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Pase 2a Notes > Intro To Clinical Sciences > Flashcards

Intro To Clinical Sciences Flashcards

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1
Q

2 types of modern autopsies

A

Hospital < 10%
- for audit, teaching, research
Medico-legal > 90%
- Coronial for standard
- forensic for crime

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2
Q

Types of deaths referred to coroner

A

Presumed natural - cause not known / not seen by doctor for 14 days
Presumed iatrogenic - Illegal Abortion, peri/post operative, anaesthetic, complication of therapy
Presumed unnatural - accident, Industrial, Suicide, neglect, custody

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3
Q

Who makes referrals?

A

GMC
Registrar of BDM
Relatives
Police
Pathologycal technicians
Other properly interested parties

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4
Q

5 main coronial laws

A

Coroners Act1988 - allows natural or unnatural death autopsies
Coroners Rules 1984 - autopsy ASAP on suitable premise and report immediately
Amendment Rules. 2005 - Choice and precise record of tissue retention
Coroners Justice Act 2009 - conclusions not verdicts
Human Tissue Act 2004 - more consent and only on licensed premises

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5
Q

Most deaths are:

A

From natural causes performed by medico-legal authority

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6
Q

Role of coronal autopsy to answer 4 Qs

A

Who was the deceased
When did they die
Where did they die
How did their death come about

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7
Q

Who performs autopsies?

A

Histopathologist - hospital + coronial e.g. fire, road traffic, suicide, drowning

Forensic pathologist - coronial e.g. homicide, neglect, custody

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8
Q

3 steps of an autopsy

A

External examination - Identification, Injuries and disease
Evisceration - Yshaped incision to remove all organs
Internal examination - View all but GI

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9
Q

Define inflammation

A

Local physiological response to tissue injury or infection involving inflammatory cells such as neutrophils and macrophages

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10
Q

Adv and Dis of Inflammation

A

Adv - destructs invading microorganisms and walls of abscess to prevent spreading.
Dis
- Autoimmunity
- An over reaction (TB)
- May compress vital structures
- Chronic inflammation leads to fibrosis distorting tissue permanently

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11
Q

Acute vs Chronic inflammation

A

Acute- Sudden onset, short duration and resolves
Chronic - Slow onset, long duration, May never resolve

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12
Q

What cells are involved in inflammation?

A

Neutrophils
Macrophages
Lymphocytes
Endothelial cells
Fibroblasts

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13
Q

Describe neutrophil polymorphs

A

First on scene for acute inflammation and release chemicals that attracts other inflammatory cells.

Short lived and dies at scene
Nucleus has many lobes and cytoplasmic granules release analytic enzymes
Mobile and phagocytic

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14
Q

Describe macrophages

A

Binds to specific antibodies and phagocytoses bacteria and debris.
May present antigen to lymphocytes and called differently (liver = kupffer)

Long lived with big round nucleus
(May be brown due to ingesting iron)

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15
Q

Describe lymphocytes

A

Produces chemicals which attract other inflammatory cells and may become plasma cells = memory + antibodies

Long lives and big nucleus with little cytoplasm

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16
Q

Describe endothelial cells in infection

A

Become sticky so inflammatory cells adhere to capillary lining. Also becomes porous to allow cells to pass into tissue and grows into damaged areas = new vessels
Capillary sphincters open so more blood= more inflammatory cells to area

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17
Q

Describe fibroblasts

A

Long lived cells switched on in inflammation to form collagen in areas of chronic inflammation and repair

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18
Q

Causes of acute inflammation

A

Microbial infections - virus, bacteria
Hypersensitivity reactions - excess
Physical agents - UV, trauma
Chemicals - corrosive
Bacteria toxins
Tissue necrosis - infarction

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19
Q

Steps during acute inflammation (appendicitis)

A

Unknown precipitating factor
Neutrophils appear
Blood vessels dilate
Capillary sphincters open
Inflammation of Serosa surface
Pain felt
Appendix bursts or removed

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20
Q

4 Outcomes of acute inflammation

A

Resolution - complete restoration
Suppuration - formation of pus, mixture of dead neutrophils, bacteria and cellular debris
Organisation - tissue replacement by fibrosis then granulation (scarring)
Progression to chronic inflammation

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21
Q

3 processes of response to acute inflammation

A

Change in vessel calibre or flow (dilation)
Increased vascular permeability + formation of exudate
Emigration of neutrophils into extra vascular space

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22
Q

Causes of chronic inflammation

A

Primary chronic inflammation
Transplant rejection
Progression from acute
Recurrent episodes of acute

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23
Q

Steps during chronic inflammation (tuberculosis)

A

No initial acute inflammation
Waxy cell wall mycobacteria ingested by macrophages (mostly fails)
Lymphocytes and macrophages appear
Fibrosis occurs

