Homeostasis Flashcards
draw a feel back system for high calcium and low calcium
low blood calcium STIMULUS Low Blood Calcium Levels RECEPTOR Chemoreceptors on Parathyroid Gland MODULATOR Parathyroid Gland RELEASES Parathyroid Hormone into bloodstream EFFECTOR Bone Kidneys Intestines RESPONSE Bone- osteoclasts break down bone. Kidneys increase reabsorption of calcium from filtrate. Intestines- increase absorption of calcium from diet. FEEDBACK negative Increased Blood Calcium Levels
high calcium STIMULUS High Blood Calcium Levels RECEPTOR Chemoreceptors on Parathyroid Gland MODULATOR Thyroid Gland RELEASES Calcitonin EFFECTOR Bone Kidneys Intestines RESPONSE Bone- osteoblasts build down bone, storing excess calcium. Kidneys decrease reabsorption of calcium from filtrate, so calcium is removed in urine. Intestines- decrease absorption of calcium from diet, so calcium is removed via defaecation. FEEDBACK negative Decreased Blood Calcium Levels
draw a feed back system for metabolism
low metabolism STIMULUS Low metabolism – Low levels of thyroxine. RECEPTOR Chemoreceptors on Hypothalamus MODULATOR Hypothalamus TSH Releasing Factor Anterior Pituitary Gland Thyroid Stimulating Hormone Released EFFECTOR Thyroid Gland RESPONSE Increased production of thyroxine. FEEDBACK Increased levels of thyroxine – increased metabolism
high metabolism STIMULUS High metabolism – high levels of thyroxine. RECEPTOR Chemoreceptors on Hypothalamus MODULATOR Hypothalamus TSH Inhibiting Factor Anterior Pituitary Gland Thyroid Stimulating Hormone Inhibited EFFECTOR Thyroid Gland RESPONSE Decreased production of thyroxine FEEDBACK Decreased levels of thyroxine – decreased metabolism
outline the diseases causes effects and treatment for hyperthyroidism and hypothyroidism
HYPERTHYROIDISM
(over-production of thyroxine)
disease
Grave’s Disease
causes
Autoimmune condition causing an enlargement of thyroid gland.
effect Rapid heart rate. Weight loss. Increased appetite. Fatigue. Sweating. Anxiety. Protruding eyeballs.
treatment
Drugs- block iodine to reduce thyroxine production.
Surgery- remove thyroid gland.
Radioactive iodine destroys thyroid.
HYPOTHYROIDISM
(under-production of thyroxine)
disease
Hashimoto’s Disease
causes
Issues - hypothalamus/ pituitary gland/ thyroid.
Lack iodine in diet- reduced thyroxine.
Autoimmune response that destroys thyroid.
Surgery that removes thyroid (i.e. cancer).
effects Goitre. Low heart rate. Weight gain. Fatigue. Lethargy. Cold intolerance. Foetus- cretinism.
treatment
Thyroxine tablets.
Iodine supplements in diet.
show the dysfunction loop for hyperthyroidism
STIMULUS
High metabolism – high levels of thyroxine.
RECEPTOR
Chemoreceptors on Hypothalamus
MODULATOR
Hypothalamus TSH Inhibiting Factor Anterior Pituitary Gland Thyroid Stimulating Hormone Inhibited.
EFFECTOR
Thyroid Gland
ISSUE: Autoimmune disease- enlarged thyroid gland
TREATMENT: Drugs, surgery, radioactive iodine.
RESPONSE
Decreased production of thyroxine.
issue: Thyroid CONTINUES to produce thyroxine.
treatment: Reduced thyroxine
FEEDBACK
Decreased levels of thyroxine – decreased metabolism.
issue
Thyroxine levels remain HIGH- metabolism remains high.
treatment:Reduced thyroxine, reduced metabolism
outline what occurs surfing conduction, convection, radiation and evaporation
conduction,
This type of heat transfer involves heat energy moving from a warmer object to a cooler object when they are in direct physical contact.
If you touch a cold object heat passes from your body to the object
The reverse happens when you touch something hotter than your body
convection
An object will heat or cool the air as it passes over the object.
