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ΩΩ 3b Bateman - Acute and Critical Care > Acute Care > Flashcards

Acute Care Flashcards

1
Q

WHAT DOES SODIUM DO IN THE BODY?

A

Nerve conduction

Biocarbonate buffer system

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2
Q

What is the reference range of sodium?

A

135-145 mmol/L

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3
Q

What are some causes of hypernatraemia?

A

MODEL gets FRIED

2 C Conn’s + Cushing

Medications

Osmotic diuresis - for example, diabetic coma, diuretics

Diabetes insipidus

Excessive H2O loss

Low H2O intake

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4
Q

What are the symptoms of hypernatraemia?

A

MODEL gets FRIED

Flushed skin and fever

Restless, irritable, anxious

Increased blood pressure + fluid retention

Edema - peripheral and pitting

Decreased urine output and dry mouth

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5
Q

What is the treatment for hypernatraemia?

A
  1. IV 0.9% saline solution
  2. Slowly over 48 hours
  3. Too much fluid too fast can cause cerebreral oedema
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6
Q

What are some causes of hyponatraemia?

A

4 D’s + S cause SALT LOSS

Drugs (Diuretics e.g. furosemide, carbamazepine)

Diarrhoea

Dehydration

Drains

SIADH/Heart failure

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7
Q

What are the symptoms of hyponatraemia?

A

4 D’s cause SALT LOSS

Stupor/coma

Anorexia

Lethargy

Tendon Reflexes (decreased)

Limp muscles

Orthostatic hypotension

Seizures/headache

Stomach cramping

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8
Q

What is the treatment for hyponatraemia?

A

Treat underlying cause

  • *Hypovolaemic hyponatraemia**
    0. 5-1L 0.9% Saline

Normovolaemic (euvolaemic) hyponatraemia
Restriction of fluid intake to 500 ml per day to raise plasma sodium to 130 mM
Frequent measurements of plasma osmolality and sodium

Hypervolaemic hyponatraemia
Dietary sodium restriction and diuretic therapy are the mainstays of therapy

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9
Q

What can excessively rapid correction of hyponatraemia cause?

A

Central pontine myelinolysis

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10
Q

WHAT IS THE REFERENCE RANGE OF POTASSIUM?

A

3.5-5.0 mmol/L

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11
Q

What are some causes of hyperkalaemia?

A

Hyperkalaemia CARED for MURDER

  1. Cellular movement of K+ from intracellular to extracellular (burns, tissue damahge)
  2. Adrenal insufficiency - Addison’s disease/AKI/rhabdomyolysis
  3. Renal failure
  4. Excessive K+ intake
  5. Drugs (potassium-sparing drugs - spironolactone, Heparin)
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12
Q

What are the symptoms of hyperkalaemia?

A

hyperkalaemia CARED for MURDER

  1. Muscle weakness
  2. Urine output little or none
  3. Respiratory failure
  4. Decreased cardiac contractility
  5. Early: muscle twitches/cramps
  6. Rythm changes
    Tall peaked T waves, prolonged PR interval
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13
Q

What is the management of hyperkalaemia?

A
  1. Cardiac protection
    IV Calcium gluconate
  2. Shift potassium into cells
    Insulin-glucose infusion - 10 units soluble insulin in 25g glucose
    Nebulised salbutamol
  3. Remove potassium from body
    Stop exaccerbating drugs e.g. ACE inhibitor
    Calcium resonium (orally or enema)
    Loop diuretics
    Dialysis

​​All patients with severe hyperkalaemia (≥ 6.5 mmol/L) or with ECG changes should have emergency treatment

  1. IV calcium gluconate: to stabilise the myocardium
  2. Insulin/dextrose infusion: short-term shift in potassium from ECF to ICF
  3. other treatments such as nebulised salbutamol may be given to temporarily lower the serum potassium
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14
Q

What are the ECG changes in hyperkalaemia?

A

Hyperkalaemia causes a rapid reduction in resting membrane potential leading to increased cardiac depolarization, and muscle excitability which in turn causes ECG changes

  1. Tall tented T waves [T wave larger than R wave in > 1 lead]
  2. Widened QRS [>0.12 s]
    * *P WAVES + PR interval**
  3. Flattened or absent P waves
  4. First degree heart block (prolonged PR interval) [>0.2 s];
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15
Q

What are some causes of hypokalaemia?

