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Year 3 SBOM > ABCDE > Flashcards

ABCDE Flashcards

1
Q

What is SIRS?

A

Systemic Inflammatory Response Syndrome
- Hyper/hypothermic, tachycardia, tachypnoea, high or low WCC

Causes = sepsis, pancreatitis, trauma, burns

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2
Q

What is the pathophysiology of sepsis?

A

Get invading organisms => activation of macrophages - release pro-inflammatory molecules (cytokines, thrombin and NO) => combination of hyper coagulability and hypocoagulability, inflammation, endothelial dysfunction.

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3
Q

Why do we get sepsis?

A

Normally - needs to be a pro-inflammatory response to microorganisms and a counter-response by the body of anti-inflammatories to keep inflammation localised to the area it is needed.

In septic shock - the pro-inflammation molecules overwhelm the anti-inflammatory ones

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4
Q

What are micro-emboli called that end up the in small capillaries due to sepsis?

A

Purpura fulminans

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5
Q

What do pro-inflammatory cytokines cause?

A

Endothelium of BVs connected with tight junctions - infection - then these become less tight for migration of pro-inflammatory factors. Want the WBCs to get to the infection.

Vascular system becomes very permeable
Early stages of sepsis - they are already hypovolemic. When you add fluid - it doesn’t stay in the vasculature as a result.
P becomes hypotensive. Causes negative inotropy - reduces cardiac contractility

Has fever - high temp - body losing water and heat - generating massive amounts of energy and losing it. Diarrhoea as well = further fluid losses and electrolyes.

Initially - get hypercoagulability - can cause microemboli. Forming the clot - body uses up the coag factors - uses up the fibrin etc - cant keep up with the consumption of these ingredients - even though the body wants to coagulate, the body runs out of materials to form clots = hypocoaguable state.

Get increased WBCs - esp Ns - massive inc - get to site of infection, adhere.

Metabolic changes - see insulin resistance v quickly - because the body wants lots of glucose circulating in order to supply the energy needs. Body also quickly starts to consume proteins in order to meet energy demands to fight the infection and to rebuild after the infection

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6
Q

What cardiovascular changes occur in sepsis?

A

Initially warm and dry or warm and sweaty

Can get vasoconstriction at this point as the body tries to stop the loss. Still resuscitatable - bolus of fluid or leg raise will bring them round.

End - very cold, very shut down. Heart is very dysregulated - when you fill them with fluid, the venous system fills up. Its not going into the arterial system because the heart is not pumping to move the fluid into the arterial system = this is not fluid responsive.

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7
Q

What metabolic changes occur in sepsis?

A

Fundamentally - driven by evolution
Sepsis - body thinks we cant do anything - tries to reduce the amount of energy that it needs apart from fighting the infection - and self-cannibalises in order to do so.

In ITU - these mechanics act against interventions

Mitochondria function differently - in areas where there is no inflammation the mitochondria are downregulated. Ps to begin are hyperglycaemic.

Get circulatory changes - vasoconstriction and dilation in the appropriate areas - as it becomes dysregulated you get generalised vasodilation. Leads to tissue hypoxia in the areas where the mitochondria are not working. Instead you get anaerobic respiration and lactic acidosis.

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8
Q

How can you identify sepsis?

A

Suspected infection

+

An acute change in SOFA score of more than 2 points consequent to infection

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9
Q

How can you identify sceptic shock in Ps?

A

Persisting hypotension requiring vasopressors to maintain a MAP of 65mmHg

Serum lactate >2mmol/L

despite volume resuscitation

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10
Q

If a patient has problems breathing - how can you identify this?

A
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11
Q

What do you give a patient who has problems breathing in septic shock?

A

A 15L non-rebreather mask

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12
Q

What signs are concerning regarding circulation in a sceptic patient?

A

Cap refill > 2 seconds (very sensitive indicator)
Core v. peripheral temperature differences (cool peripheries = not good)
HR, BP
Oliguria
Confusion

Mottled, cold and dry = bad - person is about to die.

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13
Q

What is usually the first evidence of organ dysfunction in the CVS/Respiratory system?

A

The appearance of ALI or ARDS (acute lung injury or acute respiratory distress syndrome)

Not pneumonia - caused by sepsis. Get inflamed capillaries in the lungs - fluid is pouring out of the capillaries and into the air spaces in the lungs.

Do sequential CXRs

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14
Q

What is shock?

A

The body cannot provide enough glucose for its metabolic demands. Starts to shut down circulation to underperfusing parts of its circulation (evolutionary response).

= Massive cellular dysregulation. Lose K+ and Na+ = fluids in interstitium. Lysosomes release -> cell death.

