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MRCS B - Critical Care (Kanani and Lammy) > Exposure (everything else) > Flashcards

Exposure (everything else) Flashcards

1
Q

Define pH?

A

log^10 [H+]

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2
Q

Where does acid load come from in the body?

A

Predominantly generated via CO2 being turned into carbonic acid and in turn giving H+.
- Via enzyme carbonic anhydrase

Also via:

  1. Metabolism of sulphur containing amino acids
  2. Generation of lactic acid during anaerobic respiration
  3. Generating ketone bodies in DKA
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3
Q

Main acidic buffers?

A

HCO3-
Phosphate
Plasma proteins
globin of Hb

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4
Q

What is Henderson hasselbalch equation?

A

Describes relationship between dissociate and undissociated acids and bases.

Allowing us to identify pH of a buffer solution.

pH = pK + Log [HCO3-/CO2]

Means we can analyse what happens of CO2 changes for example

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5
Q

Which organs are involved inn acid base balance?

A

Respiratory:

  • Controls PCO2 via ventilation.
  • Increased PCO2 stimulates chemoreceptors in medulla by releasing H+ which crosses BBB

Renal:
Controls bicarb

Haematology:
Plasma proteins and globin chains buffer acids

GI:
Liver can generate bicarb and ammonia
In kidneys, ammonia secretion generates more bicarb

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6
Q

How do the kidneys regulate acid base balance?

A

• Tubular cells of nephron secrete H+, and in doing so facilitate the reabsorption of bicarbonate.
-80% of this is reabsorbed in the proximal tubule.
• Tubule cells can also generate de novo bicarbonate from glutamine, which it metabolises to 2 ammonia and 2 bicarb.
-Generally, bicarb returned to blood, and NH4 secreted into urine
• Kidney also excretes urinary buffers  phosphate being the predominant buffer
-Phosphate is excreted, meaning more H+ can be excreted which also generates more bicarbonate to be reabsorbed.
-Acidosis stimulates increased PTH which causes increased phosphate excretion.

• Tubular cells in the collecting duct can also conversely excrete bicarbonate and reabsorb H+

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7
Q

Define base excess?

A

This is the amount of strong acid needed to return 1L of fully oxygenated blood to a normal pH at a PCO2 of 5.3kPA at 37 degrees.

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8
Q

What is metabolic acidosis?

A

low pH, with a fall in bicarbonate

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9
Q

How can bicarbonate ions be lost?

A

Excreted e.g. D+V, fistula

Depleted via buffering, if overwhelming H+

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10
Q

How can we classify the causes of metabolic acidosis?

A

Via anion gap.
Anion gap = (Na+K) - (Bicarb + Cl)

normal anion gap = hyperchloraemic metabolic acidosis, is due to loss of bicarb NOT GAIN OF ACID.
It is normal because with loss of bicarb, the body is very good at displacing a different. negative ion to extracellular space e.g. chloride, so it balances it out.

Raised anion gap = impaired H+ secretion / accumulated organic acids
In this case you will have an increase in UNMEASURED ions. So raised anion gap as chloride not raised.

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11
Q

Causes of normal anion gap vs raised anion gap?

A

Normal anion gap = bicarb loss:
GI loss e.g. D+V, fistula, stoma
Renal loss = Renal failure, RTA type 2 and 4

Raised anion gap: KUSMEL

Ketoacidosis
Uraemia
Salicylate poisoning
Methanol 
Ethylene glycol poisoning 
Lactic acidosis
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12
Q

Physiological effects an acidosis has on the body?

A
  1. Shifts oxygen dissociation curve to the left = lower affinity to oxygen = readily available oxygen to perfuse tissues.
  2. Acids causes reduced myocardial contractility and risk of arrhythmias
  3. Acids cause pulmonary vasoconstriction = pulmonary hypertension
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13
Q

What is a metabolic alkalosis?

A

a pH >7.45, with bicarbonate >28.

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14
Q

Other ions implicated in a metabolic alkalosis?