Warm air created by contact with a warm body rises and is replaced by cool air.
The currents of moving air remove heat energy from the object
radiation
Heat energy moves from a warmer object to a cooler object across space.
No contact between bodies is necessary
If your body has a higher temperature than the environment you will radiate heat into the environment, which cools the body and vice versa
evaporation
This occurs when liquid water is converted to water vapour
This process requires energy which is taken from the body in the form of heat, thus cooling the body.
As we sweat the evaporation of sweat from the skin cools the body
out line what occurs when regulating high body Temperature
behaviour response
stimulus: high body temperature
receptor: thermoreceptors in the skin and hypothalamus
modulator: thermoregulotary center in the hypothalamus ‘heat loss center’
effector: cerebral cortex
response: remove clothing, reduce activity, cool environment, sprawl out
feedback: decreased body temperature
sweating
stimulus: high body temperature
receptor: thermoreceptors in the skin and hypothalamus
modulator: hypothalamus transmits nerve impulse too the sweat glands
effector: sweat glands
response: release sweat water evaporates as the body heats it up heat energy in the body is removed
feedback: decreased body temperature
vasodilation
stimulus: high body temperature
receptor: thermoreceptors in the skin and hypothalamus
modulator: hypothalamus transmits nerve impulse to arterioles
effector: smooth muscle in blood vessels (arterioles)
response: increase blood flow to extremities and warm blood looses heat via radiation
feedback: decreased body temperature
decreasing metabolism
stimulus: high body temperature
receptor: thermoreceptors in the skin and hypothalamus
modulator: hypothalamus releases thyroid stimulating hormone inhibiting factor allowing for thyroid stimulating hormone to be released from the ant pit gland and thryroxine will be released from from the thyroid
effector: somatic body cells
response: reduced cellular respiration and there is a decreased heat produced
feedback: decreased body temperature
outline what occurs when regulating low body temperature
behaviour response
stimulus: low body temperature
receptor: thermoreceptors in the skin and hypothalamus
modulator: thermoregulotary center in the hypothalamus ‘heat production center
effector: nerve impulse is transmitted to the cerebral cortex frontal lobe
response: delibrate movement, putting clothes on, turn oh a heater, find shelter
feedback: increased body temperature
shivering
stimulus: low body temperature
receptor: thermoreceptors in the skin and hypothalamus
modulator: hypothalamus sends nerve impulse to skeletal muscle
effector: skeletal muscle
response: mussels repeatedly contract and relax to generate heat via friction and cellular respiration
feedback: increased body temperature
vasoconstriction
stimulus: low body temperature
receptor: thermoreceptors in the skin and hypothalamus
modulator: hypothalmus transmits nerve impulse to blood vessels
effector: smooth muscle in blood vessels (arterioles)
response: vasoconstriction blood flow released to extemities warm blood circulates the core of the body and heat loss is reduced
feedback: increased body temperature
increasing metabolism
stimulus: low body temperature
receptor: thermoreceptors in the skin and hypothalamus
modulator: hypothalamus releases thyroid stimulation hormone realeasing factor this stimulates the release of TSH from the posterior lobe of the pituitary gland thyroid will realease thyroxine
effector: somatic body cells
response: increase rate of cellular respiration and heat is produced as a by product
feedback: increased body temperature
release of adrenaline and noradrenaline
stimulus: low body temperature
receptor: thermoreceptors in the skin and hypothalamus
modulator: hypothalamus transmits nerve impulse
effector: adrenal medulla
response: release of adrenaline and Nora adrenaline and increased cell respiration
feedback: increased body temperature
what is the normal reading of glucose levels and why do they need to be regulated
Normal reading 4.0-7.8 mmol/L.
Nervous tissue – sensitive to changes in glucose levels.
Excess or deficiency of blood glucose levels for more than a few hours can result in the loss of consciousness and brain damage
The storage form of glucose (glycogen) does not harm the tissues
what is the function of the pancreas and the islets of langerhans and outline the difference between alpha and beta cells
The pancreas is a large mass of glandular tissue enclosed by the duodenum.
