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PSIO220 Integrated Physiology > Learning objectives > Flashcards

Learning objectives Flashcards

1
Q

Briefly define the nervous system hierarchy

A

CNS & PNS
Efferent neurons split into Autonomic & somatic
Autonomic split into sympathetic & parasympathetic

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2
Q

Briefly define the mechanism of action of the
endocrine system

A

Signalling via hormones in the blood. Endocrine system is amplitude modulated - increase [ ] hormone to increase response

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3
Q

Compare and contrast the endocrine and nervous
systems

A

NS is electrical signalling, ES is hormonal signalling
NS is faster

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4
Q

Briefly describe the relationship between energy
and metabolism.

A

energy is a fundamental requirement to complete any “work”. metabolism is the sum of all reactions to maintain life, primarily transforming energy to carry out work

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5
Q

Briefly describe the different types of metabolic
rates and energy expenditure.

A

BMR - basal metabolic rate (rate of energy consumption used to maintain the body)

RMR - resting metabolic rate (BMR plus approx 10% for eating and prior activity

MMR - rate of energy consumption by the body

TEF/DIT - thermic effect of food/dietary induced thermogenensis - energy required to break down food

TDEE - total daily energy expenditure (sum of basal energy, resting energy, thermic effect of food & thermic effect of exercise)

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6
Q

Briefly describe the thermic effect of food (i.e. the
energy required to digest food).

A

the amount of energy above BMR required to process & store food. magnitude depends on food composition

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7
Q

Briefly describe the concept of the Body Mass Index (BMI).

A

weight divided by height squared

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8
Q

Briefly describe the methods for measuring metabolic rate.

A

can measure the amount of O2 consumed or the amount of CO2 produced (indirect calorimetry) using open circuit (diuglas bag) or closed circuit (benedit roth spirometer)

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9
Q

what is direct vs indirect calorimetry

A

direct - measures the heat produced
indirect - measures the gast exchange to calculate the heat

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10
Q

Briefly describe the calculations for metabolic rate.

A

RQ is moves CO2 produced / moles O2 consumed

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11
Q

Briefly describe hypothalamus & pituitary structures and functions

A

Hypothalamus link nervous system & endocrine system via pituitary . Hypothalamus reglation metabolic processes ie body temp, hunger, fatigue etc.

Hypothalamus has 3 main structures - supraoptic nucleus, paraventricular nucleus & median eminence

Pituitary hangs off the bottom, 2 fused glands (anterior & posterior) Posterior Pituitary = Part of the brain, storage of neurohormones vasopressin (ADH) and oxytocin.
Anteruir Pituitary = attached true gland, prolactic, TSH, ACTH, GH, FSH, LH.

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12
Q

Briefly describe the regulation of metabolism by the hypothalamus & pituitary gland

A

Hypothalamus releases TRH, stimulates anterior pituitary release of TSH, TSH stimulates thyroid release of T3 and T4, T3 and T4 then have a negative feedback loop& inhibit TRH from hypithalamus & TSH from anterior pituitary

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13
Q

Briefly describe the regulation of thyroxine secretion

A

feedback loop - t3 and t4 inhibit hypoithalamus TRH and anterior pituitary TSH

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14
Q

Briefly describe the regulation of metabolism by thyroxine

A

Thyroxine (t4 is the less active form, longer half life, gets converted to more potent T3 in cells).

Thyroxine is thermogenic, increased O2 consumption, protein catabolismn, increase metabolic rate

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15
Q

Briefly summarise liver metabolism associated with
fed, fasted and starvation states

A

Fed: anabolic processes.
* carbs used immediately, lipoprotein synthesis, glycogenesis, lipogenesis
* Proteins - amino acids in liver intermediates for aerobic metabolism, excess lipogenesis
* Fats - triglycerides in liver/adipose tissue, cholesterol used for steroid sythemsis, lipoprotein synthesis

Fasted: starting to catabolise storage molecules
* carbs - glycogenolysis in liver for use in glycolysis
* Fats - triglycerides broekn down (lipolysis), fatty axids used for ATP through beta oxidation

Starvation: proteolysis
* proteins broken down, deaminated for ATP production or for gluconeogenesis

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16
Q

Briefly describe the roles of the adrenal gland and
pancreatic hormones in the regulation of
metabolism

A

Pancreatic hormones
* insulin from beta cells. insulin allows glucose into cells & drives anabolism
* glucagon from alpha cells. opposes insulin function, increases blood glucose.

