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MRCS Critical care > Critical care: GI > Flashcards

Critical care: GI Flashcards

1
Q

What is a metabolic acidosis

A

Decrease in pH due to metabolic cause

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2
Q

What is the anion gap? how is it calculated? What is a normal anion gap?

A

-Difference between cations (+ve-cats are positive) and anions (-ve) in your blood
-(Na+ + K+) - (Cl- + HCO3-)
-Should be 8-16/ around 12

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3
Q

What is a high anion gap acidosis? What are the causes?

A

Increase in unmeasured anions: LKTR
Lactate
Ketones
Toxins (salicylates, metformin)
Renal failure (impairment of H+ excretion)

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4
Q

What are the causes of normal anion gap metabolic acidosis?

A

-Loss of bicarb, i.e. high bowel output
–> fistulas
–> stomas
–> diarrhoea

Too much Nacl
Renal tubular acidosis (kidneys excrete bicarb)

Bicarb is replaced by chloride which is also a buffer

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5
Q

Indications for RRT

A

Refractory uraemic encephalopathy
Refractory acidosis
Refractory fluid overload
Refractory hyperkalaemia
Toxins

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6
Q

Complications of dialysis

A

-Hypotension: losing fluid
-Electrolyte shift
-Coagulopathy: citrate chelates calcium –> cofactor –> stops clotting
-Complications from line: bleeding, damage to local structure, pneumothorax

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7
Q

Why is anion gap corrected for albumin? how is this done?

A

the normal AG = 0.2 x [albumin] (g/L) + 1.5 x [phosphate] (mmol/L)

Albumin is major unmeasured anion: changes in albumin levels can significantly change equation

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8
Q

Describe patholphysiology of NAGMA vs HAGMA

A

High anion gap metabolic acidosis: bicarb is consumed by unmeasured cation (e.g. h+) as a result of its action as a buffer–> high anion gap

normal anion gap metabolic acidosis: Loss of bicarb is primary pathology, gets replaced by Cl- (also a buffer): therefore is hyperchloraemic metabolic acidosis

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9
Q

What is dialysis

A

Countercurrent exchange between blood and dialysate, exchange accross semipermeable membrane
Molecules are removed via diffusion

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10
Q

What is haemofiltration

A

-Haemofiltration - fluid is driven across the
semipermeable membrane by convection (pressure gradient)
-The solutecontaining plasma water is removed from the body and replaced with clean fluid.

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11
Q

How would gastric outlet obstruction present?

A

-Projectile vomiting undigested food
-Early satiety
-Unintentional weight loss
-Bloating

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12
Q

What would differentials be for gastric outlet obstruction?

A

Large gastric polyp in antrum/pylorus
Peptic ulcer disease
Carcinoma of stomach/head of pancreas/duodenum

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13
Q

What are the causes of metabolic alkalosis?

A

-Persistent vomiting (loss of HCL, hypokalaemia, hyponatremia–> kidneys retain sodium at expense of H+ to preserve Na/K+ pumps, worsening alkalosis
-Contraction alkalosis: e.g. due to dehydration: aldosterone causes renal H+ excretion
-Use of loop diuretics and thiazides: loss of sodium and water causes contraction alkalosis
-Primary hyperaldosteronism (conn’s)

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14
Q

Explain the phenomenon of aciduria in gastric outlet obstruction

A

-Prolonged vomiting leads to loss of HCL and K+: hypochloraemic hypokalaemic metabolic alkalosis
-K+ is shifted from intracellular to extracellular compartment, depleting body’s store of K further
-As dehydration worsens, kidneys preferentially reabsorbs Na and water, over K+ and H+–> paradoxical aciduria

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15
Q

What are ecg changes with hypo and hypercalcaemia

A

Hyper: Short QT
Hypo: prolonged QT

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16
Q

What are ecg changes of hyper/hypokalaemia

A

Hypo: small/inverted t waves
U waves after t waves
Prolonged pr
ST depression

Hyper:
Tall tented t waves
Broad QRS
Flattened P wave

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17
Q

What do gastrin and pepsinogen do?

A

Gastrin: stimulates secretion of gastric acid
Pepsinogen: protein digesting enzyme. Converted to pepsin by hydrochloric acid

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18
Q

What hormones are produced and by which cell type in stomach?

A

G cells in pyloric antrum of stomach, duodenum and pancrease: Gastrin
Parietal cells: HCL and intrinsic factor
Pepsinogen: chief cells

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19
Q

In what syndrome is gastrin produced in excessive levels? What are its features?

