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60 Second Viva Practice > Physiology > Flashcards

Physiology Flashcards

1
Q

What factors influence cerebral blood flow?

A

Defined as the volume of blood per 100g of brain tissue/min
Normal = 50ml/100g/min

—Autoregulation
—Cerebral perfusion pressure
—CMRO2
—PaO2
—PaCO2
—Drugs used in anaesthesia
—Temperature
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2
Q

What are the functions of the stomach?

A

Range of functions:
—Storage of large meals
—Mixing
—Secretory function: HCl, Gastrin, pepsinogen, Intrinsic Factor
—Hormonal/endocrine: secretion of hormones for GI tract function
—Immune: barrier to infective pathogens

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3
Q

What is myasthenia gravis?

A

Autoimmune disease with IgG auto-antibodies produced against the nicotinic ACh receptors in the neuromuscular junction.
Symptoms range from ocular, bulbar, respiratory or widespread.

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4
Q

How would you anaesthetise for a mediastinal mass?

A

Considerations:

—Change from negative pressure to positive pressure ventilation may cause tracheobronchial obstruction
Maintain SPONTANEOUS VENTILATION
—Changes in patient position may compress everything
—Compression of SVC - SVC obstruction
—Indications for anaesthetic (e.g. thymoma = Myasthenia Gravis and considerations for that)

Pre:
—CT/MRI to establish where mass is in relation to airways/vessels
—ECHO
—high dose steroids pre-op (e.g. lymphoma)
Peri:
—Anti-sialogogue
—Gas induction in head up position
—Maintain spontaneous ventilation
—Awake extubation
—If compresses - lateral or prone positioning, use of rigid bronchoscopy may be required

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5
Q

What is aldosterone?

A

Aldosterone is a mineralocorticoid steroid hormone synthesised in the zona glomerulosa of the adrenal gland to act on the distal tubules/collecting ducts of the nephron to conserve Na/H2O and increase BP

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6
Q

What is insulin?

A

Insulin is a polypeptide hormone formed in beta cells of islets of Langerhans
Bind to tyrosine kinase receptors to cause increased uptake of glucose into cells

Formed from breakdown of pro-insulin by cleaving C peptide
Released in 2 phases - rapid release from vesicles followed by release as it is synthesised
Released in response to:
—rise in plasma glucose concentration (facilitated diffusion into beta-islet cells)
—adrenaline/beta-2adrenergic activation

Effects are:
—facilitate glucose uptake
—encourage storage of glycogen/fatty acids
—inhibit breakdown of stored glucose

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7
Q

What do we mean by the ‘stress response to surgery’?

A

Refers to a series of hormonal, inflammatory, metabolic and psychological changes occurring in response to surgery/trauma

—Hypothalamic stimulation causes ACTH, GH, ADH, adrenaline, RAAS
—Immune response: inflammation/cytokines, suppressed T cells

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8
Q

What is glucagon?

A

A peptide hormone produced in alpha cells in islets of Langerhans
Stimulated by hypoglycaemia and adrenaline
Inhibited by: insulin, somatostatin, ketones/fatty acids

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9
Q

What factors affect cerebral blood flow?

A

Cerebral blood flow is proportional to CPP and inversely proportional to cerebral vascular resistance

PO2
PCO2
CMRO2
Temperature
CPP
CVR - anaesthetic drugs
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10
Q

What is the oxygen cascade?

A

The sequential reduction in PO2 from the atmosphere to cellular mitochondria

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11
Q

How is CO2 transported in the blood?

A

Bound to bicarbonate
Bound to carbamino compounds (Hb; Bohr shift and Haldane shift)
Dissolved

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12
Q

Describe the control of ventilation

A

Mainly done by central chemoreceptors
Controlled to maintain homeostasis of pH, PaO2 and PaCO2

Respiratory centre in the brainstem:
—Dorsal respiratory group (inspiration)
—Pneumotaxic centre
—Ventral respiratory group (expiration)
—Apneustic centre
Peripheral chemoreceptors (aortic arch/carotid bodies)
Central chemoreceptors (ventral medulla)
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13
Q

How is coronary blood flow autoregulated?

A

Metabolic: H+, K+, CO2 release
Myogenic: stretch
Endothelial: NO, prostaglandin (PGI2)
Autonomic: ANS (minor role)
Hormonal: ANP, Angiotensin II

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14
Q

What factors affect myocardial oxygen supply?

