Unit 5- Introduction To Disease Flashcards

1
Q

What is the definition of pathology?

A

The study of disease processes with the aim of understanding their nature & cause.

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2
Q

How can pathology be studied?

A

By examining urine samples (to check kidney function), blood samples (e.g. lipid levels), & tissue biopsies (e.g. liver biopsy).

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3
Q

What is aetiology?

A

The study of the cause of diseases.

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4
Q

What is pathogenesis?

A

The process by which a cause alters an existing process to produce a disease.

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5
Q

What’s the difference between signs & symptoms?

A

Signs: Detected by a clinician but not necessarily evident to the patient.
* Symptoms: The damage caused by the disease combined with the body’s response.

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6
Q

What are the 4 variations in the manifestation of diseases over a lifetime?

A

Developmental, inflammatory, neoplasticism, & degenerative diseases.

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7
Q

What is senescence?

A

The gradual deterioration in vitality associated with aging & tissue/cell atrophy.

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8
Q

What are 2 main origins of diseases?

A

Environmental and genetic factors.

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9
Q

Name some environmental factors causing disease

A
  • Physical agents: Trauma, radiation, electricity, constant pressure.
  • Chemical: Arsenic, acids/alkalis, toxins, & medicines
  • Reduced oxygen supply: Hypoxia or anoxia
  • Nutritional deficiencies: Starvation, vitamin deficiencies, dietary excess.
  • Viruses
  • Abnormal immune reactions: Hypersensitivity, autoimmune diseases.
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10
Q

What is an iatrogenic effect?

A

An unexpected consequence of medical treatment causing disease.

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11
Q

What are the effects of reduced oxygen supply on tissues?

A

*Hypoxia: Reduced blood flow due to atherosclerosis
* Anoxia: Complete blockage of blood flow.

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12
Q

What are hypersensitivity reactions?

A

Overactive immune responses, such as anaphylactic shock or asthma.

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13
Q

What are immune diseases?

A

Diseases caused by the immune system attacking the body e.g. thyroiditis, pernicious anemia.

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14
Q

How do genetic factors contribute to disease?

A
  • Normal genes: Variability in genetic polymorphism & environmental influences.
  • Abnormal genes: Mutations, chromosome translocations, or duplications.
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15
Q

Give examples of diseases linked to genetic abnormalities.

A
  • Sickle cell anaemia (point mutation).
  • Burkitt’s lymphoma (chromosome translocation)
  • Down’s syndrome (trisomy 21)
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16
Q

What is ulcerative colitis?

A

A chronic inflammatory disease of the colon, characterised by diarrhoea with mucus & blood, cramping abdominal pain & mucus membrane ulceration.

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17
Q

What is necrosis?

A

The death of cells due to infection, injury, hypoxia, physical trauma, or chemical trauma, leading to unregulated cell disintegration.

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18
Q

What are the characteristics of necrosis?

A

Disassembly of cell membranes, protein denaturation, coagulation, & uncontrolled enzymatic activity.

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19
Q

What is apoptosis?

A

Programmed cell death that removes cells in an orderly manner, playing a role in development, maintenance, & tissue renewal.

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20
Q

What is the key difference between necrosis & apoptosis?

A

Necrosis involves unregulated cell leakage, while apoptosis involves bundled apoptotic bodies safely removed by phagocytic cells.

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21
Q

What are apoptotic bodies?

A

Packaged cellular fragments produced during apoptosis for safe destruction by phagocytic cells.

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22
Q

What is sub-lethal cell damage?

A

Damage that does not kill the cell but contributes to disease morbidity, e.g. amyloid accumulation.

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23
Q

How does amyloid accumulation affect tissues?

A

It causes stiffness in tissues like the heart. Reducing cardiac efficiency & output.

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24
Q

What are the 2 types of classification in connective tissues?

A

Dystrophic classification: Occurs after necrotic damage (e.g. lunge infection).
Metastatic classification: secondary to hypercalcemia, often due to parathyroid hormone imbalance.

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25
Q

What is haemostatis?

A

The process of forming a clot to prevent blood loss & promote wound healing.

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26
Q

What role do clots play in wound healing?

A

Clots provide a matrix for cell to move & repair tissue while depositing plasma & cell-secreted components.

27
Q

What is clotting cascade?

A

A series of enzymatic reactions where fibrinogen is cleaved into fibrin threads by thrombin to form a clot.

28
Q

What are the 2 pathways of blood clotting?

A

Intrinsic pathway: Activated by internal endothelial damage, slower.
Extrinsic pathway: Activated by external trauma, faster, involving tissue factor.

29
Q

What is fibrinolyses?

A

The breakdown of clots to allow tissue regeneration & healing.

30
Q

What is thrombosis?

A

The formation of thrombus (blood clot) within a blood vessel or heart, often leading pathological complications.

31
Q

What is Virchow’s triad?

A

The 3 factors that cause thrombosis:
* Alterations in blood flow
* Damage to the endothelial lining.
* Changes in blood composition.

32
Q

What aid an example of necrosis to ischemia?

A

Cardiac muscle cell death from a heart attack caused by a blood clot.

