Cell adaptations

Mind Map by , created over 6 years ago

Blood Science Mind Map on Cell adaptations, created by maisie_oj on 04/28/2013.

Created by maisie_oj over 6 years ago
Bone marrow failure syndromes
Haemostasis (part 2: secondary haemostasis)
Haematopoietic System Malignancies 2
Flame tests
Joshua Rees
Chapter 16: The Cold War
Becca Strobbe
Acute Inflammation
Rheumatoid Arthritis
Haemopoietic System Malignancies
Blood transfusion and haematopoietic stem cell transplantation
Haemostasis (part 1: primary haemostasis)
Cell adaptations
1 Introduction
1.1 Normal cell (homeostasis)
1.1.1 Stress, increased demand Adaptation Inability to adapt
1.1.2 Injurous stimulus Cell injury -> cell death
1.2 Cell adaptation
1.2.1 Many cell adaptations involve changes in cell growth, size or even differentiation
1.2.2 Adaptations are a physiological event but also occur in response to pathological/abnormal stimuli
2 Adaptive mechanisms
2.1 Hyperplasia
2.1.1 Increase in the number of cells in a tissue resulting in an increase in the size of the organ
2.1.2 Physiological (normal) Hormonal Breast tissue at puberty/pregnancy Uterine smooth muscle during pregnancy Compensatory Following partial hepatectomy Chronic hypoxia (increase in RBCs)
2.1.3 Pathological Hormonal Unopposed effect of oestrogens on endometrium Despite pathological hyperplasia being reversible it may be a risk for developing malignancy Wound healing Kelloid formation
2.2 Hypertrophy
2.2.1 Physiological Hormonal Uterus in pregnancy Compensatory Increase in skeletal muscle in body builders
2.2.2 Increase in the size of the cells in response to an increased demand Not accompanied by cell division, although hypertrophy and hyperplasia may co-exist
2.2.3 Pathological Increase in the size of cardiac muscle in response to obstruction (valvular disease) or ioncreased resistance (hypertension) Hypertrophy of the cardiac muscle is accompanied by a change in gene expression - e.g. fetal contractile genes re-activated aloha-myosin heavy chain (MHC) expressed in normal adults and beta-MHC in fetal heart - this fetal version has a lower level of ATPase activity ... It also contracts more slowly. The switch from alpha to beta form is associated with hypertrophy Hypertrophy of bladder muscle due to prostate disease
2.3 Atrophy
2.3.1 Pathological Decreased workload Disuse atrophy (e.g. skeletal muscle wasting following a fracture and immobilisation) Loss of innervation Denervation atrophy Diminished blood supply Brain atrophies with age as supplying blood vessels become narrower
2.3.2 Partial or complete wasting of tissue due to pathological process
2.4 Hypoplasia
2.4.1 Failure to achieve normal size of organ due to developmental abnormality (e.g. hypoplastic left heart)
2.5 Metaplasia
2.5.1 A reversible event in which one adult, fully differentiated tissue type is replaced by a different fully differentiated type Which is better suited to the new environmental conditions
2.5.2 Physiological Change in endocervical epithelium from glandular to squamous (squamous metaplasia) This area is called the transformation zone From glandular tissue (vagina) to the cerical tissue (stratified squamous)
2.5.3 Pathological (adaptation to stimulus) Squamous metaplasia in respiratory tract due to chronic irritation Squamous metaplasia of salivary gland ducts/bile ducts (due to obstruction) Squamous metaplasia of urinary bladder due to chronic infection Squamous to columnar metaplasia in oesophagus (Barrett's oesophagus) - - due to chronic acid reflux
2.5.4 Although regarded as an adaptive response, metaplastic tissue is 'unstable', and areas of metaplasia are frequent sites for neoplastic development Cervical cancer Barrett's oesophagus Lung carcinoma on the back of squamous metaplasia
3 Dysplasia and anaplasia
3.1 Dysplasia is disordered differentiation (classic malignant appearance)
3.2 Anaplasia is a lack of differentiation
3.3 Characterised by several features
3.3.1 Pleomorphism Variation in size and shape
3.3.2 Abnormal nuclear morphology Nuclei contain abundant DNA and are dark staining - hyperchromatic
3.3.3 Mitoses Reflecting increased proliferation
3.3.4 Loss of polarity Orientation of cells is disturbed
4 What determines a cell's response?
4.1 Major factor is the cell type
4.2 Three populations identified
4.2.1 Labile cells Continually dividing cells Squamous epithelium (skin, mouth and other mucous membrabes) Glandular epithelium of the intestines Haemopoietic cells
4.2.2 Stable cells Normal rate of growth/turnover is very slow - but can be accelerated in response to stimuli e.g. liver, renal tubular epithelium and endocrine glands
4.2.3 Permanent cells Cells unable to divide e.g. neurones, heart and skeletal muscle
4.3 Susceptability to cell injury
4.3.1 Depends on... Cell type (active membrane exchange - renal tubular cells; neurones have very little ability to use anaerobic respiration) Metabolic state of the cell (depleted reserves of glycogen - liver damaged by alcohol/drugs)
4.3.2 Susceptability to hypoxia (low O2) High Neurones (3-5mins) Medium Myocardium, hepatocytes, renal tubules (30mins - 2hrs) Low Fibroblasts, skeletal muscle (many hours)

Media attachments