Function:
Exocrine- produces digestive enzymes
Endocrine- ‘Islets of Langerhans’ – produce hormones.
Islets of Langerhans
Special cells in the Islets of Langerhans have chemoreceptors that detect the glucose level of the blood – alpha and beta cells
Alpha cells detect low glucose levels
Beta cells detect high levels of glucose in the blood
what are the function of alpha and beta cells
ALPHA cells – low blood glucose levels
GLUCAGON – increases blood glucose levels.
BETA cells- high blood glucose levels
INSULIN- decreases blood glucose levels
what is the role of the the liver in glucose regulation
Major role in glucose regulation.
Blood supply is from the ‘HEPATIC PORTAL VEIN’ – comes directly from the digestive system
Rich in nutrients
Glucose is
Removed by the liver for energy
Stored as glycogen in the liver and skeletal muscles
Circulated the body to provide cells with energy
Converted to fat for long term storage
define what Glycogenolysis, Lipolysis, Gluconeogenesis Glycogenesis ,Translocation, Lipogenesis do
Glucagon causes the following effects;
Glycogenolysis
Breakdown of glycogen into glucose
Lipolysis
Lipids are broken down
Gluconeogenesis
Fats and amino acids combine to produce glucose
Insulin causes the following;
Glycogenesis
Glucose molecules combine to produce glycogen which is then stored in the liver
Translocation
Glucose moves from the blood into the cells (increase cellular uptake)
Lipogenesis
Glucose is converted into lipids
outline what occurs when Low blood glucose levels eg. during exercise also outline what occurs when High blood glucose levels eg after a meal
draw the feed back loop
low glucose
Stimulus
Low blood glucose levels
Receptors
`Islets of Langerhans
Modulator
Alpha cells produce glucagon
Effectors
Liver and body cell
Response
Glycogenolysis, gluconeogenesis, lipolysis
Feedback
Higher glucose in blood
high glucose
Stimulus
High blood glucose levels
Receptors
Islets of Langerhans
Modulator
Beta cells produce insulin
Effectors
Liver, body cell and muscles cells
Response
Glycogenesis, translocation, lipogenesis
Feedback
Lower glucose in blood
these are both negative feeback
how can adrenaline and cortisol affect glucose production display in feedback loop
Effects of Adrenalin
Stimulus
Stress/Exercise
Reduced glucose.
Receptors
Amygdala interprets stressor
Modulator
Hypothalamus- nerve impulse along sympathetic n.d. to adrenal medulla- releases adrenalin
Effectors
Liver, skeletal muscles cells, adipose tissue
Response Glycogenolysis Lipolysis Gluconeogenesis Increased metabolism Increased HR, BP Reduced inflammatory response
Feedback
All responses aimed to enhance body to over stress.
Increased glucose for energy.
Effects of Cortisol
Stimulus
Stress
Low blood glucose
Receptors
Amygdala interprets stressor.
Modulator
Hypothalamus- ACTH RF- Anterior Pituitary Gland – ACTH – Adrenal Cortex - Cortisol
Effectors
Liver, skeletal muscles cells, adipose tissue
Response Glycogenolysis Lipolysis Gluconeogenesis Increased metabolism Increased HR, BP Reduced inflammatory response
Feedback
All responses aimed to enhance body to over stress.
Increased glucose for energy.
these are both negative feedback
how can the hypothalamus regulate glucose levels
Behaviour can also change in response to blood sugar levels
HIGH blood glucose levels-
Hypothalamus acts through the cerebral cortex to decrease appetite
LOW blood glucose levels-
Hypothalamus acts through the cerebral cortex to increase appetite
draw the dysfunction loops for both diabetes mellitus type 1 and type 2
diabetes mellitus type 1
Stimulus
High blood glucose levels
Receptors
Islets of Langerhans Issue: Beta cells destroyed by autoimmune response. Can not detect levels.
Modulator
Beta cells produce insulin Issue: Beta cells destroyed by autoimmune response. Can not produce insulin. Treatment: Regular self-monitor of blood glucose levels and insulin injection
Effectors
Liver, body cell and muscles cells treatment Effectors respond to insulin.
Response
Glycogenesis, translocation, lipogenesis treatment Responses can take place.
