Introduction to Clinical Science Flashcards
1
Q
What are the 4 signs of inflammation?
A
Rubor - redness
Calor - heat
Tumor - swelling
Dolor - pain
2
Q
What is inflammation?
A
A reaction to injury or infection involving cells such as macrophages and neutrophils
3
Q
What is the difference between Acute and Chronic inflammation?
A
Acute - short lasting, sudden, usually resolves.
Chronic - long lasting, slow onset, may not resolve
4
Q
Give one example of Chronic and acute inflammation
A
Acute - Appendicitis
Chronic - TB
5
Q
What cells are involved in inflammation?
A
Neutrophils Macrophages Lymphocytes Endothelial cells Fibroblasts
6
Q
What is the role of Neutrophils in inflammation?
A
Cytoplasmic granules w/ enzymes to kill bacteria and can signal for macrophages.
They are the first there and first to die at the site.
7
Q
What is the role of Macrophages in inflammation?
A
Long lasting, phagocytic and can present antigens.
They ingest bacteria and carry it away.
8
Q
What is the role of Lymphocytes in inflammation?
A
Long lasting - produce chemicals to attract other inflam cells.
They provide immunological memory for past infections.
9
Q
What is the role of Endothelial cells in inflammation
A
They line capillary blood vessels.
They become sticky, allowing adhesion of inflam cells, can also become porous to let cells pass into tissue.
10
Q
Is inflammation always good?
A
It can be during infection/injury.
It is problematic in hypersensitivity reactions or AI disease.
11
Q
What are endogenous chemical mediators of inflammation (with examples)
A
They are secreted and mediate the inflammatory response.
Examples - histamine, prostaglandins, bradykinin and Nitric Oxide.
12
Q
How would you treat inflammation?
A
You need to treat the route cause e.g. bact infection w/ antibiotics.
You would prescribe NSAIDs which inhibit prostaglandin synthetase.
You could also prescribe Corticosteroids to down regulate chemical mediators.
13
Q
Why might somebody be refered for an autopsy?
A
Medico legal reasons - coronial
Hospital autopsy - teaching/confirmation of COD.
(Presumed natural, presumed unnatural and presumed iatrogenic)
14
Q
Who can make request an autopsy?
A
Relatives, police, registrar of BDM, coroner.
15
Q
What is an embolus?
A
Mass of material in the vascular system able to become lodged within a vessel and block it.
16
Q
What are three causes of Emboli?
A
Thrombus
Air
Cholesterol Crystals
17
Q
How do the lungs act as a filter for venous emboli?
A
BV from the lungs are capillaries which means that it cannot reach the arteries as it will get caught in the vein/cap network.
18
Q
What is Thrombosis?
A
solid mass of blood constituents formed within an intact vascular system during life.
19
Q
What is Virchow’s triad?
Reasons for Thrombotic formation
A
Change in vessel wall
Change in blood flow
Change in blood constituents
20
Q
Process of Thrombus formation
A
- Damage to endothelial cells cause platelets to stick to collagen –> Platelet aggregation, + Feedback
- Endothelial injury disrupts laminar flow
Formation of a thrombus causes fibrin polymerase to be released –> keeps it together.
21
Q
What is the reason clots are fairly rare?
A
Laminar flow - blood travels in the center and doesn’t touch the side.
Endothelial cells are not sticky when healthy.
22
Q
What are the outcome of Thromboses?
A
Break down and lysis
Recanalisation - new capillaries grow through it
Break off and embolise
23
Q
How can you prevent thrombosis?
A
Exercise
Stockings
Aspirin - inhibits platelet aggregation.
24
Q
What is Ischaemia?
A
Reduction of blood flow to a tissue without any other implications.
25
What is the risk of Reperfusion post ischaemia?
Can produce super oxide radicals which damage the cells.
26
What is the difference between Ischaemia and Infarction?
In Ischaemia there is reduction of blood flow w/o implications and in infarction there is tissue death.
27
What is Infarction?
Reduction in blood flow means that cell's cannot support maintenance and will die.
28
Is Infarction always deadly?