Adrenal hormone
* epinephrine - stress hormone, acts @ liver to increase Blood glucose
* cortisol - acts to increase blood glucose by increasing lipolysis & proteolysis to liberate substrates for gluconeogenesis

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17
Q

Briefly describe the role of growth hormone in the
regulation of metabolism

A
  • released by anterior pituitary
  • results in increase in blood glucose
  • effect exerted by hormones released from liver (IGFs)
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18
Q
  • Describe the two major functions of the respiratory system
    and the four processes involved in respiration
A

2 main processes - supply O2 to body & dispose of CO2

4 processes:
1. pulmonary ventilation
2. external respiration
3. gas transport
4. internal respiration

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19
Q

Describe how gas exchange occurs across the respiratory membrane

A

simple diffusion - gas moves from high [ ] to low [ ]

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20
Q

Describe the structural characteristics of the alveoli in
human lungs which allow for optimal gas exchange

A
  • large surface area
  • thin
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21
Q

Define partial pressure and describe how the gas
composition of alveolar air differs from atmospheric air

A

partial pressure is the pressure due to the component gas. alveolar air gas composition is different due to humidity & gas exchange )more CO2)

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22
Q

Describe how gas exchange occurs between the systemic
capillary blood and the interstitial fluid

A

O2 is being used in the cells, therefore Po2 of cells is lower than Po2 in blood, O2 moves into tissue by diffusion. CO2 is opposite.

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23
Q

Quantitatively describe how the blood PO2 and PCO2 changes as the blood moves between the systemic and pulmonary
circulations, and how these levels are dependent on the PO2 and PCO2 in the alveolar air and the interstitial fluid

A

ALveoli Po2 100mmHg, Pco2 40mmHg
aterial blood Po2 100mmHg, Pco2 40mmHg
cell Po2 < 40mmHg, Pco2 > 46mmHg
venous blood Po2 <40mmHg, PCo2 >46mmHg

partial pressure gradient for CO2 smaller than O2 but it is way more soluble

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24
Q

Define the conformational changes of
deoxyhaemoglobin and oxyhaemoglobin

A

Tense - no O2 bound (deoxy), not a lot of access to haem groups
Relaxed - at least 1 O2 bound (oxy), loosens up a lil, increases ability of O2 to access haem group (increases O2 affinity)

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25
Q

Relate the structure of haemoglobin to its ability to
function in transport O2 and CO2

A

4 globin chains - 2 alpha, 2 beta
each globin chain has 1 haem group
haem group has the Fe which binds the oxygen

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26
Q

Compare and contrast the transport of CO2 and O2
in blood

A

O2 has poor plasma solubility, so relies on Hb for transport
CO2 way more soluble in plasma, so some does that, small amount travels bound to proteins including Hb, but most as HCO3-

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27
Q

Draw and briefly describe the haemoglobin
dissociation curve

A

Hb dissociation curve is sigmoidal
curve fairly flat up to 25%, coresponding to tense state Hb
25-75% saturation steep curve - increase affinity as transitioning to relaxed state

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28
Q

Define cyanosis and briefly describe its biochemical
and physiologic basis

A

cyanosis is blue tinged tissues caused by hypoxaemia (less O2 bound Hb changes refractive index and colour looks blue

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29
Q

Describe the stimuli that influence respiratory rate
and depth

A
  1. emotion (limbic system)
  2. Pco2 in blood & tissues
  3. pH & Po2 (pH normally more important but P02 in very low saturation circumstances)
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30
Q

Describe the stimuli that influence respiratory rate
and depth

A
  1. emotion (limbic system)
  2. Pco2 in blood & tissues
  3. pH & Po2 (pH normally more important but P02 in very low saturation circumstances)
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31
Q

Describe the neural pathways involved in influencing respiratory rate and depth

A
  1. Limbic - “stress response” .activates sympathetic nervous system. to hypothalamus/brainsteam via thalamus. causes increases respiration anticipating O2 demand via adrenal gland adrenaline release, binds to adrenergic receptors in lungs, increase T4 to T3 conversion
  2. Pco2 - chemoreceptors in carotid bodies signal via CNIX & CNX, as PCo2 increases, increase depth and rate of respiration to help expel CO2 and bring in O2
  3. pH - closely linked to PCo2 (bc increased PCo2 = increase H2CO3 = pH drop. pH change also detected in carotid bodies & aortic arch via CNIX & CNX. increased resp rate decreases CO2 & decreases acid buildup
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32
Q