A

DITCH the 7 L’s

  1. Drugs - loop diuretics e.g. furosemide / laxatives, glucocorticoids, hydrocortiosne
  2. Inadequate consumption of K+
  3. Too much water intake
  4. Cushing/Conn’s syndrome (causes kidneys to excrete K+)
  5. Heavy fluid loss (nasogastric tube suction, vomiting, diarrhoea, wound drainage)
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16
Q

What are the symptoms of hypokalaemia?

A

DITCH the 7 L’s

  1. Lethargic
  2. Low, shallow respirations
  3. Lethal cardiac dysrhythmias
    ST depression, shallow T wave, projecting U wave
  4. Lots of urine
  5. Leg cramps
  6. Limp muscles
  7. Low blood pressure
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17
Q

What is a complication of hypokalaemia?

A

Hypokalaemia predisposes to arrhythmia, which could ultimately cause a myocardial infarction

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18
Q

What is the management of hypokalaemia?

A

Treat underlying cause

Replacement of potassium either IV or orally

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19
Q

What are the ECG changes in hypokalaemia?

A

After the QRS complex

  1. Flattened T waves
  2. ST segment depression
  3. Prolonged QT interval
  4. Tall U waves

Ventricular tachycardia or ventricular fibrillation and torsade de pointes

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20
Q

What is the maximum rate potassium can be given?

A

10 mmol/hour

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21
Q

WHAT IS THE REFERENCE RANGE OF CALCIUM?

A

2-2.60 mmol/l

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22
Q

What are the causes of hypercalcaemia?

A

CHIMP gets STONES, MOANS, GRAONS

Calcium supplements

Hyperparathyroidism

Iatrogenic

Multiple myeloma

Parathyroid hyperplasia

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23
Q

What are the symptoms of hypercalcaemia?

A

CHIMP gets Stones, bones, abdominal moans, and psychic groans

GI problems ‘moans’
Constiaption
Nausea and vomiting

Renal ‘stones’
Polyuria
Nephrolithiasis

Skeleton ‘bones’
Bone pain
Arthritis

Neuromuscular ‘psychic groans’
Lethargy and fatigue
Weakness

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24
Q

What is the treatment of hypercalcaemia?

A
  1. Normal saline - typically 3-4 litres/day.
  2. Following rehydration bisphosphonates may be used. They typically take 2-3 days to work with maximal effect being seen at 7 days
  3. Other options include:
    * *Calcitonin** - quicker effect than bisphosphonates
    * *Steroids** in sarcoidosis

Loop diuretics such as furosemide are sometimes used in hypercalcaemia, particularly in patients who cannot tolerate aggressive fluid rehydration. However, they should be used with caution as they may worsen electrolyte derangement and volume depletion.

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25
Q

What are the ECG changes for hypercalcaemia?

A

Shortening of the QT interval

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26
Q

What are the causes for hypocalcaemia?

A
  1. Vitamin D deficiency (osteomalacia)
  2. Chronic kidney disease
  3. Hypoparathyroidism (e.g. post thyroid/parathyroid surgery)
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27
Q

What are the symptoms of hypocalcaemia?

A

Convulsions

Arrhythmias

Tetany

Spasms and stridor (Chvostek - FACE, Trosseau - HAND)

Numbness in the fingers

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28
Q

What is the diagnosis of some conditions that cause hypocalcaemia?

A

Uraemia and an elevated serum creatinine indicate chronic renal failure

Elevated serum phosphate and normal renal function indicate hypoparathyroidism - skeletal abnormalities will indicate pseudohypoparathyroidism

Hypoparathyroidism due to hypomagnesaemia produces a hypocalcaemia uncorrected by calcium

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29
Q

What is the treatment of hypocalcaemia?

A
  1. IV calcium gluconate, 10ml of 10% solution over 10 minutes
  2. ECG monitoring is recommended
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30
Q

What are the ECG changes in hypocalcaemia?

