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Pase 2a Notes > Intro To Clinical Sciences > Flashcards

Intro To Clinical Sciences Flashcards

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
Q

Definition of granulation tissue

A

Small blood vessels in a connective tissue matrix with myofibroblasts, contracts to reduce wound size

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26
Q

How to treat inflammation?

A

Ice closes capillaries and swelling

Ibuprofen inhibits prostaglandin release (chemical mediators of inflammation)

Antihistamines
Anti-inflammatories
Corticosteroids
Antibiotics

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27
Q

Macroscopic appearance of acute inflammation

A

Red - dilation
Heat - hyperaemia
Swelling - exudate oedema
Pain - distortion of tissue
Loss of function

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28
Q

Define repair vs resolution

A

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

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29
Q

Example of repair vs resolution

A

Repair - liver cirrhosis (drinking every day starts fibrotic repair) or Covid (alveolar walls are damaged)
Resolution - Lobar pneumonia (pneumocytes lining alveoli can regenerate)

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30
Q

Normal abrasion healing

A

Scab formed over surface
Epidermis grows from adnexa produced by scab
Thin confluent epidermis
Final epidermal regrowth

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31
Q

1st vs 2nd Intention healing

A

1st - suture skin together so fibrin then collagen fills gap
2nd - when skin is lost, granulation tissue (capillaries + endothelial) grow from both sides

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32
Q

Cells that can regenerate

A

Hepatocytes
Pneumocytes
All blood cells
Gut epithelium
Skin epithelium
Osteocytes

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33
Q

Cells that don’t regenerate

A

Myocardial cells
Neurones

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34
Q

Define organisation in inflammation

A

Formation of fibrovascular connective tissue by production of granulation tissue and phagocytosis of dead tissue

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35
Q

Define thrombosis

A

A solid mass of blood constituents formed within an intact vascular system during life

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36
Q

Why are clots rare?

A

Laminar flow - cells travel in centre of arterial vessels
Endothelial cells - not sticky when healthy

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37
Q

How is a thrombosis formed?

A

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.

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38
Q

What is Virchow’s triad?

A

Causes of thrombosis:
Change in vessel wall (smoking)
Change in blood flow (stasis)
Change in blood constituents (clotting factors)

39
Q

What is prescribed to reduce risk of thrombosis?

A

Aspirin - inhibits platelet aggregation

40
Q

Define an embolus

A

Mass of material in the vascular system able to become lodged within a vessel and block it
(Occurs via embolism)

41
Q

Causes of an embolus

A

Air
Tumour
Amniotic fluid
Fat (severe trauma)
DVT
Bacteria
Intravenous drug use

42
Q

What happens to an embolus in arterial vs venous system

A

Arterial - travels anywhere downstream
Venous - lodges in pulmonary arteries

43
Q

Define ischaemia

A

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
Q

Define infarction

A

A reduction of blood flow with subsequent death of cells

45
Q

What is an end artery supply?

A

Organ that receives blood from only one artery
(Problematic as thrombus leads to infarction)

46
Q

Define an atheroma

A

Fatty material forms deposits and damages arterial walls, leading to restriction of circulation and risk of thrombosis. This then establishes an atherosclerosis

47
Q

Distribution of atherosclerosis

A

Common in high pressure systems (aorta + systemic arteries) and never in low (pulmonary arteries)

48
Q

What is in an atheroma plaque?

A

Fibrous tissue like collagen
Lots of cholesterol crystals
Surrounded by lymphocytes

49
Q

Mechanism of atherosclerosis formation

A

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
Q

Risk factors of atherosclerosis

A

Smoking - nicotine, free radicals and CO damage endothelial
High BP - shearing force on cells
Diabetes - damage cells
Hyperlipidaemia -high cholesterol damages cells

51
Q

Define apoptosis

A

Programmes cell death

52
Q

Triggers of apoptosis

A

DNA damage is constantly monitored before replication. If molecules like p53 detect damage, capsase enzymes digest DNA, nuclear membrane and other organelles

53
Q

Apoptosis in diseases and development

A

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
Q

Define necrosis

A

Traumatic cell death in an organ or tissue

55
Q

Examples of necrosis

A

Toxic spider venom
Frostbite
Cerebral infarction
Pancreatitis
Avascular necrosis of bone

56
Q

When do most chromosome abnormalities occur?

A

Early after conception leading to loss of zygote

57
Q

Single vs polygenic gene disorder

A

Abnormality of a single gene causes disease
Vs
Interaction of several different genes cause disease

58
Q

What are homebox genes?