Name the major respiratory centres and describe
their roles

A
  • PRG = pontine respiratory group. no direct link to respiratory muscles, input from thalamus & DRG, output to DRG&VRG
  • DRG = dorsal respiratory group in NTS (nucleus tractus solitarius) pf medulla. major regulator of breathing. input from CNIX, CNX & PRG. output to PRG & respiratory muscles
  • VRG = ventral respiratory group in medulla oblongata. pacemaker & pre-botzinger complex, important at rest.
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33
Q

Briefly define the relationships of the energy metabolic pathways in the muscle.

A

At the onset of exercise, immediately endogenous ATP will be used up (1-2 seconds).
Then phosphagen system - around 30sec activity
Anaerobic glycolysis boots up around 30sec, tapers off after a couple of minutes
aerobic kicks in around 1min and goes for a while.

At low intensity exercise, fats more utilised. high intensity, carbs utilised

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34
Q

Briefly define the phosphocreatine system and how this relates to the adenylate kinase and purine nucleotide cycle

A

All are trying to regenerate ATP by moving phosphates around.

  • PCr system - takes the P from PCr, puts it on an ADP leaving ATP & Cr
  • Adenylate kinnase system turns 2 ADP into an AMP and an ATP
  • purine nucleotide system - as AMP builds up (acidic), converts to IMP & NH4 - helps make ADP which can go back into the other 2 systems to make ATP
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35
Q

Briefly define muscle-centric glycogenesis and gluconeogenesis.

A

glucose gets converted to lactate in the muscles (anaerobic glycolysis). this also produces NAD+ for further glycolysis.

Lactate then goes to liver to get turned back into glucose. glucose goes back to muscles.

hepatic gluconeogenesis means glycolysis can continue and be supported for longer than relying on glycogenolysis

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36
Q

Describe the production of new glucose in the liver from alanine & lactate.

A

both lactate and alanine are transported to the liver (lactate via Cori cycle, alanine via glucose-alanine shuttle). in the liver they are both converted to pyruvate.

Pyruvate is then converted to G6P and then glucose for transport back to active tissues.

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37
Q

Define the types of muscle fibres where anaerobic metabolism is the dominant form of glycolysis

A

fast-twitch glycolytic fibers - low mitochondria for less efficient at using oxygen, primarily use anaerobic glycolysis for high intensity short duration exercise

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38
Q

Briefly define muscle-centric Aerobic glycolysis

A

pyruvate from glycolysis forms acetyl CoA

Acetyl CoA goes into TCA cycle then ETC (oxidative phosphorylation)
yeilds 32 ATPs including the 5 from glycolysis. occurs in the mitochondria

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39
Q

Briefly describe Fatty acid oxidation

A

process of using fatty acids to get Acetyl CoA which can then enter TCA & ETC. occurs inthe mitochondria

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40
Q

Briefly describe the muscle fibre types that employ aerobic glycolysis, and how this increases ATP yield.

A

oxidative fibres - slow twitch fibres mostly& some fast twitch oxidative fibres.
Lots of mitochondria where aerobic metabolism takes place which has higher yield

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41
Q

briefly describe ketogenesis

A

Acetyle Coa - inst4ead of going into TCA, gets converted into ketone bodies for use in brain & heart. ketones can be converted back tinto Acetyl CoA. happens in liver mitochondria.
nervous system activates hormones, hormones activate enzymes to make this happen.

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42
Q

Understand the involvement of sympathoadrenal system with exercise and fed-fasted metabolic supply of fuel.

A

exercise causes increased depth/rate of breathing

this stimulates HPA axis
causes epunephrine release
causes CRH release which causes cortisol release

cortison causes glucagon & GH release which increase blood glucose availability

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43
Q

Touch on the role of exercise and other hormone that regulate human physiology.

A
  • during exercise insulin secretion reduced (increase blood glucose)
  • resistance training induces transient testosterone rise & cortisol fall
44
Q

Describe the adaptations the body makes in response to exercise.

A

resistance training increases frequency and amplitude of GH & testosterone release

45
Q

Describe how the body is able to maintain relatively constant levels of oxygen and carbon dioxide when metabolic rate is increased during exercise.