Feedback
Lower glucose in blood treatment Glucose levels are lowered- neg. feedback. (if not treated glucose will remain high and the feedback will be positive but if treated negative)
Diabetes Mellitus Type 2
Stimulus
High blood glucose levels
Treatment: Prevent high blood glucose levels to begin with. exercise
Receptors
Islets of Langerhans
Modulator
Beta cells produce insulin
Effectors
Liver, body cell and muscles cells
Issue: Effectors DO NOT RESPOND to insulin.
Treatment: Medications make receptors on effectors more sensitive, and thus respond to insuli
Response
Glycogenesis, translocation, lipogenesis
treatment: Rate of responses increases.
Feedback
Lower glucose in blood
treatment: Glucose levels are reduced- Neg. feedback.
outline the cases symptoms treatments of type 1 and type 2 diabetes mellitus
1) Insulin dependent diabetes
cause
A fault in the individual’s immune system caused by a destruction of beta cells in the islets Langerhans of the pancreas so you can’t produce insulin
Symptoms They don’t produce insulin Long term Kidney failure Hearst attack Stroke Blindness Nerve damage Amputations
Treatments
Insulin cannot be taken from tablet because it is absorbed in the alimentary canal Regular injections of insulin, they do not actually treat the diabetes it just fulfills the role to maintain homeostasis
An insulin pump is also used
2) Adult-onset diabetes
causes Cells not responding to insulin because of -Lack of physical activity -Being overweight or obese -Diet high in fat -Smoking -High blood cholesterol Causing There cells do not respond to insulin the insulin receptors open up too much so they become worn out over time insulin receptors become worn and torn so there will be reduced levels of glucose, so their cells begin to produce too much glucose
symtoms
No symptoms but can lead to kidney failure, heart attach blindness
treatment
- Careful diet
- Regular physical activity’s
- Maintaining healthy weight
- Medication to control glucose levels main king the receptors more sensitive
out line what glomerus filtration tubular reabsorption and tubular secretion are
glomerulus filtration
the movement of substance from the blood within the the glomerulus in to the capsular space
tubular reabsorption
the movement of substances from the tubular fluid back into the blood
tubular secretion
the movement of substances from the blood into the tubular fluid
to the table test of the nephron
rate on the performance
draw a feed back loop for breathing at rest or active breathing
Breathing at rest- inspiratory centre switches off, and exhalation occurs passively
STIMULUS
High carbon dioxide = increased hydrogen ions = low pH.
Extremely low oxygen
RECEPTOR
Chemoreceptors- Medulla oblongata; aortic & carotid bodies.
MODULATOR
Medulla oblongata ‘Respiratory Centre- Inspiration Centre’
Nerve impulse along intercostal nerve and phenic nerve
EFFECTOR
External Intercostal muscles & diaphragm
RESPONSE
Inhalation/increased depth and rate of breathing.
FEEDBACK
Reduced carbon dioxide, decreased hydrogen ions, increased pH.
Increased oxygen levels
Breathing when Exercising- inspiratory centre switches off, and expiration centre turns on to push air out of lungs.
STIMULUS
High carbon dioxide = increased hydrogen ions = low pH.
Extremely low oxygen
RECEPTOR
Chemoreceptors- Medulla oblongata; aortic & carotid bodies
MODULATOR
Medulla oblongata ‘Respiratory Centre- EXPIRATION Centre’
Nerve impulse along intercostal nerve and phenic nerve
EFFECTOR
Internal Intercostal muscles & Abdominal muscles
RESPONSE
Forced expiration of air from lungs.
FEEDBACK
Reduced carbon dioxide, decreased hydrogen ions, increased pH.
Increased oxygen levels
explain what antidiuretic hormone does
ADH controls the permeability of the walls of the DCT and CD.
Increased ADH in blood stream DCT/CD permeability increases water actively reabsorbed from filtrate back into the blood stream.