A

Zollinger ellison syndrome (gastric acid hypersecretion, peptic ulceration, gastrinoma)

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20
Q

How would you diagnose and treat zollinger-ellison

A

Investigations:
-Secretin stimulation test–> measures evoked gastrin levels
-Fasting gastrin levels, on 3 separate occasions
-Increased level of chromogranin A (common marker neuroendocrine tumour)

Treatment
-PPI (omeprazole, lansoprazole)
-Octreotide (mimics somatostatin)
Surgery +/- chemotherapy

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21
Q

What would you find on examination of baby with congnital hypertrophic pyloric stenosis?

A

Dehydration
Olive shaped mass right upper quadrant/epigastrium

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22
Q

What would be your initial management of pyloric stenosis

A

NBM
NG tube
Fluid resuscitation, correct electrolytes
UO monitoring
Bloods + capillary blood gas

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23
Q

What investigations would you carry out to confirm diagnosis of pyloric stenosis?

A

US
Feeding test

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24
Q

What would be definitive management of pyloric stenosis?

A

Open/laparascopic pyloromyotomy

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25
Q

What are the functions of the spleen?

A

FISH
Filtration and removal of old/abnormal red cells/white cells/platelets
Immunological properties: antibody synthesis
Storage of platelets
Haematological properties: extramedullary erythropoiesis in adults, erythropoeisis in foetus

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26
Q

What is grade 1 splenic haematoma?

A

Subcapsular haematoma <10% surface area
Capsular laceration <1cm in depth

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27
Q

What is grade 2 splenic haematoma?

A

Subcapsular haematoma 10-50% surface area
Intraparenchymal haematoma <5cm in diameter
Laceration 1-3cm depth not involving trabecular vessels

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28
Q

What is grade 3 splenic haematoma?

A

Subcapsular haematoma >50% of surface area/expanding
Intraparenchymal haematoma >5cm or expanding
Laceration >3cm depth or involving trabecular vessels
Ruptured subcapsular/parenchymal haematoma

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29
Q

Grade 4 splenic haematoma

A

Laceration involving segmental/hilar vessels with major devascularisation (>25% spleen)

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30
Q

Grade 5 splenic haematoma

A

Shattered spleen: hilar vascular injury with devascularisation spleen

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31
Q

How would you classify splenic injury?

A

Grade 1-5

32
Q

What are options for management of splenic injuries?

A

Isolated grade 1/2 splenic injury may be suitable for conservative management

Grade 3-5
-If haemodynamically unstable, early resuscitation and emergency surgery
-If haemodynamically stagble with signs of bleeding (dropping serial hb: consider IR/surgery

33
Q

What specific problems may occur post splenectomy?

A

Severe infection following splenectomy by encapsulated organism
Strep pneumonia, haemophilus, neisseria meningitidis
Malaria parasites
Greatest risk during first 2 years, but persists throughout life

34
Q

What measures would you consider in patients post splenectomy?

A

Haemophilus influenza type b vaccine
Meningococcal group c vaccine
Pneumococcal vaccine
Antibiotics for minimum 2 years, preferably lifelong (oral pen v/clarithromycin if pen allergic)
Children: until minimum age 16 (as well as minimum 2 years and preferebly lifelong)

35
Q

What maintenance fluid would you use in children?

A

0.9% sodium chloride + 5% glucose

36
Q

What type of fluid would you use for replacement of NG losses in children?

A

0.9% sodium chloride with 10mmol K

37
Q

How would you calculate maintenance fluids in children?

A

4ml/kg for first 10kg
2ml/kg for next 10kg
1ml/kg for subsequent kgs

38
Q

How would you give fluid bolus in child?

A

20ml/kg 0.9% saline

39
Q

Causes of pancreatitis

A

Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps and other viruses (epstein barr, cmv)
Autoimmune
Scorpion sting, snake bites
Hyperlipidaemia
ERCP
Drgus (steroids, NSAIDs, diuretics-furosemide and thiazides)

40
Q

Glasgow criteria for pancreatitis

A

PaO2 <8
Age >55
Neutrophils (WCC) >15
Calcium <2
Renal (urea- >16
Enzymes (LDH > 600/AST >200)
Albumin <32
Sugar >10

> 2 = severe pancreatitis

41
Q

What is a tips procedure?

A

Interventional radiology procedure which establishes communication between inflow portal vein and outflow hepatic vein
-Access via internal jugular vein
-Used to treat portal hypertension and varices
-Reduces blood pressure in portal venous system

42
Q

What parameters are accounted for in classes of shock?