A

by increasing perfusion as metabolic rate increases, and increasing minute ventilation as metabolic rate increases.

46
Q

Describe the mechanisms whereby blood flow to a tissue can vary according to metabolic need.

A

cardiac output can be increased 4-7x resting amount. Vasoactive mechanisms - changes to dilation to shunt blood towards active tissues

47
Q

Describe the relative importance of increased heart rate and increased stroke volume when cardiac output increases at different exercise intensities.

A

CO is a function of both SV & HR.
At low intensity, increasing SV is primary mechanism to increase CO (Frank Starling mechanism).
At high intensity, increasing heart rate is primary mechanism to increase CO (SV plateaus)

48
Q

Briefly discuss how heart rate measurements can be useful in determining energy expenditure during physical activities and in determining exercise training intensity.

A

due to linear relationship of HR & VO2, measurements of HR allows VO2 calculation by:
* y=mx+b where y=HR, m=slope of line, x = VO2, b = intervept & solve for x
* wearable devices to measure metabolic rate

49
Q

Briefly discuss why systemic arterial blood pressure does not normally reach dangerously high levels during intense exercise, and why different types of exercise can elicit different effects on blood pressure.

A

large decrease in peripheral vascular resistance from arteriole vasodilation mediates BP.
Work by smaller muscle mass evokes a greater BP & HR response compared to equivalent work with a larger muscle mass.

50
Q

Describe the relative importance of increased respiratory rate and increased tidal volume when minute ventilation increases at different exercise intensities.

A

similar to cardiac output, minute ventilation = respiratory rate x tidal volume.

low intensity exercise, increase minute ventilation is due to increased tidal volume.
high intensity exercise, increase minute ventilation is due to increased respiratory rate

51
Q

Briefly describe the anaerobic threshold (lactate inflection point) and how it can be measured.

A

lactate inflection point = exercise intensity at which lactate production exceeds clearance, measured by blood lactate testing, ventilatory parameters or heart rate deflection.

52
Q

Describe the way in which systolic and diastolic arterial blood pressure is created.

A

systolic BP is generated by the force of ventricular contraction.
diastolic BP occurs during ventricular relaxation

53
Q

Describe the structure and dimensions of the different types of blood vessels, with particular emphasis on the vascular smooth muscle.

A

3 types of blood vessels:
1. Arteries: thick walls, smooth muscle & elastic fibres to withstand high pressure
2. veins: thinner walls, contrain valves to ensure 1-way flow
3. capillaries: smallest, thin endothelial later, facilitate exchange with surrounding tissue

54
Q

Relate the structural differences of the different types of blood vessels to the different functions of these vessels.

A

Arteries are designed to withstand high pressure. veins have larger lumens and valves to help get blood back to the heart against gravity. capillaries have thin walls to allow exchange.

55
Q

Outline how blood pressure changes in different parts of systemic
circulation.

A

BP decreases as blood moves away from the heart (due to resistance)

56
Q

Briefly describe how tissues autoregulate their local perfusion

A

Dilation or constriction of arterioles to maintain optimal perfusion (NO)

57
Q

Describe the distribution of blood in different parts of the
cardiovascular system

A

distribution matches demans. tissues with higher metabolic rate receive greater blood flow.

58
Q

Describe how the venous skeletal muscle pump promotes venous return of blood to the heart and the importance of these capacitance vessels in combating circulatory shock.

A

Venous skeletal muscle pump: contraction of skeletal muscles compressing nearby veins helping to propel blood back to the heart against gravity.

Veins can expand & store large amounts of blood to maintain venous return and prevent circulatory shock

59
Q

Briefly describe the non-immunological structure and function of the lymphatic system.

A

lymphatic system consists of lymphatic vessels, lymph nodes & lymphoid organs. it collects & transports excess fluid (lymph) from tissues back to circulatory system. helps in immune responses & aids in absorption of fats from the digestive system.

60
Q

Explain what is meant by “mean arterial pressure”

A

MAP refers to the average pressue exerted on the arterial walls during a cardiac cycle. It is a crucial parameter in determining tissue perfusion. Calculated by adding 1/3 pulse pressure (diff between systolic & diastolic) to the diastolic pressure.

61
Q

Outline how cardiac output and total peripheral resistance are the mainfactors influencing mean arterial pressure in terms of Ohm’s law.