No
Some organs have two artery supplies e.g. COW, Liver, Lung whereas others only have one.
29
What is usually the cause of infarction?
Thrombosis breaking off from other areas or a tumour.
30
What is granulation tissue?
Composed of small BV in a connective matrix with myofibroblasts.
31
What is a granuloma?
An aggregate of epitheliod histocytes
32
What are the definitions of Resolution and Repair?
Resolution - initiating factor is removed and the tissue regenerates.
Repair - the initiating factor is still present, tissue is damaged and unable to regenerate.
33
What cells can regenerate?
```
Hepatocytes
Pneumocytes
All blood cells
Epithelium of Gut and Skin
Osteocytes
```
34
What cells cannot regenerate?
Myocardial cells
| Neurones
35
What is the process of Repair?
replacement of damaged tissue by fibrous tissue which is collagen produced by fibroblasts.
36
What produces collagen?
Fibroblasts
37
What is lobar pneumonia?
Pneumonia specific to one lobe in the Lungs, can recover as pneumocytes can regenerate.
38
What is the process of Skin repair?
Abrasion - scab formation - epidermis grows and is protected by the scab.
39
What is the process of Skin repair post surgery?
Exudation of fibrinogen causes a weak fibrin joint. Epidermal growth causes collagen synthesis --> stronger collagen joint
40
What is Atherosclerosis?
A disease in which plaque builds up in the artery.
41
Who tends to get Atherosclerosis more often?
Men in industrial areas.
42
Where do Atheroma's develop?
In arteries with high pressure, e.g. the aorta, and less in the arteries with low pressure e.g. pulmonary arteries.
43
What increases the risk of Atherosclerosis?
Smoking - damages endothelium using free radicals
Hypertension - shearing forces on endothelial cells
Diabetes ( poorly controlled) - super anions damage cells
Hyperlipidaemia - direct damage to endothelial cells.
44
What is the Endothelial Damage theory?
Recurrent endothelial cell injury causes microthrombi formation which builds atheroscleroma over years.
45
What are some of the Complications of Atherosclerosis?
MI
Gangrene
Peripheral Vasc disease
Aneurysm
46
How can you reduce the risk of Atherosclerosis?
Low dose aspirin can prevent platelet aggregation.
47
What is Apoptosis?
Programmed cell death
48
What is Necrosis?
Traumatic cell death which is unprogrammed
49
What are some examples of Necrosis?
Avascular necrosis of bone
Pancreatitis
Frost bite
50
What are the different types of Necrosis?
Caseous necrosis - linked w/ TB
Liquifactive necrosis - thin liquid
Coagulation necrosis - thick and goey
51
What is a disease in which too much apoptosis occurs?
HIV (gets rid of T helper cells)
52
What is a disease in which too little apoptosis occurs?
Cancer
53
What protein Initiates apoptosis?
P53
54
What is the role of Capases?
They are the effectors of apoptosis
55
What are the effectors of apoptosis?
Capases
56
What switches on Capases?
BAX protein
57
What switches off Capases?
Bcl2 protein
58
What can trigger apoptosis?
DNA damage
59
What is the process of apoptosis?
1. A trigger causes a release of enzymes
| 2. These enzymes cause the nucleus to shrink and organelles are carried out by vesicles
60
Why don't adult cells divide very often?
The telomeres get shorter after every division.
61
What causes cells to 'wear out'?
Free radical generation
Free radical absorption
Cross linking of proteins via UV light
Shortening telomeres
62
What are some diseases associated with aging?
Deafness --> Ciliated hair cells are not replaceable
Osteoporosis - bone matrix is decreased
Senile dementia --> brain atrophy
Sarcopenia --> loss of skeletal muscle mass
63
Define congenital
Present at birth
64
Define Inherited disease
Caused by an inherited genetic abnormality, not always present early e.g. huntingtons
65
Define acquired disease
caused by non-genetic environmental factors e.g. FAS
66
What is a homeobox gene?
A gene sequence that codes for different parts of the body.
67
What is Mendelian inheritance?
