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2nd Year - systems 2 > Systems 2 - Integrated Physiology > Flashcards

Systems 2 - Integrated Physiology Flashcards

1
Q

Equivalents

A

= moles x valence

So 1 mol Na⁺ = 1 eq/L
1 mol Ca²⁺ = 2 eq/L

Moles are unit of quantity, 6 x 10²³

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2
Q

PaCO₂

A

PaCO₂ (arterial) = Rate of CO₂ production / alveolar ventilation rate

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3
Q

Quantity of moles

A

1 mole =
10³ mmol
10⁶ μmol
10⁹ nmol

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4
Q

pH equations

A

pH = -log[H⁺]
So minor changes in pH -> major changes in [H⁺]

pH = pk + log[A⁻]/[HA]

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5
Q

Importance of pH in body

A
  • enzyme activity/protein strucure affected
  • Ca²⁺ ions - 50% are free in blood, ionised, to stabilise nerve and muscle membranes. 50% are bound to albumin, which competes with H⁺ for binding. -> when decreased H⁺, less free Ca²⁺, so less of a membrane stabilising effect
  • –> so in hyperventilation, increased pH, hyperexcitable nerves
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6
Q

Trousseau sign, Chvostek’s sign

A

Trousseau - hand cramped forward, claw
Chvostek - muscle twitch when tap facial nerve

-> indicate disturbance of plasma calcium, or acid/base balance disruption

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7
Q

Buffers

A

Resist a change in pH by absorbing or releasing H⁺ when an acid or base is added

pH will still change slightly - buffer pair is weak acid and its conjugate base

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8
Q

pk

A

= the pH where an acid is 50% dissociated, [A⁻]/[HA] = 1

Lower pk -> stronger acid

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9
Q

Extracellular buffers

A

Bicarbonate
Haemoglobin
Phosphate
Plasma proteins

-> work together to resist change, isohydric principle

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10
Q

Bicarbonate buffer system

A

pk = 6.1 CO₂ + H₂O = H₂CO₃ = H⁺ + HCO₃⁻

BUT rarely know [H₂CO₃], so use solubility coefficient of 0.03 - [H₂CO₃] = 0.03 x PCO₂

  • > pH ∝ [HCO₃⁻]/PaCO₂
  • > pH depends on the ratio of bicarbonate to carbon dioxide

IMPORTANT

  • high conc of buffer pair in plasma
  • PaCO₂ regulated by respiratory system
  • [HCO₃⁻] regulated by kidney
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11
Q

Acid production in body

A

Body is net producer of acid

Kreb’s cycle makes CO₂
Metabolism makes H⁺
Gut below pylorus -> HCO₃⁻ to lumen in alkaline tide, H⁺ into blood

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12
Q

Renal handling of bicarbonate

A

Reabsorption - of bicarbonate ions by glomerular filtration. If too high, exceeds tubular threshold and spills into urine

Regeneration - of bicarbonate lost in buffering, by secreting protons into nephron to be trapped and excreted by non-bicarbonate buffers, and by secreting ammonium

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13
Q

-aemia

A

Acidaemia - acidic blood, pH less than 7.35

Alkalaemia - alkaline blood, pH more than 7.45

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14
Q

-osis

A

Acidosis/alkalosis - processes that cause a change in pH of blood

Usually -> -aemia

‘osis-without-aemia’ when pH in normal range

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15
Q

Compensation

A

Attempts to return pH to normal

Pathological chronic change in PCO₂ or HCO₃⁻ is compensated by homeostatic change in the other

Renal compensation (adjusting HCO₃⁻) is more effective than respiratory compensation (adjusting CO₂) but takes longer to get effect, days

-> if renal and lung disease, big problem

Change in same direction, if increase in HCO₃⁻, body will increase CO₂ to compensate