A

MAP = CO x TPR. CO is volume of blood pumped by the heart per minute, TPR is resistance encountered by blood flow in systemic circulation. increasing the CO or the TPR increases the MAP

62
Q

Describe the importance of internal radius on the resistance to blood flow.

A

internal radius has impact on resistance - Poiseville’s Law. resistance is inversely proportional to the 4th power of the4 radius, therefore small change in radius has substantial effect on resistance.

63
Q

Describe how blood flow through individual blood vessels is determined by the resistance of each blood vessel.

A

blood flow is determined by resistance of each blood vessel. Resistance is influenced by radius, length, viscosity. increasing resistance decreases blood flow.

64
Q

Describe why the velocity of blood flow is lowest in the capillaries and
why this is useful.

A

Due to the vast total cross-sectional area of capillary network. Large area means more surface for exchange with tissues. slow flow means more time for exchange.

65
Q

Provide an outline of the effects of the autonomic nervous system
(sympathetic and parasympathetic arms) on cardiovascular function.

A

sympathetic: increase HR, increase contractility, increase vasoconstriction = all resulting in increased BP.

parasympathetic: decrease HR, less influence on vessel diameter

66
Q

Outline the role of peripheral neural receptors (baroreceptors and
chemoreceptors) in the modulation of cardiovascular function.

A

to provide feedback to regulate cardiovascular function

67
Q

Describe the baroreceptor reflex

A
  • Baroreceptor detect increased BP (aorta & carotid bodies)
  • signal goes to cvcc in medulla
  • reduces sympathetic output, increase parasympathetic activity - causes arterial dilation
  • return to normal BP

if BP low,
* responds by increasing sympathetic output to increase BP

short term reflex, can adapt over 1-2 days

68
Q

Describe the chemoreceptor reflex

A
  • chemoreceptor detect low O2 in aorta/carotid bodies)
  • sends signald to CVCC in medulla
  • increases sympathetic output
  • causes vascoconstriction to increase cardiac return, increases HR & SV
  • doesnt work well when bloop pressure above 80mmHg
69
Q

Describe how blood pressure is measured.

A
  • directly - highly invasive, normally in ICU only
  • sphygmomanometry (korotkoff sounds)
  • electric BPM
70
Q

Briefly explain the relationship between blood volume and blood
pressure.

A

Higher blood pressure drives fluid into bowman’s capsule & increases urine formation, to gradually decrease blood volume. reduced blood volume affects cardiac return affecting BP.

71
Q

Describe how the Frank-Starling mechanism and the Bainbridge reflex operate to ensure that cardiac output is matched to venous return.

A

Frank-starling mechanism states that the greater the preload (ventricular filling), the greater the force of contraction, allowing the heart to respond to changes in venous return.

Bainbridge reflex increases HR in response to atrial stretch.

Both reflexes allow heart to adapt to changes in preload - Frank-starling changes contractile force & bainbridge changes HR

72
Q

Describe the process of exchange at the capillaries and how Starling’s forces acting across the capillary wall determine the direction and rate of such exchange.

A

at the arteriolar end of capillary, blood hydrostatic pressure is very big and pushes fluid out of capillary (net filtration pressure is positive = filtration).

At the venous end, blood hydrostatic pressure has decreased cause of resistance and is now lower than blood osmotic pressure, pulling fluid into capillary (net filtration pressure is negative = reabsorption)

73
Q

Describe the effect of hydrostatic blood pressure changes on glomerular filtration rate, urinary output and arterial blood pressure.

A

increased blood pressure increases glomerular filtration, increases urine output & reduces blood volume to reduce BP. occurs over hours to days. opposite occurs with low BP.

74
Q

Describe two important characteristics of the kidneys that ensure that the filtration rate in renal capillaries is very high compared to that which occurs in other capillaries.

A
  1. fenestrated capillaries - highly permeable
  2. high BP compared to other capillaries (by having larger afferent arteriole than efferent, and mesangial cells to control dilation)
75
Q

Describe the structure and function of the nephron,
associated capillary beds and collecting duct with reference
to the 3 major functions of the kidneys – filtration,
reabsorption and secretion.

