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MRCS PART B > cRIT CARE > Flashcards

cRIT CARE Flashcards

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1
Q

What is pulse pressure?

A

Difference between systolic and diastolic
Represents force of the heart

Low - reduced stroke volume as preload decreased

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2
Q

Compartment syndrome

A

increased pressure within a closed osteofascial compartment, resulting in impaired local circulation and necrosis of muscle

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3
Q

Rhabdo tx

A
  • Fluid resuscitation: Ensure good hydration to support urine output > 300 ml/h using IV
    crystalloid until myoglobinuria has ceased.
  • Diuretics, e.g. mannitol, may also be used.
  • Alkalinisation : Sodium bicarbonate infusion has been used to limit myoglobin- induced
    tubular injury in the presence of acidic urine. It alkalinises the urine >
    6.5 pH.
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4
Q

Preload

A

End diastolic volume of the ventricles

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5
Q

Regulation of BP

A

Short term - Baroreceptors (sensors located in the carotid sinus or aortic arch), sensing blood pressure via stretch .

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6
Q

Angiotensin II

A

Vasocontrictor
increases sodium reabsorption

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7
Q

Fasciotomy

A

Anterolateral - 15-20cm incision anterior to shaft of fibula. LM -TT - careful of SPN

Posteriomedial - 15-20cm incision, MM- TT

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8
Q

Pancreatitis station - management

A

I will resuscitate this patient by giving him a fluid bolus and providing analgesia!!

Nutrition
fluid

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9
Q

Cause of retroperitoneal bleeding

A

AAA, pancreatitis

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10
Q

Which factors stimulate pancreatic secreation

A

Vagal, secretin, CCK, gastrin

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11
Q

Pathogenesis of pancreatitis

A

Duct obstruction -> premature activation of pancreatic digestive enzymes -> autodigestion -> trypsin -> increase in vascular permeability

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12
Q

Why NJ tube feeding in pancreatitis

A

Passes duodenojejunal flexure - prevents CCK being released

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13
Q

Transmission of pain

A

1st order - Nociceptors -> alpha fast, delta slow
2nd order - spinal cord - spinotholamic tract
3rd order - primary somatosensory cortex - thalamus

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14
Q

ADH

A

released due to increase serum osmalirity and decreases in volume

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15
Q

Afterload

A

Pressure heart must work during systole

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16
Q

Signs of As

A

Ejection systolic murmur
Pardoxical splitting of S2
narrowed pulse pressure

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17
Q

CPP

A

Systemic diastolic arterial pressure - LVED Pressure

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18
Q

Hypocalcemia signs

A

Paraesthesia, tetany, larygospasm, seizure, confusion

QT prolongation, bradycardia, dilated cardiomyopathy

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19
Q

Hypercalcemia ECG

A

Short QT, Wide T, ST elevation, prominent U

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20
Q

How is CO2 carried in the blood

A

Bicarbonate
carboxyheamoglobin
dissolved

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21
Q

ABG - resp acidois compensation

A
  1. cellular bicarb - small amount
  2. renal - takes 3-5 days
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22
Q

Clinical markers of cardiac index

A

Pulse rate, systolic BP, CRT, Temp, urine output

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23
Q

what are the different types of pelvic fractures

Study These Flashcards
A

Young Burgess
- Lateral compression
-Anteroposterior compression
- Vertical shear

