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YEAR 3 TCD > WEEK 8 - an acutely unwell patient > Flashcards

WEEK 8 - an acutely unwell patient Flashcards

1
Q

cardiac output equation

A

CO = HR x stroke volume

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2
Q

BP equation

A

BP = CO x systemic vascular resistance

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3
Q

In a normal physiological state:

Increased blood volume stimulates _________ in the aortic arch and carotid sinuses to _______ their firing. This stimulates cardio-_______ centres, whilst also inhibiting cardio–__________ centres and vasomotor centres. The net effect is to __________ heart rate and stroke volume, hence cardiac output; as well as increasing vasodilation in order to restore homeostasis

Decreased blood volume stimulates ___________ in the aortic arch and carotid sinuses to _________ their firing. This stimulates cardio-acceleratory centres and vasomotor centres, whilst inhibiting cardio-inhibitory centres. This increases heart rate and stroke volume (hence cardiac output), as well as increasing vasoconstriction; in order to restore homeostasis

A
  • baroreceptors
  • increase
  • inhibitory
  • acceleratory
  • decrease
  • baroreceptors
  • decrease
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4
Q

vasodilators or vasoconstrictors?

  • adrenaline
  • angiotensin II
  • adenosine
  • ATP
  • mechanism increased CA ion conc within vascular smooth muscle
  • mechanism calcium ion sequestration within vascular smooth muscle via reuptake into the sarcoplasmic reticulum and expulsion across the plasma membrane
A
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5
Q

alpha 1 receptors location and effect of stimulation

A

heart, liver, smooth muscle

— vasoconstriction, intestinal relaxation, uterine contraction, pupillary dilatation

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6
Q

alpha 2 receptor location and effect of stimulation

A

vascular smooth muscle, neurones, pancreatic islet cells, and on platelets

—> vasoconstriction, inhibition of noradrenaline release, insulin secretion, platelet aggregation

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7
Q

beta 1 receptors location and effect of stimulation

A

heart

tachycardia

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8
Q

beta 2 receptors location and effect of stimulation

A

lungs, GIT, liver, uterus, vascular smooth muscle and skeletal muscle

—> bronchodilation, smooth muscle relaxation, sphincter constriction

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9
Q

beta 3 receptors location and effect of stimulation

A

fat cells

lipolysis

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10
Q

Which pathologies are relevant to the right hypochondrium abdominal quadrant (RH)?

A
  • acute hepatitis
  • biliary colic
  • cholangitis
  • cholecystitis
  • pneumonia (referred pain)
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11
Q

Which pathologies are relevant to the left hypochondrium abdominal quadrant (LH)?

A
  • pneumonia (referred pain)
  • splenomegaly
  • splenic abscess
  • splenic infarction
  • splenic rupture
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12
Q

Which pathologies are relevant to the epigastrium abdominal quadrant (E)?

A
  • acute MI
  • acute/chronic pancreatitis
  • GORD
  • peptic ulcer
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13
Q

Which pathologies are relevant to the right iliac fossa abdominal quadrant (RIF)?

A
  • appendicitis
  • hernias
  • renal calculi
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14
Q

Which pathologies are relevant to the left iliac fossa abdominal quadrant (LIF)?

A
  • diverticulitis
  • hernias
  • renal calculi
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15
Q

Which pathologies are relevant to the hypogastrium (suprapubic region) abdominal quadrant (H)?

A
  • bladder retention
  • cystitis
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16
Q

Which pathologies are relevant to diffuse abdominal pain?

A

Acute/Chronic Mesenteric Ischemia
Adrenal Insufficiency
Bowel Obstruction
Constipation
Inflammatory Bowel Disease
Ketoacidosis
Perforation of Gastrointestinal Tract
Spontaneous Bacterial Peritonitis
Viral Gastroenteritis

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17
Q

What validated tool can be used to screen for frailty?

A

Rockwood Frailty Score

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18
Q

sepsis 6 summary

A

take 3 give 3

take — VBG for lactate, urine output and blood culture
give — IV fluids, IV antibiotics, oxygen

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19
Q

what is septic shock?

A

sepsis with persistent hypotension despite fluid correction and inotropes and a serum lactate of greater than 2mmol/L

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20
Q

what could be source of infections be in the CNS?

