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Human Bio > homeostasis - glucose and temperature (chapter 5) > Flashcards

homeostasis - glucose and temperature (chapter 5) Flashcards

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Biology 101 flashcards
1
Q

homeostasis

A
  • is the body’s ability to maintain relatively stable internal environment (a steady state) even with an outside world that’s constantly changing
  • a dynamic state of equilibrium (36.7), but within the range of 36.5 - 37.5
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2
Q

aspects of internal environment that is regulated

A
  • core body temperature
  • pH and concentration of dissolved substances in the body fluid
  • concentration of glucose in blood
  • concentration of O2 and CO2 in blood and other body fluids
  • blood pressure
  • concentration of metabolic wastes
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3
Q

role of receptors

A
  • is a type of sensor that detect and monitors changes in the environment = the stimulus
  • they send information to the modulator/control centre along efferent pathway
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4
Q

role of modulators

A
  • it determines the level at which the variable is to be maintained, analyses the information it receives and then determines the appropriate response
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5
Q

role of effectors

A
  • carries out response - information flows from the modulator to effector via efferent pathway (motor neuron)
  • the results of the response feedback to stimuli (to increase or decrease)
  • most homeostatic control mechanisms are negative, used to shut off stimulus or reduce its intensity
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6
Q

thermoregulation receptors

A

thermoreceptors:

  • central: located in the hypothalamus and detects the temperature of internal environment
  • peripheral: located in skin and some mucous membranes - it detects temperature changes in external environment and sends this information to the hypothalamus
  • cold: are stimulated by temperatures lower than normal - when they are stimulated, the hypothalamus receives the info and initiates heat conservation and heat production
  • heat: are stimulated by temperatures higher than normal, when they are stimulated mechanisms operate to reduce heat production and increase heat loss
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7
Q

heat production (inputs)

A
  • body processes: metabolism (cellular respiration) and exercise
  • illness
  • stress/emotions
  • increased thyroxine levels
  • medications
  • heat gained from environment: conduction or radiation
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8
Q

heat loss (output)

A
  • evaporation: water/liquid from skin and lungs
  • warm air breathed out
  • voiding of warm urine and faeces
  • decreases in secretions og adrenaline (from adrenal medulla)
  • radiation of body heat to the cooler surroundings
  • heat loss to environment (conduction and convection)
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9
Q

heat transfers

A

radiation:
- transfer of heat from an object to another without direct contact
- e.g. gain heat when sitting in sun/loss when in cold room

convection:
- flow of warm, less dense air upwards, which is replaced with cooler, more dense air. The faster the flow the faster the cooling
- e.g. electric fan helps to move warm air from our skin to be replaced with cool air

conduction:
- heat transfer to another object through physical contact (energy passes from molecule to molecule in contact)
- e.g. placing hand in warm water

evaporation:
- heat is removed from the body when liquid turns into vapour (which carried with it the heat)
- e.g. sweating

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10
Q

responses to decreased temperatures

A
  • shivering: involuntary contractions of skeletal muscles (increased activity produces heat)
  • vasoconstriction: decreases heat loss to surroundings via radiation
  • increased metabolic rate: increased production of thyroxine
  • increased secretion of adrenalin
  • decreased surface area: curls into ball
  • behavioural: wear thicker clothes, take warm shower, sit in front of heater and increase in voluntary activity.
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11
Q

responses to increased temperatures

A
  • sweating: increases heat loss by evaporative cooling
  • vasodilation: increases heat loss by radiation
  • decrease in metabolic rate: decreased production of thyroxine
  • increased surface area: spreading limbs out
  • behavioural: wear less clothing, taking a cold shower, sit in shade, fan yourself, reduction of voluntary movement
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12
Q

vasoconstriction vs vasodilation

A

vasodilation:
- the arterioles’ diameter thicken, increasing blood flow closer to the skin (though the arterioles don’t move closer to the skin)

vasoconstriction:
- the arterioles’ diameter thin out, decreasing the blood flow close to the skin

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13
Q

negative feedback loop (vasoconstriction)

A

stimulus:
- a decrease in body temperature

receptors:
- the central (cold) thermoreceptors in hypothalamus
- the peripheral (cold) thermoreceptors in skin

modulator:
- hypothalamus (nerve impulse sent to peripheral blood vessels in skin)

effectors:
- muscles in the walls of skin arterioles

response:
- vasoconstriction (muscles constrict away from surface, less heat lost by radiation and convection)

negative reaction:
- an increase in body temperature

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14
Q

negative feedback loop (vasodilation)

A

stimulus:
- an increase in body temperature

receptors:
- the central (hot) thermoreceptors in hypothalamus
- the peripheral (hot) thermoreceptors in skin

modulator:
- hypothalamus (nerve impulse sent to peripheral blood vessels in skin)

effectors:
- muscles in the walls of skin arterioles

response:
- vasodilation (arterioles dilate and are closer to surface, increasing heat loss through convection and radiation)

negative reaction:
- a decrease in body temperature

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15
Q

negative feedback loop (sweating)

