homeostasis

Question 1

intrinsic vs extrinsic controls of homeostasis

Answer 1

Intrinsic controls
Local controls that are inherent in an organ

Extrinsic controls
Regulatory mechanisms initiated outside an organ
Accomplished by nervous and endocrine systems

Question 2

feedforward vs feedback control

Answer 2

Feedforward
Responses made in anticipation of a change

Feedback
Responses made after change has been detected
Positive feedback systems amplify the initial change
Negative feedback systems oppose the initial change

Question 3

negative feedback systems

Answer 3

Negative feedback systems are the main type of physiological control mechanisms. They promote stability by regulating a variable through the flow of information along a closed loop. The effector opposes the initial change and aims to return the system to its setpoint.

sensor, control centre, effector

ex blood gases, blood H+, MABP, temp, blood glucose

Question 4

normothermia vs fever vs hyperthermia vs hypothermia

Answer 4

about 37.8 is normothermia
Fever is 38-40
above 40 is hyperthermia
below 35 is hypothermia

Question 5

increased vs decreased body temp effects

Answer 5

Overheating causes protein denaturation, nerve malfunction, convulsions, and death. Decreased body temperature slows down cellular metabolism and function, and can be fatal

Question 6

sources of heart gain vs loss

Answer 6

Heat gain can come from the internal environment (metabolism) or from the external environment.

The basal metabolic rate is the minimum amount of energy needed to sustain vital body functions. This is linked to the basic level of heat production. BMR can be increased by adrenaline, noradrenaline and thyroxine. Muscle activity also increases metabolism.
Heat loss is to the external environment. These must be balanced.

About half of heat loss comes from radiation. The rest is via conduction, convection and evaporation. Evaporation can be passive (skin and respiratory linings; not physiologically controlled) or active (sweating; controlled by sympathetics). Humidity of atmosphere impacts extent of evaporation.

Question 7

sensors, control centre and effectors of body temperature homeostasis

Answer 7

sensors:
central thermoreceptors (hypothalamus, abdominal organs, elsewhere)
peripheral thermoreceptors (skin)

control centre:
hypothalamus

effectors:
skeletal muscles
skin arterioles
sweat glands

Question 8

the hypothalamus as a control centre for temperature

Answer 8

The hypothalamus receives neural inputs. The posterior hypothalamus is activated by cold. The anterior hypothalamus is activated by warmth. In response to these inputs, signals are sent to the limbic system and cerebral cortex, the motor neurons to skeletal muscles and the sympathetic nervous system.

Question 9

skin arterioles, sweat glands and skeletal muscles in response to high vs low temp

Answer 9

arterioles: vasocontriction in cold; dilation in heat

skeletal muscles: increased tone and shivering in cold, decreased tone and decreased voluntary movement in heat

sweat glands: increased sweating in heat

Question 10

temperature setpoint changes in fever

Answer 10

In response to infection or inflammation there are chemicals released from macrophages (ex interleukins). These act as an endogenous pyrogens. These pyrogens stimulate the release of prostaglandins from the hypothalamus. The prostaglandins cause the hypothalamus’ thermoregulation centre to ‘reset’ the thermostat at a higher temperature. As a result mechanisms are initiated to heat the body “cold response” (ex shivering and skin vasoconstriction) to raise the body temperature to the new set point. The body temperature increases to reach the new set point resulting in ‘fever’.

The hypothalamic set point would be restored to normal if the pyrogen release is reduced/stopped or the prostaglandins synthesis is decreased/ceased.

The hypothalamus then initiate mechanisms to cool the body ‘hot response’ (ex sweating and skin vasodilatation) to reduce the body temperature to the normal hypothalamic set point.

Question 11

stimuli for control of respiration

Answer 11

hypercapnia
hypoxia
acidosis
increased temperature, central arousal, pain
amphetamines
joint movements in exercise

Question 12

sensors for respiratory controls

Answer 12

Central chemoreceptors (H+ (from CO2 only … not lactic acid/ketones etc) in CSF)
Medulla

Peripheral chemoreceptors (O2, CO2, H+)
Carotid bodies/aortic bodies

Joint receptors

Baroreceptors

note O2 only really relevant when under 8kPa

Question 13

what is the strongest stimuli for respiration?

Answer 13

arterial PCO2 (via H+ in CSF) in central chemoreceptors

Question 14

explain danger in giving oxygen to chronic respiratory failure patients

Answer 14

giving oxygen means that haemoglobin will release bound CO2. in type 2 respiratory failure the lungs do not have the capacity to blow off this CO2. Hypercapnia.

Giving oxygen leads to an increased V/Q mismatch as blood flow is directed to poorly ventilated alveoli. There is then increased release of CO2. Which the lungs cannot deal with.

Question 15

mechanical issues with respiration (x4)

Answer 15

Neuromuscular weakness (diaphragm & external intercostals - see notes)

Decreased compliance of the chest wall (kyphoscoliosis)

Loss of transmural pressure gradient across the lungs (pneumothorax)

Increased airway resistance (asthma, COPD)

NOTE: in respiratory disease expiration is more difficult than inspiration

Question 16

sympathetic vs parasympathetics and bronchi

Answer 16

sympathetic = bronchodilation; parasympathetic = bronchoconstriction

Question 17

long term vs short term management of heart failure

Answer 17

Long term medication for heart failure = DAB
(loop Diuretic ACE inhibitor Beta blocker)

Short term management (if SOB) = loop diuretic + nitrate infusion

Recall: nitrates (ex. GTN) decrease preload. They cause vasodilation.

