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Success Flashcards

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1
Q

What does SCAPE stand for?

And other names?

A

Sympathetic Crashing Acute Pulmonary Edema

Flash pulmonary edema, hypertensive cardiogenic pulmonary edema, hypertensive acute heart failure, acute pulmonary edema.

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2
Q

What does FOSPE stand for?

A

Fluid Overload Subacute Pulmonary Edema

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3
Q

What is another name for FOSPE?

A

Congestive heart failure exacerbation, Decompensated heart failure

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4
Q

What is the acuity of SCAPE?

A

Occurs rapidly (within minutes to hours)

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5
Q

What is the acuity of FOSPE?

A

Gradual onset over days

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6
Q

What is the key physiological problem in SCAPE?

A

Volume status

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7
Q

What is the key physiological problem in FOSPE?

A

Fluid overload

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8
Q

What type of congestion is associated with SCAPE?

A

Systemic congestion

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9
Q

What type of congestion is associated with FOSPE?

A

Hypertensive cardiogenic

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10
Q

What are common treatments for SCAPE?

A

CPAP or BIPAP, Nitroglycerine

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11
Q

What are common signs of FOSPE?

A

Ascites and/or peripheral edema are more commonly seen

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12
Q

What is the blood pressure status in SCAPE?

A

May be hypotensive, normotensive, or hypertensive

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13
Q

What is the characteristic ECG change associated with digitalis effect?

A

Downsloping ST depression with characteristic ‘sagging’ appearance

# flattened , inverted or biphasic T WAVE
# Shortened QT interval

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14
Q

What is a common effect of acute digoxin overdose?

A

Marked bradycardia with PR and QRS prolongation

Acute overdose effects can significantly alter heart rate and conduction.

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15
Q

What arrhythmias may occur due to digoxin toxicity?

A

Sinus arrest, varying degrees of AV block, paroxysmal atrial tachycardia with AV block, junctional tachycardia, frequent ventricular ectopics, bigeminy

These arrhythmias can complicate the clinical picture of digoxin toxicity.

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16
Q

What severe complications can arise from digoxin toxicity?

A

Ventricular tachycardia and ventricular fibrillation

These are critical conditions that may necessitate immediate medical intervention.

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17
Q

Clinical features of digitalis toxicity

A

Clinical features :

General features (may develop within 1 -2 hours of acute overdose) : Nausea, vomiting, diarrhoea and general malaise

CNS features : Anorexia, headache, weakness and rarely blurred vision or alteration in colour perception (classically xanthopsia)

Cardiac effects (may take 6 hours or more to develop) :Marked bradycardia, hypotension, arrhythmias

Metabolic effects : Hyperkalaemia (common in severe poisoning), metabolic acidosis

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18
Q

four recognised temporal patterns of anaphylaxis

A

*Uniphasic anaphylaxis — Uniphasic anaphylactic reactions are the most common type, accounting for an estimated 80 to 94 percent of all episodes. A uniphasic response typically peaks within hours after symptom onset and then either resolves spontaneously or after treatment, usually within several hours.

*Protracted anaphylaxis — A protracted or persistent anaphylactic reaction lasts hours to days without clearly resolving completely. The exact frequency of protracted episodes of anaphylaxis is unknown, although they appear to be uncommon. The literature consists only of case reports and small series.

*Refractory anaphylaxis — Refractory anaphylaxis can be defined as continued symptoms of anaphylaxis despite appropriate epinephrine dosing and symptom-directed treatment (e.g. intravenous fluids for hypotension).

*Biphasic anaphylaxis — Biphasic reactions are characterised by an initial reaction that meets criteria for anaphylaxis, followed by an asymptomatic period of one hour or more, and then a subsequent return of symptoms meeting the criteria for anaphylaxis without further exposure to antigen. Biphasic reactions have been reported with an array of allergens, including ingested, injected, and intravenously administered substances, as well as in idiopathic anaphylaxis. The time period between the resolution of the first reaction and the start of the second can range from 1 hour to up to 48 hours. The severity of recurrent symptoms in biphasic reactions is unpredictable. In most patients, recurrent symptoms are less severe than the initial symptoms. However, in a minority of patients, recurrent symptoms are more severe or even fatal.