A

stimulus:
- an increase in body temperature

receptors:
- the central (hot) thermoreceptors in hypothalamus
- the peripheral (hot) thermoreceptors in skin

modulator:
- hypothalamus (nerve impulse sent to sweat glands)

effectors:
- sweat glands produce and secrete sweat onto surface of skin

response:
- sweating (layer of sweat on skin will evaporate removing heat energy from skin with it)

negative response:
- a decrease in body temperature

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16
Q

negative feedback loop (shivering)

A

stimulus:
- a decrease in body temperature

receptors:
- the central (cold) thermoreceptors in hypothalamus
- the peripheral (cold) thermoreceptors in skin

modulator:
- hypothalamus (nerve impulse sent to skeletal muscles)

effectors:
- skeletal muscles

response:
- shivering (muscles rhythmically contract and relax which create energy and heat)

negative response:
- an increase in body temperature

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17
Q

reaction to a decrease in body temperature

A

nervous system:
- skeletal muscles (sympathetic): contraction of muscles - shivering - heat generation
- blood vessels (sympathetic): muscles of arteriole walls - vasoconstriction - reduced heat loss through radiation

endocrine system:
- adrenal medulla: secrete adrenaline and noradrenaline - increased metabolic rate - increase body temperature
- anterior pituitary gland: secretes thyroid stimulating hormone - increased production of thyroxine - increase in metabolic rate - increased body temperature

behavioural:
- wear thicker clothes
- sit in front of heater
- take warm showers etc.

18
Q

reaction to an increase in body temperature

A

nervous system:
- skeletal muscles (sympathetic): sweat glands - sweating - increase heat loss through evaporation
- blood vessels (sympathetic): muscles of arteriole walls - vasodilation - increased heat loss through radiation

endocrine system:
- adrenal medulla: decreased secrete adrenaline and noradrenaline - decreased metabolic rate - decrease body temperature
- anterior pituitary gland: decreased secretion of thyroid stimulating hormone - decreased production of thyroxine - decrease in metabolic rate - decreased body temperature

behavioural:
- wear less clothes
- find shade
- take cold showers etc.

19
Q

why is piloerection ineffective in humans

A
  • a.k.a goosebumps
  • is a physiological reaction in mammals, triggered by various stimuli (like cold temperatures or arousal)
  • is contraction of small muscles (erector pili) which are attached to hair follicles (make hair erect)
  • works in other mammals due to the amount of fur (it is effective to trap body temperature)
  • though humans have sparse hairs covering their bodies, so it is ineffective
20
Q

glucose

A
  • most simple form of sugar in the blood (a simple carbohydrate)
  • main source of energy for all cells
  • absorbed in the small intestines
  • after a meal blood glucose levels can spike
  • cells require energy for activities such as reproduction, movement and synthesising molecules
21
Q

cellular respiration

A

glucose + oxygen = carbon dioxide + water + ATP

22
Q

glycogen

A
  • glucose is stored as glycogen
  • it is a complex carbohydrate
  • can store up to 500g:
    - 100g in the liver
    - 400g in the skeletal muscles
23
Q

glycogen to glucose

A
  • glycogen stored in the liver is a short-term energy supply
  • provides glucose for the body’s use for 6 hours if no other means of supply is available
  • occurs between meals (to maintain blood sugar levels)
  • conversion is stimulated by hormone glucagon

glucose - glycogen (after a spike of glucose), then glycogen - glucose (after a decrease of glucose)

24
Q

role of the liver

A
  • converts glucose to glycogen for storage
  • converts glycogen to glucose for release into blood
  • majority of its blood supply comes from the hepatic portal vein directly from the stomach, spleen, pancreas, small and large intestines.

glucose may:
- be removed from blood by liver to provide energy for liver functions
- be removed by liver and/or muscles and converted into glycogen for storage
- continue to circulate in blood, available for body cells to absorb and use as a source of energy (cellular respiration)
- be converted into fat for long-term storage, it’s in excess of that is required to maintain normal blood sugar and tissue glycogen levels.

25
Q

glycogenesis

A

glucose to glycogen

  • effects liver and muscles
  • lowers blood glucose levels using insulin
26
Q

glycogenolysis

A

glycogen to glucose

  • goes back into blood
  • increases glucose levels using glucagon
27
Q

lipogenesis

A

glucose to fats

28
Q

gluconeogenesis

A

fats and amino acids to glucose

  • goes back into blood
  • raises blood glucose level using glucagon
29
Q

role of pancreas

A

endocrine tissue within the pancreas, specifically the Islets of Langerhans, releases hormones responsible for controlling blood sugar levels:

beta cells:
- chemoreceptors detect blood glucose levels rise above normal
- beta cells secrete insulin
- insulin decreases blood sugar levels

alpha cells:
- chemoreceptors detect blood glucose levels fall below normal
- alpha cells secrete glucagon
- it increases blood sugar levels