A
  • meningitis
  • encephalitis
  • cerebral or epidural abscesses
  • discitis
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21
Q

what could be source of infections be in the integumentary (skin/soft tissue) ?

A
  • cellulitis
  • infected bites/ulcers/wounds
  • necrotising fasciitis
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22
Q

what could be source of infections be in the genitourinary tract?

A
  • cystitis
  • pyelonephritis
  • obstructed renal calculus
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23
Q

what could be source of infections be in the GIT?

A
  • gallbladder infections (cholecytitis, cholangitis)
  • diverticulitis
  • infective colitis
  • appendicitis
  • tonsillitis
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24
Q

what orthopaedic things could be source of infections?

A
  • septic arthritis
  • prosthetic joint infections
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25
Q

in patients with sepsis, what is initial fluid resuscitation with?

A

a crystalloid given as a bolus over less than 15 minutes

eg. 500mL of 0.9% sodium chloride
500 mL of Hartmann’s solution over 10 minutes

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26
Q

what can IV fluid be divided into?

A

crystalloids and colloids

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27
Q

crystalloids vs colloids

A

Crystalloids are solutions containing small molecules in water (e.g. sodium chloride, glucose, Hartmann’s)

Colloids are solutions with large molecular weight substances (e.g. albumin, gelatins)

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28
Q

what is raised lactate a sign of>

A

Lactate is raised as a result of tissue hypoxia in sepsis; as a result of widespread systemic inflammation, there is organ hypoperfusion and subsequently the cells turn to anaerobic metabolism, which produce lactate. A raised lactate of > 4.0mmol/L is considered a high risk criteria for sepsis (these patients are at high risk of deterioration)

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29
Q

what does this ecg show?

A

tall, tented T waves, and broad QRS complexes (>0.12ms), with no discernible P waves

These are all ECG changes seen in hyperkalaemia

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30
Q

what can hyperkalaemia be due to?

A

Hyperkalaemia can be due to several causes:

  • Reduced renal excretion of potassium
  • Increased circulating serum potassium – this can be exogenous (from potassium supplementation) or endogenous (tumour lysis syndrome, rhabdomyolysis, burns)
  • Pseudohyperkalaemia – where there isn’t a true elevation in serum potassium; suspect this and repeat bloods as soon as possible for serum potassium in patients with isolated, unexpected blood results of hyperkalaemia who are well and have no ECG signs, as it may be due to test tube haemolysis or prolonged torniquet time

Of those listed, it is most often due to acute renal failure and medications (e.g. ACE-inhibitors) in hospitalised patients.

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31
Q

hyperkalaemia treatment: Most guidelines suggest urgent treatment when serum potassium exceeds ____, and/or there are ___ changes.

A
  • 6.5
  • ECG
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32
Q

what are the 3 priorities with regards to management of acute hyperkalaemia?

A
  1. Protecting the cardiac membrane – IV calcium gluconate acts by reducing membrane excitatory effects of K on cardiac tissue rapidly, therefore reducing the potential for cardiac arrhythmias such as ventricular fibrillation, but has minimal effect on lowering serum K concentrations.
  2. Shifting potassium intracellularly – give 10 units Insulin with 25g glucose (an example of a treatment regime for this would be 10 units Actrapid in 250mls of 10% dextrose at 50ml/hr for 5 hours (25g)). You will see in some guidelines the recommendation of 50ml 50% Dextrose over 15minutes however this requires a central line and risks extravasation and tissue damage if used peripherally. This regime is generally avoided in clinical practise and it should only be used after senior advise if there are concerns about the volume of fluid you are giving patients who are fluid overloaded. Nebulised salbutamol 10 – 20mg is also given alongside insulin and glucose in severe, life-threatening hyperkalaemia (Avoid salbutamol if tachyarrhythmia present)
  3. Stopping any contributing medications – such as ACE-inhibitors, potassium-sparing diuretics.
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33
Q

In 2020, NICE approved the use of potassium binders (_______give 2 examples______ ), which act by _______________, for managing hyperkalaemia in adults. However, these medications have specific additional criteria for their usage, and should only be instituted in the emergency setting alongside standard care

A
  • sodium zirconium cyclosilicate and patiromer
  • promoting potassium excretion
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34
Q

what are the kidneys main functions?

