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Primary FRCA > Physiology 8 > Flashcards

Physiology 8 Flashcards

1
Q

Outline the characteristics of bronchial arteries

A
  • Supply tracheobronchial tree as far as the terminal bronchioles
  • Originate from the thoracic aorta
  • Have the features of systemic arteries
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2
Q

What is the drainage of the bronchial veins? Why is this significant?

A
  • Into the left atrium via the pulmonary veins
  • Into the right atrium via the azygos veins

-Drainage via pulmonary veins contributes to physiological shunt and also accounts for the slightly higher CO of the left compared to right ventricles

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3
Q

What are the origins of physiological shunt?

A
  1. Thebesian/small myocardial circulation
  2. Bronchial circulation (via pulmonary veins)
  3. Intrapulmonary shunt
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4
Q

Outline the typical BP profile in the pulmonary circulation

A

Pulmonary artery: 25/8 (MAP 15) mmHg
Pulmonary capillaries: 8 mmHg
LA: 4 mmHg

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5
Q

How does the pulmonary vasculature respond to increased CO during exercise?

A

PVR decreases to keep pressure (relatively) constant through 2 mechanisms:

  1. Recruitment of unperfused pulmonary capillaries
  2. Dilatation of pulmonary vessels
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6
Q

What would happen if pulmonary artery pressure could not be regulated?

A

As CO increases, RV strain and pulmonary oedema would occur

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7
Q

What is the relationship between lung volume and pulmonary vascular resistance?

A

Complex and not yet fully understood.

J shaped curve as volume increases.

At low lung volumes vessels are narrow due to smooth muscle tone

At high lung volumes, alveolar capillaries stretch lengthways, increasing PVR

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8
Q

Outline the relationship between intraalveolar and intravascular pressures throughout the lung (when upright)

A

Three-zone model:

Zone 1: (Top) Intravascular pressures are lower than alveolar pressures due to gravity, thus there is no flow. PA>Pa>Pv

Zone 2: (Middle) Intermittent blood flow according to phase of cardiac cycle. Pa>PA>Pv

Zone 3: (Bottom) Continuous blood flow due to arterial and venous pressures exceeding alveolar pressures due to gravity. Pa>Pv>PA

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9
Q

What active control mechanisms are there in the pulmonary circulation? How does this differ from the systemic circulation?

A

-Hypoxic pulmonary vasoconstriction (V/Q matching)

This is the opposite to the effect of hypoxia on vascular tone systemically

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10
Q

How does chronic hypoxia lead to pulmonary hypertension?

A

Through proliferation of pulmonary vascular smooth muscle

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11
Q

At what phase of life is hypoxic vasoconstriction maximal?

A

During foetal life - Pulmonary blood flow is less than 15% of cardiac output

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12
Q

What is an approximate value for pulmonary vascular resistance in health?

A

160 dyn/sec/cm^5

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13
Q

Outline and explain the phases of the cardiac pacemaker action potential

A

Phase 4: Repolarisation ends at a membrane potential of around -60 mV. Funny channels allow slow sodium influx (If), allowing gradual depolarisation. When membrane potential reaches -50 mV, transient type (T) Ca2+ channels open, further depolarising the membrane. When the potential reaches -40 mV, long-lasting (L) type Ca2+ channels open, causing further depolarisation until the AP threshold is reached (between -40 and -30 mV)

Phase 0: Rapid depolarisation through continued flow of Ca2+ through open channels

Phase 3: Closure of Ca2+ channels and opening of K+ channels, returning membrane potential to normal.

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14
Q

How may sick sinus syndrome present?

A
  • Bradycardia (episodic or persistent), sinus arrest
  • Inability to increase HR with exercise
  • Tachy-brady syndrome
  • Intermittent AF
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15
Q

What conditions are associated with sinoatrial node dysfunction?

A 
Idiopathic fibrosis
IHD/MI
High vagal tone
Myocarditis
Digoxin toxicity
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16
Q

Why may a broad QRS complex follow an atrial premature beat?

A

The right bundle has a longer refractory period than the left bundle, thus a RBBB may follow a premature atrial depolarisation

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17
Q

How does adenosine work to terminate SVT?