30
Q

insulin

A
  • glycogenesis
  • lipogenesis
  • promotes protein synthesis (which requires energy and uses glucose)
  • accelerating the transport go glucose from blood into body cells (mainly skeletal muscles)
31
Q

glucagon

A
  • glycogenesis
  • gluconeogenesis
32
Q

role of adrenal glands

A

adrenal cortex (cortisol):
- they regulate carbohydrate metabolism by stimulating the conversion of glycogen into glucose (glycogenolysis)
- increase the rate at which amino acids are removed from cells and transported to the liver - these may be converted into glucose (through gluconeogenesis) if glycogen and fat levels are low
- they promote the mobilisation of fatty acids from adipose tissue - allowing muscles cells to shift from using glucose to fatty acids for much of their metabolic energy

adrenal medulla (adrenaline/noradrenaline):
- produce the same effect as those brought about by the sympathetic nerves of the autonomic nervous system
- adrenaline increases blood glucose levels through glycogenolysis and counteracts the effects of insulin
- stimulated production of lactic acid from glycogen in muscles cells, can be utilised by liver to manufacture glucose

33
Q

negative feedback loop (increasing blood glucose)

A

stimulus:
- increase in blood glucose

receptors:
- chemoreceptors in beta cells in Islets of Langerhans

modulator:
- beta cells in islet of langerhans (which secrete insulin)

effector:
- skeletal muscles
- liver

response:
- skeletal muscles increase their uptake of glucose
- liver performs glycogenesis

negative response:
- a decrease in blood glucose

34
Q

negative feedback loop (decreasing blood glucose)

A

stimulus:
- a decrease in blood glucose

receptors:
- chemoreceptors in alpha cells in Islets of Langerhans

modulator:
- alpha cells in islet of langerhans (which secrete glucagon)

effector:
- skeletal muscles
- liver
- fat

response:
- the increase in fat mobility
- glycogenolysis occurs

negative response:
- an increase in blood glucose

35
Q

hyperglycaemia

A
  • medical condition characterised by abnormally high levels of glucose in the bloodstream
  • it occurs when the body either produces too little insulin, or when cells become less responsive to it’s effects
  • it is a hallmark feature of diabetes mellitus, but can also occur due to other factors such as stress, illness, certain medications to hormonal imbalances
36
Q

causes of hyperglycaemia

A

insufficient insulin production:
- dysfunction or damage to pancreatic beta-cells, auto-immune destruction of beta cells (type 1 diabetes), reduction in insulin due to pancreatic disease/surgeries

insulin resistance:
- cells become less responsive to insulin, commonly associated with obesity, physical inactivity and generic predisposition. Causes elevated blood glucose levels due to inability to efficiently utilise glucose

excessive glucose production by the liver:
- live dysfunction or hormonal imbalances can lead to an increase in glucose synthesis and release, this overproduction, especially during fasting periods contributes to hyperglycaemia

inadequate uptake by cells:
insulin facilitates the entry of glucose into cells for energy production or storage, however defects in insulin signalising pathways or cellular glucose transporters can hinder glucose uptake leading to elevated levels

stress and illness:
- physiological stress responses, like infection or surgery, can lead to increased release of stress hormones like adrenaline and cortisol, which promote gluconeogenesis and glycogenolysis - raising blood glucose levels

medications and hormone imbalances:
- certain medication such as corticosteroids, diuretics and some antipsychotics can interfere with insulin action or promotion of glucose and it’s release. Hormonal imbalances seen in disorders in adrenal/thyroid glands can disrupt glucose regulation

dietary factors:
- consumption of high-carbohydrate meals or sugary foods can cause temporary spikes in sugar levels, particularly with impaired insulin function

37
Q

diabetes mellitus

A
  • it is a chronic disorder characterised by elevated levels of glucose
  • insulin regulates blood sugar levels by facilitating the uptake of glucose into cells for energy production or storage - though this is impacted in people with diabetes
  • this inability can lead to various complications affecting the eyes, kidneys, nerves and cardiovascular system
  • there are different types of diabetes; 1, 2 and gestational diabetes.
38
Q

type 1 diabetes

A

what:
- chronic auto-immune condition resulting in the destruction of insulin-producing beta-cells in the islets of langerhans
- leading to no insulin being produced

causes:
- autoimmune reaction, genetic predisposition and environment triggers (e.g. viral infections)

treatments:
- gene therapy
- continuous glucose monitoring
- insulin replacement surgery 9insulin pump or injections)
- carbohydrate counting with insulin adjustments

39
Q

type 2 diabetes

A

what:
- chronic metabolic disorder characterised by insulin resistance, impaired insulin secretions and elevated blood sugar levels

causes:
- insulin resistance
- impaired insulin secretions
- obesity
- sedentary lifestyle
- genetic factors
- aging

treatments:
- lifestyle modifications (diet, exercise, weightless)
- oral medications (e.g. metformin)
- regular monitoring of glucose levels

40
Q

gene therapy

A
  • involves the introduction, modification or deletion of genetic material to treat/prevent it.
  • for type 1, gene therapy involves introducing genes that encode insulin-producing beta cells or promoting the survival and function of existing beta cells

Human Bio (6 decks)

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