A
  1. filter and excrete nitrogenous waste products
  2. Maintain acid-base balance, by controlling reabsorption and excretion of electrolytes (e.g., sodium, potassium, chloride, etc.)
  3. Produce certain hormones (erythropoietin, renin, calcitriol)
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35
Q

Among the kidneys’ waste products, ___________, in particular, is a useful marker of glomerular filtration because it is completely filtered in the glomerulus. When there is damage to the kidneys, __________ levels rise.

A

creatinine

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36
Q

what is GFR proportional to?

A

1/creatinine

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37
Q

how does RAAS increase overall effective circulating volume (ECV)?

A
  1. increasing re absorption of sodium ions
  2. vasoconstriction the efferent arterioles
38
Q

The kidneys receive up to __% of cardiac output, have very sluggish blood flow in the renal medulla (to maintain the countercurrent mechanism), and have high oxygen requirements for ion transporters to work. This means that they are highly susceptible to ischaemic damage and necrosis if renal blood flow is reduced (as with pre-renal AKI). Apart from __________ and reduced renal blood flow from diarrhoea or dehydration, remember that certain medications (___________ and ________) will also inhibit the kidneys’ protective mechanism (_____), therefore making ischaemia and necrosis more likely

A
  • 25%
  • hypovolaemia
  • ACE-inhibitors and NSAIDs
  • RAAS
39
Q

what is acute tubular necrosis (ATN)? describe

A

This condition is usually the result of a combination of factors which have caused renal ischaemia and toxicity, e.g., hypotension and dehydration or sepsis with associated nephrotoxic drugs.

The histology of ATN does not usually show frankly necrotic cells, but sloughing of the renal tubular epithelium causing dilation and obstruction of tubules and some mild leukocyte infiltration.

Treatment is supportive, there are no specific drug treatments, and withdrawal of nephrotoxic agents or treatment of associated sepsis.

Usually there is recovery after 2-3 weeks (maximum 6 weeks). There is a high mortality associated with ATN (approx 50%), but this is usually because of the associated illnesses (e.g., septic shock), age, etc. Once recovered only a very small proportion of people are left with chronic kidney disease. The severity of this illness is the reason such effort is made to recognise risk factors and prevent this disease.

40
Q

what are the 3 phases of ATN?

A
  1. oligouric phase
  2. maintenance phase
  3. polyuric recovery phase
41
Q

describe the first phase of ATN

A

= oligouric phase

the kidneys produce less than 500mls of urine per day. patients in this phase are vulnerable to fluid overload and electrolyte imbalance esp K+. creatinine levels usually rise quite rapidly during this phase

42
Q

describe the second phase of ATN

A

= maintenance phase

the patient is no longer oligouric and this increased urinary output helps maintain fluid and electrolyte balance. creatinine levels are usually stable or rise very slowly

43
Q

describe the third phase of ATN

A

= polyuric recovery phase

In this phase the kidneys produce large quantities of dilute urine, so large in fact patients can become hypovolaemic and unwell. There are a number of causes for this phase postulated, but one explanation is that the distal tubules and collecting ducts recover last and in particular their aquaporin channels. These damaged aquaporin channels do not allow water to be reabsorbed and therefore high quantities of dilute urine are produced. Patients are also susceptible to electrolyte loss (e.g. hypokalemia) in this phase. Creatinine levels falls swiftly in this phase.

44
Q

what are the 2 complications of AKI?

A

The loss of the kidneys’ homeostatic functions in AKI will mean that the kidneys are:

  1. Unable to regulate acid-base balance, leading to hyperkalaemia, fluid retention and metabolic acidosis
  2. Unable to excrete metabolic waste products, leading to build-up of urea and creatinine

Eventually, this may lead to multi-organ failure.

45
Q

why is clotting measured in a patient with sepsis?

A

sepsis can be a cause of disseminated intravascular coagulation (DIC)

46
Q

what is DIC?

A

disseminated intravascular coagulation

  • a clinical syndrome characterised by dysregulated coagulation
  • several causes inc: sepsis, trauma, malignancy, obstetric complications (eg amniotic fluid embolism, placental abruption)
  • in these conditions, tissue factor (TF) is released into the bloodstream as a result of cytokine release, endotoxin release or endothelial damage, which activates the coagulation pathway
  • this widespread coagulation consumes clotting factors, which causes bleeding in addition to micro vascular thrombosis
  • management involves treating the underlying cause, and supportive blood product (platelet or FFP) transfusions in life-threatening bleeding, severe thrombocytopenia or when patients need to undergo urgent invasive interventions without delay.
47
Q

what are the 3 stages of AKI?