A
  1. Loss of H+, e.g. by vomiting = relative increase in bicarb.
  2. Chloride ions lost, causes renal tubules to take up more bicarb.
  3. Loss of potassium, causes increased bicarbonate absorption in renal tubules
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15
Q

How can we classify metabolic alkalosis and its causes?

A

Chloride responsive with urinary chloride <10, due to:

  • loss of hydrogen via the GI tract ,
  • diuretic therapy
  • post-hypercapnia syndrome
  • Contraction alkalosis - diuresis or severe dehydration…. means reduced water, means RAAS activation = water and Na retention but at expense of H+
  • Cystic fibrosis due to excess loss of NaCl in sweat

Chloride unresponsive with urinary chloride >40, due to:

  • Retention of bicarbonate
  • Intracellular shift of H+ e.g. in. hypokalaemia
  • Hyperaldosteronism - aldosterone increase Na and Water retention but at expense of H+
  • Barters and Gittlemans
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16
Q

Why does metabolic acidosis develop in pyloric stenosis?

A

Gastric acid is lost which contains protons and electrons
Reduction in pancreatic juice secretion due to reduced acid load at duodenum = retain bicarb
So currently we have lost H+, and retain bicarb.

Volume depletion maintains the alkalosis by leading to bicarbonate absorption over chloride e.g. contraction alkalosis

Also as we lose chloride, there is increased uptake of bicarb in renal tubules to maintain neutrality

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17
Q

Why alkaloid patients have poor oxygen perfusion?

A

Alkalotic means reduced H+, so oxygen dissociation curve shifts to the left = greater affinity = reduced perfusion

Also as part of compensatory mechanism = hypoventilation to increase PCO2.

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18
Q

Defining features of lactic acidosis?

A

pH <7.35

Lactate >2

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19
Q

How can you classify lactic acidosis?

A

Cohen and Woods classification:
Type A = due to inadequate tissue oxygenation:
1. Anaerobic metabolism e.g. sprinting, seizures. Lactate from pyruvate
2. Shock - poor tissue perfusion = cellular hypoxia = anaerobic
3. Reduced oxygenation e.g. Severe anaemia or carbon monoxide poisoning

Type B = No clinical evidence of poor tissue oxygenation

  1. Chronic disease = renal / liver / malignancy
  2. Drug induced e.g. paracetamol, salicylate, metformin
  3. Inborn errors of metabolism e.g. pyruvate dehydrogenase deficiency
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20
Q

Precautions in using therapeutic bicarbonate ?

A
  1. Need to carefully titrate - can overshoot and cause alkalosis
  2. Infuse slowly as can alter myocardial contractility
  3. Can get a respiratory acidosis as extra CO2 generated to balance equation
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21
Q

Distribution of calcium within the body?

A

99% in bone

1% readily exchangeable as calciums phosphate salts

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22
Q

State of calcium within the blood?

A

50% unbound and ionised
45% bound to plasma proteins
5% associated with anions such as citrate and lactate

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23
Q

Outline the hormonal control of calcium?

A

Parathyroid releases PTH:

  1. Increases calcium via increased bone resorption + increased synthesis of 1,25(OH)D2 which causes increased gut absorption
  2. Causes reduced phosphate via decreased renal absorption + reduces renal calcium loss
  3. 25(OH)D2:
  4. Increased plasma calcium and phosphate
  5. Increased renal absorption of both calcium and phosphate
  6. Increased gut absorption
  7. Increased bone resorption at high levels

CALCITONIN: from thyroid C cells

  1. Inhibits gut absorption of calcium
  2. Osteoclast activity inhibited
  3. Inhibits renal absorption
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24
Q

Features of hypercalcaemia?

A

Stones - renal, polyuria and polydipsia
Bones - Pain / cysts
Moans - depression / confusion
Groans - Pancreatitis, constipation and peptic ulcers (Ca causes increased gastric acid secretion)

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25
Q

Hypercalcaemia ECG changes?

A

Shortened QT
Increased PR
Flattened t-waves

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26
Q

Causes of hypercalcaemia?