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16
Q

Normal range of pH, PCO₂, HCO₃⁻

A

pH - 7.35-7.45

PCO₂ - 35-45

HCO₃⁻ - 21-29

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17
Q

Alkalaemia

A

pH > 7.45

HCO₃⁻ raised, metabolic alkalosis

PCO₂ decreased, respiratory alkalosis

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18
Q

Acidaemia

A

pH < 7.45

HCO₃⁻ decreased, metabolic acidosis

PCO₂ raised, respiratory acidosis

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19
Q

Acid base map

A
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20
Q

Electroneutrality

A

Total [cations] = total [anions] in body fluids, can’t have net charge

Anion gap in -ve ions, unsure where from
Normally 8-16mEq/L

Other anions are Cl⁻ and HCO₃⁻

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21
Q

Hyperchloraemic metabolic acidosis with normal anion gap

A

As cations have increased, to fill in gap, Cl⁻ increases

Anion gap remains unchanged

Caused by too much bicarb out

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22
Q

Increased anion gap metabolic acidosis

A

As bicarbonate has decreased, to fill in gap, anion gap increasases

Cl⁻ remains unchanged

Caused by too much acid in

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23
Q

Causes of increased anion gap metabolic acidosis

A
  • more fixed acid production, eg lactic acidosis/ketoacidosis
  • ingestion of fixed acids, eg aspirin
  • inability to excrete fixed acids, eg in renal failure
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24
Q

Causes of hyperchloraemic metabolic acidosis with normal anion gap

A
  • loss of bicarb from gut, eg diarrhoea, ileostomy
  • loss of bicarb via kidney, eg renal tubular acidosis
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25
Q

Causes of metabolic alkalosis

A

SALINE RESPONSIVE

  • vomiting, diuretic use, volume contraction
  • treated with saline to decrease RAAS activity

SALINE UNRESPONSIVE
- primary hyperaldosteronism

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26
Q

Causes of respiratory alkalosis

A

Decreased PCO₂, caused by:

  • mechanical ventilation, hyperventilation
  • stimulation of respiratory centre
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27
Q

Causes of respiratory acidosis

A

Increased PCO₂, caused by ALVEOLAR HYPOVENTILATION

  • defects in neuromuscular chain
  • work of breathing exceeds the strength of respiratory pump, eg in obstruction to airflow, restrictive lung diseases, decreased lung compliance, so increased CO₂ production
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28
Q

Constant body temperature

A

Homeotherms (birds and mammals) have physiological mechanisms to regulate temperature

  • allows them to inhabit physiological niches
  • enzyme reactions work in narrow range so good to keep constant

Humans do vary by location in body in order to preserve core temperature (isotherms areas of equal heat), and also varies with time

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29
Q

BMR

A

Basal metabolic rate

  • without doing anything, we produce heat, ~100W
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30
Q

Clinical measurement of body temperature

A

Must be a representative site (into core)

Must be easily accessible

External auditory meatus most common now

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31
Q

Major routes for heat gain and loss equation

A

Metabolism - Evaporation ± Conduction ± Convection ± Radiation = 0, when heat gain = heat loss

20% loss by evaporation
40% loss by radiation
40% loss by convection

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32
Q

Thermoreceptors

A

SKIN (peripheral)

  • specific
  • sensitive to dynamic and absolute changes
  • small receptive fields
  • more cold receptors than warm

CENTRAL (posterior hypothalamus)

  • more warm receptors than cold
  • also in midbrain, medulla, spinal cord
33
Q

Central controller of temperature

A

Posterior hypothalamus

Set point generated here

ACh main transmitter

Increase Na⁺, increase set point, increase body temp
Increase Ca²⁺, decrease set point

Peripheral and central input are integrated to fine tune response (eg in cool temps, there must be a greater core temp increase to stimulate sweating)

34
Q

Adaptation/acclimatisation to heat

A

Lower sweating threshold
Increased sweat rate
Decreased electrolyte content of sweat
Behavioural changes

35
Q

Adaptation/acclimatisation to cold

A

Decreased skin blood flow
Decreased shiver threshold
Thyroid hormones
Behavioural changes

36
Q

Pyrexia

A

= fever

Above 38 degrees is significant

Infection -> toxins -> WBC reaction -> pyrogens (IL family) -> increased set point in hypothalamus –> shivering, vasoconstriction, pyloerection -> increase in core temperature