A

Lengthening of the QT interval

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31
Q

What is the transfusion threshold for patients?

How long should the blood be given?

A

Patients without ACS Patients with ACS

Transfusion threshold 70 g/L 80 g/L

Target after transfusion 70-90 g/L 80-100 g/L

90-120 mins

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32
Q

What must be prescribed between two units of packed red blood cells?

A

Furosemiude to prevent fluid overload

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33
Q

What is the rate of infusion of an insulin drip in DKA?

A

0.1 unit/kg/hour

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34
Q

What is the maintenance fluids for a child?

A
  1. 1st 10kg of body weight = 100 ml/kg/day
  2. 2nd 10kg of bodyweight = 50 ml/kg/day
  3. Remainder of bodyweight = 20 ml/kg/day
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35
Q

What is the maintenance fluids for an adult?

What is the maintenance ions for an adult?

What is the maintenance of glucose for an adult?

A
  1. 25 ml/kg/day
  2. 1 mmol/kg/day - potassium, sodium + chloride
  3. 50-100g/day of glucose
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36
Q

WHAT IS HAPPENING IN DKA?

A

DKA is caused by uncontrolled lipolysis (not proteolysis) which results in an excess of free fatty acids that are ultimately converted to ketone bodies

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37
Q

What are the features of DKA?

A
  1. Abdominal pain
  2. Polyuria, polydipsia, dehydration
  3. Kussmaul respiration (deep hyperventilation)
  4. Acetone-smelling breath (‘pear drops’ smell)
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38
Q

What are the diagnostic criteria for DKA?

A
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39
Q

What is the management of a DKA?

A
  1. Fluid replacement
    isotonic saline is used initially, even if the patient is severely acidotic
  2. Insulin
    An intravenous infusion should be started at 0.1 unit/kg/hour
    Oonce blood glucose is < 15 mmol/l an infusion of 5% dextrose should be started
  3. Correction of electrolyte disturbance
    Serum potassium is often high on admission despite total body potassium being low
    This often falls quickly following treatment with insulin resulting in hypokalaemia
  4. Long-acting insulin should be continued, short-acting insulin should be stopped
40
Q

What is DKA resolution defined as?

A
  1. pH >7.3 and
  2. Blood ketones < 0.6 mmol/L and
  3. Bicarbonate > 15.0mmol/L
41
Q

What are some complications of DKA?

A
  1. Gastric stasis
  2. Thromboembolism
  3. Arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
  4. Iatrogenic due to incorrect fluid therapy: cerebral oedema*, hypokalaemia, hypoglycaemia
  5. Acute respiratory distress syndrome
  6. Acute kidney injury
42
Q

WHAT IS THE PATHOPHYSIOLOGY OF HYPEROSMOLAR HYPERGLYCAEMIC STATE?

A
  1. Hyperglycaemia results in osmotic diuresis with associated loss of sodium and potassium
  2. Severe volume depletion results in a significant raised serum osmolarity (typically > than 320 mosmol/kg), resulting in hyperviscosity of blood.
  3. Despite these severe electrolyte losses and total body volume depletion, the typical patient with HHS, may not look as dehydrated as they are, because hypertonicity leads to preservation of intravascular volume.
43
Q

What are the clinical features of HHS?

A
  1. General: fatigue, lethargy, nausea and vomiting
  2. Neurological: altered level of consciousness, headaches, papilloedema, weakness
  3. Haematological: hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)
  4. Cardiovascular: dehydration, hypotension, tachycardia
44
Q

How do you diangose HHS?

A
  1. Hypovolaemia
  2. Marked Hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis
  3. Significantly raised serum osmolarity (> 320 mosmol/kg)
45
Q

How do you manage HHS?

A
  1. Normalise the osmolality (gradually)
    • ​​The serum osmolality is the key parameter to monitor
    • If not available it can be estimated by 2 * Na+ + glucose + urea
  2. Replace fluid and electrolyte losses
  3. Normalise blood glucose (gradually)
46
Q

WHAT ARE THE SYMPTOMS OF AN MI?