A
  • glomerulus is the bundle of capillaries, inside the bowman’s capsule. filtration occurs at glomerulus - fluid from blood plasma goes through but proteins too big.
  • then proximal tubule, loop of henle and distal tubule to collecting duct. resorption of fluid & dissolved products happens along renal tubules/collecting duct. peritubular capillaries lies along tubules.
  • Secretion of dissolved products/some water happens along various parts of renal tubules.
76
Q

differentiate cortical and juxtamedullary nephrons

A
  • cortical are all in the cortex, juxtamedullary loop of henle down into medulla.
  • Cortical nephrons always active, juxtamedullary more active when concentrated urine needs to be formed
77
Q

Describe the renin-angiotensin-aldosterone system.

A
  • activated when BP falls
  • drop in BP stimulates renin release from renal arterioles
  • renin catalyses angiotensinogen into angiotensin I
  • angiotensin goes through lungs & gets converted to angiotensin II by ACE (angiotensin converting enzyme)
  • angiotensin II increases blood pressure
78
Q

Discuss how angiotensin II increases arterial blood pressure

A
  • angiotensin II strong vasoconstrictor - rapidly increases BP (within 20mins).
  • longer term continued action of RAAS:
  • angiotensin II reduces glomerular filtration, reducing urine formation
  • it also stimulated adrenal cortex to release aldosterone
  • aldosterone promotes Na+ resorption, water follows salt, reduces water loss via kidneys.
79
Q

Outline the factors influencing the release of aldosterone.

A

Aldosterone released in response to angiotensin II and elevated K+ extracellular

80
Q

Briefly describe the role of the kidney in the regulation of
the sodium concentration in the body and how aldosterone
influences this.

A

Na+ is important for exerting osmotic pressure. aldosterone makes almost all Na+ get resorbed. in the nephron tubules. when Na+ resorbed, water also resorbed. Often K+ excreted to allow Na+ resorption.

81
Q
  • Describe the way in which the regulation of water and
    sodium balance by the kidneys influences blood pressure.
A

aldosterone, released due to the RAAS system, causes Na+ resorption, water follows salt, causes water resorbtion. this increases blood volume which increases blood pressure.

82
Q

Describe how the kidneys maintain an osmotic gradient from the renal cortex to the renal medullary region

A
  • solutes like Na+ pumped from filtrate into interstitial fluid around renal medulla, more concentrated deeper into the medulla
  • the concentration of solutes causes the osmotic pressure
  • it is maintained by selective permeability of loop of henle - descending permeable to water only, ascending permeable to sodium (actively pumped out of ascending, this draws water from nearby descending)
  • countercurrent exchange with vasa recta removes water that leaves loop of henle, maintaining solute concentrations
83
Q

Describe the role of antidiuretic hormone (ADH) in the
regulation of water levels in the body.

A
  • It triggers resorption of water in the kidneys, results in lower output urine, more concentrated urine
84
Q

Describe the role of the collecting duct in reabsorption of water from the renal filtrate and how ADH regulates this.

A
  • collecting ducts where fine tuning of water levels happens
  • ADH aka vasopressin regulates permeability of collecting ducts
  • does this by triggering aquaporin-2 channel insertion into collecting duct wall which allow water to flow along gradient (resorption)
  • less ADH = less permeability = less water resorption = higher urine volume, less concentrated
85
Q

Outline the factors that influence the release of ADH and describe how these factors operate to maintain water balance and arterial blood pressure homeostasis.

A

ADH aka vasopressin secreted from posterior pituitary in response to:
* low baroreceptor reading in heart (low BP - low stretch in atrium) - fixes this by increasing blood volume
* or high osmolarity (ie dehydration), increased water resorption lowers solute concentrations
* nausea - ADH prevents excess fluid loss with vomiting

86
Q

Briefly outline how atrial natriuretic peptide (ANP) is
released.

A
  • peptide hormone released by atria of the heart in response to atrial stretch
  • (atrial stretch can indicate high cardiac preload, could be because of high blood volume and/or BP)
  • reduces BP and volume
87
Q

Briefly outline how ANP reduces arterial blood pressure.

A
  • reduces vasoconstriction caused by angiotensin II
  • promotes renal secretion of Na+, water follows salt, more urine excreted, lower blood volume.

does this by inhibiting production/release of angiotensin II, aldosterone & ADH

88
Q

Briefly outline how diuretics and other antihypertensive drugs affect the kidney’s control of arterial blood pressure.

A
  • diuretics primarily increase solute (mostly Na+) concentration of renal filtrate
  • this interferes with water resorbtion, urinary output increases, reduces blood volume, which reduces blood pressure.