A 
Is PTH suppressed?
YES = appropriate
1. Malignancy e.g. myeloma or bony mets
2. Small cell lung Ca producing PTH-rP
3. Sarcoidosis with exogenous vitamin D
No = inappropriate = primary hyperparathyroidism 
80% = solitary adenoma 
20% = MEN1
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27
Q

Differentials of abdominal pain with hypercalcaemia?

A

Peptic ulceration, could be perforated
Renal colic
Pancreatitis
Constipation

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28
Q

Emergency management of hypercalcaemia?

A

ABCDE
IVF usually 3-6L within 24 hours
- if worried about overload can give furosemide, which would also lower calcium

Meds:
Bisphosphonates
Steroids if malignancy

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29
Q

Features of hypocalcaemia?

A

Muscle spasms / cramp
Irritability
Chvosteks = tap facial nerve anterior to tragus
Trousseaus = Hand spasm when having BP taken

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30
Q

Causes of hypocalcaemia?

A

Is it PTH driven?

Yes = low PTH:

  1. Autoimmune hypothyroid
  2. DiGeorge syndrome
  3. Surgical removal parathyroids

No = PTH normal / raised

  1. Low vitamin D e.g. malabsorption, osteomalacia, rickets
  2. Chronic renal failure
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31
Q

Management of hypocalcaemia?

A

ABCDE

10ml 10% calcium gluconate

Treat any hypomagnaesaemia as well

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32
Q

normal magnesium level ?

A

0.7 - 1.0

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33
Q

What is magnesium distribution within the body?

A

Most abundant intracellular cation after potassium, so serum levels are poor indicator of total body store

65% located in bone
1% found in serum

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34
Q

Purpose of magnesium?

A

cofactor for number of enzymes

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35
Q

Relationship between magnesium and calcium?

A

High magnesium prevents calcium entering cells. For this reason low magnesium can lead to bradycardia and sluggish reflexes

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36
Q

Management of severe hypermagnesaemia is….

A

Calcium gluconate

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37
Q

Which organ largely responsible for magnesium homeostasis?

A

Kidney:
It is freely filtered at glomerulus
Reabsorbed at PCT and thick ascending limb

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38
Q

Causes of hypomagnesaemia?

A
  1. Low intake e.g. ETOH, malnutrition
  2. Increased excretion:
    GI = diarrhoea, bowel resection, bypasses
    Renal = any state of diuresis e.g. diuretics or acute renal failure
    Endocrine e.g. diabetes mellitus, hyperPTH

Occurs in 60% of critically ill patients, often due to diuretics

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39
Q

Features of hypomagnesaemia?

A

Arrhythmias e.g. AF
ECG changes = prolonged PR and wide QRS
Muscular weakness
Confusion

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40
Q

Potassium distribution in the body?

A

98% intracellular

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41
Q

How is potassium regulated?

A

GI - dietary intake

Endocrine:
1. Aldosterone = Mineralocorticoid produced in zone glomerulosa of adrenal gland.
Causes K excretion in DCT and cortical collecting duct, to allow reabsorption of sodium

  1. Insulin = stimulates uptake into cells

Renal:
K and H+ are readily exchanged
So if acidotic K goes up
If alkalotic potassium lowered

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42
Q

Causes of hyperkalaemia?

A

Renal:

  • reduced GFR = no filter
  • Reduced renin in NSAID use

Drugs e.g. NSAIDS, ACEI, K-sparing diuretics

Low aldosterone = Addisons

Cellular release = rhabdomyolysis in burns/trauma, any acidosis or massive transfusion

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43
Q

Hyperkalaemia ECG changes?

A

Tall tented t-waves
Small p waves
Widened QRS

Eventually VF

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44
Q

Management of hyperkalaemia?

A

Calcium gluconate 10ml 10%
50ml 50% dextrose with 10iU of insulin over 30 mins

Treat underlying cause

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45
Q

How is potassium used in surgery?

A

Potassium rich cardioplegic fluid is used to arrest the heart in bypass surgery

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46
Q

Causes of low potassium?