37
Q

Temperature regulation in the newborn

A

Can’t shiver, will develop at a few months old

And small size, so large SA:volume ratio, lose heat easily

  • > brown adipose tissue instead, on scapulae and around major arteries
  • abundant mitochondria here, for uncoupled oxidative phosphorylation
38
Q

Ageing

A

= maturation and deterioration

Maturation dominant until around 30

Maximum survival roughly constant, so intrinsic as well as extrinsic factors

Senescence = post-reproductive decline in viability, accompanying biological age

39
Q

Causes of ageing

A

Free radicals
Apoptosis
Genetics

40
Q

Causes of ageing - free radicals

A

Occur in normal chemical reactions

Normally involve molecular oxygen, making OH. and O₂.

Production increased by environmental agents - UV, gamma, Xrays -MAINLY SMOKING

-> lipid peroxidation - breakdown products react with DNA -> mutations -> impaired protein function

Enzymes can control:

  • superoxide dismutase, catalase
  • vitamins C and E are antioxidants, trap free radicals
41
Q

Causes of ageing - apoptosis

A

Shrinkage, degrade nuclear DNA, breakdown mitochondria, break down cell, phagocytosis

Useful in development, eg tissue remodelling

In ageing - neurons, cardiac tissue, cells of immune system all die

42
Q

Causes of ageing - genetics

A

DNA redundancy failure
- non-error sequences will eventually be exhausted, so errors will be expressed

Failure in chromosome replication

  • telomeres shorten with each division, if small enough cell will die
  • evidenced by progeria/Werner’s syndrome - genetic condition -> accelerated ageing
43
Q

Homeostasis and ageing

A

Corrections to normal take longer to occur in older people

  • eg blood glucose, recovery from exertion, temperature acclimatisation
  • > physiological effectiveness reduced
44
Q

Structural cardiovascular changes in ageing

A

HEART
Fewer cardiac myocytes - necrosis and apoptosis
Increased collagen, so stiffer

VASCULATURE
Arteries - more collagen and smooth muscle, less elastic tissue, collagen cross linked, calcium deposited (so stiffer) -> increased afterload on left ventricle
Veins - fibrosis, intima thickening, loss of elastic tissues, so -> varicosities under high pressure

45
Q

Functional cardiovascular changes in ageing

A
  • Reduced maximum heart rate, and reduced stroke volume -> so reduced cardiac output
  • Increased bp, as stiffness in arteries increases resistance
  • Baroreflex sensitivity reduced, so postural hypotension
46
Q

Renal changes in ageing

A

Decrease in kidney mass with age, loss of nephron units
Reduced glomerular filtration rate
Fewer glomerular capillary loops, change in vascular tone

-> respiratory adjustments needed to maintain pH, impaired ability by kidney to restore buffer systems

47
Q

Thermoregulation and age

A

Reduced metabolic rate
Reduced muscle mass
Increased adipose tissue
Reduced activity
-> so less heat generated by metabolism

Also

  • less evaporation loss (sweat glands atrophy)
  • more radiation loss (less thermal insulation, thinner skin and subcutaneous fat)
  • less convection/conduction loss (reduced skin blood flow to compensate for reduced cardiac output)
  • > so elderly are less able to cope with hot/cold challenges, though core temperature should not change
  • sweat later, and shiver later than would in young (though once established can do)

Ideal temperature not changed, just precision lost

48
Q

Hypoxia vs hypoxaemia

A

Hypoxia - low tissue O₂ content

Hypoxaemia - low O₂ in blood

PᴀO₂ = alveolar pressure
PaO₂ = arterial pressure
49
Q

Types of hypoxia

A

Hypoxaemic - ventilatory defect, alveolar diffusion problems

Anaemic - reduced O₂ carriage in blood

Stagnant - cardiovascular shock, shunts

Toxic - reduced extraction of O₂ by tissues

50
Q

Symptoms of hypoxia

A
  • dyspnoea (SOB), laboured breathing
  • fatigue, lethargy
  • confusion
  • tachycardia
  • deterioration of vision
  • headaches
  • peripheral cyanosis
  • euphoria, moodiness, dizziness
  • pins and needles
  • > loss of consciousness
51
Q