A

6 parameters
-Amount of blood lost
-Pulse
-Blood pressure
-Respiratory rate
-Urine output
-Mental state

43
Q

Class 1 shock

A

<750ml blood loss
Pulse <100
bp normal
rr 14-20 ml
UO >30ml/hr
slightly anxious

44
Q

Class 2 shock

A

750-1500 ml blood loss
Pulse 100-120
BP normal
RR 20-30
UO 20-30ml/hr
increasingly anxious

45
Q

Class 3 shock

A

1500-2000 ml blood loss
Pulse 120-140
BP reduced
RR 30-40
UO 5-15ml/hr
Confused

46
Q

Class 4 shock

A

> 2000 ml/hr
Pulse >140
BP reduced
RR >40
UO negligible
Drowsy

47
Q

What blood products are avaiable for transfusion in shocked patient? How soon are these available?

A

Packed red cells (o negative: available immediately, type specific blood: available after 10 mins, cross matched blood available after 1 hr)
Platelets
FFP

1:1:1 ratio

48
Q

What is the difference between ffp and cryoprecipitate?

A

-FFP: fluid portion of 1 unit blood that has been separated and frozen at -18 degrees within 6 hrs collection
-Used to reverse warfarin, in massive transfusion and to replace specific clotting factor deficiencies

Cyropreceipate: prepared from plasma. One unit is formed from 4-6 units of blood
-used in Bleeding from excessive anticoagulation, massive haemorrhage, von willebrand, haemophillia, DIC
-Composed of factor 8, factor 13,fibrinogen, von willebrand

49
Q

Describe transfusion reactions

A

Immediate;
-Anaplylactic
-Febrile

Within 6 hours
-Trali: non cardiogenic pulmonary oedema due to activation of immune cells in lungs
-TACO: volume overload

Within 24 hrs
-Acute haemolytic reaction (chills, fever, hypotension, hyperbilirubinaemia)

> 24 hrs
-Graft versus host (rash, liver dysfunction, diarrhoea)
-Post transfusion purpura

4- 8 days
-Delayed haemolytic reaction

50
Q

How would you reverse warfarin in an emergency?

A

Product would depend on inr and level of bleeding
-discuss with haematology
-Vitamin K and pcc if active bleeding
-FFP produces suboptimal anticoagulation: only if PCC unavailable

51
Q

Define hypotheramia

A

Core body temperature <35 degrees

52
Q

Which part of brain regulates temperature?

A

Anterior hypothalamus

53
Q

What are signs of hypothermia?

A

Shivering
Change in HR
Change in RR
Altered GCS
Pallor
Cyanosis

54
Q

Why is surgical pt at increased risk of hypothermia?

A

-General/regional anaesthesia causes loss of behavioural response to cold and impaired thermoregulatory heat preserving mechanisms
-Anaesthetic induced peripheral vasodilatation
-Use of un-warmed blood/iv fluids and cold anaesthetic gases
-Reduced metabolic activity
-Environmental factors (e.g. low theatre temp)
-Increased head loss - environmental exposure

55
Q

What measures can be taken to minimise hypothermia intraoperatively?

A

-Maintain optimum ambient temp above 21 degrees
-Adequate/appropriate clothing
-Minimise exposure of operating field
-Warmed fluids/blood/anaesthetic gas
-Insulating drapes
-Warming blankets
-Bair hugger

56
Q

What is the body’s response to hypothermia?

A

-Piloerection
-Vasoconstriction
-Increased basal metabolic rate (shivering thermogenesis)
-Increase metabolism (due to hyroid hormones and catecholamine-mediated ‘brown fat metabolism’ (non shivering thermogenesis)
-Behavioural e.g. moving to warm environment, wearing more layers of clothes, turning heating on

57
Q

What are the physiological effects of hypothermia?

A

Respiratory
-Oxyhaemoglobin curve shifts to left
-non cardiogenic pulmonary oedema

Haematological
-Increased blood viscosity
-Coagulopathy

Renal
-Cold diuresis
-Immobilisation and rhabdomyelysis

Cardiac
-Arrhythmia

Systemic
-Sympathetic excitation

-Sympathetic excitation
-Oxyhaemoglobin curve shifts to left
-Cold diuresis
-Coagulopathy
-Increased blood viscosity
-Immobilisation
-arrythmias
-Non cardiogenic pulmonary oedema

-Sympathetic nervous system excitation (shivering, hypertension, tachycardia, tachypnoea, vasoconstriction)
-Cold diuresis (inability to concentrate urine due to renal cell dysfunction, decreased levels adh) –> leakage of fluid into interstitial tissues leading to hypovolaemia
-Confusion (neurons initially stimulated, but are then depressed)
-Immobilisation –> muscle necrosis, myoglobinuria, ATN
-Pulse and respiration decrease, major organs fail
-Oxyhaemoglobin curve shifts to left
-Haemoconcentration and inreased viscosity that can result in thrombotic and embolic complications
-Coagulopathy due to thrombocytopaenia, decreased tnzymatic actions
-non-cardiogenic pulmonary oedema
-Arrhythmias

58
Q

What are the metabolic effects of hypothermia?