A
  1. Chesgt pain - typically central/left-sided
  2. May radiate to the jaw or the left arm
  3. Often described as ‘heavy’ or constricting, ‘like an elephant on my chest’
  4. It should be noted however in real clinical practice patients present with a wide variety of types of chest pain and patients/doctors may confuse ischaemic pain for other causes such as dyspepsia
  5. Certain patients e.g. diabetics/elderly may not experience any chest pain
47
Q

What leads on an ECG correspond to the infarction in the heart?

A
48
Q

What is the treatment for ACS?

A
  1. M - Morphine
  2. O - Oxygen (if sats <94%)
  3. N - Nitrates
  4. A - Aspirin

If STEMI then a second anitplatlet should be added (e.g. clopidogrel, ticagrelor)

Then patients go for PCI if done in <120 minutes of when fibrinolysis could have been given

49
Q

What is the secondary prevention after an MI?

A

All of these as a minimum

  1. Aspirin
  2. A second antiplatelet if appropriate (e.g. clopidogrel)
  3. A beta-blocker
  4. An ACE inhibitor
  5. A statin
50
Q

When should defibrillation be given in cardiac arrest?

A
  1. A single shock for VF/pulseless VT followed by 2 minutes of CPR
  2. If the cardiac arrested is witnessed in a monitored patient (e.g. in a coronary care unit) then the 2015 guidelines recommend ‘up to three quick successive (stacked) shocks’, rather than 1 shock followed by CPR
51
Q

When should adrenaline be given in cardiac arrest?

A
  1. Adrenaline 1 mg as soon as possible for non-shockable rhythms
  2. During a VF/VT cardiac arrest, adrenaline 1 mg is given once chest compressions have restarted after the third shock
  3. Repeat adrenaline 1mg every 3-5 minutes whilst ALS continues
52
Q

When should amiodarone be given in cardiac arrest?

A
  1. Amiodarone 300 mg should be given to patients who are in VF/pulseless VT after 3 shocks have been administered
  2. A further dose of amiodarone 150 mg should be given to patients who are in VF/pulseless VT after 5 shocks have been administered
53
Q

When should thrombolytic drugs be given in cardiac arrest?

A
  1. Should be considered if a pulmonary embolus is suspected
  2. If given, CPR should be continued for an extended period of 60-90 minutes
54
Q

When should chest compressions be given in an arrest?

A

In a non-shockable rhythm

55
Q

What is the treatment for asystole?

A

CPR + check rhythm every 2 minutes

56
Q

What is the treatment of sinus bradycardia?

A
  1. Atropine (500mcg IV) is the first line treatment in this situation.

If there is an unsatisfactory response the following interventions may be used:

  1. Atropine, up to maximum of 3mg
  2. Transcutaneous pacing
  3. Isoprenaline/adrenaline infusion titrated to response

Specialist help should be sought for consideration of transvenous pacing if there is no response to the above measures.

57
Q

What is used after atropine when it fails?

A

External pacing

58
Q

WHAT ARE THE DIFFERENT CATEGORIES FOR ACUTE ASTHMA ATTACK?

A
59
Q

What is the management for an acute asthma attack?

A
  1. Oxygen 15L
  2. Salbutamol
  3. Hydrocortisone
  4. Ipatropium
  5. Theophylline
  6. Magnesium sulphate
  7. Esclate care
    • IV aminophylline after consultation with senior staff
    • Intubation and ventilation
    • Extracorporeal membrane oxygenation (ECMO)
60
Q

What is the criteria for discharge after a person has had an acute asthma attack?

A
  1. Been stable on their discharge medication (i.e. no nebulisers or oxygen) for 12–24 hours
  2. Inhaler technique checked and recorded
  3. PEF >75% of best or predicted
61
Q

What do you need to withhold while a patient is having regular nebuliers?

A

Their salbutamol inhaler

62
Q

WHAT ARE SOME CAUSES OF NEUTROPHILIA?

A
  1. Bacterial infection
  2. Tissue damage (inflammation/infarct/malignancy)
  3. Steroids
63
Q

What are some causes of neutropenia?

A
  1. Viral infection
  2. Chemotherapy
  3. Clozapine
  4. Carbimazole
64
Q

What are some causes of lymphocytosis?