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19
Q

What is the location of the Dorsal columns?

A

Posteromedial aspect of cord

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20
Q

What is the function of the Dorsal columns?

A

Transmits ipsilateral proprioception, vibration and fine-touch sensation

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21
Q

What is the location of the Spinothalamic tract?

A

Anterolateral aspect of cord

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22
Q

What is the function of the Spinothalamic tract?

A

Transmits contralateral pain, crude-touch and temperature sensation

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23
Q

What is the location of the Lateral corticospinal tract?

A

Posterolateral aspect of cord

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24
Q

What is the function of the Lateral corticospinal tract?

A

Controls ipsilateral motor power

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25
What are the types of spinal cord syndromes?
Central cord syndrome, anterior cord syndrome, Brown-Séquard syndrome, complete cord transection, posterior cord syndrome.
26
What is the mechanism of complete cord transection?
Major trauma.
27
What tracts are affected in complete cord transection?
All tracts.
28
What is Brown-Séquard syndrome?
Hemitransection due to penetrating trauma or unilateral compression of the cord.
29
What tracts are affected in Brown-Séquard syndrome?
All tracts on one side.
30
What are the clinical features of Brown-Séquard syndrome?
Ipsilateral hemiparesis, ipsilateral loss of proprioception/vibration/touch sensation, contralateral loss of touch/pain/temperature sensation.
31
What is central cord syndrome?
Involves the corticospinal tract and spinothalamic tract.
32
What are the clinical features of central cord syndrome?
Quadriplegia (above C), paraplegia (below C), varying degrees of motor and sensory loss, greater loss in upper than lower limbs.
33
What is anterior cord syndrome?
Caused by occlusion of anterior spinal artery with infarction of anterior cord.
34
What tracts are affected in anterior cord syndrome?
Corticospinal, spinothalamic, and spinocerebellar tracts.
35
What are the clinical features of anterior cord syndrome?
Bilateral motor loss, loss of pain and temperature sensation, preserved proprioception and vibration sense.
36
What is posterior cord syndrome?
Caused by penetrating trauma to the back or hyperextension injury associated with vertebral arch fractures.
37
What tracts are affected in posterior cord syndrome?
Dorsal column.
38
What are the clinical features of posterior cord syndrome?
Bilateral loss of proprioception/vibration/touch sensation.
39
What is neurogenic shock?
Neurogenic shock results in the loss of vasomotor tone and sympathetic innervation to the heart.
40
What causes neurogenic shock?
Injury to the cervical or upper thoracic spinal cord (T1 and above) can cause impairment of the descending sympathetic pathways.
41
What are the physiological effects of neurogenic shock?
The resultant loss of vasomotor tone causes vasodilation of visceral and peripheral blood vessels, pooling of blood, and hypotension.
42
How does neurogenic shock affect heart rate?
Loss of sympathetic innervation to the heart can cause bradycardia or the inability to mount a tachycardic response to hypovolaemia.
43
Is fluid resuscitation effective in neurogenic shock?
The physiologic effects of neurogenic shock are not reversed with fluid resuscitation alone.
44
What can massive fluid resuscitation lead to in neurogenic shock?
Massive resuscitation can result in fluid overload and/or pulmonary oedema.
45
What treatments may be required after moderate volume replacement in neurogenic shock?
Judicious use of vasopressors may be required after moderate volume replacement.
46
What medication can be used to counteract significant bradycardia in neurogenic shock?
Atropine may be used to counteract haemodynamically significant bradycardia.
47
Why is dobutamine not used in neurogenic shock?