Ventilatory response to hypoxaemia

A

Gaseous exchange stops at PᴀO₂ of 40

Hypoxaemia -> hyperventilation

PᴀO₂ declines at a disproportionate rate, but more breathing also decreases CO₂ though, so more space for O₂ if CO₂ reduced
- carotid bodies monitor PaO₂ (innervated by glossopharyngeal nerve), and direct to hyperventilate when gets too low

52
Q

Limit to hyperventilation

A

Can’t cope with very low PaO₂

  • as blood-brain barrier is permeable to CO₂ - as PaCO₂ decreases, CO₂ also decreases in CSF
  • > respiratory alkalosis, rise in pH
  • central chemoreceptor on medulla will inhibit drive to hyperventilation
  • contradicts with peripheral chemoreceptor (carotid bodies) drive

-> therefore hyperventilatory response not as high as should be

Few days later, renal compensation will kick in, decreasing HCO₃⁻ to maintain pH another way - ACCLIMATISATION

53
Q

Cardiovascular response to hypoxia

A

Transient rise in cardiac output
Heart rate and stroke volume then decrease

-> can’t adapt well

Long term, better

  • increased capillarity to muscles
  • reduced muscle fibre diameter, so reduced O₂ diffusion distance
  • increased myoglobin content of muscle
54
Q

Immediate response to hypoxia

A

(seconds)

Increased ventilation
Pulmonary vasoconstriction
Tachycardia, increase in systemic bp

55
Q

Intermediate response to hypoxia

A

(days)

Increased ventilation, though with CSF compensation
Renal compensation of respiratory alkalosis, HCO₃⁻ elimination
O₂ dissociation curve shifts to right, reduced HbO₂ affinity, so easier to offload O₂
Increased urine loss

56
Q

Long term response to hypoxia

A

(weeks-months)

Polycythaemia - more RBCs, high haematocrit
Increased muscle capillarity
Increased muscle myoglobin/rate of anaerobic metabolism

57
Q

Tissue hypoxia -> erythropoiesis

A

Increased expression of hypoxia-inducible factor (HIF-1)

  • stimulates production of erythropoietin by kidney
  • increases liver production of transferrin
  • increases absorption of iron from intestine by regulation of hepatic mediators

-> more haemoglobin, more RBCs (BUT, increases blood viscosity, raised afterload on heart)

58
Q

Increased urinary output at high altitude

A

Reduced aldosterone, so urine loss

  • > risk of significant dehydration
  • blood volume may allow circulation to accomodate increase in RBCs -
59
Q

Acute mountain sickness symptoms

A
  • headache + one of:
  • dizziness
  • fatigue
  • sleep disturbance
  • GI disturbance

Rarely progresses to pulmonary and cerebral oedema

60
Q

Acute mountain sickness treatment

A

DESCENT

Oxygen therapy
Hyperventilation
Acetazolamide

61
Q

High altitude pulmonary oedema

A
  • potentially fatal
  • around 3 days after ascent
  • hypoxaemia
  • > pulmonary vasoconstriction
  • pulmonary pressures increase to maintain cardiac output
  • > transudation of fluid into alveoli

Symptoms - dyspnoea, fatigue, persistent dry cough (with pink frothy sputem)

62
Q

High altitude cerebral oedema

A
  • potentially fatal
  • even more dangerous but very rare
  • around 3 days after ascent
  • hypoxaemia
  • > cerebral vasoconstriction
  • cerebral pressures increase to maintain cardiac output
  • > transudation of fluid onto brain tissue

Same symptoms as acute mountain sickness, + ataxia, altered consciousness/mental status, retinal haemmorhage

63
Q

Stress response

A

Physiological changes that occur in response to stressors such as trauma, surgery, burns and sepsis, to aid survival and eventual repair

  • signalled via afferent neuronal impulses from site of injury, and release of cytokines by macrophages and monocytes in damaged tissues
64
Q