A
48
Q

the causes of AKI can be divided into what 3 categories?

A
  1. pre-renal (85%) — reduced perfusion of the kidneys, either from hypovolaemia, reduced renal blood flow or reduced cardiac output, which leads to reduced glomerular filtration rate (GFR)
  2. renal (intrinsic) — structural damage to the glomeruli, interstitial, and/or tubules
  3. post-renal AKI — acute obstruction of urinary flow, which increases intra-tubular pressures and subsequently decreases GFR
49
Q

What are the risk factors for developing AKI?

A

Age 65 years or over;
History of AKI;
CKD (eGFR < 60mL/min/1.73m2);
Symptoms or history of urological obstruction, or conditions which may lead to obstruction;
Chronic conditions such as heart failure, liver disease, diabetes mellitus;
Neurological or cognitive impairment or disability (which may limit fluid intake because of reliance on a carer);
Sepsis;
Hypovolaemia;
Oliguria (urine output < 0.5 mL/kg/h);
Nephrotoxic drug use within the last week;
Exposure to iodinated contrast agents within the past week

50
Q

what would the key features on history and examination be in a pre-renal AKI?

A

history: poor oral intake or dehydration, diarrhoea or vomiting

examination: signs of sepsis, assessment of volume status - HR, cap refill, BP, JVP, poor skin turgor, signs of renovascular disease - abdominal bruits, impalpable peripheral pulses

51
Q

what would the key features on history and examination be in a renal AKI?

A

history : Constitutional symptoms – fever, rash, joint pains, nasal crusting, weight loss; History of fall with long lie (may cause rhabdomyolysis); Use of OTC medications such as NSAIDs; Use of nephrotoxic medications

examination : rash, uveitis, joint swelling

52
Q

what would the key features on history and examination be in a post- renal AKI?

A

history : Lower Urinary Tract Symptoms (LUTS) in men – urinary frequency, urgency – may be secondary to enlarged prostate; History of renal calculi – may cause hydronephrosis and obstruction

examination : abdo exam - palpable bladder

53
Q

In ALL patients with an AKI, remember to always:

  1. Obtain a ________
  2. Monitor __________
  3. Compare the current renal function to historical records (if available)
A
  • urine dipstick
  • urine output
54
Q

> __+ proteinuria in urine dipstick indicates intrinsic renal disease

A

3

55
Q

urine dipstick: If blood and protein +ve - consider _________

A

glomerulonephritis

56
Q

Dipstick positive for blood and no RBC - consider _______

A

myoglobin

57
Q

what are the urgent indications for starting dialysis in patients with AKI?

A

if any of the following features are present AND they are refractory to medical therapy:

  1. Hyperkalaemia
  2. Pulmonary oedema
  3. Severe metabolic acidosis
  4. Uraemia – uraemic pericarditis or encephalopathy
  5. Ingestion of certain toxins
58
Q
A
59
Q

Both gliclazide and insulin should be used cautiously, as they can __________ in renal impairment and increase the risk of ______________ in diabetic patients

A
  • accumulate
  • hypoglycaemia
60
Q

Opioids that are considered safer to use in those with renal impairment include ____________, __________ and ___________; however, these patients are at high risk of opiate toxicity and adverse effects, and will require close monitoring, dose titration and input from specialist teams such as the pain team, renal team or the palliative care team

A

oxycodone, fentanyl and hydromorphone

61
Q

furosemide in AKI?

A

Furosemide may actually improve renal function in patients who have AKI secondary to cardiorenal syndrome. In these patients, the heart fails to pump adequately, leading to reduced cardiac output and systemic hypotension. The renin-angiotensin system is activated, which causes renal efferent arteriolar vasoconstriction and inadequate glomerular perfusion.

If furosemide is given to achieve diuresis in someone with fluid overload, this decreases ventricular filling pressures and improves their symptoms. The glomerular filtration will eventually improve as there will be more blood flow through the kidneys from improved cardiac output and efferent arteriolar vasodilatation. However, you may notice that there is initially a worsening of their AKI, as creatinine levels are diluted in fluid overload; removal of the excess fluid unmasks their true kidney function. In certain circumstances of AKI you may withhold a loop diuretic.

