Review posters 17/05/2016

Question 1

Energy homeostasis

Answer 1

Physiological process of matching energy intake to energy output

Question 2

Obesity

Answer 2

Due to small constant mismatch between energy expenditure and energy intake.

Question 3

Causes of obesity

Answer 3

Higher levels of inactivity

Increased consumption of fatty foods

Question 4

Factors influencing obesity

Answer 4

Genetics- susceptibility to genes

Environment

Question 5

Diseases associated with obesity

Answer 5

Type II diabetes
Hypertension
High cholesterol
Certain cancers e.g. colonic
MI
Stroke
Obstructive sleep apnoea 
Non-alcoholic fatty liver disease

Question 6

Why do we need fat?

Answer 6

Energy storage
Prevention of starvation
Energy buffer during prolonged illness

Question 7

Starvation

Answer 7

Threat to human survival. Adipose tissue accumulation is a survival adaptation.

Question 8

The brain and obesity

Answer 8

Obesity is a disease of the brain. Increased body fat alters brain function. It thinks that the fat level is normal and that reducing this (dieting) is a threat (starvation).

Question 9

Factors that control energy intake

Answer 9

The CNS influences energy balance and body weight.

Behaviour- feeding and physical activity
ANS activity- regulates energy expenditure
Neuroendocrine system- secretion of hormones

Integration of these determines feeding behaviour

Question 10

Which neural centre is responsible for integration of the CNS signals?

Answer 10

The hypothalamus

Question 11

Three basic concepts underlying the control of energy storage system:

Answer 11

Satiety signalling
Adiposity negative feedback signalling
Food reward

Question 12

Satiety

Answer 12

Period of time between termination of one meal and initiation of the next

Question 13

Satiation

Answer 13

Sensation of fullness generated during a meal

Question 14

Adiposity

Answer 14

The state of being obese

Question 15

What happens to satiation signals during a meal

Answer 15

They increase to prevent too big a meal size

Question 16

Satiation signals include:

Answer 16

CCK, Peptide YY, glucagon line peptide-1, oxyntomodulin, obestatin, ghrenlin.

Question 17

CCK as a satiation signal

Answer 17

Secreted by neuroendocrine cells in the gut

Signals via sensory nerves to hindbrain and stimulates hindbrain directly (nucleus tractus solitares)

Question 18

Peptide YY as a satiation signal

Answer 18

Secreted from endocrine mucosal L cells of the GI tract. Levels increase rapidly after a meal. Inhibits gastric motility, slows gastric emptying and reduces food intake.

Question 19

Glucagon line peptide- 1 as a satiation signal

Answer 19

Product of proglucagon gene. Also released from L cells in response to food ingestion. Inhibits gastric emptying and reduces food intake.

Question 20

Oxyntomodulin (OXM) as a satiation signal

Answer 20

Also from pro-glucagon gene and released from oxyntic cells of the small intestine after a meal.

Question 21

Obestatin as a satiation signal

Answer 21

Peptide produced from gene that encodes ghrenlin and released from cells lining the stomach/small intestine. Suggested that it reduces food intake, however may act to antagonise ghrelin.

Question 22

Ghrelin as a satiation signal

Answer 22

Octonoylated peptide, produced and secreted by oxyntic cells in the stomach. Ghrelin levels increase before a meal and decrease after meals. Levels are raised by fasting and hypoglycaemia.
Peripheral ghrelin stimulated food intake and decreased fat utilisation.
Ghrelin containing neurones in the hypothalamous- help control fat metabolism.
‘HUNGER HORMONE’- promotes food intake, promotes fat storage.

Question 23

Central appetite controls (drugs)

Answer 23

Glutamate, Gaba and Opioid’s.

When injected into the hypothalamous centre- effects are modest but short lasting

Question 24

Monamines

Answer 24

Act to suppress food intake.

Question 25

How is fat storage controlled?

