagulability (sepsis, atherosclerosis, COCP, preggomalignancy)
  • Decreased blood flow (AF, immobility)
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6
Q

Arterial thrombosis

A
  • By atherogenesis and plaque rupture
  • High pressure, low pulse
  • Thin cool skin, intermittent claudication
  • Mainly made of platelets - so treat with antiplatelet (aspirin)
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7
Q

Venous thrombosis

A
  • Caused by venous stasis
  • Low pressure, high pulse
  • Rubor, tumour and pain
  • Mainly fibrin - so treated by anticoagulants (DOACs, warfarin)
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8
Q

Fate of thrombi

A
  • Resolution (dissolves and clears, normal/best case scenario)
  • Organisation (leaves scar tissue, slight narrowing of vessel lumen)
  • Recanalisation (intimal cells may proliferate, capillaries may grow into the thrombus and fuse to form larger vessels)
  • Embolism (fragments of the thrombus break off into circulation)
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9
Q

Formation of the secondary platelet plug (coagulation cascade)

A

Prothrombin -> thrombin
Fibrinogen -> fibrin

Intrinsic - 12, 11, 9, 8, 10, 1(5), 2, 1

Extrinsic - 3, 7, 10, 1(5), 2, 1

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10
Q

What is an embolism

A

A mass of material in the vascular system able to block in a vessel and block its lumen

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11
Q

Arterial vs venous embolism

A

Arterial
- Lodges in systemic circulation (from left heart)
- eg: AF thrombus lodges in carotid artery -> ischaemic stroke
Venous
- Lodges in pulmonary circulation (from right heart)
- eg: DVT thrombus embolises and lodges in pulmonary artery -> pulmonary embolism

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12
Q

Ischaemia

A

The reduction in blood flow to a tissue or part of the body caused by constriction or blockage of the blood vessels supplying it
- Effects can be reversible
- Brief attack
- Cardiomyocytes and cerebral neurons are most vulnerable

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13
Q

Infarction

A

The necrosis of part of the whole of an organ that occurs when the artery supplying it becomes obstructed
- Usually macroscopic
- Reperfusion injury = damage to tissue during reoxygenation

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14
Q

What organs are susceptible to infarcts?

A
  • Most organs as they only have a single artery supplying them
  • Liver, brain and lungs are less susceptible as they have a dual supply
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15
Q

What is atherosclerosis?

A
  • Fibrolipid plaques forming in the intima and media of systemic arteries
  • More in high pressure arteries, eg: aorta and bifurcations
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16
Q

What is in an atherosclerotic plaque?

A

Lipids (cholesterol)
- Smooth muscle
- Macrophages (+foam cells)
- Platelets
- Fibroblasts

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17
Q

What are foam cells?

A

Macrophages that phagocytose LDLs (form fatty streaks in plaque)

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18
Q

Atherosclerosis formation

A
  • Macrophages form foam cells from lipids in arterial wall - fatty streak formation (platelets) > intermediate lesion
  • Plaque protrudes into artery lumen and disrupts laminar flow - medial thinning and platelet aggregation
  • Secondary platelet plug forms fibrin mesh over itself and traps red blood cells
  • Fibroblasts form smooth muscle ‘fibrous cap’ over this
  • Continuous formation of secondary platelet plug, this is a stable atheroma - plaque stabilisation/( fibrous cap formation)
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19
Q

Risk factors for atherosclerosis

A
  • Smoking
  • High bp
  • Hyperlipidemia
  • Increasing age
  • Male
  • Poorly controlled diabetes mellitus

(all risk factors for MI!!)

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20
Q

Complications of atherosclerosis

A
  • Cerebral infarction
  • Carotid atheroma, leading to TIAs and cerebral infarcts
  • MI
  • Aortic aneurysm
  • Peripheral vascular disease
  • Gangrene
  • Cardiac failure
  • Ischaemic collitis in colon
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21
Q

Preventative measures for atherosclerosis

A
  • Smoking cessation
  • Blood pressure control
  • Weight reduction
  • Low dose aspirin
  • Statins
  • Control diabetes
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22
Q

What is apoptosis?

A

Non-inflammatory, controlled cell death in single cells
- Cells shrink, organelles retained, CSM intact
- Chromatin unaltered, fragmented for easy phagocytosis

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23
Q

What is necrosis?