Other classes of antihypertensives:
* ACE inhibitors - results in less formation of angiotensin II
* Beta blockers - block beta-1 adrenergic receptors on heart reducing cardiac output, but same receptors are in kidneys & causes reduced renin release as well

89
Q

Define pH and briefly describe the main physiologic sources of acid

A
  • pH is inverse log of [H+]
  • low pH = acidic, high pH = alkaline
  • normal blood pH 7.35-7.45
  • main sources of acid are products of metabolism (ie lactic acid, amino acids), transport of CO2 (as carbonic acid)
90
Q

Describe the role of buffers in maintaining physiological pH

A

buffers resist large pH changes. blood has large buffering capacity. work by binding excess H+ when pH drops and releasing h+ when pH rises.

Chemical Buffer systems in blood, less than 1 sec to respond):
* bicarbonate buffer system (H2CO3 (weak acid) and HCO3- (weak base)
* phosphate buffer system (H2PO4- (weak acid) and HPO4 2- (weak base)
* protein buffer system (amino acid side chains as weak acids (-COOH) and weak bases (-NH2) ) only contributes 20% of buffering in blood

91
Q

Describe the role respiration plays in maintaining
physiological pH

A
  • Respiratory buffer - 2nd to respond after chemical, takes minutes
  • changes the rate and depth of breathing to regulate removal of CO2
  • ie drop in pH = increase in respiratory depth & rate to increase external respiration & remove CO2 from blood to bring up pH
  • can’t completely correct acid-base status
92
Q

Describe the role the kidneys play in maintaining
physiological pH

A
  • Renal buffer - 3rd to respond after chemical & respiratory, takes hours to days
  • changes renal H+ secretion & reabsorption/production of bicarbonate (uses bicarbonate buffer, phosphate buffer & ammonia buffer system
  • v slow but can completely correct acid-base status
93
Q

Familiar with the following terms – hypobaric, hyperbaric, hypoxia, hypoxaemia, and describe the 4 types of hypoxia.

A
  • hypobaric = low pressure (eg high altitude)
  • hyperbaric = high pressure (eg diving)
  • hypoxia = inadequate O2 supply in tissues
  • hypoxaemia = deficient O2 in arterial blood (reduced pO2)

4 types of hypoxia
1. hypoxic (low arterial PO2)
2. anaemic (normal arterial PO2 but insufficient available Hb)
3. ischaemic (normal arterial PO2 but inadequate perfusion)
4. histotoxic (normal arterial PO2 but cells unable to utilise oxygen eg cyanide poisoning)

94
Q

Discuss the relationship between altitude and atmospheric pressure.

A

higher altitude has lower atmospheric pressure. gas molecules more spread out.

95
Q

Discuss the partial pressure of gasses and the relationship between altitude and partial pressure of oxygen in the air.

A

% concentration remains constant ie O2 stays around 21%, but as altitude increases air is less dense around so 21% is a lower number of molecules per breath.

Partial pressure is better measure - %v/v x atmospheric pressure
(ie at atmospheric pressire 760mmHg, PO2 = 21% x 760 mmHg = 160mmHg)

as altitude increases, atmospheric PO2 falls because atmospheric pressure changes, causes alveolar PO2 to call, causes arterial PO2 to fall, causes hypoxaemia.
eg atmospheric pressure at Mt E = 253mmHg, 21% x 253 = PO2 of 53mmHg

96
Q

Discuss the major adverse effects of acute exposure to high altitude.

A
  • starts at 2500m (~75% PO2 at sea level)
  • tissue hypoxia (cognitive symptoms of brain - confusion, impaired judgement, unconsciousness)
  • pulmonary vascular resistance - hypoxia can cause pulmonary vasoconstriction, blood flow reduces to alveoli with low PO2, increases resistance in pulmonary circulation up to 300%, can cause puolmonary oedema in severe cases
  • respiratory alkalosis - reduced arterial PO2 causes increased respiratory rate & depth, reduced PCO2, pH increases
97
Q

Discuss how the body can adapt (acclimatise) to chronic exposure to high altitude and the human limits of such adaptation.