Cell contents are released - these are pro-inflammatory = start to magnify the response => causes inflammatory cascade.

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15
Q

What is biofilm?

A

Is a community of microorganisms in which cells stick to each other and often also to a surface. These adherent cells become embedded within a slimy extracellular matrix that is composed of extracellular polymeric substances (EPSs)

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16
Q

What type of bacteria is Staph aureus?

A

Gram positive

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17
Q

Which is harder to treat - gram positive or gram negative bacteria?

A

Gram-Negative Bacteria

Their peptidoglycan layer (LPS) is much thinner than that of gram-positive bacilli. Gram-negative bacteria are harder to kill because of their harder cell wall. When their cell wall is disturbed, gram-negative bacteria release endotoxins that can make your symptoms worse.

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18
Q

What proportion of sceptic patients are a result of gram positive bacteria?

A

50% (mostly staph aureus)

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19
Q

How do macrophages recognise S aureus?

A

By their peptidoglycans and lipoteichoic acids - recognised on Macs TLRs -> inflammatory response

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20
Q

Why does TSS occur?

A

Certain bacteria produce toxins which function as super antigens = trigger responses in up to 20% of all T cells (rather than just the tiny proportions of resting T cells).

Superantigens are big molecules - locks a T cell into a pro-inflammatory position, no disassociation = massive and prolonged response.

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21
Q

Which inflammatory factors are released during TSS?

A

IL1
IL2
TNF

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22
Q

What does C Diff do?

A

Causes severe epithelial and mucosal damage - esp in the colon where it can cause massive sloughing of cells

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23
Q

What is the difference between sepsis, SIRS and septic shock?

A
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24
Q

What were the problems with the SIRS criteria?