A

Induces inflammation and repair, traumatic cell death
- Cells burst, organelles splurge, CSM damaged
- Chromatin altered, cell is f*cked

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24
Q

Intrinsic apoptosis mechanism

A
  • Bax is a protein, inhibited by BCl-2 gene
  • It acts on mitochondrial membrane to promote cytochrome C reusase
  • This activates caspases
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25
Q

Extrinsic apoptosis mechanism

A

Fas-L or TNF-L binds to CSM receptors which activate caspases

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26
Q

Cytotoxic apopstosis mechanism

A
  • CD8+ binding releases Granzyme B from CD8+ cells
  • Granzyme B -> Perforin -> Caspases
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27
Q

Types of necrosis

A

Coagulative, liquifactive, caseous and gangrene

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28
Q

Coagulative necrosis

A
  • Most common type
  • Can occur in most organs
  • Caused by ischaemia
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29
Q

Liquefactive necrosis

A

Occurs in the brain due to its lack of substantial supporting stroma

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30
Q

Gangrene necrosis

A
  • Necrosis from rotting of the tissue
  • Affected tissue appears black due to deposition of iron sulphide from degraded haemoglobin
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31
Q

Caseous necrosis

A

Causes a cheese pattern
- eg: TB

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32
Q

What is inflammation?

A

Acute/chronic tissue injury response

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32
Q

What is hypertrophy?

A
  • Increase in cell size without cell division
  • eg: skeletal muscle
33
Q

What are polymorphs?

A
  • What neutrophils are referred to as sometimes
  • Because they have a varying number of lobulated nuclei
34
Q

What is hyperplasia?

A
  • Increase in cell number by mitosis
  • eg: bone marrow at high alititudes, prostate at older age
35
Q

What is atrophy?

A
  • Decrease in tissue/organ size caused by a decrease in the number or size of constituent cells
  • eg: brain in Alzheimer’s, muscular atrophy in ALS
36
Q

What is metaplasia?

A

-The change in differentiation of a cell from one fully-differentiated cell type to another
- eg: GORD (squamous -> columnar epithelia)

37
Q

What is dysplasia?

A

Morphological changes seen in cells in the progression to becoming cancer

38
Q

What is carcinogenesis?

A

Transformation of normal cells to neoplastic (malignant) cells through permanent genetic alterations or mutations

39
Q

What is a neoplasm?

A

An autonomous, abnormal and persistent growth

40
Q

What is a tumour?

A

Any abnormal swelling; neoplasm, inflammation, hypertrophy, hyperplasm

41
Q

What can a neoplasm arise from?

A
  • Nucleated cells
  • So can’t arise from erythrocytes but can arise from their precursor
42
Q

Properties of benign tumours

A

Non-invasive
- Localised
- Slow growth rate, low mitotic activity
- Close resemblance to normal tissue
- Well circumscribed
- Rare necrosis and ulceration
- Growth on mucosal surfaces
- Often exophytic (outward growth)

43
Q

Properties of malignant tumours

A
  • Invasive
  • Rapid growth rate, high mitotic activity
  • Poorly defined + irregular border
  • Hyperchromatic and pleomorphic nuclei
  • Common necrosis and ulceration
  • Growth on mucosal surfaces and skin
  • Often endophytic (inward growth)
44
Q

Complications of benign tumours

A
  • Hormone secreting (eg: prolactinoma)
  • Pressure on local structures (eg: pituitary -> optic chiasm)
  • Obstruct flow
  • Transformation to malignant neoplasm
  • Anxiety
45
Q

Complications of malignant tumours

A
  • All of the issues of benign tumours +
  • Destroy surrounding tissue
  • Metastasise (spread around the body)
  • Blood loss from ulcers
  • Pain
  • Paraneoplastic (eg: SCLC, SIADH)
  • Form secondary tumours
46
Q

Benign epithelial neoplasms

A
  • Papilloma - non-glandular, non-secretory, eg: squamous cell papilloma
  • Adenoma - glandular, secretory, eg: colonic adenoma
47
Q

Malignant epithelial neoplasms (carcinomas)

A

glandular epithelium -> adenocarcinoma
eg: urothelial carcinoma

48
Q
A
49
Q

Malignant connective tissue neoplasms

A
  • Lipoma - adipocytes
  • Chondroma - cartilage
  • Osteoma - bone
  • Angioma - vascular
  • Rhabdomyoma - striated muscle (rare)
  • Leiomyoma - smooth muscle (more common)
  • Neuroma - nerves

Same as benign ones, but followed by ‘sarcoma’ instead of ‘myoma’

49
Q

adipocytes
cartilage
bone
vascular
- striated muscle (rare)
- smooth muscle (more common)
- nerves

A
  • Lipoma - adipocytes
  • Chondroma - cartilage
  • Osteoma - bone
  • Angioma - vascular
  • Rhabdomyoma - striated muscle (rare)
  • Leiomyoma - smooth muscle (more common)
  • Neuroma - nerves
49
Q

Host factors for cancer

A
  • Race
  • Diet
  • Age
  • Gender
  • Inheritance
  • Premalignant lesions
  • Transplacental exposure
49
Q

What is a tumour called where the cell origin is unknown?

