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Flashcards in Biology Exam Deck (65):
1

What is atrophy

wasting away of body tissue or an organ, especially as a result of the degeneration of cells.

2

What is hypertrophy

An enlargement of an organ or tissue in response to an increase in the size of its cells

3

What is hyperplasia

the enlargement of an organ or tissue caused by an increase in the reproduction rate of its cells, often as an initial stage in the development of cancer.

4

What is metaplasia

abnormal change in the nature of a tissue

5

What is dysplasia

the presence of cells of an abnormal type within a tissue, which may signify a stage preceding the development of cancer

6

What is apoptosis

the death of cells which occurs as a normal and controlled part of an organism's growth or development

7

What is necrosis

the death of most or all of the cells in an organ or tissue due to disease, injury, or failure of the blood supply.

8

Define and describe Pharmacodynamics in detail

Pharmacodynamics is the branch of pharmacology concerned with the action of drugs on the body or on microorganisms within or on the body; and how the drug binds to receptors.

9

Define and describe Pharmacokinetics in detail

Pharmacokinetics is the scientific study of how the body processes drugs and is normally broken down into 4 stages: Absorption, Distribution, Metabolism and excretion.

10

What is Bioavailability

The proportion of the administered dose which reaches the systemic circulation.

11

What is Therapeutic Range or Therapeutic index

The difference between the level of a drug in the blood to be effective and the level where the drug becomes toxic.

12

What is the definition of commensal microorganisms

A microorganism that lives harmlessly (usually) on the skin

13

What is Aetiology

The scientific study of the causes of disease.

14

Identify the signs and symptoms of inflammation (see Ashelford et al P36).

Redness.
Heat.
Swelling.
Pain.
Loss of function

15

provide a biological rationale for inflammation (see Ashelford et al P36).

1) The release of Inflammatory mediators
2) A vascular response
3) A cellular response

16

Describe the acute inflammatory processes with reference to cellular physiological and pathophysiological detail. (Ashelford et al, chapter 2).

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17

Describe chronic inflammatory processes with reference to cellular pathophysiological detail (Ashelford et al, chapter 2).

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18

Discuss inflammation and corticosteroids (Ashelford et al, P43).

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19

Discuss inflammation, pain and Non-Steroidal Anti-inflammatory Drugs (NSAIDs) ((Ashelford et al, P152) and demonstrate an awareness of potential side effects and contraindications.

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20

List the innate immune system defences against infection (Ashelford et al P77)

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21

Demonstrate a general understanding of the adaptive immune system response to infection (Ashelford et al P76 to P89).

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22

Provide a short account of the types and characteristics of potentially infectious organisms (See Ashelford et al P54 to P59).

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23

Demonstrate a detailed understanding of the mechanism of action of antibacterial drugs (Ashelford et al P65).

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24

Describe antimicrobial resistance at a cellular level, and account for the effects of healthcare behaviours (Ashelford et al P67 to P70.

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25

Describe the components of the pain experience including transduction, transmission, perception and modulation (see powerpoint slideset on Moodle and Ashelford et al P139 -P147).

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26

Identify types of pain (see Ashelford et al essential textbook P149) including nociceptive and neuropathic pain types and provide a brief description of how these may occur.

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27

Provide an account of the gate control theory of pain and its effect on pain modulation. (Ashelford et al P145).

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28

Discuss the pharmacological and physiological aspects of Non-Steroidal anti-inflammatory (NSAID) and opiate medications, including an understanding of common side effects (see Ashelford et al chapter 5 and Moodle resources).

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29

Draw a diagram or table summary of the World Health Organisation Analgesic Ladder (see Ashelford et al P151)

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30

Discuss cardiovascular disease as a common condition

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31

Provide a short description of blood cholesterol variation

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32

Describe the development of atheroma and advanced or unstable plaques.

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33

Demonstrate an understanding of the biological processes resulting in Hypertension.

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34

Discuss pathological process leading to acute coronary syndromes (ACS) and myocardial infarction (MI)

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35

Provide an explanation of the effects of common cardiovascular medications.

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36

Provide a short description of heart failure

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37

Provide a short description of atrial fibrillation

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38

Discuss renin-angiotensin-aldosterone-system effects in health and illness

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39

Provide a detailed account of acute kidney injury (AKI) pathophysiology and treatment

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40

Provide a detailed pathophysiological rationale for the monitoring, care and treatment of chronic kidney disease (CKD)

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41

Demonstrate a detailed understanding of the biological basis of urinary tract infections (UTIs)

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42

Describe issues related to the conditions: benign prostatic hyperplasia, urinary retention and bladder cancers

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43

Understand key aspects of blood glucose regulation.
(see p288 in essential text).

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44

Describe the pathophysiological processes related to Type 1 diabetes mellitus (p291 in essential text)

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45

Describe the pathophysiological processes related to Type 2 diabetes mellitus (p291 in essential text)

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46

Demonstrate a detailed pathophysiological understanding of three diabetes mellitus emergencies including hypoglycaemia, diabetic ketoacidosis and hyperosmolar hyperglycaemic state (p294 in essential text).

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47

Understand the microvascular and macrovascular complications resulting from long term poor control of blood glucose

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48

Understand the key pharmacological effects of insulin and metformin

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49

identify and discuss the issues apparent in normal neurological function. This is essential to recognising pathophysiological dysfunction (P267 to P269 in the Ashelford text)

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50

Explain the pathophysiological process of Parkinson’s disease, including the location of the cellular dysfunction, the neurotransmitter involved, the cellular changes occurring and the presenting symptoms (P269 to P271 in the Ashelford text)

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51

Understand the effects of Levodopa on the brain cells and the specific medication administration considerations. (P271 to P273 in the Ashelford text)

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52

Demonstrate a basic understanding of the pathophysiological effects of Multiple Sclerosis on nerve tissue and the subsequent effects on the function of the tissues and cells involved.

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53

Provide a short account of the differences between osteoarthritis and osteoporosis and identify suitable treatment options including an explanation of how these work at the level of cells and tissues

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54

List the hallmarks and provide a detailed understanding of these features of carcinogenesis (see P107-P108 table in Ashelford et al essential text)

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55

Discuss the role of cell mutations in proto oncogenes, tumour suppressor genes and oncogenes resulting in unregulated cell growth. (Ashelford et al P113-P117)

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56

Provide a short description of the pathophysiological process resulting in metastasis ( P118-P119 Ashelford et al).

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57

Describe the staging and grading systems of cancer (P120-P121 Ashelford et al).

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58

Provide a brief account of cancer chemotherapy effects at a cellular level (P124-124).

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59

What is the smallest living unit of the body

Cell

60

Endocrine signalling involves the release of what?

Hormones

61

The transition of a molecular signal from a cell's exterior to its interior is known as what?

Signal transduction

62

Prokaryotic cells (bacteria) differ from eukaryotic cells (human) for what reason?

Prokaryotic (bacteria) cells have no nucleus

63

Symptoms of infection can be caused by what?

the immune system
toxins produced by microorganisms
the death of invaded human cells

64

how long does a cough usually last for

21 days

65

Give 2 examples of strategies to prevent antibiotic resistance

1) Preventing infections by good hygiene
2) ensuring doses of antibiotics are not missed