A

Adenosine binds to the A1 receptor, coupled to Gi which inhibits adenylyl cyclase, reducing cAMP and increasing Ca2+ efflux, resulting in hyperpolarisation and inhibiting Ca2+ current.

This transiently blocks transmission of AP at the AV node, terminating any AV/nodal re-entrant tachycardia.

SVTs not involving the AVN will not be terminated, but the conduction rate will be reduced, which may make atrial flutter/fibrillation clearer.

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18
Q

What is the pathophysiology of the Wolff-Parkinson-White syndrome?

A

An accessory conductive pathway (the bundle of Kent) breaches the fibrous atrioventricular barrier.

The accessory pathway does not have the normal AV conduction delay, thus PR interval is short. The atypical ventricular conduction pathway is slower and thus delta-waves are seen on the R wave.

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19
Q

How are AVNRTs classified?

A

Into those with orthodromic and those with antidromic flow.

Orthodromic: atria activated retrogradely through the accessory pathway, causing flow through the AVN and a narrow QRS.

Antidromic: ventricles activated via accessory pathway causing wide QRS. Retrograde flow through AVN causes atrial stimulation.

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20
Q

What is a typical cause of VT?

A

post-MI

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21
Q

What is a typical cause of VF?

A

Hypoxia

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22
Q

Outline the international code for pacemaker function

A

Five letters:
Position 1: Chambers paced (O, A, V, D)
Position 2: Chambers sensed (O, A, V, D)
Position 3: Response to sensing (O, T - Triggered, I - Inhibited, D)
Position 4: Rate modulation (O, R - Rate modulated)
Position 5: Multisite pacing (O, A, V, D)

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23
Q

First choice type of pacemaker for sinus node disease with chronotropic incompetence?

A

DDDR + AVM

24
Q

First choice pacemaker for sinus node disease without chronotropic incompetence?

A

DDD + AVM

25
Q

First choice pacemaker for AV block without SAN disease?

A

DDD

26
Q

First choice pacemaker for AV block with SAN disease?

A

DDDR

27
Q

First choice pacemaker for AF

A

VVIR

28
Q

What is the significance of reciprocal changes in the context of STEMI?

A

Reciprocal changes are associated with increased likelihood of cardiac complications, and may represent a large mass of myocardium at risk and thus greater potential to salvage ischaemic tissue through revascularisation.

29
Q

Which types of pacemakers are safe for surgery?

A

Asynchronous PPMs which do not have a sensing function cannot be affected by diathermy and are thus safe for surgery

30
Q

How are nephrons distributed throughout the renal parenchyma?

A

85% of nephrons are cortical, with glomeruli in the outer 2/3 of the cortex and short loops of Henle

15% are juxtamedullary, with long loops extending deep into the medulla.

31
Q

What level of perfusion do the kidneys receive?

How is this distributed within the renal parenchyma?

A

20-25% of CO

500ml/min/100g

90% supplies the cortex, 10% supplies the medulla and capsule.

84% of medullary flow supplies the outer medulla, and 16% supplies the inner medulla

32
Q

Describe the renal vascular tree

A

Renal artery -> interlobar arteries -> arcuate arteries -> interlobular arteries -> afferent arterioles -> glomeruli -> efferent arterioles.

Outer cortical efferent arterioles -> peritubular capillaries

Inner cortical efferent arterioles -> peritubular capillaries + vasa recta

33
Q

Where do the renal vasa recta travel?

A

The vasa recta are closely associated with the loops of Henle of the juxtamedullary nephrons and collecting tubules

34
Q

What is the purpose of renal autoregulation of perfusion?

A

To maintain flow at varying pressures

35
Q

Which mechanisms are involved in autoregulation of renal perfusion?

A

Sympathetic ANS
Renal prostaglandins
Angiotensin II
Tubulo-glomerular feedback

36
Q

What are the main roles of mesangial cells?

A
  1. Structural support for the glomerulus

2. The ability to contract and relax, modifying the surface area for filtration

37
Q

What percentage of sodium efflux from the proximal tubule is ultimately reabsorbed into the peritubular capillaries?

A

20%

38
Q

What is the main driver of transport in and out of the proximal tubule?

A

Sodium movement down an electrochemical gradient

The Na+/K+ ATPase pump extrudes sodium at the basal and basolateral surfaces of the tubular epithelial cells

80% enters tubular cells in exchange for H+ ions

H+ secretion leads to Cl- and HCO3- reabsorption (as CO2) through various mechanisms.