A
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25
How is sepsis now defined?
Life threatening organ dysfunction caused by a dysregulated host response to infection.
26
What NEWS score can indicate possible sepsis?
NEWS >7
27
What are the qSOFA score criteria?
SBP <100mmHg RR >22 Altered mental status - GCS <15
28
What are the sepsis six?
29
What type of antibiotics should you use in sepsis?
Broad spectrum bacterio-cidal ABx NOT bacteriostatic ones Check local guidelines
30
What should you do before starting systemic Abx?
Send blood cultures!
31
How does normal glucose metabolism occur?
Glucose enters body and goes to the liver through the mesenteric circulation - enters metabolic pathways - brain, blood, muscle, fat, pancreas and liver.
32
What is the first phase of starvation? What happens in this phase?
Simple starvation - occurs 4-6 hours after the last meal. Involves adaptive metabolic responses - - consumption of glycogen (glycogenolysis) - gluconeogenesis (FAs and glycerol) Lean tissue is conserved (i.e. protein)
33
What is the second phase of starvation? What happens in this phase?
Phase 2 = catabolic weight loss (adipolysis) Uses mainly stored fat for energy (occurs 12-18 hours after last meal) Generates ketones form fat stores = ketotic state (mild ketosis) Body starts to consume bicarb to balance out the acidosis from the ketones = bicarb levels fall
34
What is the third phase of starvation? What happens in this phase?
Phase 3 = catabolic weight loss via proteolysis Fat stores are gone - proteins used to produce AAs. Not uniform loss - muscles, liver and spleen are catabolised first. Tries to maintain basal metabolism. Poor wound healing, immune response, GI integrity etc common at this phase.
35
When is ketosis not pathological?
When conc is only mildly elevated (<3mmol) above baseline Due to a normal response to low glucose availability.
36
What happens when the body is in a state of ketosis?
Machinery of glucose production shifts to the liver Insulin inhibits lipolysis Feedback mechanism - the more ketones you have, the more lipolysis is inhibited
37
What is ketoacidosis?
A metabolic state associated with metabolic acidosis and pathologically high serum and urine concs of ketone bodies.
38
What causes ketoacidosis?
- DKA - Alcoholic ketoacidosis (AKA) - Salicylate poisoning - Isopropyl alcohol ingestion - Starvation ketoacidiosis (>3 w of starvation)
39
What is the difference between starvation and injury?
In injury - metabolic rate is increased for repair whereas in starvation it is decreased to conserve calories. In injury - protein is used for catabolism as the products from its breakdown are used for repair. In starvation - fats and ketones are used for catabolism as they are the least useful materials needed by the body and are therefore expendable.
40
What is the difference between SIRS and Sepsis?
SIRS = exaggerated defence response of the body to a noxious stressor - intended to localise and eliminate the source of assault. Sepsis = life-threatening organ dysfunction caused by a dysregulated host response to infection.
41
What causes sepsis and septic shock?
An imbalance between the proinflamamtory and anti-inflammatory responses. Both pathways occur but should stay in balance. When they get out of balance and you get too much proinflammation - this causes sepsis and septic shock.
42
By how much do energy requirements increase in sepsis?
Energy requirements can go up by 30% in sepsis
43
How is the post-shock metabolic response categorised?
Into the ebb phase and flow phase. Ebb phase - starts immediately and lasts for 24 hours as the body conserves energy. Flow phase - the body expends energy and massive catabolic efforts take place.
44
What causes a huge rise in nitrogen excretion after stressful insults to the body?
Protein catabolism used for repair of the body
45
What do you need to beware when feeding sick Ps?
If you underfeed or overfeed a P - the mortality rates go up. Is a "goldilocks feeding point" = need to provide the right number of calories which is only a little bit more than the cumulative normal basal metabolic rate.
46
Why do Patients go off their food when they are unwell?
Stress mediators oppose the anabolic actions of insulin. Get peripheral insulin resistance in these patients.
47
In times of illness, which places stress on the body, there are additional glucose requirements - how does the body obtain these?
48
What is the hypermetaboic response to injury?
The flow phase of recovery - HT, tachycardia, Nitrates in urine, mild pyrexia, albumin v high Pro inflammatory condition. Massively consumes lean body mass - muscle, bone, parenchyma (liver and spleen) - results in very high energy metabolites (lactate and Fas) being released - body floods itself in the absence of being able to take food in. Get hyperglycaemia, plus ketones and lactic acid create acidosis as well.
49
What is lactate used for in the body?
Used both in the cori cycle and the Krebs cycle to make energy
50
What can cause a high serum lactate?
Lots of things - Exercise - Critical illness - Sepsis - Cardiogenic shock - Liver failure - Open heart surgery
51
Why do you get hyperlactatemia in sickness?
Is not always due to tissue hypoperfusion (response to this is to increase tissue perfusion by increasing fluids). Fluid challenge is not always the right response to a raised lactate. Initial problem of high lactate can be due to both overproduction from sickness OR inability of the body to clear the lactate it has. Over production happens due to massive inflammation - accelerates glycolysis and proteolysis - catabolic state - mobilisation of substrates to increasing the production of pyruvate and lactate. Happens in skeletal muscle - supply source that the body turns to when it has run out of glycogen. Lactate is moved in the circulation from skeletal muscle to places like the liver where it can be utilised. High lactate - body is deliberately producing it as an energy source for increased demand. In sepsis - vast majority is oxidised = limited uptake by the Cori cycle - remainder is turned into glycogen by gluconeogenesis in the liver. Not efficient energy supply.
52
What is it called when you have 2+ altered organ functions in acutely ill patients -> homeostasis cannot be maintained without intervention.
Multiple Organ Dysfunction Syndrome
53
Where does MODS usually appear first?
Cardiovascular and respiratory systems - can manifest as acute lung injury ./ acute respiratory distress syndrome. This leads to hepatic and renal dysfunction Then disorders of haemostats, GI and CNS Finally bone marrow failure and myocardial dysfunction are usually late manifestations.