A
  1. Viral infection
  2. Lymphoma
  3. Chronic lymphocytic leukaemia
65
Q

What are the causes of thrombocytopenia?

A
  1. Reduced production
    Infection
    Drugs
    Myelodysplasia
  2. Increased destruction
    Herpain
    Hypersplenism
    DIC
    ITP
    Haemolytic uraemic syndrome
66
Q

What are the causes of thrombocytosis?

A
  1. Reactive
    Bleeding
    Tissue damage
    Postslenectomy
  2. Primary
    Myeloproliferative disorders
67
Q

What does a raised urea normally mean?

A

Kidney injury or upper GI haemorrhage

68
Q

In an AKI what indicates where the pathology is coming from?

A
  1. Urea > Creatinine = prerenal
  2. Urea < Creatinine = Intrinsic renal
  3. Urea < Creatinine = postrenal
69
Q

WHAT THE MARKERS ARE PREHEPATIC JAUNDICE?

WHAT CAN CAUSE THIS?

A
  1. Solely increased bilirubin
  2. Haemolyisis + Gilbert’s
70
Q

What are the markers for intrahepatic jaundice?

What can cause this?

A
  1. Increased bilirubin and AST/ALT increase.
  2. Fatty Liver
  3. Hepatitis
  4. Cirrhosis
  5. Malignancy
  6. Metabolic (Wilson’s disease)
71
Q

What are the markers for posthepatic jaundice?

What is this caused in?

A
  1. Increased bilirubin and increased ALP
  2. Gallstone, drugs causing cholestasis
  3. Tumour, primary biliary cirrhosis
  4. Pancreatic or gastric cancer

Normal LFTs apart from ALP think bone metastases

72
Q

WHAT DOES PRIMARY HYPOTHYROIDISM DO TO T4 AND TSH?

WHAT CAUSES THIS?

A
  1. Low T4
  2. High TSH
  3. Hashimoto’s thyroiditis, drug-induced hypothyroidism
73
Q

What does secondary hypothyroidsm do to T4 TSH?

What causes secondary hypothyroidsm?

A
  1. Low T4 and Low TSH
  2. Pituitary tumour or damage
74
Q

What does primary hyperthyroidism do to T4 and TSH?

What causes hyperthyroidism?

A
  1. High T4 and LOW TSH
  2. Graves disease, toxic nodular goiter, drug-induced hyperthyroidism
75
Q

What does secondary hyperthyroidism do to T4 and TSH?

What causes this?

A
  1. High T4 and High TSH
  2. Pituitary tumour
76
Q

WHAT IS THE DEFINITION OF ANAPHYLAXIS?

A

Anaphylaxis may be defined as a severe, life-threatening, generalised or systemichypersensitivity reaction.

77
Q

What are some triggers of anaphylaxis?

A
  1. Food (e.g. nuts) - the most common cause in children
  2. Drugs
  3. Venom (e.g. wasp sting)
78
Q

What does the Resus Council UK define anaphylaxis as?

A

The Resus Council UK define anaphylaxis as:

  • The sudden onset and rapid progression of symptoms
  • Airway and/or Breathing and/or Circulation problems
  1. Airway problems may include:
    • swelling of the throat and tongue →hoarse voice and stridor
  2. Breathing problems may include:
    • respiratory wheeze
    • dyspnoea
  3. Circulation problems may include:
    • hypotension
    • tachycardia

This means that if there are no ABC problems then the patient is technically not having anaphylaxis.

79
Q

What dose of adrenaline is given to a <6 month old in anaphylaxis?

A

100-150 microgram - 1 in 1000

80
Q

What dose of adrenaline is given to a 6 month - 6 years in anaphylaxis?

A

150 micrograms - 1 in 1000

81
Q

What dose of adrenaline is given to a 6-12 year old in anaphylaxis?

A

300 micrograms - 1 in 1000

82
Q

What dose of adrenaline is given to an adult and child >12 years in anaphylaxis?

A

500 micrograms 1 in 1000

83
Q

How often can adrenaline be given in anaphylaxis?

A

Every 5 minutes

84
Q

What is refractory anaphylaxis defined as?