Single gene inheritence
68
What is autosomal inheritance?
Non sex cell, autosomal dominant (FAP) and recessive (CF)
69
What is polygenic inheritance?
When one characteristic is associated with two or more genes.
70
What is Hypertrophy, with an example?
Increase in size of tissue caused by an increase in size of constituent cells.
e.g. Muscles getting bigger.
71
What is Hyperplasia, with an example?
Increase in size of a tissue caused by an increase in number of the constituent cells
e.g. Benign prostatic hyperplasia.
72
What is Atrophy, with an example?
Decrease in size of a tissue caused by a crease in the number of constituent cells or a decrease in their size .
e.g. Muscular atrophy and alzheimers.
73
What is metaplasia, with an example?
Change in differentiation of a cell from one fully differentiated type to a different fully differentiated type.
e.g. change from cilliated columnar epithelium to squamous in bronchi (barretts oesophagus thanks to smoking)
74
What is Dysplasia, with an example?
Imprecise term for the morphological changes seen in the progression to becoming cancer.
e.g. epithelial cells changing as a precursor to cancer.
75
Define carcinogenesis.
The transformation of normal cells to neoplastic cells through permanent alterations/mutations.
76
Define Oncogenesis
Formation of benign and malignant tumours
77
Define Mutagenic
Something which acts on the DNA
78
How much of cancer is due to the environment?
85%
79
What are some behavioral risks of cancer?
Smoking - Lung cancer
| Rubber industries - bladder cancer
80
What is radiating energy?
ionising radiation w/ long term effects
e.g. Thyroid cancer post chernobyl and exposure to UV --> Increase in skin cancer, BCC and melanoma
81
What are the classes of Carcinogens?
```
Chemical
Viral
Ionising/non ionising radiation
Host
Miscellaneous
```
82
What is a chemical carcinogen?
It has no common structure, some act directly some need to be metabolised from pro-carcinogenic to ultimate carcinogenic.
83
Examples of Chemical carcinogens
Polycyclic aromatic HC - lung and skin cancer - smoking
Aromatic amines - bladder cancer - rubber workers
Nitrosamines - gut cancer
Alkylating agents - Leukaemia
84
Miscellaneous examples of carcinogens
Asbestos and metals
85
What are Host factors?
Race - oral cancer in indians
Diet
Constitutional factors - increases w/age, inherited predisposition + gender
premalignant lesions - Ulcerative collitis
86
What are the Biological factors?
Hormones - Oestrogen - mammary/endometrial cancer
Mycotoxins - alfatoxin B1 - Hepatocellular Carcinoma
Parasites - Clonorchis sinesis - Cholanginocarcinoma
87
What does Asbestos cause?
Malignant Mesothelioma
Lung cancer
Asbestosis
88
What is Basal cell carcinoma and how would you treat it?
Only invades the skin locally, doesn't spread to other parts of the body. You can excise it locally.
89
How is leukemia spread around the body?
WBC circulate around the body and so will any tumour of the WBC.
Chemotherapy is the appropriate treatment
90
What is a Carcinoma?
They spread to the lymph nodes that drain the site of the carcinoma (can spread from blood to bone)
91
What cancers can be spread from blood to bone?
```
Breast
Prostate
Lung
Thyroid
Kidney
```
92
How would you treat Breast cancer?
1. Confirm the cancer using a biopsy
2. Check if its spread to the axilla - if so clear it.
3. if it's spread to the body chemo
4. If it hasn't surgery w/wo axillary clearence
93
What is adjuvant therapy?
Extra treatment given post surgical excision to prevent a secondary tumour.
94
What is the route of mets?
1. Through BM to EC
2. EC to vessels, travels in to the vessels
3. Adheres and breaks int othe EC then grows
95
What is the growth of mets limited to, and what is it dependent on?
1mm in diameter.
GF and blood supply
96
What is required to invade the basement membrane?
Requires collagenase and cell motility
Collagenase required to break through the collagen layers of the BM
97
What is required to enter the blood stream (Intravasation)?
Collagenase + cell motility
98
What is required to exit the blood stream?