A

Anaplastic

49
Q

Metastasis pathway

A
  1. Detachment of tumour cell
  2. Invasion of surrounding connective tissue
  3. Intravasation into blood vessels
  4. Evasion of host defence mechanisms
  5. Adherance to endothelium at a remote location
  6. Extravasation to distant site
  7. Angiogenesis - growth of own blood supply
49
Q

Benign connective tissue neoplasm

A
  • Lipoma - adipocytes
  • Chondroma - cartilage
  • Osteoma - bone
  • Angioma - vascular
  • Rhabdomyoma - striated muscle (rare)
  • Leiomyoma - smooth muscle (more common)
  • Neuroma - nerves
49
Q

Tumour differentiation grading

A
  • Graded based on similarity to parent cell
    1. >75% cells resemble parent - well differentiated
    2. 10-75%
    3. <10% cells resemble parent - poorly differentiated
49
Q

Other tumours

A
  • Melanoma (melanocyte malignancy)
  • Mesothelioma (mesothelial malignancy - typically pleural)
  • Teratoma - cancer of all 3 embryonic germ layers
  • Blastoma - embryonal tumours
49
Q

Lymphoid tumours (always malignant)

A
  • Leukemia, lymphoma
  • Need to be treated by systemic chemotherapy
49
Q

Eponymously named tumours (people names)

A
  • Burkitt’s lymphoma (B cell malignany cause by EBV)
  • Kaposi sarcoma (vascular endothelial malignancy, HIV associated)
  • Ewing’s sarcoma (bone malignancy)
49
Q

Characteristics of the neoplastic cell

A

Autocrine growth stimulation (overexpression of GF and mutation of tumour suppressor genes, eg: p53, and underexpression of growth inhibitors)
- Evasion of apoptosis
- Telomerase - prevents shortening of telomeres with each replication

49
Q

Classes of carcinogens

A
  • Chemical - eg: paints, dyes, rubber, soot
  • Viruses - eg: EBV, HPV
  • Ionising and non-ionising radiation - eg: UVA and UVB, ionising radiation
  • Hormones, parasites, mycotoxics - eg: high oestrogen, anabolic steroids
  • Misc - eg: asbestos, arsenic
49
Q

Methods of cancer spread

A
  • Haematogenous - via blood, bone, breast, lung, liver
  • Lymphatic - secondary formation in lymph nodes
  • Transcolemic - via exudative fluid accumulation, spread through pleural, pericardial, peritoneal effusions
50
Q

Method of spread for sarcomas (mesenchymal cells)

A

Mostly haematogenous

50
Q

Method of spread for carcinomas (epithelial cells)

A
  • Mostly lymphatic
  • Exceptions: follicular thyroid, choriocarcinoma, RCC, HCC
50
Q

Tumour staging

A
  • Spread determined by histopthological and clinical examination
  • TNM: primary tumour, lymph node, metastases
  • Different for leukemias, lymphomas and CNS cancers
50
Q

Screening in the UK

A
  • Cervical cancer (cervical swab test)
  • Breast cancer (mammogram)
  • Colorectal cancer (fecal occult)
  • Heel prick test at birth for sickle cell, CF and hypothyroid
50
Q

Mutation involved in colorectal cancer

A
  • FAP (familial adenamatous polyposis)
  • HNPCC (lynch syndrome)
50
Q

Which tumours are most likely to metastasise via bone?

A

Breast
Lung/lymphoma
Thyroid
Kidney
Prostate

…and multiple myeloma

51
Q

FAP (mutation in colorectal cancer)

A
  • Autosomal dominant
  • Mutated APC (adenomatous polyposis coli) gene, millions of colorectal adenomas inevitable
  • Adenocarcinoma by 35 years old
  • Overexpression of x-MYC and point mutation in KRAS
51
Q

HNPCC (mutation in colorectal cancer)

A
  • Autosomal dominant
  • Mutated MSH gene
  • Involved in DNA mismatch repair
51
Q

Lifespan of neutrophil polymorphs

A

2-3 days

52
Q

Cellular sequence of acute inflammation

A
  • Injury or infection
  • Neutrophils arrive and phagocytose and release enzymes
  • Marophages arrive and phagocytose
  • Either resolution with clearance of inflammation or progression to chronic inflammation
53
Q

Examples of acute inflammation

A
  • Acute appendicitis
  • Frostbite
  • Streptococcal sore throat
  • Lobar pneumonia
54
Q

Treating inflammation

A
  • Ice/cold
  • Antihistamines
  • Aspirin/ibuprofen - inhibit prostaglandins
  • Corticosteroids - upregulate inhibitors of inflammation and downregulate chemical mediators of inflammation
55
Q

What is the acute mediator of inflammation?

