Review posters 17/05/2016 Flashcards Preview

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Flashcards in Review posters 17/05/2016 Deck (40):
1

Energy homeostasis

Physiological process of matching energy intake to energy output

2

Obesity

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

3

Causes of obesity

Higher levels of inactivity
Increased consumption of fatty foods

4

Factors influencing obesity

Genetics- susceptibility to genes
Environment

5

Diseases associated with obesity

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

6

Why do we need fat?

Energy storage
Prevention of starvation
Energy buffer during prolonged illness

7

Starvation

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

8

The brain and obesity

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).

9

Factors that control energy intake

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

10

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

The hypothalamus

11

Three basic concepts underlying the control of energy storage system:

Satiety signalling
Adiposity negative feedback signalling
Food reward

12

Satiety

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

13

Satiation

Sensation of fullness generated during a meal

14

Adiposity

The state of being obese

15

What happens to satiation signals during a meal

They increase to prevent too big a meal size

16

Satiation signals include:

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

17

CCK as a satiation signal

Secreted by neuroendocrine cells in the gut
Signals via sensory nerves to hindbrain and stimulates hindbrain directly (nucleus tractus solitares)

18

Peptide YY as a satiation signal

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.

19

Glucagon line peptide- 1 as a satiation signal

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

20

Oxyntomodulin (OXM) as a satiation signal

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

21

Obestatin as a satiation signal

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.

22

Ghrelin as a satiation signal

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.

23

Central appetite controls (drugs)

Glutamate, Gaba and Opioid's.
When injected into the hypothalamous centre- effects are modest but short lasting

24

Monamines

Act to suppress food intake.

25

How is fat storage controlled?

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.

26

Insulin

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

27

Orlistat

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.

28

Lorcaserin

5-HT2 receptor agonist.

29

Types of shock

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.

30

What is shock?

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

31

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

30

32

Management of shock

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

33

What is the humoral response?

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

34

Describe the divisions of the immune system.

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.

35

Where are B cells produced?

Bone marrow

36

Where are T cells produced?

Produced in the bone marrow, mature in the thymus.

37

Describe the action of B lymphocytes?

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.

38

T lymphocytes are further divided into...

Cytotoxic T cells and T helper cells

39

Describe the action of T helper cells

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

40

Describe the action of cytotoxic T cells?

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.