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Hypovolaemi Flashcards

1
Q

How do you measure TBW?

A

Deuterium oxide (D2O)

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2
Q

How do you measure ECF?

A

Inulin

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3
Q

How do you measure ICF?

A

TBW - ECF

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4
Q

What are the two methods of regulation of ECF?

A

Osmoregulation & volume regulation

Osmoregulation:

  • osmoreceptors in hypothalamus
  • respond to NaCl in blood
  • stimulate thirst
  • release ADH
Volume regulation:
- baroreceptors in arteries; AA, CS
- respond to decreased stretch with:
Sympathetic drive: increased HR, vasoconstriction, venoconstriction
Atrial natriuretic peptide
Vasopressin
Endogenous digitalis like factor (pressure natriuresis)
RAAS
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5
Q

What do elastic arteries do?

A

WINDKESSEL EFFECT

Act like springs; store up energy from stretch and then release it through whole phase of cycle

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6
Q

What do arterioles do?

A

RESISTANCE

Allow shunting of blood

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7
Q

What do capillaries do?

A

EXCHANGE

High surface area

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8
Q

What do venules do?

A

CAPACITANCE

Hold 2/3 of CBV

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9
Q

Darcy’s law is…

A

Change in pressure = Flow * resistance

Therefore

ABP-CVP=CO*TPR
CVP

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10
Q

Describe baroreceptor reflex

A

CBV (ABP) detected by baroreceptors in aortic arch / carotid sinus

Signal sent via vagus / IX (hering’s) to medulla oblongata

HR / TPR adjusted: darcy’s law

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11
Q

What affects local blood flow?

A

Local vascular resistance

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12
Q

How do you measure renal plasma flow

A

P-aminohippurate (PAH)

PAH passes freely across the glomerular membrane and is not reabsorbed

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13
Q

How much blood perfuses the kidney?

A

25% of cardiac output… 90% of which goes to the cortex

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14
Q

How can you measure GFR (2 ways)

A
  • Inulin
  • Creatinine

Inulin is administered IV and isn’t reabsorbed so measure as it appears in urine

Creatinine is a muscle breakdown product and is fairly constant in blood so can be measured

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15
Q

What goes into measuring eGFR

A

Serum creatinine, age, sex, ethnicity

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16
Q

Where is the highest amount of protein in the body compartments?

A

IVF: 70g/L

ISF has around 20-30g/L

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17
Q

What are the two main regulators of water in the body?

A

Osmoregulation = regulation of concentration = movement of WATER

Volume regulation = regulation of volume = movement of SALT

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18
Q

What is shock?

A

Inadequate delivery of oxygen to critical organs and tissues, and inadequate waste disposal

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19
Q

Non-progressive shock compensation mechanisms

A
  1. Baroreceptor reflex
  2. Osmoreceptors
  3. CNS ischaemic response
  4. Sympathetic activation
  5. Atrial NP
  6. Vasopressin
  7. E (Pressure natriuresis)
  8. RAAS
  9. Starling forces
  10. Liver -> increased plasma proteins
  11. Kidneys produce more EPO -> RBCs up
  12. Thirst / salt appetite (hypothalamus)
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20
Q

When is progressive shock expected?

A

When 30% of blood volume is lost and treatment is delayed (golden hour)

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21
Q

What are two common complications of progressive shock?

A

DIC and SIRS

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22
Q

What is SIRS? A common complication of SIRS?

A

Widespread release of inflammatory mediators in response to an insult, without resolution, resulting in a vicious circle:

  • widespread vasodilation
  • widespread increased capillary permeablity
  • -> decreased MAP, CO –> MOF/death

LPS of gram(-) (“endotoxin”)

RDS: alveoli become filled with fludi and cells

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23
Q

What is DIC?

A

Clotting cascade is activated, and this leads to using up of all of the clotting factors.

The clots form and are broken down leading to thromboemboli formation, and then widespread bleeding occurs due to lack of clotting fators.

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24
Q

What is arterial compliance?

A

Change in V / change in P

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25
Q

How do you calc ABP?

A

dBP + PP/3

26
Q

What is PP?

27
Q

What is CVP average?

28
Q

What is Starling’s law / Frank Starling mechanism?

A

Increased venous return (EDV) causes increased stroke volume (SV) due to increased volume stretching the ventricular wall which causes more forceful cardiac muscle contraction

29
Q

What is Boyle’s law?

A

PxV=constant therefore lower P = higher V

30
Q

What does local blood flow rely on?

A

Local arteriole resistance

31
Q

Draw the pacemaker cell action potential and describe what causes each phase

A

Phase 4 around -60mV:

  • If (Slow inward Na open)
  • ICa(T) at -50mV
  • ICa(L) at -40mv

Phase 0 around -40mV:

  • ICa(L) primarily [note slow influx so not steep]
  • ICa(T) and INa start to close

Phase 3 around +5mV?:

  • Ik
  • ICa(L) close

Phase 4: -60mV must be reached before it starts again

32
Q

What happens in the cardiac pacemaker cell during hypoxia?