Adhesion
Cell motility
Collagenase
99
How does a tumour hide from the immune system?
Shed surface antigens
adhese to other cells
aggregate w/ platelets.
100
What are 2 angiogenesis promoters?
Vascular endothelial growth factor
| Basic fibroblast growth factor
101
What are 3 angiogenesis inhibitors?
Angiotensin, endostatin, vasculostatin
102
How could a cancer spread to the lung?
Tumour enters vein and R side of heart to capillary level which acts a filter so it goes to the Lung
103
How could a cancer spread to the liver?
PV to liver which branches to capillary level and acts as a filter
Colon stomach and pancreatic can all spread via PV.
104
What is chemotherapy suitable for?
Fast dividing tumours - lymphoma, acute leukemia, germ cell tumour of testis
Not good for slow dividing.
105
What is conventional chemotherapy and what are some problems?
Not selective to tumour cells
It will hit normal cells that are dividing - hair loss myelosuppresion and diarrhea
106
What is the difference between conventional chemotherapy and targeted chemotherapy?
Targeted is more effective and comes w/ less side effects.
107
What is a tumour?
Any abnormal swelling - could be down to hyperplasia, hypertrophy, neoplasm or inflammation.
108
What is a neoplasm?
A lesion resulting from relatively autonomous abnormal growth of cells that persist after the initiating stimulus is removed.
109
What is the structure of a Neoplasm?
Neoplastic cells - derivded from nucleated cells, growth pattern and activity is related to parent cells
Stroma - connective tissue framework w/ mechanical support and nutrition.
110
Why might central necrosis of a tumour occur?
Due to a lack of blood supply.
111
How would you classify neoplasms?
Treatment and prognosis
112
Why should we classify neoplasms?
Appropriate treatment and informed prognosis
113
What is a benign neoplasm?
Localised, low mitotic activity, non invasive and often bare close resemblance to normal tissue.
They are exophytic (grow up and out)
Rare necrosis + ulceration.
114
Is necrosis and ulceration more common in benign or malignant tumours?
Malignant.
115
Why would a benign neoplasm cause worry?
Pressures adjacent structures, can become malignant, can produce hormones and causes anxiety.
116
Why would a malignant neoplasm cause worry?
Destruction of adjacent tissue, mets, blood loss from ulcers + obstruction of flow, can also produce hormones and causes anxiety.
117
What is a malignant neoplasm?
Invasive, mets with a rapid growth rate.
They have hyperchromatic + pleomorphic nuclei
Poorly defined with variable resemblance to the normal tissue
Endophytic growth (grow down and in)
118
What can neoplasms arise from?
Epithelial cells
connective tissues
Lymphoid/haemopoietic regions
119
What is a papilloma?
Benign tumour of non secretory, non glandular epithelium - prefixed with its origin.
e.g. squamous cell papilloma
120
What is a adenoma?
Benign tumour of secretory or glandular epithelium, prefied with its origin.
e.g. Thyroid adenoma.
121
What is a carcinoma?
Malignant tumour of epithelial cells, prefixed by the epithelial cell type.
Adenocarcinoma (glandular)
122
What are 2 benign epithelial neoplasms?
Papilloma and Adenoma.
123
What is a metastatic epithelial neoplasm?
Carcinoma
124
What are the benign neoplasms of the connective tissue?
Lipoma - adipocytes
chondroma - cartilage
Osteoma - bone
Angioma - vascular
Rhabdomyoma - striated muscle
leiomyoma - smooth muscle
125
What is a neuroma?
Benign neoplasm of the nerves
126
What is an aplastic tumour?
When the cell type of origin is unknown.
127
How are tumours classified?
Often by their degree of differentiation.
128
What are some malignant connective tissue neoplasms?
```
Liposarcoma - adipose
Rhabdosarcoma - striated muscle
Leiomyosarcoma - Smooth muscle
Chondrosarcoma - cartilage
Osteosarcoma - bone
Angiosarcoma - vascular
```
129
What is innate immunity?
Instinctive, non specific not dependent on lymphocytes.