62
Q

what is AIN?

A

acute interstitial nephritis

Many medications can cause acute interstitial nephritis (AIN). This is a clinical syndrome characterised by inflammatory infiltrates in the renal interstitium (seen on renal biopsy), in response to a drug, infection or autoimmune process. Patients rapidly develop an AKI within 2 weeks of starting the medication, and can either be asymptomatic, or present with constitutional symptoms (rash, malaise, fever). Some examples of medications which can rarely cause AIN include proton pump inhibitors, penicillins, NSAIDs, allopurinol, aciclovir.

63
Q

what is pyonephrosis?

A

pus in the renal pelvis

characterized by the accumulation of purulent debris and sediment in the renal pelvis and urinary collecting system

64
Q

what % of patients progress to develop CKD after an acute episode of AKI?

A

5-10%

65
Q
A
66
Q

what are indications for renal replacement therapy in patients with AKI?

A
  • refractory metabolic acidosis
  • refractory pulmonary oedema
  • refractory hyperkalaemia
  • uraemia encephalopathy
67
Q
A

5

  • age
  • diabetes
  • NSAID use
  • hypertension
  • history of AKI
68
Q
A

weight

69
Q

what is the equation for shock index?

A

heart rate / BP

70
Q

a shock index of what is normal and suggests that a patient is haemodynamically stable?

A

0.5-0.7

71
Q

what is a mnemonic for remembering the different categories of shock?

A

‘how fast you fill the pump and squeeze’:

  • The ‘fast’ is the heart rate
  • The ‘fill’ is the blood volume
  • The ‘pump’ is the heart
  • The ‘squeeze’ is the blood pressure
72
Q

what is shock?

A

Shock is a descriptive term used to describe the state that results when circulatory insufficiency leads to inadequate tissue perfusion and thus inadequate oxygen delivery to tissues. This shortage of oxygen means that aerobic metabolism cannot occur, resulting in organ dysfunction

73
Q

what are 5 signs that the circulatory system is not working?

A
  • altered mental state
  • mottled and clammy skin
  • oliguria
  • elevated blood lactate
  • tachycardia
74
Q

what are some broad categories of types of shock?

A
  • Hypovolaemic (e.g., haemorrhagic, dehydration)
  • Distributive (e.g., sepsis, anaphylaxis)
  • Obstructive (e.g., pulmonary embolism, tension pneumothorax)
  • Cardiogenic (e.g., myocardial infarction)
  • Neurogenic (e.g., cervical spinal cord injury)
75
Q

Hypovolaemic shock is suggested by signs of shock plus history or examination evidence of __________ or fluid ____, ____ peripheries, a ____ response to fluid or blood resuscitation

A
  • bleeding
  • loss
  • cool
  • good
76
Q

Distributive shock may be suggested by signs of shock plus peripheral vasodilation i.e. warm, dilated peripheries. There may be clues in the history like a recent _________ that has been getting worse (sepsis) or a known exposure to an allergen (anaphylaxis). The patient may be ________. It may respond to fluid resuscitation, but as this is not the underlying cause, your patient may remain ___________.

A
  • infection
  • febrile
  • hypotension
77
Q

Obstructive shock is suggested by signs of shock plus signs of a problem inside the ______ that is impeding cardiac output

A

thorax

78
Q

what are typical examination findings in a tension pneumothorax?

A

respiratory distress, asymmetric chest expansion, dilated neck veins, tracheal deviation away from affected side, absent breath sounds on affected side, hyperresonant percussion note on affected side

79
Q

what are typical examination findings in cardiac tamponade?

A

dilated neck veins, muffled heart sounds

80
Q

describe neurogenic shock

A
  • a specific syndrome that happens in trauma
  • different to spinal shock
  • happens in high (cervical or high thoracic) spinal cord injuries where the patient loses their sympathetic outflow, hence their normal sympathetic responses to blood loss:
  • instead of tachycardic, they will be bradycardic
  • and instead of hypotension and peripherally vasoconstricted/cold, they will be hypotensive but peripherally dilated/warm
81
Q

what is the Glasgow-Blatchford score?

A

a screening tool to assess the likelihood that a person with an acute upper GI bleed will need to have a medical intervention such as a blood transfusion or endoscopic intervention

82
Q

what is the Rockall score?