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24
Q

Granuloma definition

A

A collection of epithelia histiocytes (macrophages) surrounded by lymphocytes
= Have a specific appearance

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25
Definition of granulation tissue
Small blood vessels in a connective tissue matrix with myofibroblasts, contracts to reduce wound size
26
How to treat inflammation?
Ice closes capillaries and swelling Ibuprofen inhibits prostaglandin release (chemical mediators of inflammation) Antihistamines Anti-inflammatories Corticosteroids Antibiotics
27
Macroscopic appearance of acute inflammation
Red - dilation Heat - hyperaemia Swelling - exudate oedema Pain - distortion of tissue Loss of function
28
Define repair vs resolution
Repair - Initiating factor still present and damaged tissue is replaced by fibrous tissue + collagen produced by fibroblasts Resolution - Initiating factor removed and tissue undamaged or able to regenerate
29
Example of repair vs resolution
Repair - liver cirrhosis (drinking every day starts fibrotic repair) or Covid (alveolar walls are damaged) Resolution - Lobar pneumonia (pneumocytes lining alveoli can regenerate)
30
Normal abrasion healing
Scab formed over surface Epidermis grows from adnexa produced by scab Thin confluent epidermis Final epidermal regrowth
31
1st vs 2nd Intention healing
1st - suture skin together so fibrin then collagen fills gap 2nd - when skin is lost, granulation tissue (capillaries + endothelial) grow from both sides
32
Cells that can regenerate
Hepatocytes Pneumocytes All blood cells Gut epithelium Skin epithelium Osteocytes
33
Cells that don’t regenerate
Myocardial cells Neurones
34
Define organisation in inflammation
Formation of fibrovascular connective tissue by production of granulation tissue and phagocytosis of dead tissue
35
Define thrombosis
A solid mass of blood constituents formed within an intact vascular system during life
36
Why are clots rare?
Laminar flow - cells travel in centre of arterial vessels Endothelial cells - not sticky when healthy
37
How is a thrombosis formed?
Damage to endothelial cells exposes collagen underneath and as platelets stick, they release chemicals which cause aggregation. RBCs also get trapped and clotting factors produce fibrin to bind cells. Positive feedback causes thrombosis to completely block vessel.
38
What is Virchow’s triad?
Causes of thrombosis: Change in vessel wall (smoking) Change in blood flow (stasis) Change in blood constituents (clotting factors)
39
What is prescribed to reduce risk of thrombosis?
Aspirin - inhibits platelet aggregation
40
Define an embolus
Mass of material in the vascular system able to become lodged within a vessel and block it (Occurs via embolism)
41
Causes of an embolus
Air Tumour Amniotic fluid Fat (severe trauma) DVT Bacteria Intravenous drug use
42
What happens to an embolus in arterial vs venous system
Arterial - travels anywhere downstream Venous - lodges in pulmonary arteries
43
Define ischaemia
Reduction in blood flow to a tissue without any other complications (Can be due to an embolism, can be restored and means cells further away die from low oxygen)
44
Define infarction
A reduction of blood flow with subsequent death of cells
45
What is an end artery supply?
Organ that receives blood from only one artery (Problematic as thrombus leads to infarction)
46
Define an atheroma
Fatty material forms deposits and damages arterial walls, leading to restriction of circulation and risk of thrombosis. This then establishes an atherosclerosis
47
Distribution of atherosclerosis
Common in high pressure systems (aorta + systemic arteries) and never in low (pulmonary arteries)
48
What is in an atheroma plaque?
Fibrous tissue like collagen Lots of cholesterol crystals Surrounded by lymphocytes
49
Mechanism of atherosclerosis formation
Endothelial damage theory - Cannot produce nitric oxide (inhibits platelet aggregation) so fatty streaks in intima and migration of leukocytes cause more endothelial cells to form over the thrombosis.
50
Risk factors of atherosclerosis
Smoking - nicotine, free radicals and CO damage endothelial High BP - shearing force on cells Diabetes - damage cells Hyperlipidaemia -high cholesterol damages cells
51
Define apoptosis
Programmes cell death
52
Triggers of apoptosis
DNA damage is constantly monitored before replication. If molecules like p53 detect damage, capsase enzymes digest DNA, nuclear membrane and other organelles
53
Apoptosis in diseases and development
Disease - HIV = virus injects genetic and too much apoptosis - Cancer = lack of apoptosis Development - Apoptosis avoids web-like fingers - Duodenal villi cells wear out, apoptose and are replaced
54
Define necrosis
Traumatic cell death in an organ or tissue
55
Examples of necrosis
Toxic spider venom Frostbite Cerebral infarction Pancreatitis Avascular necrosis of bone
56
When do most chromosome abnormalities occur?
Early after conception leading to loss of zygote