A

Contain information about migration of cells

59
Q

Examples of growth disorders

A

Cleft lip palate
Spina bifida
Meningocele
VSD / Hole in heart

60
Q

Congenital vs inherited

A

Inherited - caused by an inherited genetic abnormality
Continental - present at birth (not always inherited e.g. club foot)

61
Q

Example of late onset

A

May not manifest until later life e.g. Huntingtons

62
Q

Acquired diseases

A

Caused by non-genetic environmental factors, but may be congenital e.g. foetal alcohol syndrome

63
Q

Hypertrophy vs Hyperplasia

A

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
Q

Combined Hypertrophy and hyperplasia can occur where?

A

In smooth muscle of uterus during pregnancy

65
Q

Define atrophy

A

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
Q

Define metaplasia

A

Change in differentiation of a cell from one fully - differentiated type to another
E.g. Barrett’s oesophagus

67
Q

Define dysplasia

A

Morphological changes seen in cells in the progression to becoming cancer
(Seen in biopsies with abnormal architecture and arrangement)

68
Q

Describe the hayflick limit

A

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
Q

What happens in dermal elastosis?

A

Prolonged UV-B light causes protein cross-linking and accumulation of abnormal elastic in dermis of skin (wrinkles)

70
Q

What happens in osteoporosis?

A

Increased bone resorption or decreased bone formation due to a lock of oestrogen. Can cause wide holes and osteopenia which fractures easily

71
Q

What happens in cataracts?

A

UV-B light causes protein cross-linking and formation of opaque proteins in the lens which leads to loss of elasticity

72
Q

What happens in senile dementia?

A

Plaques and neurofibrillary tangles occur

73
Q

What happens in deafness?

A

Loss of delicate hair cells in cochlea (cannot divide/regenerate)

74
Q

What happens in sarcopenia?

A

Loss of muscle due to decreased growth hormone, decreased testosterone and increased catabolic cytokines. E.g. causes falls

75
Q

NSAID Related gastritis pathophysiology

A

NSAIDs like ibuprofen, aspirin diminish mucin secretion which exfoliate surface epithelium. Damage elicits acute inflammation.

76
Q

How to lower NSAID related gastritis?

A

Proton pump inhibitors
Alternative pain management
Discussion about food

77
Q

Helicobacter associated gastritis pathophysiology

A

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
Q

Acute inflammation involves

A

Compliment cascade
Kinin System
Fibrinolytic system
Coagulation cascade

79
Q

Acute inflammation causes

A

Chronic inflammation
Emphyma = pus collection
Resolves
Repairs and reorganises
Perforation leading to sepsis

80
Q

Causes of chronic inflammation

A

Resistance of infective agent to phagocytosis
Response to endogenous or exogenous material
Autoimmune disease
Primary granulomatus disease

81
Q

Histology of acute vs chronic inflammation

A

Acute = neutrophils
Chronic = no neutrophils, but lymphocytes, macrophages and eosinophils present

82
Q

Why does chronic inflammation cause cancer?

A

Chronic inflammation - cause cellular changes and proliferation (increased mutations), release of ROS
Metaplasia
Dysplasia
Carcinoma in situ
Invasive carcinoma

83
Q

Osteoarthritis vs Rheumatoid arthiritis

A

Osteo - primarily degenerative
Rheumatoid - systemic chronic inflammation (auto antibody)

84
Q

3 main factors of thrombosis

A

Vasoconstriction
Platelet plug - damaged cells release VWF
Coagulation cascade - GP 2b/3G expression binds to fibrinogen

85
Q

Secondary haemostasis intrinsic pathway

A

Thrombin enzyme amplifies feedback loop

86
Q

Secondary haemostasis extrinsic pathway

A

Factor 7 tissue activation

87
Q

Final activation in coagulation

A

Factor x

88
Q

Intrinsic vs extrinsic coagulation pathway

A

I - activated by factors in blood
12-11-9-8

E - activated by tissue factor 7

89
Q

What is the common pathway of coagulation

A

Converts fibrinogen to fibrin
10-5-2-1-13

90
Q

What is PT (thrombosis)

A

Measures time taken for blood to clot via extrinsic pathway

91
Q

What is APTT (thrombosis)

A

Time taken for blood to clot via intrinsic pathway

92
Q

What is TT (thrombosis)

A

Time taken for thrombin to convert fibrinogen to fibrin

93
Q

What is disseminated intravascular coagulation?

A

Uncontrolled activation of clotting factors
Widespread clotting
Body uses up fibrin/platelets/coagulation factors
= Hemorrhage

Pase 2a Notes (6 decks)

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