54
How much water do we require each day?
30ml/kg
55
What are water losses via breathing and sweating called?
Insensible losses
56
What test can you do to see whether a P will respond to fluids?
Straight left lift - arterial pressure should go up and HR come down - as CVS has blood entering the circulation. When legs go back out - they refill - then the hypotension and tachycardia should come back = P is relatively hypovolaemic AND the circulation system should respond if you give fluids. In the later stages of shock, it wont respond! Preferable to do to intubated Ps - otherwise risk of reflux and aspiration.
57
How can you assess a P's volume status?
58
What clinical signs can you use to monitor volume status?
Cap refill - really sensitive measure of fluid refill If in bed for a long time - fluid can accumulate in flanks and sacrum - get pitting oedema Are they warm, cold? Do they have swollen knees? Breathless - because fluid overloaded or because they are hypovolaemic? Arterial line - look for a swing in systolic pressure - does the systolic pressure move up and down in line with respiration - sign that someone needs fluid. JVP - not useful in determining fluid balance
59
What does haematocrit measure? What does a high Hb and high crit indicate?
Haematocrit = absolute conc of vol of a ml of blood that is taken up with RBCs If Hb high and crit low - P has high amount of Hb but they arent dehydrated. If Hb high and crit high - blood is conc - could do with more plasma.
60
Where is the best place to take a lactate reading from?
Take a mixed venous lactate from central line that sits at the entrance to the right atrium - where the blood mixes from the SVC and IVC - meaning you get an indication of the lactatemia in the total circulation. Lactate taken from a cannula - not very useful.
61
How do we calculate serum osmolality?
2xNa + 2xK + Glucose + Urea Want to know absolute value and trend over time - going up (P drying out), going down (P getting wetter)
62
What investigations can you do to assess a P's volume status?
63
Why do we not give pure water IV to Ps?
Would go into the cells & can lyse the cells. Na & Cl are added to give similar osmolality.
64
What happens if you give too much normal saline?
If you give Ps enough normal saline they become hypertensive - massive salt load - kidneys want to get rid of it - so they increase the perfusion pressure in order to push the Na out.
65
What does 0.9% saline contain?
154 mmol/L Na and Cl
66
What does 5% glucose contain?
50g of glucose/L
67
What affect does 5% glucose have on Ps?
Contains no Na or Cl - just glucose. Therefore makes Ps hypotonic - reduces blood Na and Cl. Glucose is metabolised to H20 and CO2. Gives energy but adds a lot of water.
68
What does Hartman's contain?
Na (131) K (5) Cl (111) Ca (<0.5) Lactate (5.16) HCO3 (29)
69
Why do neurologists not like lactate?
They worry about the cells in the brain around an injury - brain cells like to use glucose for energy - if you make the brain use anaerobic respiration (in an hypoxic area) - is very bad and produces a lot of lactate - neuro worries that if the brain is injured the lactate might make damaged areas more damaged because the brain will utilise the lactate to respire in the areas that are injured.
70
What is the osmolality of the extracellular and intracellular spaces?
280-310
71
Which crystalloid fluids is the most similar to normal physiological fluids?
Haartman's Hartmann's = Na, K, Cl - closer to physiological normal levels - small amount of Ca - isnt much Ca IC - so this amount of Ca maintains normal body levels. Is no glucose but there is lactate. Lactate - is a useful molecule for metabolism. Also has HCO3 in it - good for buffering and metabolism.
72
What fluids would you give in this case?
73
How much fluid should be given as maintenance?
30mls H20 /kg/day (approx 2.5L) Doesn't work in real world. Standard surgical regime = 1L 0.9% saline with 20 mmol KCL 1L 0.9% saline with 40 mmol KCL + 1L glucose which may or may not have 20mmol KCL
74
What do you want to do now?
Non-rebreathe mask @ 15L High flow O2 Blood cultures taken now Proper Abs - double check the Abs - are they bacteriacidal? Needs a fluid challenge - 500ml bolus as fast as you can get it in - squeeze it in Measure lactate - arterial sample. Put catheter in and measure urine output
75
What is the aim of fluid administration in the following scenarios - Maintenance - Resuscitation - Vomiting deficit - Diarrhoea deficit
Maintenance = replace daily requirements Resus = replace intravascular levels, restore physiology and perfusion Vomiting = replace water, Na, H+ and K+ Diarrhoea = replace water, Na, HCO3 and K+
76
How much fluid should be given in resus?
500ml over 15-20mins, 250ml over 30mins if frail Keep on giving until they dont need any more or if they stop responding (if they stop responding - they are getting worse).
77
How much of the following do you need on a daily basis as an adult? - Na - K - Ca - H20 - Carbs
Na+ – 2mmol/kg K+ – 1mmol/kg Ca2+ – 0.1mmol/kg H2O – 30 mL/kg Carbohydrate – 4g/kg
78
How can you re-assess the response to a fluid challenge?
Straight leg raise
79
What can be used as a marker of tissue hypoxia / perfusion?
Lactate
80
When you give crystalloid fluids - how much stays in the intravascular space?
1/4
81
Why does dextrose distribute much further than normal fluids?
The glucose is taken up by all compartments - only 1/12 will remain intravascular.
82
Why is dextrose not used for resus?
Only 1/12 remains intravascualr It can cause electrolyte dilution - esp hyponatremia Will lyse cells as well due to hypotonic status - not good
83
What types of colloid fluids are there?
Colloid = fluid with big molecules in there - Succinylated gelatin - Albumin - Blood products
84
Where do colloid fluids redistribute to?
They dont - they stay in the intravascular space - have high oncotic pressure and therefore stay intravascular.
85
When are colloids used?
In specific situations - when you need rapid volume expansion or when protein loss is high. - Replacement (ascitic / pleural losses) - Trauma resus if blood loss - Balanced resus in severe sceptic shock ( in sepsis the tight junctions fail and even the big molecules can leak out. Give colloids for specific therapeutic indication - e.g. RBCs for anaemia or FFP for coagulopathy)
86
What do you need to complement giving 0.9% saline with?
5% dextrose Otherwise P can develop acidosis and hypernatremia as saline does not contain K+
87
What must you complement 5% dextrose with?
0.9% saline
88
What do vasopressors do?
Make BVs constrict to increase BP.
89

Year 3 SBOM (7 decks)

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