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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
What is haemostatis?
The process of forming a clot to prevent blood loss & promote wound healing.
26
What role do clots play in wound healing?
Clots provide a matrix for cell to move & repair tissue while depositing plasma & cell-secreted components.
27
What is clotting cascade?
A series of enzymatic reactions where fibrinogen is cleaved into fibrin threads by thrombin to form a clot.
28
What are the 2 pathways of blood clotting?
Intrinsic pathway: Activated by internal endothelial damage, slower. Extrinsic pathway: Activated by external trauma, faster, involving tissue factor.
29
What is fibrinolyses?
The breakdown of clots to allow tissue regeneration & healing.
30
What is thrombosis?
The formation of thrombus (blood clot) within a blood vessel or heart, often leading pathological complications.
31
What is Virchow’s triad?
The 3 factors that cause thrombosis: * Alterations in blood flow * Damage to the endothelial lining. * Changes in blood composition.
32
What aid an example of necrosis to ischemia?
Cardiac muscle cell death from a heart attack caused by a blood clot.
33
What is an example of a hereditary disease caused by genetic mutations?
Cystic fibrosis: An autosomal disease recessive disorder affecting exocrine glands, leading to faulty digestion, respiratory issues, & salt loss through sweating.
34
How do genetic mutations affect DNA repair rates?
Variations in DNA repair genes influence the rate of mutations, affecting disease susceptibility.
35
How can alterations in blood flow increase the likelihood of thrombus formation?
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
What are common causes of slowed blood flow that increases thrombosis risk?
* Cardiac failure * Immobility (e.g. prolonged bed rest)
37
What effect does turbulence & shear stress have on endothelial function?
They cause altered endothelial function & increase production of pro-thrombotic agents.
38
What are common causes of endothelial damage?
* Disease of the vessel wall (e.g. atheroma) * Toxins from inflammatory processes. * Local compression (e.g. during or after surgery)
39
What changes in blood composition can promote thrombosis?
* 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
Where are thrombi most commonly formed?
* Capillaries near tissues affected by acute inflammation. * Heart (atria, ventricles, & valves), particularly atrial fibrillation.
41
What is embolism?
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
What happens if a thrombus remains attached?
Capillaries grow toward the thrombus, attracting fibroblasts & phagocytic cells, leading to thrombus degradation & replacement by fibrovascular tissue.
43
What is a phlebolith?
A classified thrombus residue formed when calcium salts deposit within a shrinking thrombus, visible on x-ray images.
44
What is prophylaxis in the context of thrombosis prevention?
The use of anticoagulant (e.g. warfarin, heparin) or drugs that inhibit prostaglandin synthesis (e.g. aspirin) to reduce blood clottability.
45
How is an existing thrombus treated?
By stimulating fibrinolysis using exogenous fibrinolytic agents, such as streptokinase.
46
How does atheroma predispose ill-health?
* Reduction in blood flow (hypoxia) * Increased peripheral resistance (hypertension) * Precipitation of thrombosis (intravascular clotting)
47
What do atherosclerosis plaques consist of histologically?
Patchy collections of lipid-like substances in the tunica intima of vascular walls.
48
What are the risk factors of atheroma?
* Obesity * Heavy smoking * hypertension * Sedentary lifestyles
49
What is inflammation?
A dynamic process by which living tissues initially react to injury, starting with changes to vasculature & connective tissues.
50
What are the phases of inflammation?
Acute phase, followed by sub-acute or chronic phase if the reaction persists.
51
What causes redness and heat in inflammation?
Hyperaemia (increased blood flow).
52
What causes swelling & pain in inflammation?
Exudation of fluid (bleeding, vascular fluid leakage, & interstitial fluid accumulation).
53
What is phagocytosis?
The removal of damaged cells or debris by phagocytes, essential for clearing infections.
54
Name some chemical mediators involved in inflammation?
* Histamine (mast cells) * Leukotrienes & prostaglandins (arachidonic acid derivatives) * Cytokines, kinins, & platelet-activating factor.
55
What is chronic inflammation?
Long-standing inflammation following acute inflammation or caused by persistent agents, foreign materials, or autoimmune diseases.
56
What is granuloma?
Clusters of macrophages surrounded by lymphocytes, often in chronic inflammation.
57
What leads to fibrosis i chronic inflammation?
Angiogenesis due to vascular endothelium proliferation & collagen build-up by fibroblasts.
58
What is an abscess?
Localised pus accumulation within a pyogenic membrane, isolating infection until discharge.
59
What is neoplasia?
Unregulated cell division lading to tumour formation.
60
What differentiates benign and malignant neoplasms?
Benign: Slow-grading, well-differentiated, localised. Malignant: Rapid-growing, undifferentiated, invasive, & capable of metastasis.
61
What are 4 main modes of tumor spread?
* Local invasion * Lymphatic spread * Vascular spread * Trans-coelomic spread
62
How are tumors classified?
By tissue origin
63
How do monoclonal antibodies interact with the immune system?
* Flag cancer cell for immune attack * Trigger membrane destruction. * Block immune inhibitors. * Bind cancer & immune cells for targeted response.

Pharmacy Science (9 decks)

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