A

Renal loss:
Loop diuretics / barters = NA/K/Cl transporter blocked, so no K or Na. But Na absorbed further downstream at sake of K
Thiazides / Gittlemans = Block Na/Cl transporter, so further downstream Na absorbed at expense of K

GI loss e.g. D+V

Excess aldosterone e.g. Conns

Cellular redistribution e.g. Alkalosis or insulin

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47
Q

ECG changes in hypokalaemia?

A

Flattened T waves, U-waves, prolonged PR.

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48
Q

Distribution of sodium within the body?

A

50% extracellular, 45% bone, 5% intracellular

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49
Q

Major physiological effects of sodium?

A

Osmotic force

Generating action potentials

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50
Q

Daily requirement?

A

1mmol/kg/day

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51
Q

Classifying hyponatraemia?

A

Hypovolaemic, euvolaemic and hypervolaemic

Hypovolaemic = lose Na+H20 = ADH = reabsorb water but not sodium

  1. Renal losses (Urinary sodium >20)
    - Diuretics
    - Salt losing nephropathy
  2. Extra-renal loss (urinary sodium <20)
    - Fistula / D+V / burns

Euvolaemic:

  1. SIADH e.g. lung Ca, meningitis
  2. Adrenal insufficiency = Addisons - low cortisol means low BP = ADH release
  3. Hypothyroid = reduced cardiac output = reduced BP = ADH release

Hypervolaemic:

  1. Cardiac failure = low BP = ADH release
  2. Cirrhosis = NO release = low BP = ADH
  3. Renal failure
  4. Excess dextrose / TURP syndrome
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52
Q

What is pseudohyponatraemia?

A

Falsely low sodium as serum volume is raised due to increased lipid/protein levels

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53
Q

TURP syndrome?

A

Following transurethral resection of prostate, use of hypotonic fluid for irrigation. Fluid s absorbed through inured vessels producing a dilutional hyponatraemia.

PC = haemodynamic instability, confusion and severe cases have convulsions and comas.

54
Q

Features of low Na?

A 
<135. = malaise 
<130 = headache and confused
<125 = seizures and coma
55
Q

Causes of hypernatraemia?

A

Unreplaced water loss e.g. GI losses
Diuresis in diabetes
Reduced ADH receptors in diabetes insipidus

56
Q

What is diabetes insidious, tests and Mx?

A

Diabetes insipidus is polyuria ceasing severe thirst and dehydration, leading to hypernatraemia

Causes can be central = no vasopressin produced, or nephropgenic when kidneys cannot respond

Ix:
Fluid deprivation test - still will not concentrate urine
Then give Desmopressin - if responds means it is central, if does not means it is nephrogenic

Mx:
Central = desmopressin
Nephrogenic = thiazide diuretic

57
Q

Why measure urine output?

A
  1. indicator of renal perfusion pressure = therefore cardiac output + ability to perfuse peripheral tissue
  2. Indicator of renal tubular function
  3. Indicator urinary tract is functional with no blockage
58
Q

what is normal urine output?

A

0.5ml/kg/hour

Kids = 1ml

59
Q

Common causes of post reduced urine output?

A

Physiological stress response

Poor renal perfusion:

  • Dehydration
  • Bleeding
  • Low CO e.g. MI, PE, arrhythmia, excess IVF causing CCF
  • Vasodilated

Renal tubular dysfunction

Renal tract blockage

Intra-abdominal HTN (>20mmHg) = compresses renal parenchyma

60
Q

Most common cause of post op oliguria?

A

Physiological stress in first 36 hours

- Circulating glucocorticoids and MR’s inducing salt and. water retention

61
Q

Clinical signs you would look for when examining oliguria patient?

A

A - nil
B - tachypnoeic, wet crackles
C:
Dry mouth, drains and fluid chart, drug chart
Cool peripheries, tachycardia, low BP / CVP

62
Q

Acute tubular necrosis vs pre-renal AKI investigations?

A

ATN: Na = >20, urine osm <500, Urine:plasma osm <1.2

Pre-renal: Na <40, urine osm >350, Urine:plasma osm >1.2

63
Q

Management of poor urine output?