130
What is adaptive immunity?
Specific acquired immunity, requiring lymphocytes
131
Where do leukocytes originate from?
Multipotent haematopoietic stem cells (haemocytoblast)
132
Give 3 examples of Polymorphonuclear leukocytes
Neutrophils
Eosinophils
Basophils
133
Give 3 examples of mononuclear Leukocytes
Monocyte
T cell - thymus
B cell - Bone marrow
134
What do monocytes turn into usually in tissue?
Macrophages
135
What do B cells turn into usually?
Plasma cells that secrete Ab
136
What do T cells turn into usually?
T reg cells
T Helper Cells (CD4)
Cytotoxic T cells (CD8)
137
What are mast cells?
Natural killer cells e.g. Langerhans/dendritic cells.
138
What are the soluble factors in the blood?
Complement
Antibodies
Cytokines
Chemokines
139
What is complement?
Group of proteins secreted by the liver that needs to be activated to work.
140
What are the 3 functions of complement?
Lysis
chemotaxes of leukocytes
Opsonisation
141
What do antibodies bind to?
Antigens
142
What are immunoglobulins bound to?
B cells
They are soluable and secreted.
143
Which Immunoglobulin is secreted?
IgA (15%)
144
Give 3 functions of antibodies
1. Neutralise toxins
2. Opsonisation of pathogens
3. Activation of complement system (classical)
145
What are the 2 most common Ig?
IgG and IgM
146
What region of an antibody binds to an antigen?
Fab region.
147
What region of an antibody binds to a B cell?
Fc region.
148
Where is IgD present?
mature B cells
149
Where is IgE present?
On basophils and Mast cells.
150
What are cytokines?
Proteins secreted by immune and non-immune cells.
151
Give 4 examples of Cytokines
Interferons
Interleukins
Colony stimulating factors
Tumour Necrosis Factors
152
What do Interferons do?
Induce Anti-viral resistance in non affected cells.
153
What do Interleukins do?
Pro or anti-inflammatory affects
154
What do Colony stimulating factors do?
Directs division + differentiation of bone marrow and stem cells.
155
What does Tumour Necrosis Factor do?
mediates inflammation.
156
What are Chemokines?
Substances that attract leukocytes to the site of infection e.g. CXCL - Neutrophils.
157
What are 3 O2 dependent ways of microbial killing?
Using ROI
Superoxides can be converted to H2O2 and OH Free radicals
NO causes vasodilation and increased extravascation.
158
What are 3 O2 independent ways of microbial killing?
Enzymes
Proteins - defensins + TNF
pH
159
What is the process of phagocytosis?
1. Pathogen binds to macrophage/neutrophil
2. Engulfment of pathogen
3. Phagosome formation then phagolysosome
4. Pathogen is destroyed.
160
What are the 3 complement activation pathways?
Classical - Antibody binds to microbe
Alternative - C binds to microbe.
Lectin - activated by mannose binding lectin bound to microbe.
161
How can pathogens be sensed?
Pathogen associated molecular patterns (PAMP) (on microbe)
Pattern Recognition Receptors (PRR) (On cells)
162
How can microbes be sensed;
a - in the blood
b - in tissues
in the blood - monocytes+neutrophils
in tissues - macrophages + dendritic cells
163
What are the Hallmarks of inflammation?
Increased vasc supply
increased vasc permeability
Increased leukocyte migration
164
What are some physical and chemical barriers?
Skin
Mucocillary escalator
Gastric acid
Lysozymes and pH
165
What does a lysozyme do?
Destroy bacterial cell walls
166
What is the inflammatory response?
1. Coagulation
| 2. Acute inflammation
167
What is the purpose of the inflammatory response?
Kill pathogens, stop the spread and neutralise toxins.
Proliferation of cell to repair damage
Removal of clot - remodelling extracellular matrix
Establish normal tissue function.
168
What are some of the defence mechanisms in innate immunity?
Physical + chemical barriers
Blood proteins - complement
Phagocytic cells - Macrophages + neutrophils.
169
What is extravasation?