24
Q

What is inside a neutrophil

Study These Flashcards
A

lysomal granuals

25
How do neutrophils bind
Margination - adhesion - transmigration - migration
26
What is cerebral perfusion pressure?
Net pressure gradient causing blood flow to the brain CPP = MAP - ICPSV
27
Why does dilation occur in raised ICP?
Uncus of the temporal lobe of brain herniates through the tentorium cerebelli occulomotor nerve compresed parasympathetic paralysis unopposed sympathetic - mydriasis
28
Burns: How do you assess adequacy of fluid?
1. Clinical measures of cardiac index 2. Central venous pressure - reflection of right heart 3. Hemotocrit
29
Types of burns
Superficial - Dry, red, no blisters, pain , brisk CRT Superficial partial thickness - moist, red/pink, blisters, sluggish Superfical deep -moist, blotchy, pain, no CRT Full thickness - dry, black, no pain, no CRT,
30
Why no colloids in burns
Burns can lead to capillary leak colloids leak into extravascular space, exerts oncotic pressure and triggers third space loss
31
What is cushings response?
physiological nervous system response (mixed vagal and sympathetic stimulation) to an elevated ICP that results in cushing’s triad. Increased sytolic bP and widened PP Bradycarida irregular bretahing
32
Raised ICP clinical picture
Headache N+V Papiloedema Dilated pupil - occulomotor Lateral gaze - abducens
33
What are the effects of raised ICP?
Decreased CPP - ischemia Midline shift - ventricular outflow obstruction Herniation - occulomotor damage compression of medulla - ventilation
34
Difference between neurogenic and spinal shock?
Neuorgenic is a form of distbutive shock - autonimic dysfucntion - lack of sympathetic This leads to hypotension, bradycardia and vasodilation spinal shock - transient Loss of sensormotor physiological repsonse - can improve lack of reflexes and muscle some featurres of neuor shock - bradyacraida and hypotension
35
Function of potassium
Fluid balance nerve impulse function muscles function cardiac muscle function
36
Homeostasis of potassium
Potassium = intracellular Na/k pump - insulin Na/k - DCT- Aldosterone Acid base stasis of blood
37
hyperkalemia on heart
Depolirasation of resting membrane -> BRADYCARDIA -> Cardiac arrest, decrease action potential
38
High urine output post AKI
Initially reduced GFR, then recovers, distal tubules do not recover - plasma filtered at glomerulus is not reabsorbed - extreme polyuria
39
Chronic renal failure and anaemia
Reduced production of EPO Circulating bone marrow toxins -> bone marrow supression ureamia increases cell wall fragidity
40
What leads to an increase in Aldosterone
Increased angiotensin ii reduced sodium Increased potassium
41
Counter current
Thick ascending limb imperable to water -
42
Stages of wound healing
1. Heamostasis - vasoconstriction, platelets, activation of cascade 2. inflammation - neutrophils 3. inflammation - macrophages 4. proliferative - fibroblasts , epitherlisation 5. maturation, remnodelling
43
How does vascular surgery interfere with heamostasis?
Easier platelet activation, higher fibrinogen, shutdown of fibrinolysis
44
What is DIC
Pathological consumpative coagulopathy due to activation of the coagulation and fibrolynitc system. This leads to formation fo mico thrombi and consumption of clotting factors and fibronogen.
45
Signs of DIC
1. Widespread heamorrhage 2. Thombocytopenia , decreased fibrinogen and increased FDP
46
What is necrotising facsitis
Necrotising fasciitis is a life-threatening rapidly-progressing infection that spreads along the fascial planes and subcutaneous tissue.
47
fever
pyogenes -> IL1 and TNF alphas -> prostaglandin in hypothamus -> fever
48
Crystalloids
Water soulable moleulces
49
Colloids
Contain larger insoluable molecules
50
Why no colloids in trauma
in SIRS - Endothelial dysfunction - capillary leak. colloids can seap through and pull out water
51
What is MAP?
Average arterial pressure mainatined throughout a cardiac cycle
52
Compents of TPN
Water, carbohydrates (50%), lipids (30%), proteins, vitamins, nitrogen, trace elements
53
Negatives of complete carbohydrate feed
glucose intolerance: as part of the stress response, critically unwell patients are often in a state of hyperglycemia and glucose intolerance. * Fatty liver: the excess glucose occurring as a consequence of the above is converted to lipid in the liver * Respiratory failure: the extra CO2 released upon oxidation of the glucose may lead to respiratory failure and increased ventilatory requirements * Relying solely on glucose may lead to a deficiency of the essential fatty acids.
54
How would you manage hypovalemic shock
1. Fluids and bloods 2. Control bleeding - pelvic binder, stabilising fractures, laparotomy
55
Pathophysiology of ARDS
* An acute phase, characterized by 1) Widespread destruction of the capillary endothelium, extravasation of protein-rich fluid and interstitial edema 2) Migration of neutrophils and extensive release of cytokines 3) The alveolar basement membrane is also damaged, and fluid seeps into the airspaces, stiffening the lungs and causing ventilation/perfusion mismatch. * A later reparative phase, characterized by 4) Fibroproliferation, and organization of lung tissue. 5) If resolution does not occur, disordered collagen deposition occurs leading to extensive lung scarring.
56
Portal HTN
Cirrhosis resulting from chronic liver disease and is characterized by liver cell damage, fibrosis and nodular regeneration. The fibrosis obstructs portal venous return and portal hypertension develops. * Arteriovenous shunts within the liver also contribute to the hypertension

MRCS PART B (10 decks)

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