A

Flush catheter
Fluid challenge and response to CVP
Inotropes if required - dopamine increase renal blood flow as well as being inotropic

Drug review

Renal support if severe

64
Q

Definition of AKI?

A

abrupt reduction of kidney function inn <48 hours

Loosely biochemically defied as:
Oliguria <30ml/hour for >6 hours
Creatinine rise of 1.5x

65
Q

what is acute tubular necrosis?

A

Renal failure due to injury of tubular epithelial cells

Can be ischaemic injury e.g. due to shock
Can be nephrogenic e.g. drugs, toxins, myoglobin

66
Q

Major causes of AKI?

A

Renal = ATN, glomerulonephritis and tubulointerstitial nephritis

Post-renal = stones, obstruction secondary to tumour, renal tumours, iatrogenic injury, BPH

67
Q

Which part of the kidney is most susceptible to injury?

A

cells of thick ascending limb for two reasons:

  1. Cells reside in medulla, which has less oxygenation vs cortex
  2. Active NA/K ATP-ase pump on the cell membranes has high oxygen demand
68
Q

Pathogenesis of AKI?

A
  1. Vasoconstriction:
    - Compensatory response to fall in renal perfusion pressure of efferent arteriole
    - Maintains capillary filtration pressure, at expense of reduced blood supply to the tubules perfused by efferent arteriole
  2. Obstruction:
    - Tubular cell ischaemia and necrosis = shed cells = obstruction
  3. Pressure changes:
    - obstruction cases back weak of tubular fluid into parenchyma = increases interstitial hydrostatic pressure.
69
Q

Drugs causing AKI?

A

Paracetamol = ATN

NSAIDS = reduces protective effect of PGE during ischaemia

Aminoglycosides

70
Q

How to distinguish AKI vs CKD?

A

Historic blood results

CKD has features such as anaemia, nocturia, pruritus. As well as radiological features e.g. small scarred kidney

71
Q

2 most life threatening complications of AKI?

A

Acute pulmonary oedema due to fluid retention form over hydration

Hyperkalaemia: Can lead to metabolic acidosis and arrhythmias

72
Q

Definition of CKD?

A

Kidney. damage for > 3 months based on proven. structural / functional abnormality

Most commonly caused by diabetes and HTN

73
Q

What is creatinine?

A

Creatine minus a water molecule

Formed in muscle by non-enzymatic and irreversible degradation of creatine phosphate

74
Q

Why is serum creatinine better marker of kidney function than urea?

A

50% of serum urea that is filtered gets reabsorbed, which means you underestimate GFR

75
Q

Classification of CKD?

A

Stage 1 = >90

Stage 2 = 89-60

Stage 3A = 59-45

Stage 3B = 44-30

Stage 4 = 29-15

Stage 5 <15

76
Q

Causes of CKD?

A

Congenital - PCKD

Glomerular disease e.g. diabetes, glomerulonephritis

Renovascular e.g. vasculitis

Chronic outflow obstruction e.g. tumour / BPH

Tubular e.g. nephritis

77
Q

Clinical features of CKD?

A
  1. HTN secondary to fluid retention
  2. Polyuria and nocturia due to osmotic diuresis caused by uraemia
  3. Oedema - due to fluid retention and proteinuria
  4. Features of uraemia e.g. skin pigmentation, anorexia, nausea, malaise and constipation
  5. Haematological = normocytic normochromic anaemia
  6. Renal osteodystrophy
  7. Neurological deficit
78
Q

Acid base disturbances in CKD?

A

Low sodium and calcium
Raised phosphate and potassium

Produces a resistant metabolic acidosis with increased anion gap. Due to chronicity has a low bicarbonate and raised creatinine

79
Q

What is renal osteodystrophy pathophysiology?

A

Kidneys that are damaged cannot produce 1-alpha hydroxylase = reduced 1,25(OH)D3
This causes secondary hyperparathyroidism
This increases bone resorption, cyst formation and osteitis fibrosa

Hyperphosphataemia develops as a direct result of renal dysfunction, cannot excrete it.

80
Q

Why are uraemia patients anaemic?