A

Histamine

56
Q

Ischaemia vs infarction

A

Ischaemia - reduction in blood flow
Infarction - reduction in blood flow with subsequent cell death

57
Q

Endothelial damage theory for atherosclerosis

A

Endothelial cells are delicate
- Easily damaged by cigarette smoke, shesring forces as arterial divisions, hyperlipidemia, glycosylation products

58
Q

p53 DNA damage pathway

A

Resting cell. Is there DNA damage?

Yes- apoptose
No- divide

59
Q

Apoptosis in HIV

A
  • Can induce apoptosis in CD4 helper cells
  • Reduces their numbers enormously to produce an immunodeficient state
60
Q

Examples of necrosis-

A

Infarction due to lack of blood supply
- Frostbite
- Toxic venom from reptiles and insects
- Pancreatitis
- Avascular necrosis of bone- cuts off blood supply

61
Q

Why do we get deafer as we get older?

A

Hair cells in cochlea can’t divide

62
Q

Basal cell carcinoma

A
  • The skin only invades locally
  • Can be cured by complete local excision
63
Q

What is adjuvant therapy?

A

Extra treatment given after surgical excision
Eg: radiotherapy in breast cancer

64
Q

Example of chronic inflammatory process from the start

A

Infectous mononucleosis

65
Q

Metaplasia in smoking

A

Cilliated bronchial epithelium with mucocillary escalator -> squamous epithelium

66
Q

What is oncogenesis?

A

What is oncogenesis?
The transformation of normal cells to benign or malignant tumours through permanent genetic alterations or mutations

67
Q

Carcinogen definitions

A

Carcinogenic = cancer causing
Oncogenesis = tumour causing
Mutagenic = act on DNA

68
Q

Types of carcinoma

A

In situ and invasive

69
Q

Angiogenesis promoters (new blood vessels)

A
  • Vascular endothelial growth factor
  • Basic fibroblast growth factor
70
Q

Angiogenesis inhibitors

A
  • Angiostatin
  • Endostatin
  • Vasculoatatin
71
Q

Tumours that are most likely to metastasise to the lung

A

Sarcomas, any common cancers

72
Q

Tumours that are most likely to metastasise to the liver

A
  • GI tract tumours
  • Carcinoid tumours lf intestine
  • Pancreatic
  • Breast
  • Bronchial
72
Q

Cons of conventional chemotherapy

A
  • Not selective for tumour cells
  • Targets other cells, causing hair loss, diarrhoea and myelosuppresion
72
Q

What tumours is chemotherapy good for?

A

Fast dividing ones:
- Germ cell tumours of testis
- Acute leukemia
- Lymphomas
- Embryonal paediatric tumours
- Choriocarcinoma

73
Q

What is targeted chemotherapy?

A
  • Exploits some difference between cancer cells and normal cells to target drugs to the cancer cells
  • More effective
  • Less side effects
74
Q

Arterial ulcers

A
  • Punched out holes
  • Little exudate
  • Tips of toes + lateral maleolus
  • Pale cool skin
  • Low distal pulse
  • Peripheral vascular disease
75
Q

Venous ulcers

A
  • Less demarcated
  • Lots of exudate
  • Medial malleolus + inner calf
  • Warm erythematous skin
  • Deep vein thrombosis
76
Q

Stages of atherogenesis

A
  1. Endothelial demage
  2. Fatty streaks
  3. Intermediate lesions
  4. Fibrous plaques/advanced lesions
  5. Plaque erosion
  6. Plaque rupture
77
Q

Cell wall and nucleic acid synthesis (MEMORISE)

A

antibiotics picture thing

78
Q

Risk factors for developing tuberculosis

A
  • HIV
  • Born in high prevalance area
  • Close contact with TB positive person
  • Children under 5
  • History of TB
  • Immunosippression
  • Homelessness
  • Prison
  • Excessive alcohol
  • IVDU
  • Smokers
  • Co-morbidities
  • Diabetes
  • End stage CKD receiving RRT
  • Malignancy
79
Q

Which cell type is the primary receptor for HIV?

A

CD4+
Retroviral therapy targets within this cell type:
- Fusion/entry inhibitors
- Reverse transcriptase inhibitors
- Integrase inhibitors
- Protease inhibitors

80
Q

What blood markers are secreted in sarcoidosis?

A

ACE and calcium

80
Q

When does apoptosis take place?

A
  • Development - removal of cells during development, eg: interdigital webs
  • Cell turnover - removal of cells during normal turnover, eg: cells in the intestinal villi at the tips are replaces by cells from below
80
Q

Cells that regenerate

A
  • Hepatocytes
  • Pneumocytes
  • All blood cells
  • Gut epithelium
  • Skin epithelium
  • Osteocytes

Haroon flashcards (10 decks)

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