33
Q

What is an example of a hereditary disease caused by genetic mutations?

A

Cystic fibrosis: An autosomal disease recessive disorder affecting exocrine glands, leading to faulty digestion, respiratory issues, & salt loss through sweating.

34
Q

How do genetic mutations affect DNA repair rates?

A

Variations in DNA repair genes influence the rate of mutations, affecting disease susceptibility.

35
Q

How can alterations in blood flow increase the likelihood of thrombus formation?

A

Altered flow increases platelet collisions with vessel walls, initiating the clotting cascade. Slow blood flow disrupts laminar flow, causing turbulence & shear stress, which promote thrombosis.

36
Q

What are common causes of slowed blood flow that increases thrombosis risk?

A
  • Cardiac failure
  • Immobility (e.g. prolonged bed rest)
37
Q

What effect does turbulence & shear stress have on endothelial function?

A

They cause altered endothelial function & increase production of pro-thrombotic agents.

38
Q

What are common causes of endothelial damage?

A
  • Disease of the vessel wall (e.g. atheroma)
  • Toxins from inflammatory processes.
  • Local compression (e.g. during or after surgery)
39
Q

What changes in blood composition can promote thrombosis?

A
  • Increased platelets, fibrinogen, or pro-thrombin (e.g. post surgery)
  • Increased platelet adhesiveness
  • Inherited genetic abnormalities reducing thrombus inhibition.
  • Factors like contraceptives, smoking, & some cancers.
40
Q

Where are thrombi most commonly formed?

A
  • Capillaries near tissues affected by acute inflammation.
  • Heart (atria, ventricles, & valves), particularly atrial fibrillation.
41
Q

What is embolism?

A

When part or all of a thrombus detaches, becoming a free-floating embolus that can occlude blood flow elsewhere, such as causing a pulmonary embolism in the lungs.

42
Q

What happens if a thrombus remains attached?

A

Capillaries grow toward the thrombus, attracting fibroblasts & phagocytic cells, leading to thrombus degradation & replacement by fibrovascular tissue.

43
Q

What is a phlebolith?

A

A classified thrombus residue formed when calcium salts deposit within a shrinking thrombus, visible on x-ray images.

44
Q

What is prophylaxis in the context of thrombosis prevention?

A

The use of anticoagulant (e.g. warfarin, heparin) or drugs that inhibit prostaglandin synthesis (e.g. aspirin) to reduce blood clottability.

45
Q

How is an existing thrombus treated?

A

By stimulating fibrinolysis using exogenous fibrinolytic agents, such as streptokinase.

46
Q

How does atheroma predispose ill-health?

A
  • Reduction in blood flow (hypoxia)
  • Increased peripheral resistance (hypertension)
  • Precipitation of thrombosis (intravascular clotting)
47
Q

What do atherosclerosis plaques consist of histologically?

A

Patchy collections of lipid-like substances in the tunica intima of vascular walls.

48
Q

What are the risk factors of atheroma?

A
  • Obesity
  • Heavy smoking
  • hypertension
  • Sedentary lifestyles
49
Q

What is inflammation?

A

A dynamic process by which living tissues initially react to injury, starting with changes to vasculature & connective tissues.

50
Q

What are the phases of inflammation?

A

Acute phase, followed by sub-acute or chronic phase if the reaction persists.

51
Q

What causes redness and heat in inflammation?

A

Hyperaemia (increased blood flow).

52
Q

What causes swelling & pain in inflammation?

A

Exudation of fluid (bleeding, vascular fluid leakage, & interstitial fluid accumulation).

53
Q

What is phagocytosis?

A

The removal of damaged cells or debris by phagocytes, essential for clearing infections.

54
Q

Name some chemical mediators involved in inflammation?

A
  • Histamine (mast cells)
  • Leukotrienes & prostaglandins (arachidonic acid derivatives)
  • Cytokines, kinins, & platelet-activating factor.
55
Q

What is chronic inflammation?

A

Long-standing inflammation following acute inflammation or caused by persistent agents, foreign materials, or autoimmune diseases.

56
Q

What is granuloma?

A

Clusters of macrophages surrounded by lymphocytes, often in chronic inflammation.

57
Q

What leads to fibrosis i chronic inflammation?

A

Angiogenesis due to vascular endothelium proliferation & collagen build-up by fibroblasts.

58
Q

What is an abscess?

A

Localised pus accumulation within a pyogenic membrane, isolating infection until discharge.

59
Q

What is neoplasia?

A

Unregulated cell division lading to tumour formation.

60
Q

What differentiates benign and malignant neoplasms?

A

Benign: Slow-grading, well-differentiated, localised.

Malignant: Rapid-growing, undifferentiated, invasive, & capable of metastasis.

61
Q

What are 4 main modes of tumor spread?

A
  • Local invasion
  • Lymphatic spread
  • Vascular spread
  • Trans-coelomic spread
62
Q

How are tumors classified?

A

By tissue origin

63
Q

How do monoclonal antibodies interact with the immune system?

A
  • Flag cancer cell for immune attack
  • Trigger membrane destruction.
  • Block immune inhibitors.
  • Bind cancer & immune cells for targeted response.