A
  • acute changes - breathing increase in response to low PO2, causes low PCO2 and increase pH. response to low PCO2 and high pH limites increase in breathing
  • after several days, brain respiratory centre loses 80% sensitivity to PCO2 and pH changes, allowinf breathing to increase to approrpiate level to achieve PO2
  • after couple days, low CO2 causes renal pH control, reduces urinary H+ secretion & increase bicarb excretion to increase [H+] and lower pH
  • renal increased erythropoeisis so blood can carry more O2

Long term (weeks to years) acclimatisation
* renal - increase erythropoeisis to increase O2 carrying capacity
* respiratory - change in resistance of respiratory membrane, increase O2 diffusion (mechanism unclear)
* vascular - increased vascular growth factors = more capillary density = more perfusion
* increased ability of cells to use O2 when PO2 is low (involves haldane effect -Hb affinity for O2)

98
Q

Discuss the relationship between underwater depth and pressure

A

pressure doubles for every 10 metres below surface

increasing atmospheric pressure raises partial pressure (because PO2 = % concenration inhaled O2 x inhaled gas pressure)

99
Q

Discuss the problems associated with breathing under pressure and when a person ascends too rapidly from deep underwater.

A

ascent problems:
* pulmonary overinflation/pneumothorax - gas takes up more space as pressure decreases, when ascending gas in alveroli can expand and rip them apart
* air embolism/decompression sickness - Henry’s law that amount of gas that dissolves is directly proportional to the pressure. When ascending, bgases esp. nitrogen become less soluble, bubbles form, can be in joints & cause pain or in blood & cause emboli
* pain/damage to ears/sinuses/teeth - air-filled cavities, because gases expand or form bubbles but cannot escape

100
Q

Be familiar with the following terms - homeotherms,
thermoregulation, thermogenesis, hyperthermia, hypothermia.

A
  • homeotherm = organism that maintain body temp despite environmental changes
  • thermoregulation = homeostatic process enabling homeotherms to maintain body temp
  • thermogenesis = heat production
  • hyperthermia = increase body temp above normal range
  • hypothermia = decrease body temp below normal range
101
Q

discuss the different heat input and heat loss factors that influence the human body’s heat balance and body temperature

A

heat inputs:
* metabolic heat production
* environmental ie radient heat from sun

heat loss:
* evaporative from skin & lungs (humidity & temp impact)
* radiating heat from body as electromagnetic waves
* convective heat loss - movement of molecules on body surface (tiny contribution)
* conductive heat loss - transfer of heat from body to environment if environment is cooler than body

102
Q

briefly describe major mechanisms which allow the body to maintain a relatively constant temperature under hot and cold external environments.

A

decrease core temp by sympathetic NS:
* sweating (increase evaporative heat loss)
* peripheral vasodilation (increase radiant heat from skin)

increase core temp by:
* shivering & norepinephrine release (increase metabolic heat generated) (somatic motor)
* peripheral vasoconstriction (minimise radiant heat from skin) (sympathetic adrenergic)

103
Q

describe the role of the hypothalamus as the body’s
thermostat and how this can be altered during fever.

A
  • anterior hypothalamus responds to too hot
  • posterior hypothalamus responds to too cold
  • does this by integrating input from peripheral and central thermoreceptors
  • determines what is hot & cold based on matching body temp to ‘set point’. fever increases set point (triggers hypothalamus to maintain higher temp to match)
104
Q

describe the thermal events during exercise.

A

heat production is increased during sustained exercise, triggering cooling mechanisms to compensate

105
Q

Be able to describe how air temperature and humidity affect heat
loss during exercise.

A
  • humidity is biggest factor affecting evaporative heat loss
  • thermal/humidity gradients between body & env decrease when it is hot and humid, less gradient = less heat loss = body can’t cool down as well
  • results in more sweating, more peripheral vasodilation
  • water & salt are lost when hot, dehydration was impair sweating which makes it harfer again to lose heat
  • results in more sweating, more peripheral vasodilation
  • in cold conditions, cold causes vasoconstriction which reduces heat loss
106
Q

Be able to briefly describe how environmental factors (including
cold water immersion) can promote hypothermia.

A
  • low temp - increase gradient between body & environment, promote convective heat loss
  • low humidity - humidity gradient bigger, encourages evaporation & increases evaporative heat loss
  • wind chill - increases rate of convective heat loss if wind is colder than body
  • insulation - adipose tissue or clothing reducing radiant heat loss
  • cold water immersion - heat loss 25x greater than in water of same temp

PSIO220 Integrated Physiology (4 decks)

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