A
  1. Deficiency of EPO from kidney
  2. Presence of circulating toxins
  3. Bone marrow fibrosis drone osteitis firbosa
  4. Increased. red cell fragility due to toxins
81
Q

Clinical findings when examining a CKD patient?

A
  1. Tachypnoeic from :
    - metabolic acidosis - kussmauls (deep and laboured breathing).
    - Fluid overload
    - Anaemia
  2. Uraemia signs - pigmentation of skin, pruritic scratch. marks, anorexic
  3. Pitting oedema due to overload as well
  4. signs of renal therapy = May see fistula on arm or abdominals car from renal transplant
82
Q

management of CKD?

A

Optimise electrolytes and fluid balance
Treat the cause
ESRF = RRT or transplant

83
Q

How can we assess burns?

A 
1. According to % SA = Wallace's Rule of 9's
(-Each palm is 1%)
- Head 9%
- Each arm 9%
- Each leg 18%
- Ant/post torso each 18%
- Genitalia 1%
  1. According to depth…
    - Superficial = just epidermal layer, erythema and painful, blanche and blisters
    - Partial thickness = mid dermal, skin pale and dry, adnexae remain, painful ++
    - Deep partial = deep dermal layer, non-blanching, mottled red, NO PAIN
    - Full thickness = Leathery and charred, NO PAIN
84
Q

Why in burns are you susceptible to respiratory side effects?

A
  1. Thermal injury to airway
  2. Smoke = hypoxia + pulmonary oedema if ARDS
  3. Carbon monoxide
  4. Circumferential burns = respiratory restriction
  5. Aggressive IVF can cause pulmonary oedema
85
Q

Why is carbon monoxide toxic?

A

Its affinity for Hb is 250x greater than oxygen
So oxygen dissociation curve to the left = poor oxygenation of tissue

ALSO binds to some respiratory chain enzymes, affecting oxygen utilisation

86
Q

Whens do you suspect impending respiratory distress in burns patients?

A
  1. Fire in a confined space
  2. Soot at mouth / in sputum
  3. Burns on face / singed hair or eyebrows
  4. Vocal changes
  5. Serum carboxyhaem >10%
87
Q

Why do you get AKI in burns?

A
  1. severe loss of fluid means reduced renal perfusion = ATN

2. Circulating myoglobin = rhabdomyolysis = ATN

88
Q

Systemic complications of burns injuries?

A 
Burns shock = hypovolaemia 
Hypothermia as no skin 
Gastric stress ulcers
Coagulopathy secondary to DIC
Haemolysis = haemoglobinuria
89
Q

Management principles of burns?

A 
A = any impending distress intubate 
B = High flow oxygen early
C = IVF and CVP monitoring if necessary

Renal - catheter
Thermoreg = convection heaters
GI = stress ulcer prophylaxis such as sucralfate
Escharotomy if circumferential burns of torso

90
Q

How much IVF in burns?

A

Parklands formula:

4ml x weight (kg) x % burns = IVF inn 24 hours, half within first 8 hours

91
Q

nutritional requirements in burns?

A

Curreri formula:

Adult = 25kcal/kg + 40kcal/%BSA

Kids = 40-60kcal / kg / %BSA

92
Q

How can we assess nutrition?

A

Anthropometrics:
Height, weight, BMI
Fat indices
Lean muscle indices

Biochemical markers:
Serum proteins e.g. albumin

Clinical markers:
Appearance
Grip strength

93
Q

How much does each energy source supply?

A 
Fats = 9.3 Kcal/g
glucose = 4.1 Kcal/g
Protein = 4.1 Kcal/g
94
Q

Define the respiratory quotient…

A

Respiratory quotient is the ratio of CO2 produced to the volume of oxygen consumed for the oxidation of a given amount of nutrient

Carbs = 1
Fat = 0.7
Protein = 0.8
95
Q

Disadvantages of using glucose as main source of energy?