Urine volume decreases, solutes become more concentrated.
explain what occur when water concentration is high or low for….
thirst reflex
aldosterone
and ADH
Feedback loop – THIRST REFLEXlow water concentration in blood stream. STIMULUS Decreased water Decreased blood volume & pressure Increased salt concentration Increased osmotic pressure RECEPTORS Osmoreceptors- Hypothalamus ‘Thirst Centre’ MODULATOR (& how it works) Hypothalamus ‘Thirst Centre’ EFFECTOR Cerebral Cortex- Feel thirsty RESPONSE Feel thirsty Behavioural response- drink water/eat foods high in water FEEDBACK Increased water Increased blood vol & pressure Decreased salt concentration Decreased osmotic pressure
Feedback loop – THIRST REFLEXHIGH water concentration in blood stream. STIMULUS Increased water Increased blood volume & pressure Decreased salt concentration Decreased osmotic pressure RECEPTORS Osmoreceptors- Hypothalamus ‘Thirst Centre’ MODULATOR (& how it works) Hypothalamus ‘Thirst Centre’ EFFECTOR Cerebral Cortex RESPONSE No longer feel thirsty Behavioural response- stop drink water/eat foods high in water. FEEDBACK Decreased water Decreased blood vol & pressure Increased salt concentration Increased osmotic pressure
Feedback loop - aldosteronelow water concentration in blood stream. STIMULUS Decreased water Decreased blood volume & pressure Increased salt concentration Increased osmotic pressure RECEPTORS (x3) Osmoreceptors (Hypo + Kidney) MODULATOR (& how it works) Hypothalamus ACTHRF Anterior Lobe Pit. Glands ACTH Adrenal Cortex Release aldosterone EFFECTOR Distal convoluted tubule and collecting duct RESPONSE Increased reabsorption of sodium ions into blood. Increases osmotic pressure water moves from filtrate to blood FEEDBACK Increased water Increased blood vol. & pressure Decreased salt concentration Decreased osmotic pressure
Feedback loop - aldosteroneHIGH water concentration in blood stream. STIMULUS Increased water Increased blood volume & pressure Decreased salt concentration Decreased osmotic pressure RECEPTORS (x3) Osmoreceptors (Hypo + Kidney) MODULATOR (& how it works) Hypothalamus ACTHIF Anterior Lobe Pit. Glands Stop ATCH Adrenal Cortex Stop aldosterone EFFECTOR Distal convoluted tubule and collecting duct RESPONSE Decreased reabsorption of sodium ions into blood. Decreases osmotic pressure water stays in filtrate. FEEDBACK Decreased water Decreased blood vol. & pressure Increased salt concentration Increased osmotic pressure
Feedback loop - adh low water concentration in blood stream.
STIMULUS Decreased water Decreased blood volume & pressure Increased salt concentration Increased osmotic pressure RECEPTORS Osmoreceptors- Hypothalamus MODULATOR (& how it works) Hypothalamus Nerve Impulse Posterior Lobe Pit. Glands Release Antidiuretic Hormone EFFECTOR Distal convoluted tubule and collecting duct RESPONSE Increased permeability- water ducts open and water moves from filtrate into blood. FEEDBACK Increased water Increased blood vol & pressure Decreased salt concentration Decreased osmotic pressure
Feedback loop - adhHIGH water concentration in blood stream.
STIMULUS Increased water Increased blood volume & pressure Decreased salt concentration Decreased osmotic pressure RECEPTORS Osmoreceptors- Hypothalamus MODULATOR (& how it works) Hypothalamus No Nerve Impulse Posterior Lobe Pit. Glands No Antidiuretic Hormone EFFECTOR Distal convoluted tubule and collecting duct RESPONSE Decreased permeability- water ducts close and water remains in filtrate and exits as urine. FEEDBACK Decreased water Decreased blood vol & pressure Increased salt concentration Increased osmotic pressure
what is hyperventilation/ why is it dangerous and draw a feedback loop of the effect of hyperventilation
Hyperventilation
Quick breathing more co2 is breathed out than oxygen is breathed in Significant decrease in carbon dioxide levels.
Oxygen levels DO NOT increase.
Removes the STIMULUS to breathe
Why is Hyperventilation Dangerous?
Oxygen is used up BEFORE carbon levels build up enough to stimulate breathing response.