57
Single vs polygenic gene disorder
Abnormality of a single gene causes disease Vs Interaction of several different genes cause disease
58
What are homebox genes?
Contain information about migration of cells
59
Examples of growth disorders
Cleft lip palate Spina bifida Meningocele VSD / Hole in heart
60
Congenital vs inherited
Inherited - caused by an inherited genetic abnormality Continental - present at birth (not always inherited e.g. club foot)
61
Example of late onset
May not manifest until later life e.g. Huntingtons
62
Acquired diseases
Caused by non-genetic environmental factors, but may be congenital e.g. foetal alcohol syndrome
63
Hypertrophy vs Hyperplasia
Increase in size of a tissue caused by an increase in: Hypertrophy - size of constituent cells e.g. skeletal muscle in bodybuilders Hyperplasia - number of constituent cells E.g. benign prostatic
64
Combined Hypertrophy and hyperplasia can occur where?
In smooth muscle of uterus during pregnancy
65
Define atrophy
Decrease in size of a tissue caused by a decrease in number of, constituent cells, size or both E.g. cerebral atrophy in dementia
66
Define metaplasia
Change in differentiation of a cell from one fully - differentiated type to another E.g. Barrett’s oesophagus
67
Define dysplasia
Morphological changes seen in cells in the progression to becoming cancer (Seen in biopsies with abnormal architecture and arrangement)
68
Describe the hayflick limit
Telomeres at the end of chromosomes allow DNA to unwind for replication, but gets shorter each replication - limiting the number of divisions that occur = ageing
69
What happens in dermal elastosis?
Prolonged UV-B light causes protein cross-linking and accumulation of abnormal elastic in dermis of skin (wrinkles)
70
What happens in osteoporosis?
Increased bone resorption or decreased bone formation due to a lock of oestrogen. Can cause wide holes and osteopenia which fractures easily
71
What happens in cataracts?
UV-B light causes protein cross-linking and formation of opaque proteins in the lens which leads to loss of elasticity
72
What happens in senile dementia?
Plaques and neurofibrillary tangles occur
73
What happens in deafness?
Loss of delicate hair cells in cochlea (cannot divide/regenerate)
74
What happens in sarcopenia?
Loss of muscle due to decreased growth hormone, decreased testosterone and increased catabolic cytokines. E.g. causes falls
75
NSAID Related gastritis pathophysiology
NSAIDs like ibuprofen, aspirin diminish mucin secretion which exfoliate surface epithelium. Damage elicits acute inflammation.
76
How to lower NSAID related gastritis?
Proton pump inhibitors Alternative pain management Discussion about food
77
Helicobacter associated gastritis pathophysiology
Gram negative bacteria produces urease which hydrolyses luminal area to form ammonia. This buffers acidic environment liquifieing mucus and allowing H pylori to attach to epithelium. Toxins are released which induces damage and inflammatory response
78
Acute inflammation involves
Compliment cascade Kinin System Fibrinolytic system Coagulation cascade
79
Acute inflammation causes
Chronic inflammation Emphyma = pus collection Resolves Repairs and reorganises Perforation leading to sepsis
80
Causes of chronic inflammation
Resistance of infective agent to phagocytosis Response to endogenous or exogenous material Autoimmune disease Primary granulomatus disease
81
Histology of acute vs chronic inflammation
Acute = neutrophils Chronic = no neutrophils, but lymphocytes, macrophages and eosinophils present
82
Why does chronic inflammation cause cancer?
Chronic inflammation - cause cellular changes and proliferation (increased mutations), release of ROS Metaplasia Dysplasia Carcinoma in situ Invasive carcinoma
83
Osteoarthritis vs Rheumatoid arthiritis
Osteo - primarily degenerative Rheumatoid - systemic chronic inflammation (auto antibody)
84
3 main factors of thrombosis
Vasoconstriction Platelet plug - damaged cells release VWF Coagulation cascade - GP 2b/3G expression binds to fibrinogen
85
Secondary haemostasis intrinsic pathway
Thrombin enzyme amplifies feedback loop
86
Secondary haemostasis extrinsic pathway
Factor 7 tissue activation
87
Final activation in coagulation
Factor x
88
Intrinsic vs extrinsic coagulation pathway
I - activated by factors in blood 12-11-9-8 E - activated by tissue factor 7
89
What is the common pathway of coagulation
Converts fibrinogen to fibrin 10-5-2-1-13
90
What is PT (thrombosis)
Measures time taken for blood to clot via extrinsic pathway
91
What is APTT (thrombosis)
Time taken for blood to clot via intrinsic pathway
92
What is TT (thrombosis)
Time taken for thrombin to convert fibrinogen to fibrin
93
What is disseminated intravascular coagulation?
Uncontrolled activation of clotting factors Widespread clotting Body uses up fibrin/platelets/coagulation factors = Hemorrhage

Pase 2a Notes (6 decks)

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