A
  1. Glucose intolerance:
    - As part of the stress response, critically unwell patients are often in a state of hyperglycaemia and glucose intolerance.
  2. Fatty liver:
    - Excess glucose is converted too lipids in the liver
  3. Respiratory failure:
    - Given its higher respiratory quotient means it produces more CO2, glucose use only may lead to respiratory failure
96
Q

Recommended daily intake of nitrogen and protein?

A

Protein is 1g/kg

Nitrogen = 0.15g/kg/day

97
Q

How much protein gives 1 g of nitrogen?

A

6.25g of protein yields 1g of nitrogen

98
Q

What is an essential amino acid?

A

An amino acid that cannot be synthesised by. the body, it must be ingested
e.g. isoleucine, leucine, lysine

99
Q

What are essential minerals (elements)?

A

Copper, calcium, iron

100
Q

What are fat soluble vitamins and their function?

A

A = cell membrane stabilisation and retinal fucntion

D = Calcium homeostasis

E = Free radical scavenger

K = Involved in gamma carboxylation of glutamic acid residues of Factors 2,7,9,10

101
Q

What are the names of each vitamin B, and the result of their deficiency?

A

B1 = Thiamine = wernickes encephalopathy and beri beri

B2 = riboflavin = Glossitis + stomatitis + cheilosis

B3 = niacin = Pellagra (3 D’s dementia, diarrhoea, dermatitis)

B5 = panthothenic acid = acne and paraesthesia

B6 = Pyridoxine = stomatitis and peripheral neuropathy

B7 = biotin = rarely in isolation, but immune deficiency

B9 = Folate = Macrocytic anaemia and neural tube defects

B12 = cobalamin = megaloblastic anaemia + peripheral neuropathy

102
Q

functions of vitamin C?

A
  1. Hydroxylation of proline and lysine residues during collagen synthesis
  2. Iron absorption in gut
  3. Synthesis of adrenaline from tyrosine
  4. Antioxidant function
103
Q

Indications for enteral feeding?

A

Functionally intact GI system, but. cannot meet daily requirements

104
Q

Types of enteral feeding?

A

Oral supplements
NJ / NG
PEG / PEJ

105
Q

Polymeric vs elemental diet?

A

Polymeric = if well functioning GI tract whole protein used, glucose and fat

Elemental if poorly functional GI tract:
Free amino acids
Glucose polymers
Long chain triglycerides

106
Q

Other enteral diets?

A

Modular = enriched in particular nutrient

Specific formulation = made to requirement e.g. ventilated patients have diet rich in fat to reduce CO2

107
Q

Why do gastrically fed patients receive break periods?

A

constant feeding encourages colonisation of stomach, so if aspirate = increased risk of nosocomial infection

Continuous feeding = induces secretory response from colon = DIARRHOEA

108
Q

What happens in bowel to those not fed enterally ?

A

Atrophic changes of intestinal mucosa

Due to NO local hormonal release in response to food stimulus

109
Q

What is the result of gastric mucosal atrophy?

A

Loss of cellular adhesion and development of cellular channels
Means bacteria can translocate across bowel into the sytemic circulation = sepsis

110
Q

Complications of enteral feeding?

A

Tube displacement
Infection around PEG/PEJ
re-feeding syndrome = low phosphate, thrombocytopaenia and confusion
Hyperkalaemia if renal impairment
Hyperglycaemia if critically ill and reduced glucose tolerance

111
Q

Indications for TPN?

Which is the. only one that is an absolute indication?

A

General critical illness:
- Severe malnourishment, multiple trauma, sepsis/multi-system failure, severe burns

Gut problems:
- Enterocutaneous fistula, Short bowel syndrome, IBD

ENTEROCUTANEOUS FISTULA

112
Q

How do we administer TPN?

A

Via central line as high osmolality mixture will irritate small veins.

If given through PICC must be <900mOsm/L

113
Q

Why monitor liver in TPN admin ?

A

Can cause derangement in LFT’s

secondary to enzyme induction due to amino acid imbalances
Can also cause fatty changes

114
Q

Metabolic complications of TPN?

A

Hypo/hyperglycaemia
Hyperlipidaemia
Hyperchloraemic metabolic acidosis
Ventilatory problems if excess glucose

115
Q

What is myoglobin and its function?