Brain RUNS OUT of oxygen…person passes out until issue corrects itself.
If underwater…breathing will occur subconsciously…drowning.
‘Shallow Water Drowning’
Effect of Hyperventilation
Hyperventilation REMOVES STIMULUS as it removes significant amounts of carbon dioxide from the blood.
STIMULUS Does not exist. Carbon dioxide levels are too low, and take time to build up. Oxygen runs low before stimulus is initiated. PASS OUT. RECEPTOR Not stimulated MODULATOR Not stimulated EFFECTOR Not stimulated RESPONSE Not stimulated FEEDBACK Carbon dioxide slowly builds up, oxygen levels continue to drop.
what is emphysema what are the causes effects and treatment and draw a dysfunction feed back loop
What is Emphysema?
Lung condition
Shortness of breath
Alveoli are damaged, walls weaken and rupture.
Reduces surface area, reducing oxygen diffusion into blood stream.
Causes? Tobacco, marijuana smoke (including second-hand smoke) Air pollution Dust, chemicals and fumes Age, smoking habits increase chances
Effects? Shortness of breath Blue fingernails, lips Not mentally alert Coughing, phlegm, wheezing Swelling of limbs Collapsed lung Complications: preventing from doing daily activities, chronic problems such as asthma, back problems, cancers, diabetes, heart issues, stroke, kidney problems.
Treatments?
Medications- bronchodilators (relaxing bronchioles to address breathing issues), inhaled steroids (reduce inflammation, relieving shortness of breath), antibiotics.
Therapy- pulmonary rehabilitation (breathing exercises)
Nutritional therapy- dietary adjustments (i.e. weight-loss, weight-gain)
Supplemental oxygen
Lung volume reduction surgery
Lung transplant
Effect of Emphysema
STIMULUS
High carbon dioxide = increased hydrogen ions = low pH.
Extremely low oxygen.
RECEPTOR
Chemoreceptors- Medulla oblongata; aortic & carotid bodies.
MODULATOR
Medulla oblongata ‘Respiratory Centre- Inspiration Centre’
Nerve impulse along intercostal nerve and phenic nerve.
EFFECTOR
External Intercostal muscles & diaphragm
RESPONSE
Inhalation/increased depth and rate of breathing.
FEEDBACK
Carbon dioxide remains HIGH = increased hydrogen ions = low pH.
Extremely low oxygen.
ISSUE:
Emphysema – destruction of alveoli (reduced surface area). Inefficient gas exchange.
TREATMENT:
Additional oxygen supply to increase chances of gas exchange.
what is asthma what are the causes effects and treatment and draw a dysfunction feed back loop
What is Asthma? Lung condition Airways become inflamed, swollen, narrow and produce extra mucous. Difficult to breathe. Causes? Exposure to irritant and substances that trigger allergies, such as pollen, dust mites, spores, pet dander, etc. Induced by change in temperature, exercise. Psychological- stress, panic Effects? Unusual tiredness Trouble sitting still Pale, sweating skin Fast breathing Coughing, wheezing Shortness of breath Treatments? Incurable Inhalers with spacers- corticosteroids inhaled into lungs to clear airways to assist in breathing. Oxygen therapy- supplemental oxygen.
Effect of Asthma
STIMULUS
High carbon dioxide = increased hydrogen ions = low pH.
Extremely low oxygen
RECEPTOR
Chemoreceptors- Medulla oblongata; aortic & carotid bodies
MODULATOR
Medulla oblongata ‘Respiratory Centre- Inspiration Centre’
Nerve impulse along intercostal nerve and phenic nerve.
EFFECTOR
External Intercostal muscles & diaphragm
RESPONSE
Inhalation/increased depth and rate of breathing.
ISSUE:
Asthma- Bronchioles are constricted, air flow is prevented.
Air is unable to flow into/out of lungs, gas exchange is insufficient.
TREATMENT:
Body- Releases adrenaline- relaxes smooth muscle in bronchioles, opening airways.
Medication- I.E. Ventolin – opens airways.
FEEDBACK:
Reduces carbon dioxide = reduces hydrogen ions = increases pH.
Increases oxygen levels.