Acute phase stress response

A

IL6 produced by macrophages

  • > fever
  • > increased granulocytes, especially neutrophils and platelets
  • > liver increases production of proteins by CRP (which adheres to bacteria and promotes complement activation and phagocytosis)
65
Q

Full blood count

A

To identify cause of infection

TOTAL WHITE CELL COUNT
Neutrophils raised -> bacterial infection
Lymphocytes raised -> viral infection
Eosinophils raised -> parasitic infection/allergy

66
Q

CRP test

A

To monitor degree of inflammation

Measure CRP sequentially to see trend

67
Q

Behavioural changes in stress response

A

As brain stimulated by neuronal and cytokine signals

INCREASED

  • arousal
  • aggression
  • defence
  • vigilance

DECREASED

  • sexual activity
  • feeding
68
Q

Fight or flight response in stress response

A

Adrenaline released
-> α adrenoreceptor
- relaxation of smooth muscle in GI tract
- mydriasis (pupil dilation)
- constriction of arterioles in skin and kidney
(- hepatic gluconeogenesis and glycogenolysis)

-> β adrenoreceptor
- relaxation of smooth muscle in GI tract
- increase heart rate and contractility
- bronchodilation
- relaxation of detrusor in bladder
- dilation of arterioles in skeletal muscle
(- hepatic gluconeogenesis and glycogenolysis, lipolysis in adipose tissue, renin secretion in kidneys)

-> so blood diverted to skeletal muscle, away from gut and skin (-> glucose production, salt retention, raised bp)

69
Q

HPA axis activity in stress response

A

Hypothalmic-Pituitary-Adrenal axis

Increases activity

So hypothalamus releases CRH - corticotrophin releasing hormone
To anterior pituitary, which releases ACTH - adrenocorticotrophic hormone
To adrenal gland, which releases CORTISOL (will inhibit sequence now)

70
Q

Cortisol effects

A
  • increased gluconeogenesis
  • increased protein catabolism
  • increased lipolysis
  • > survival during fasting
  • decreased immune response
  • decreased inflammatory response (steroids use!)
  • increased vascular response to catecholamines, as increases α1 adrenoreceptors
  • decreased histamine release from mast cells
  • > treats anaphylactic shock
71
Q

Adrenocortical insufficiency

A

Primary - addison’s disease

Secondary - secondary to exogenous steroid therapy

72
Q

Salt and water metabolism in stress

A

SALT
Sympathetic stimulation of kidney
-> RAAS activation, Na⁺ retention

WATER
ADH release from posterior pituitary
-> water retention by distal nephron

-> so post op (stress), dangerous to give hypotonic solutions, as retain lots of fluid -> hyponatraemia, cerebral oedema, death

73
Q

Insulin

A

For glucose -> glycogen in liver, -> fat in adipose, -> protein in muscle

Increases glucose uptake into cells, and reduces blood glucose

74
Q

Metabolic changes to provide fuels in stress

A
  • protein catabolism
  • stimulated by cytokines and cortisol
  • > amino acids for gluconeogenesis in liver
  • gluconeogenesis and glycogenolysis
  • > glucose and ketone bodies as fuel for heart and brain
  • lipolysis
  • stimulated by cortisol, catecholamines, insulin deficiency
  • > free fatty acids and glycerol to liver
75
Q

Hyperglycaemia

A

As catecholamines and cortisol stimulate hepatic glycogenolysis and gluconeogenesis

So increased glucose in blood
Decreased insulin production, insulin resistance (very high insulin concs reduce wound healing and increase infection)

76
Q

Systemic Inflammatory Response Syndrome (SIRS)

A

Will become sepsis -> severe sepsis -> septic shock

Triggered by surgery, trauma, infections, burns, haemmorhagic shock

77
Q

Stress response a destructive force?

A

Intensive care uses drugs and machines to try to restore physiological values to normal
- may not be good; high insulin always associated with death, increased fluids following traumatic haemmorhage give death

-> so consider different therapeutic end points

78
Q

Na⁺/K⁺ levels

A

More Na⁺ extracellularly (blood tastes salty!)

More K⁺ intracellularly

2nd Year - systems 2 (7 decks)

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