A

A respiratory pigment found in cardiac and skeletal muscles = single globin chain of 8 alpha-helical regions, with a single haem component

Ready source of oxygen during increased activity

116
Q

How does oxygen dissociation curve differ for myoglobin?

A

Shape is hyperbolic

not affected by pH, CO2.

117
Q

What is rhabdomyolysis?

A

Clinical syndrome caused by release of toxic muscle cell components into circulation

Causes = trauma, drugs, metabolic and congenital conditions

118
Q

What kinds of trauma can trigger rhabdomyolysis?

A

Blunt trauma e.g. crush injury
Prolonged immobilisation on hard floor
massive burns
Acute ischaemic reperfusion injury

119
Q

Complications of rhabdomyolysis?

A

AKI - ischaemic tubular injury due to myoglobin and its breakdown products accumulating in tubules

DIC due to pathological activation of cascade

Metabolic disturbance - due to haemolysis and AKI

Compartment syndrome

Hypovolaemia - can haemorrhage into necrotic muscle

120
Q

electrolyte disturbances of rhabdomyolysis?

A

Hyperkalaemia
Hyperphosphataemia
Hyperuricaemia

Hypocalcaemia

121
Q

How do we confirm diagnosis of rhabdomyolysis?

A

CK > 1000

Elevated LDH
Elevated creatinine
Positive blood dip urine, with absence of haemoglobinuria on microscopy

122
Q

managing rhabdomyolysis?

A

IVF to ensure UO >30ml/hour
You can alkalinise using sodium bicarb
Manage any electrolyte disturbances

123
Q

Clinical features of compartment syndrome?

A

Pain out of proportion to injury

Paraesthesia

Late sign = loss of pulses

124
Q

What level of pressure may lead to compartment syndrome?

A

First clinical signs occur at pressures 20-30mmHg

125
Q

Management of compartment syndrome?

A

Fasciotomy

126
Q

Which four physiological systems are involved in stress response?

A
  1. Acute phase response = cytokines, PGE, leukotrienes, kinins
  2. Sympathetic nervous system:
    - Noradrenaline released from symp nerves and adrenaline from adrenal medulla
    - Stimulates catecholamine release = tachy and HTN
    - as well as: Bronchodilation, reduced intestinal motility, increased glucagon and glycogenolysis
  3. Vascular endothelium:
    - NO produces vasodilation
    - PGE induces vasodilation and platelet aggregation
  4. Endocrine system:
    INCREASE = GH, prolactin, ACTH, ADH, cortisol, renin, aldosterone, glucagon

DECREASE = Insulin, testosterone and oestrogen

No CHANGE = TSH, LH, FSH

127
Q

Outline the key hormonal changes in stress response?

A
  1. Cortisol increase:
    - Significant. within 4-6 hours
    Usual negative feedback fails, and concentrations of ACTH and cortisol remain high
    - Metabolic effects of cortisol are enhanced:
    * Skeletal muscle breakdown
    *lipolysis
    *anti-insulin
    * MR effects
    * anti-inflamm
  2. GH increase:
    - Important for preventing muscle breakdown and promotes tissue repair via insulin GF’s
  3. ADH increased:
    - Vasopressor and enhances haemostasis
    - Renin released causing angiotensin 1 to 2
    - Causes aldosterone secretion = sodium reabsorption
  4. Insulin decrease:
    - Inhibition of pancreatic B cells by the alpha 2 inhibitory effects of catecholamines
128
Q

what happens during the two phases of metabolic response?

A

Ebb phase = reduction in metabolic rate in 24 hours following stimulus

Flow phase = Increase in metabolic rate, with general catabolism / -ve nitrogen balance and glucose intolerance

129
Q

Why is there fall I UO post surgery?

A

Activation of RAAS = release of ADH = sodium and water reabsorption

130
Q

Post surgery why may metabolic alkalosis develop?

A

Increase in aldosterone and cortisol promote sodium retention and potassium excretion. Low potassium = excrete H+ to get K back

MRCS B - Critical Care (Kanani and Lammy) (6 decks)

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