WBC migration across the endothelium
170
What do macrophages secrete to initiate Extravasation?
TNF alpha
171
Describe the process of Extravasation
1. Macrophages release TNFa
2. Endothelium stimulated to express adhesion molecules + stimulate chemokines
3. Neutrophils bind to adhesion molecules - roll, slow and get stuck.
4. Neutrophils are activated by chemokines
5. Neutrophils pass through endothelium to combat infection
172
Why do we need cell mediated immunity?
Some viruses evade innate immunity.
IC Viruses + bacteria hide from innate immunity.
Needs memory to a specific antigen when it happens again.
173
What Cells are responsible for cell mediated immunity?
T cells - intracellular microbes
174
What cells are responsible for humoral immunity?
B cells - Extracellular microbes
175
Give 3 examples of APC
Dendritic cells
Macrophages
B cells
176
What is cell mediated immunity?
Occurs between APC and T cells and requires intimate cell to cell contact.
It controls Ab responses via contact w/ B cells to kill infected ones.
177
Which cells express MHC 1?
Glycoproteins on all nucleated cells
178
Which cells express MHC 2?
Glycoproteins only on APC.
179
What does MHC 1 bind to?
CD8 cell --> killer cell --> induce apoptosis when they bind.
180
What does MHC 2 bind to?
CD4 cells --> helper cells --> TH1 Secretes cytokines and TH2 Produces antibodies against extracellular pathogens.
181
What happens to B cells that can recognise self?
They are killed in the bone marrow as they mature.
182
Describe the process of a T helper cell binding to a B cell.
B-cell Ab binds to Ag
Epitope is displayed on the surface of B-cell bound MHC2
TH2 binds to b cell --> cytokine secretion causes B cell clonal expansion
Differentiation of plasma cells and memory B cells.
183
What happens to T cells that recognise self?
They are killed in thymus, they only respond to IC presented antigens.
184
Which T cell would respond to an IC/intrinsic antigen?
CD8
185
Which T cell would respond to an EC/Ex antigen?
CD4
186
What is needed for Cell mediated immunity?
Intimate contact between T and APC cells.
Intrinsic/endogenous/IC antigens OR Extrinsic/exogenous/EC antigens.
This helps recognise self from non-self.
187
What is a type one hypersensitivity reaction?
IgE binds to mast cells which releases histamine
e.g. Pollen and anaphylaxis
188
What is a type two hypersensitivity reaction?
IG bind to surface antigens
e.g. Transplant rejection and grave disease
189
What is a type three hypersensitivity reaction?
The activation of complement by a fungus.
190
What is a type four hypersensitivity reaction?
T cell mediated
E.g. TB
191
How can you diagnose Atopy?
Skin prick or Ras Test
192
Where would IgM be the highest?
at the beginning of Infection
193
What is IgE made against?
Made to things that we are allergic too
194
What is active immunity?
When you make your own antibodies post exposure to a pathogen.
195
What is passive immunity?
When you artificially gain the antibodies
196
Why are vaccines good?
Save lives, prevents disability and saves money.
197
What is an adverse drug reaction?
A noxious and unintended response to a drug
198
What is Rawlin-thompsons classification?
Way of classifying different drug reactions
199
What is a Type A RT?
Augmented, very common and predictable --> dose related
200
What is a Type B RT?
Bizzare, unpredictable, immunological in nature --> often allergy related
201
What is a Type C RT?
Chronic, occurs after long term therapy
202
What is a Type D RT?
Delayed and happens after many years of treatment
203
What is a Type E RT?
End of use, withdrawal action
204
What are 3 causes of ADR?
Receptor abnormality
Immunological
Abnormalities in drug metabolism
205
What are 3 risk factors for ADR?
Being a woman
Elderly
Poly-pharmacy
Many allergies
206
What is the difference between active and passive immunity?
Active - making your own antibodies post infection
Passive - Artificially gaining the antibodies
207
How can synthetic peptides be used as vaccines?
They stimulate T cell development.
208
What is the process of active immunisation?