Answer 25

Two hormones report fat store status to the brain- insulin and leptin.
Leptin is made and released from fat cells
Insulin is made and released from pancreatic cells. The levels in the blood increase as more fat is stored.

Question 26

Insulin

Answer 26

Circulates in proportion to body adiposity.
There is a transport system for insulin to enter the brain. There are high levels of insulin receptors in the hypothalamous. Intercerebro insulin inhibits food intake and decreased body weight.
Neuron specific deletion of insulin receptors leads to obesity

Question 27

Orlistat

Answer 27

Inhibits pancreatic lipase decreasing triglyceride absorption. Reduces efficiency of fat absorption in small intestine.
Side effects include, cramping, severe diarrhoea, steatorrhoea
Not to be used long term, vitamin supplements needed.

Question 28

Lorcaserin

Answer 28

5-HT2 receptor agonist.

Question 29

Types of shock

Answer 29

Cardiovascular- loss of cardiac contractility.
Hypovolaemic- loss of blood volume e.g. haemorrhagic (loss of blood) or by loss of extra cellular fluid (vomiting, diarrhoea)
Obstructive- increase in intrathoracic pressure e.g. pneumothorax.
Neurogenic- loss of sympathetic tone resulting in mass vessel dilatation.
Vasoactive- release of vasoactive mediators resulting in mass vessel dilatation.

Question 30

What is shock?

Answer 30

An abnormality of the circulatory system resulting in inadequate tissue perfusion.

Question 31

Compensatory mechanisms can maintain blood pressure if up to …% is lost?

Answer 31

30

Question 32

Management of shock

Answer 32

ABCDE
If cardiovascular- give inotropes (increase force of contractility)
If obstructive (pneumothorax)- needle aspirate chest
If anaphylactic- give adrenaline
If septic- vasopressin

Question 33

What is the humoral response?

Answer 33

A inflammatory response when they havent yet entered cells. Still in blood stream/interstitial fluid.

Question 34

Describe the divisions of the immune system.

Answer 34

the innate immune system (non-specific) and the adaptive immune system (specific) are the first divisions.
The innate immune system further divides into the first line of defence which is the skin, mucous membrane, stomach acid.
And the 2nd line of defence which is phagocytes and the inflammatory response.

The adaptive immune system is made up of lymphococytes which are both B cells and T cells.

Question 35

Where are B cells produced?

Answer 35

Bone marrow

Question 36

Where are T cells produced?

Answer 36

Produced in the bone marrow, mature in the thymus.

Question 37

Describe the action of B lymphocytes?

Answer 37

B cells bind to a virus circulating in the blood and become activated. Once activated- they proliferate to make memory B cells and effector B cells. The memory B cells will last for several years and become re-activated when the pathogens re-invade.
Effector B cells (also known as plasma cells) produce antibodies which will bind to the remaining pathogen.
Also by activation, the virus/pathogen attached to the membrane bound antibody is brought into the cell. THe contents are digested and part of this binds to the major histocompatibility complex class II. This is then presented on the B cells surface.

Question 38

T lymphocytes are further divided into…

Answer 38

Cytotoxic T cells and T helper cells

Question 39

Describe the action of T helper cells

Answer 39

ALARM CELLS
Dendritic cells are the best for activating these (antigen presenting cells activate them).
The dendritic cell has a major histocompatibility complex with a pathogen attached. THe specific interchangeable group on a specific T cell will bind to this causing activation.
Activation of T helper cells causes memory T helper cells to be produced and effector T helper cells. These effector T helper cells will release cytokines (chemical messengers) which will cause an inflammatory response

Question 40

Describe the action of cytotoxic T cells?

Answer 40

Every nucleated cell in the body has a major histocompatibility complex type 1 ability. These will present when there is a viral infection or something wrong with the cell.
This attracts cytotoxic T cells which bind to it- becoming activated. Memory T cells are produced and so are effector T cells which release proteins and granenzymes to kill the cell.