A 
Coronary perfusion pressure (=aortic pressure - intraventricular pressure or LVEDP)
Perfusion time/HR
Coronary vessel patency
Coronary vessel diameter
Blood viscosity (haematocrit)
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15
Q

What factors determine myocardial oxygen consumption?

A 
HR
Contractility
Afterload
Tissue mass
Temperature
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16
Q

What happens in pericardial tamponade?

A

Increase in pericardial space causing compression of chambers and haemodynamic instability
Starling’s forces unable to work - decreased output
Due to decreased cardiac filling. Pericardial pressure normally = to intrapleural pressure
When pericardial pressure raised it reduces filling in all 4 chambers

17
Q

What is the definition of sepsis?

How do we score it?

A 
Dysregulated host response to infection
SOFA score (RS, CNS, CVS, Liver, Coagulation, Renal)
qSOFA score >1

|Severe sepsis = above, plus organ dysfunction

|Septic shock = hypotension despite fluid resus (25% mortality)

18
Q

What is cardiac output?

A

CO = SV x HR

SV = the amount of blood ejected from the ventricle per contraction
Comprises:
—Preload (blood volume, intrathoracic pressure, body posture)
—Contractility (sympathetic stimulation, catecholamines, inotropes, calcium)
—Afterload (SVR, inotropes, intrapericardial pressure)

19
Q

What are the respiratory differences in a neonate?

A

—Immature respiratory centre so control not well developed
—Periodic breathing - rate varies; occ apnoeas
—Reduced response to hypercarbia
—Horizontal ribs; flatter diaphragm
—Fewer Type 1 fibres
—Compliant rib cage
—Small diameter airways

20
Q

Describe the autonomic regulation of cardiac function

A

Regulated by SNS and PNS
—PNS more rapid control of HR

SNS:
-from T1-T5
-R ganglia influence chronotropy (closer to SAN)
-L ganglia control inotropy (L ventricle and inotropy)
Increases membrane permeability to Ca/Na ->effect on resting membrane potential etc

PNS:
-R Vagus - SAN
-L Vagus - AVnode
Increase membrane permeability to K ->hyperpolarised membrane potential

21
Q

What is cerebral perfusion pressure?

A

Determines CBF at extremes of MAP (i.e. outside of autoregulation)

CPP = MAP - ICP

Normal = ~80 - 100mmHg

22
Q

What is preload?

How can we increase it or decrease it?

A

The initial length of cardiac muscle fibres before contraction begins
The intraluminal pressure that stretches the ventricle to its end-diastolic dimensions
-related to the diastolic length of the cardiac myocyte

Starling’s law: the force of cardiac contraction depends on the preceding diastolic length of the ventricular fibres - so an increased preload increases SV

Difficult to measure, so LVEDV/P used as a surrogate (depends on compliance)
Affected by: blood volume, intrathoracic pressure, body posture

23
Q

What is afterload?

How can you increase it/decrease it?

A
  • The stress developed in the LV wall during ejection; reflects the force opposing the shortening of cardiac myocytes
  • Resistance the LV must overcome to eject blood
  • MAP & SVR reflect LV afterload; can be increased or decreased with vascular tone alteration, intrapericardial pressure or inotropes
  • As afterload increases, both the rate and extent of sarcomere shortening decrease, resulting in a reduction in SV
  • Governed by SVR; an increase in afterload results in a reduction in SV (as less blood is ejected from the heart per beat, there is a greater volume of blood remaining in the ventricle at end-systole causing greater LVEDV
24
Q

What is contractility?

A

The intrinsic ability of the cardiac myocyte to do work for a given preload and afterload
Factors that affect contractility = inotropic
Sympathetics, catecholamines, inotropes

Drugs: inotropes, Ca; milrinone, dobutamine (inodilator - increases inotropy and vasodilates)

25
Q

What do we mean by oxygen delivery?

What do we mean by Oxygen Extraction Ratio?

A
  1. DO2 = CO x CaCO2 x 10
  2. OER = VO2/DO2
    Demonstrates what should be being taken out of blood to oxygenate tissues. Normally 25%.
    If DO2 is inadequate = anaerobic threshold
26
Q

What is the neuromuscular junction?

A 
The chemical synapse between a motor neuron and a muscle cell
Consists of:
-terminal bouton
-synaptic cleft
-motor end plate
27
Q

How is acetylcholine stored and released?