A
  1. Defined as respiratory and/or cardiovascular problems persist despite 2 doses of IM adrenaline
  2. IV fluids should be given for shock
  3. Expert help should be sought for consideration of an IV adrenaline infusion
85
Q

What is the management following stabilisation after anaphylaxis?

A
  1. Non-sedating oral antihistamines, in preference to chlorphenamine, may be given following initial stabilisation especially in patients with persisting skin symptoms (urticaria and/or angioedema)
  2. Serum tryptase levels are sometimes taken in such patients as they remain elevated for up to 12 hours following an acute episode of anaphylaxis
  3. All patients with a new diagnosis of anaphylaxis should be referred to a specialist allergy clinic
  4. An adrenaline injector should be givens an interim measure before the

Specialist allergy assessment (unless the reaction was drug-induced)

  1. Patients should be prescribed 2 adrenaline auto-injectors
  2. Training should be provided on how to use it
86
Q

How fast can a patient be discharged after anaphylaxis?

A
  1. Fast-track discharge (after 2 hours of symptom resolution):
    • good response to a single dose of adrenaline
    • complete resolution of symptoms
    • has been given an adrenaline auto-injector and trained how to use it
    • adequate supervision following discharge
  2. Minimum 6 hours after symptom resolution
    • 2 doses of IM adrenaline needed, or
    • previous biphasic reaction
  3. Minimum 12 hours after symptom resolution
    • severe reaction requiring > 2 doses of IM adrenaline
    • patient has severe asthma
    • possibility of an ongoing reaction (e.g. slow-release medication)
    • patient presents late at night
    • patient in areas where access to emergency access care may be difficult
    • observation for at 12 hours following symptom resolution
87
Q

What is skin patch testing useful for?

A
  1. Useful for contact dermatitis.
  2. Around 30-40 allergens are placed on the back. Irritants may also be tested for.
  3. The patches are removed 48 hours later with the results being read by a dermatologist after a further 48 hours
88
Q

What is a radioallergosorbent test (RAST)?

A
  1. Determines the amount of IgE that reacts specifically with suspected or known allergens, for example IgE to egg protein. Results are given in grades from 0 (negative) to 6 (strongly positive)
  2. Useful for food allergies, inhaled allergens (e.g. Pollen) and wasp/bee venom
  3. Blood tests may be used when skin prick tests are not suitable, for example if there is extensive eczema or if the patient is taking antihistamines
89
Q

How often can you give salbutamol nebulisers in anaphylaxis?

A

Back to back

90
Q

WHAT IS ORAL ALLERGY SYNDROME?

A

Oral allergy syndrome, also known as pollen-food allergy, is an IgE-mediated hypersensitivity reaction to specific raw, plant-based foods including fruits, vegetables, nuts and certain spices

91
Q

WHAT IS THE FIRST THING TO DO IN A SEIZURE?

A
  1. check the airway and apply oxygen if appropriate
  2. place the patient in the recovery position
  3. if the seizure is prolonged give benzodiazepines
92
Q

How often can rectal diazepam be repeated in a seizure?

A

Every 10-15 minutes

93
Q

What dose of benzodiazepine is given in a seizure?

A

10mg

94
Q

What are the medications which can cause a long QT?

A
  1. Amiodarone, sotalol, class 1a antiarrhythmic drugs
  2. tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram)
  3. methadone
  4. chloroquine
  5. terfenadine**
  6. erythromycin
  7. haloperidol
  8. ondanestron
95
Q

What electrolytes and conditions can cause long QT?

A
  1. electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia
  2. acute myocardial infarction
  3. myocarditis
  4. hypothermia
  5. subarachnoid haemorrhage
96
Q

WHAT ARE THE SYMPTOMS OF NIACIN DEFICIENCY?

A

Pellagra

  1. dermatitis
  2. diarrhoea
  3. dementia
97
Q

WHAT ELECTROLYTE ABNORMALITY WOULD BE SEEN IF A PATIENT IS IMMOBIBLE FOR A LONG TIME?

A

Hyperkalaemia

ΩΩ 3b Bateman - Acute and Critical Care (3 decks)

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