39
Q

What is the main way by which chloride enters tubular cells in the early proximal tubule?

A

By antiport in exchange for organic anions (bicarbonate, formate and oxalate)

These anions react with secreted H+ in the lumen, forming organic acids which are reabsorbed and then dissociate back into H+ and anions, which can be antiported again.

This system enables reabsorption of Na+ and Cl- into tubular cells at a 1:1 ratio

40
Q

How does NaCl absorption differ between the first 1/3 and latter 2/3 of the proximal tubule?

A

First 1/3: Na absorbed down electrochemical gradient, pumping out H+ which drives absorption of organic acids which dissociate and diffuse out of the cell in exchange for Cl-

Latter 2/3: In the juxtamedullary nephrons, the same processes occur as in the first 1/3. In cortical nephrons NaCl is reabsorbed paracellularly down a concentration gradient established in the first 1/3. Up to 20% of NaCl absorption occurs in this way.

41
Q

How much of the glucose content of glomerular filtrate is reabsorbed?

A

Dependent on concentration.

At normal concentrations (<11mmol/L) 100% is reabsorbed through Na+ co-transporters.

Between 11 and 22mmol/L some transporters reach their rate limit.

Above 22mmol/L all transporters reach their limit and reabsorbed glucose amounts plateau.

42
Q

What does Tm mean in relation to tubular transport.

A

Tm refers to the maximum rate of tubular transport for a particular solute

43
Q

What is the Tm for glucose?

A

Approx 380 mg/min

44
Q

How is the proximal tubule divided?

A

Into pars convoluta (early) and pars recta (late)

45
Q

How does glucose transport vary between the pars convoluta and the pars recta?

A

Different ratio of Na+:glucose reabsorption.

Pars convoluta - 1:1
Pars recta - 2:1

46
Q

How and where are amino acids reabsorbed in the nephron?

A

Proximal tubule

Tm-limited transport very similar to glucose (Na+ co-transport)

47
Q

How much of the filtered phosphate load in the renal tubule is reabsorbed?

A

around 20% in normal circumstances

48
Q

What is the relationship between plasma PO4 concentration and reabsorption/excretion?

A

Above a plasma conc. of 1.2 mmol/L, the increase in plasma conc. is matched by the increase in excretion, suggesting a Tm for PO4.

49
Q

How and where is PO4 absorbed in the nephron?

A

The proximal tubule through an electroneutral Na+ cotransporter.

The basolateral mechanism for transport of PO4 is unclear.

50
Q

What is a normal plasma urea concentration?

What percentage of renally filtered urea is reabsorbed? How?

A

2.5-7.5 mmol/L

40-50% is reabsorbed in the proximal tubule through passive diffusion out of the lumen down an increasing concentration gradient

51
Q

What proportion of renally filtered HCO3- is reabsorbed? Where?

A

Approx 90%, in the proximal tubule

52
Q

What proportion of renally filtered water is reabsorbed in the proximal tubule?
How is this accounted for?

A

60-70%

20% of this is due to relative hypertonicity of luminal fluid relative to plasma

40% of this is due to a hypertonic intermediate compartment (lateral intercellular space)

40% is due to different anion permeabilities in cortical nephrons.

53
Q

What are the main Tm-limited secreted molecules in the proximal tubule?

A
  • Organic acids including penicillin, chlorothiazide, hippurate and p-aminohippurate (PAH)
  • Organic bases including histamine, choline, thiamine, guanidine, creatinine and tetraethylammonium
  • Ethylene diamine tetraacetic acid (EDTA)
54
Q

How does peritubular capillary oncotic pressure compare to that in the afferent arteriole?
Why is this relevant to the proximal fractional reabsorption of filtrate?

A

It is much higher

This means that proximal tubular reabsorption is related to GFR, and results in a fixed percentge of filtrate being reabsorbed.

ie. more fluid filtered -> higher peritubular oncotic pressure -> more reabsorption. Less fluid filtered -> lower peritubular oncotic pressure -> less reabsorption.

55
Q

What is the rate of glucose reabsorption in the proximal tubule?

A

0.4-0.7 mmol/min

Primary FRCA (34 decks)

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