A

-Hyperglycaemia (decreased glucose consumption by cells; decreased insulin secretion; tissue sensitivity to insulin blunted; glucose released from liver).
-Hypoglycaemia (common in alcoholics as their glucose stores are depleted)
-Cellular metabolic processes shut down
-acidosis from carbon dioxide retention and lactic acidosis

59
Q

What ecg changes might be expected in hypothermia?

A

-Sinus bradycardia
-Prolonged PR
-Prolonged QT
-‘J’ waves (extra deflection at end of QRS, just overlapping beginning of ST segment)

60
Q

How would you manage mild hypothermia? What temperature classifies as mild?

A

32-34.9
-Passive rewarming
-Use of person’s own heat generating ability
-insulating dry clothing
-Warm environment

61
Q

How would you manage moderate hypothermia? What temperature is moderate hypothermia defined at?

A

28-31.9
-Active external rewarming
-Warming devices externally e.g. bair hugger

62
Q

How would you manage severe hypothermia?

A

20-27.9
-Active internal (core) rewarming
-Warmed IV fluids
-Warmed humidified inhaled air
-Irrigation of body cavities with warmed fluids
-Extracorporeal rewarming (e.g. heart lung machine-cardiopulmonary bypass

63
Q

What are the stages of hypothermia?

A

Stage 1 is characterized by a person who is awake and shivering and is associated with a core body temperature of 32-35 degrees.

Stage 2 is characterized by a person who is drowsy and not shivering, their core temperature is typically 28 to 32 degrees.

Stage 3 features include being unconscious and not shivering with a core temperature of 20-28 degrees.

In stage 4 hypothermia the core temperature is less than 20 degrees centigrade and no vital signs are seen

64
Q

Management of sepsis

A

Goal directed therapy with circulatory optimisation, with sepsis 6

65
Q

What is the pathophysiology of hyperglycaemia in pancreatitis/

A

Destruction of beta cells in islets of langerhans

66
Q

What is the pathophysiology of hypocalcaemia in pancreatitis?

A

Saponification of omental fat by released pancreatic enzymes. Released fatty acids chelate calcium, resulting in hypocalcaemia

67
Q

What are the complications of pancreatitis?

A

Local complications
-Haemorrhage
-necrosis
-Pseudocyst

Systemic
-ARDS
-Metabolic effects (hyperglycaemia, hypocalcaemia)
-Ileus
-PV thrombosis

68
Q

Sepsis

A

SIRS syndrome in the presence of an infection

69
Q

Septic shock

A

Sepsis with hypotension refractory to fluid therapy

70
Q

What are the principles of managing a pt with septic shock?

A

-Broad spectrum antibiotics, discussion with microbiologist
-Invasive cardiac monitoring and circulatory support - inotropes
-Ventilatory support - non-invasive ventilation (NIV) e.g. CPAP, intubation, ventilation
-Renal support - IV fluid resuscitation to ensure UO >0.5ml/kg/hr, haemofiltration, haemodialysis
-Nutritional support- enteral/parenteral nutrition
-Source control (surgical/radiological intervention)
-Consider higher level care

71
Q

What is the natural progression of septic shock if not managed appropriately?

A

-Dysfunction in 2or more organ systems
-Potentially reversible

-Multi-organ failure (MOF)
-Multi-organ dysfunction syndrome (MODS) = clinical syndrome characterised by development of progressive and potentially reversible physiological dysfunction in 2 or more organs or organ systems induced by variety of acute insults including sepsis

72
Q

What would be the expected mortality rate of a pateint who has developed SIRS/sepsis/severe sepsis/septic shock?

A

4 week mortality:
-SIRS 10%
-Sepsis 20%
-Severe sepsis 20-40%
-septic shock 40-60%

73
Q

Define severe sepsis

A

Sepsis with organ dysfunction (Hypotension, oliguria, lactic acidosis, alteration in gcs)

74
Q

What micro-organisms would you expect in pt with anastomotic leak?

A

E.coli
Bacteroides
Enterococcus
C.dif

75
Q

Which antibiotics are beta lactams?

A

Penicilins
carbapenems
vancomycin

76
Q

What is cryoprecipitate and how does it differ from PCC?

A

Cryoprecepitate is a frozen blood product prepared from plasma. One unit of cryo is formed from a pool of four to six units of blood instead of a single product. It is used to replace fibrinogen in patients who are at increased risk of bleeding.

PCC is combination medication of factors 2,7,9,10. Used primarily for rapid warfarin reversal prior to surgery or in those with bleeding. Trade names include beriplex.

MRCS Critical care (11 decks)

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