A

assesses the risk of death in UGIB

83
Q

The British Society of Gastroenterologists recommend that this patient be resuscitated using a mixture of __________ and ______. They recommend activating the major haemorrhage protocol if the patient is haemodynamically unstable. If the patient is stable, they recommend a blood transfusion only if the haemoglobin is less than ____/L, aiming for a haemoglobin of ___-___g/L. Remember to correct other elements of coagulopathy like low platelets or deranged clotting factors. Ultimately, this patient needs an endoscopy to diagnose the cause of the bleeding and, if there is active bleeding, to treat it. Depending on what the endoscopy shows, they may benefit from other treatments like a _______ (if they have a peptic ulcer) or _____________ (if they have a oesophageal or gastric varicies).

A
  • crystalloid and blood
  • 70g/L
  • 70-100g/L
  • PPI
  • terlipressin
84
Q

what is rhabdomyolysis?

A

Rhabdomyolysis is a syndrome whereby there is breakdown and necrosis of damaged skeletal muscle, releasing its contents (electrolytes, myoglobin, sarcoplasmic proteins such as creatinine kinase) into the circulation. It can cause multiple complications, including AKI as the myoglobin deposits in and obstructs the renal tubules.

85
Q

Anaphylaxis is a type __ hypersensitivity reaction, which causes compromise in airway, breathing, and/or circulation problems, with or without skin or mucosal changes. It is a medical emergency which requires immediate recognition and treatment.

A

1

86
Q
A

IV plasmalyte 500mL over 10 mins

this patient is dangerously dehydrated and showing sings of hypovolaemic shock. NICE guidance on IV fluids tells us that, for resuscitation, we should prescribe 250-500mL of a crystalloid IV STAT/over less than 15 mins

87
Q
A

IM adrenaline 0.5mL 1:1000

The patient is shocked and the features of tongue swelling causing airway compromise and pallor suggesting severe illness/ hypotension, as well as features of an uritcarial rash and a possible food exposure in a restaurant, suggest that his shock is due to anaphylaxis. The treatment for this is IM adrenaline 500mcg or 0.5mL of 1:1000. We use 1:1000 IM because it is more concentrated, thus a smaller amount can be injected into the muscle. In cardiac arrest, we use 1:10000 IV because it is less concentrated so it is less likely to cause phlebitis.

88
Q
A

ECG and prescribe IV calcium gluconate

A potassium of 6.7 is dangerously high and so we should immediately review the patient, undertake an ECG, and protect the cardiac membrane with IV calcium. This will usually be 10mLs of 10% calcium gluconate IV over 10 minutes which is equivalent to 2.2mmol of calcium and can be repeated if the ECG has not improved). After these initial life-saving actions have been undertaken, it would be appropriate to prescribe IV insulin-dextrose (usually 5-10 units of fast acting insulin in 50mLs of 50% glucose over 5-10 minutes) and nebulised salbutamol to drive potassium out of the serum and into the cells.

89
Q
A

raised anion gap metabolic acidosis due to elevated lactate

The pH of 7.28 shows an acidosis. However, blood gases may show several synchronous processes so don’t forget to work out the anion gap to confirm or refute the presence of raised anion gap metabolic acidosis. In this case, the acidotic pH is likely due to the addition of unmeasured anions or lactate. This is commonly due to hypoperfusion such as caused by sepsis or other causes of shock, but it can also be due to medications such as metformin or salbutamol.

90
Q
A

ramipril

Ramipril (an ACE-inhibitor) has many long-term benefits for patients with certain chronic diseases. However, many patients with acute illness have hypotension, AKI, and hyperkalaemia. Ramipril has antihypertensive effects and it also reduces renal hyperfiltration which can reduce eGFR and increase potassium, all things we want to avoid in the acutely unwell patient. Hence, NICE advises us to temporarily suspend it in the setting of acute hypotension and AKI. Remember that many drugs are renally excreted. The patient’s apixaban and metformin prescriptions will need to be reviewed if the eGFR continues to drop.

91
Q

how do you calculate the anion gap?

A

(Na+ + K+) - (Cl- + HCO3-)

= measure of acid-based balance

If the anion gap is too high, your blood is more acidic than normal. If the anion gap is too low, your blood isn’t acidic enough.

YEAR 3 TCD (15 decks)

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