A
  1. In the NMJ - stored in vesicles
    - 1% in the active zone
    - 80% in the reserve pool
    - 20% in the stationary store
  2. Action potential reaches bouton and causes Ca channels to open
    Ca diffuses in and triggers vesicles to release ACh in synapse via SNARE proteins
    ACh receptor is a nicotinic ligand gated ion channel - Na/K enter and when reach threshold potential cause action potential in the muscle cell
28
Q
  1. What is the pathophysiology of HOCM?

2. What is the mechanism leading to ischaemia?

A

1.
—LV hypertrophy causes poor compliance and diastolic dysfunction
—Septal hypertrophy causes LVOT obstruction (due to septum itself or/and indrawing of mitral valve leaflet
—Fibrosis occurs causing areas prone to arrhythmias
—Myocardial ischaemia (see below)

2.
Decreased blood supply:
—Small/obliterated vessels
—Inadequate number to supply heart
—Increased LVEDP (which means decreased coronary perfusion pressure)
—A decrease in SVR will cause reduction in coronary blood flow/coronary perfusion pressure
Increased O2 demand:
—Hypertrophy
29
Q
  1. What is the response to haemorrhage?

2. What are the physiological adaptions to anaemia?

A
  1. —Blood loss causes: decreased venous return and CO, which causes activation of baroreceptors in carotid bodies/aortic arch -> inhibition of PNS/activation of SNS
    —CO increases and SVR increases due to direct SNS, catecholamines and local tissue mediators
    —Starling’s forces encourage movement from tissues into capillaries
    —(Slower) = HPA axis: RAAS (angiotensin II is a potent vasoconstrictor that stimulates aldosterone and ADH release)
2.
—Increased O2 extraction
—Increased CO
—Redistribute CO to brain/heart
—OHDC shift to R to offload O2 (increased levels of 2,3-DPG)
—Stimulation of EPO
30
Q

Describe gastric acid secretion

A
  • Histamine, Vagus nerve at M3 receptors, Gastrin -> stimulate HCl production
  • Produced/released from parietal cells
  • Use of H+/K+ ATPase pump
  • Inhibited by somatostatin

CO2 diffuses into cell, reacts with H2O to form H+/HCO3-, which enters into the H+/K+ ATPase pump. HCO3 goes into blood in exchange for Cl-

31
Q

What factors increase contractility?

A

Sympathetic activation
Catecholamines/inotropic agents
Increased Afterload (Anrep)
Increased HR (Bowditch)

Increased cytosol Ca2+

32
Q

Why may PaO2 and PAO2 differ?

A

—V/Q mismatch
—Diffusion abnormalities/basement membrane problems
—Shunt

33
Q

What are the causes of anaemia in CKD?

A

May be due to:

  1. Low levels of EPO
  2. Functional iron deficiency (from high levels of hepcidin aka anaemia of chronic disease/inflammation)
  3. Repeat sampling
  • Low O2 levels in blood stimulate EPO release from peritubular interstitial cells in kidney
  • EPO acts on bone marrow to hasten pro-erythroblast maturation to reticulocytes/RBCs
34
Q

How do you assess dehydration in children?

A

Clinical parameters
Biochemically
Assess % dehydration (5% = 50ml/kg lost, 10% = 100ml/kg lost)

Replace over 24-48 hours
IN ADDITION TO
Maintenance = 4-2-1 rule

For shock/bolus = 10ml/kg

35
Q

Give a description of the pain pathway

A

—Tissue damage causes release of: histamine/bradykinin/serotonin/H+/K+ ions
—Stimulate nociceptors (unmyelinated nerve endings)
—Influx of Na+/Ca2+ ions causing depolarisation
—Impulse travels to dorsal root ganglia and dorsal horn
—Primary neuron synapses with second order neuron/interneurone in Rexed’s laminae (I,II,III)
—Secondary interneurone decussate and travels to thalamus (via STT)
—Synapse in thalamus with tertiary order neurones - to higher centres/limbic system
—Also to PAG, NRM, LC to initiate descending inhibition

Peripheral sensitisation:
-up-regulation of Substance P, prostaglandins

Central sensitisation:
-NMDA receptor hyperexcitability

Cortical reorganisation
Dysregulation of descending pathways

60 Second Viva Practice (6 decks)

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