A

Hypoxia is depolarising, and so it takes longer for phase 3 to hyperpolarise the cell to phase 4 for the next beat… hypoxia therefore causes pacemaker cell BRADYCARDIA

33
Q

Draw a cardiac non-pacemaker cell action potential and describe it

A

Phase 4: -90mV; Ik high (k+ efflux)

Phase 0: depolarisation from adjacent cell causes depolarisation to -70mV; INa open; Ik close

Phase 1: IK+ open

Phase 2: ICa(L) cause calcium influx which causes plateau

Phase 3: ICa(L) close and IK open

34
Q

What channels are the depolarisation of cardiac pacemaker cells primarily from?

A

Long lasting calcium channels (ICa(L))

35
Q

What channels are the depolarisation of cardiac non-pacemaker cells primarily from?

36
Q

How do you measure renal plasma flow

A

PAH - not reabsorbed but passes freely thru glom membranes

37
Q

What is glomerular selectivity?

A

Glomerulus shows selectivity for smaller and positively charged molecules - allows retention of plasma proteins such as albumin which are negatively charged

Glomerulonephritis = impairment of glom cap all electrostatic barrier which leads to proteinuria in nephrotic syndrome (loss of -vely charged components of wall)

38
Q

What makes up the glomerular filter

A

Podocytes with fenestration slits
Basement membrane
Fenestrated endothelium
Glycocalyx

39
Q

Control of GFR is via

A
  1. Myogenic response of AAs
    - expansion due to increased ABP = reflexive contraction of AAs therefore lower BP and lower GFR
  2. Tubuloglomerular feedback
    - Macula densa cells absorb more Na+/Cl- and the Na+ has to be pumped out via Na+K+ pump which uses ATP. ADP causes vasoconstriction of AA smooth muscle cells = lower GFR
40
Q

What is GFR for average 70kg man

A

125mL/minute = 180L/day

41
Q

What does the PT contribute to reabsorption?

A

ISOSMOTIC reabsorption of around 2/3 H2O and solutes

42
Q

What does the LoH contribute to reabsorption

A

Reabsorbs 1/5 NaCL to generate medullar osmotic gradient

43
Q

What does the DT and CD contribute to reabsorption

A

Fine H2O / salt reabsorption controlled by hormones e.g. ADH and aldosterone

44
Q

Where is organic solute reabsorption (glucose and AAs) reabsorbed?

A

PT

Via secdonary active transoport thru co-transporters driven by Na+ gradient out of nephron

45
Q

Which segment of the tubules regulate pH?

A

PT by citrate reabsorption

Acidosis INCREASES reabsorpton
Alkalosis decreases reabsorption

46
Q

How does the LoH work?

A

Descending limb has aquaporin 1 so permeable to water
Ascending limb actively transports ions

So the final product is hypotonic but also low in volume

47
Q

What part of the tubule does aldosterone have a large effct on ?

48
Q

What does PTH do to the tubule?

A

Increases calcium reabsorption in the DCT

49
Q

Where does furosemide affect?

50
Q

Where do thiazide diuretics effect?

51
Q

150mg/kg within last 24 hours: took them 2 hours ago

A

Wait until 4 hours post-ingestion, take a level, and give if above line

52
Q

150mg/kg within last 24 hours: took them 6 hours ago

A

Take a level if the result will come back before 8 hours has passed, give if above line

53
Q

150mg/kg within last 24 hours: took them 8 hours ago

A

Start NAC, take a level.

Stop NAC only if:

  • Normal LFTs
  • Asymptomatic
  • Level is below line
  • Normal creatinine
  • Normal INR
54
Q

150mg/kg take during the last 24 hours: spread over 16 hours

A

Start NAC, take a level

Stop NAC only if:

  • Normal LFTs
  • Normal creatinine
  • Normal INR
  • Asymptomatic
  • Level below line
55
Q

150mg/kg within last 24 hours: taken 45 mins ago

A

Administer charcoal:

  • 1g/kg children
  • 50g adults

Take level at 4h, then give if above line.

56
Q

150mg/kg within 24 hours but that was 36 hours ago

A

Poisoning is unlikely.

Take level and administer NAC if above line

57
Q

Neonate given too much paracetamol, quantity unknown

A

Give NAC and take level.

Increased risk of hepatic necrosis in below 45w

58
Q

Signs of paracetamol tox

A

First 24h: N&V, RUQ pain

24-96h: hepatic necrosis peaks e.g. encephalopathy, coagulation disorder, decreased BM, death

59
Q

Patient is being given NAC and develops hypersensitive rash.. what do you do?

A

Slow NAC down and give anti-histamine

60
Q

Patient is being given NAC and develops anaphylaxis, what do you do?

A

Stop NAC and treat anaphylaxis - medical emergency

61
Q

Patient is being given NAC and develops asthma and wheezing, what do you do?

A

Slow NAC down and give SABA nebuliser

62
Q

How does NAC work?

A

Glutathione donor

Paracetamol is pro-toxin. Gets metabolised to NAPQI when glutahtione stones are low (which usually converts it to mercapturic acid). NAPQI binds to hepatic proteins.

NAC donates glutathione and so NAPQI is de-toxified.

March (13 decks)

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