Engage the immune system
Elicits danger signals and triggers PAMPs
Engage TLR
Activate specialist APC -> Langerhans
Engage the adapative immune system - generates T+B memory cells and activates T cell helpers.
209
Give 3 examples of active immunity
1. Induces immunological memory
2. Produces high affinity AB
3. Produces a protective response against pathogens
210
Give 2 advantages of passive immunity
Immediate effect
| Useful for acute dangers
211
Give 3 disadvantages of passive immunity
Short term
No Immunological memory
Possible
212
What is the first immune response to initial exposure?
1. Innate immune response
2. IgM predominates
3. Low affinity
213
What is the second immune response to a previously met pathogen?
1. Rapid and larger than the first
2. Higher affinity IgG
3. Adaptive immunity - T cell help
214
What are 5 Features of an Ideal vaccine?
```
Safe
Induces a suitable immune response
Shouldn't require boosters
Generates immunological memory
Stable and easy to transport
```
215
What is the role of an adjuvant?
A substance added to a vaccination to stimulate an immune response.
216
What is an example of an adjuvant?
Toxoids, proteins and chemicals.
217
What are the advantages of an inactivated vaccine?
No risk of infection
| Storage is less critical
218
What are the disadvantages of an inactivated vaccine?
Response is weak
Boosters are needed
Tend to only activate humoral response --> Lack of T cell involvement.
219
Where are atherosclerotic plaques found?
Peripheral and coronary artery
220
What leads to neointima forming?
Atherosclerosis causing increased wall thickness.
221
What is the function of thyroid hormone?
1. Food metabolism
2. Protein synthesis
3. Increased sympathetic action e.g. CO and HR
4. Heat production
5. Needed for growth and development
222
How long does Thyroxine (t4) last?
Half life is 5-7 days
223
How long does Triiodothyronine last?
Half life is only 1 day
224
What does ADH do?
Acts on the CD of the nephron and increases the insertion of aquaporin 2 channels --> Causes H2O retention.
225
What are two things ADH is inhibited by?
Caffeine and Alcohol
226
When is ADH release triggered?
High osmolality and Low blood vol, nausea, vomiting, stress and exercise
227
What are two characteristics of Iodothyronines?
Not water soluble
| 99% Bound to proteins
228
How are Iodothyronines formed?
Iodine + tyrosine = Iodothyronines
229
How is Thyroxine (t4) formed?
Iodothyronines are conjugated to make T4.
230
Where is the posterior pituitary derived from?
The floor of the ventricles
231
Name two hormones that are secreted from the posterior pituitary
Oxytocin and ADH
232
Give two functions of oxytocin
Milk secretion
| Uterine contraction
233
What 4 cells make up the islets of Langerhans?
Beta cells (70%)
Alpha cells (20%)
Delta cells 8%
Polypeptide secreting cells
234
What is an example of a water soluble hormone?
Peptides e.g. TRH,LH,FSH
235
Are water soluble hormones stored in vesicles or synthesised on demand?
Water soluble hormones e.g. peptides are stored in vesicles.
236
How do water soluble hormones e.g. peptides get into cells?
They bind to cell surface receptors.
237
Give an example of a fat soluble hormone
Steroids e.g. cortisol
238
Are fat soluble hormones stored in vesicles or synthesised on demand?
Synthesised on demand
239
Give an example of an amine hormone
Noradrenaline and adrenaline
240
Where are hormones secreted from the posterior pituitary bound to?
Stored in colloid and bound to thyroglobulin.
241
What stimulates the movement of colloid into a secretory Cell?
TSH it allows T3-->T4.
242
Describe the pathway for noradrenaline synthesis
Phenylalanine --> L-tyrosine --> L-dopa --> Dopamine --> NAd and Ad
243
What two enzymes break down catecholamines
MAO and COMT
244
What are noradrenaline and adrenaline broken down into?
Normetadrenaline and metadrenaline
245
Where in a cell are peptide cell receptors located?
on the cell membrane
246
Where in a cell are thyroid/vit A and D cell receptors located?
Thyroid, Vit A and D and oestrogen act on nuclear receptors.