Question 18

interstitial lung disease

Answer 18

Interstitial lung disease (pulmonary fibrosis, farmer’s lung) is a restrictive lung condition. It is associated with a dry cough and crackles at the lung bases. There is inflammation and scarring in the lungs. There is reduced compliance and impaired gas diffusion

Question 19

gas diffusion issues effect on CO2 and O2

Answer 19

If difficulty with gas diffusion, then CO2 will not be affected majorly as it is far more soluble than O2

Question 20

effect of hyperventilation on pO2

Answer 20

none

Question 21

COPD and pH

Answer 21

Most well patients with COPD will have a high CO2, but normal pH, because they have metabolically compensated for their high CO2. COPD patients with an acute exacerbation, or another acute illness an also have an acute CO2 retention on top of their chronic retention.

Question 22

numbness/tingling around the mouth and hyperventilation

Answer 22

Numbness/tingling around the mouth … Hyperventilation can cause alkalosis (low CO2). As a result more Ca2+ and binds to albumin. This results in hypocalcaemia. There is then neuromuscular effects –> tingling in fingertips, toes, perioral

Question 23

GOLD classification of airflow limitation on COPD

Answer 23

GOLD1: mild - FEV1>= 80% predicted
GOLD2: moderate - FEV1 >=50-79% predicted
GOLD3: severe - FEV1 >= 30-49% predicted
GOLD4: very severe - FEV1 <30% predicted

Question 24

anaemia and pH

Answer 24

Anaemia is a reduced haemoglobin concentration. This results in a reduced capacity for transporting oxygen.

Despite the remaining haemoglobin having normal function, there is not enough of it to meet the body’s demands. There is there for as a result tissue hypoxia and an inability to sustain aerobic metabolism (especially during exertion). Sensors in the tissue itself signal this hypoxia. There may also be resultant lactic acid build up (from anaerobic function) that can result in compensatory measures (SOB).

This results in compensatory mechanisms such as increased cardiac output and RR to try to deliver more oxygen through increased blood flow to the lungs and body.

Question 25

anaemia; pO2 and sats

Answer 25

pO2 normal (enough oxygen issue is transport)
sats normal (all Hb saturated, just not enough)

Question 26

left vs right sided heart failure

Answer 26

LEFT: paroxysmal nocturnal dyspnoea, orthopnoea, pulmonary oedema, cough, wheeze, tachypnoea, tachycardia

RIGHT: distended jugular veins, ascites, enlarged liver and spleen, oedema, weight gain

Question 27

stroke volume, Frank-Starling, cardiac output

Answer 27

Stroke volume is the volume of blood ejected per heart beat:
End diastolic volume (EDV) - end systolic volume (ESV)

Frank-Starling Law:
The more the ventricle is filled with blood during diastole (END DIASTOLIC VOLUME), the greater the volume of ejected blood will be during the resulting systolic contraction (STROKE VOLUME)

The end diastolic volume is determined by the venous return to the left and right ventricles

Cardiac output is the volume of blood pumped by each ventricle per minute:
CO = SV X HR

Question 28

factors that increase the work of breathing (x5)

Answer 28

Decreased pulmonary compliance (pulmonary fibrosis)

Restricted chest expansion

Increased airway resistance

Decreased elastic recoil

Need for increased ventilation

Question 29

In normal lungs there is ‘dynamic airway compression’. The ‘out’ force is the air in the airways, and the ‘in’ force is the pleural pressure. The pleural pressure increases at the alveoli. In normal lungs this acts to push air out of the lungs. Patients with obstructive lung diseases (COPD/asthma) have a loss of this pleural pressure over the obstructed section. This results in a decrease in pressure within the airway, and compression occuring. This may lead to alveolar collapse. If the lungs also have decreased elasticity (emphysema), then this can be made worse.In normal lungs there is ‘dynamic airway compression’. The ‘out’ force is the air in the airways, and the ‘in’ force is the pleural pressure. The pleural pressure increases at the alveoli. In normal lungs this acts to push air out of the lungs. Patients with obstructive lung diseases (COPD/asthma) have a loss of this pleural pressure over the obstructed section. This results in a decrease in pressure within the airway, and compression occuring. This may lead to alveolar collapse. If the lungs also have decreased elasticity (emphysema), then this can be made worse.

Answer 29

Compliance is the ease of inflating the lungs. This is decreased by pulmonary fibrosis, oedema, lung collapse, pneumonia, absence of surfactant. Decreased compliance = SOB. Restrictive.

Question 30

dynamic airway compression and obstructive lung diseases

Answer 30

In normal lungs there is ‘dynamic airway compression’. The ‘out’ force is the air in the airways, and the ‘in’ force is the pleural pressure. The pleural pressure increases at the alveoli. In normal lungs this acts to push air out of the lungs. Patients with obstructive lung diseases (COPD/asthma) have a loss of this pleural pressure over the obstructed section. This results in a decrease in pressure within the airway, and compression occuring. This may lead to alveolar collapse. If the lungs also have decreased elasticity (emphysema), then this can be made worse.