Dobutamine is not used in neurogenic shock because of its peripheral vasodilatory properties and potential reflex bradycardia.
48
What are the causative agents of Neuroleptic Malignant Syndrome?
Dopamine antagonists ## Footnote Commonly associated with antipsychotic medications.
49
What is the onset time for Neuroleptic Malignant Syndrome?
Gradual (days) ## Footnote Symptoms can develop over several days.
50
List some similar features of Neuroleptic Malignant Syndrome and Serotonin Syndrome.
* Hypertension * Tachycardia * Hyperthermia (> 40°C) * Hypersalivation * Diaphoresis ## Footnote Both syndromes share several autonomic symptoms.
51
What are some distinct features of Neuroleptic Malignant Syndrome?
* Encephalopathy, stupor, coma * Hyporeflexia * 'Lead-pipe' rigidity * Normal pupils * Reduced, sluggish bowel sounds ## Footnote These features help differentiate it from Serotonin Syndrome.
52
What are the lab findings associated with Neuroleptic Malignant Syndrome?
* Increased creatine kinase * Leucocytosis * Low serum iron * Acidosis ## Footnote Lab findings can indicate muscle breakdown and other metabolic changes.
53
What is the management for Neuroleptic Malignant Syndrome?
* Dantrolene * Amantadine * Bromocriptine ## Footnote These medications help to counteract the effects of dopamine antagonism.
54
What are the causative agents of Serotonin Syndrome?
Serotonergic agents ## Footnote Commonly associated with antidepressants and certain recreational drugs.
55
What is the onset time for Serotonin Syndrome?
Rapid (hours) ## Footnote Symptoms can appear within hours of exposure to serotonergic agents.
56
List some distinct features of Serotonin Syndrome.
* Agitation * Hypervigilance * Delirium * Hyperreflexia * Rigidity with clonus * Dilated pupils * Hyperactive bowel sounds ## Footnote These features are indicative of increased serotonergic activity.
57
What are the lab findings associated with Serotonin Syndrome?
More commonly no lab findings ## Footnote Unlike Neuroleptic Malignant Syndrome, lab tests are often unremarkable.
58
What is the management for Serotonin Syndrome?
* Benzodiazepines * Cyproheptadine ## Footnote These treatments help alleviate symptoms and counteract serotonin effects.
59
What does DOACS stand for?
DOACS stands for apixaban, dabigatran, edoxaban, and rivaroxaban
60
What is the mode of action of DOACS?
DOACS are anticoagulants with a novel mode of action
61
Which DOACS are direct and reversible inhibitors of factor Xa?
Apixaban, edoxaban, and rivaroxaban
62
What is the effect of inhibiting factor Xa?
Inhibition of factor Xa prevents thrombin generation and thrombus development
63
What type of inhibitor is dabigatran?
Dabigatran is a reversible inhibitor of free thrombin, fibrin-bound thrombin, and thrombin-induced platelet aggregation
64
Reversible agents of -) heparin -) dabigatrin -) apixaban, riveroxaban
Heparin = protamine sulfate Dabigatran = Idarucizumab Apixaban = Andexanet alfa
65
Acyanotic CHDs
ASD VSD AORTIC STENOSIS COARCTATION OF AORTA
66
Cyanotic CHDs
5T’s Truncus arteriosus Transposition of great arteries Tricuspid atresia Tetrology of fallot Total anamolus pulmonary venous return
67
Dosage of IM adrenaline for Children > 12 years and adults
500 mcg (0.5 mL)
68
Dosage of IM adrenaline for Children 6 - 12 years
300 mcg (0.3 mL)
69
Dosage of IM adrenaline for Children 6 months - 6 years
150 mcg (0.15 mL)
70
Dosage of IM adrenaline for Children < 6 months
100-150 mcg (0.1 - 0.15 mL)
71
Trifasicular block includes?
RBBB LAD ( left ant.fascicular block ) First degree AV block Nothing but bifascicular block + AV block
72
What concentration should intravenous insulin infusion start at in dka
1 unit/mL
73
What is the fixed rate for insulin infusion in dka
0.1 units/kg/hour
74
How is the insulin infusion made up in dka?
Using 50 units human soluble insulin (Actrapid® or Humulin S®) made up to 50 ml with 0.9% sodium chloride solution.
75
What should happen to blood ketone concentration during treatment in dka
It should fall by at least 0.5 mmol/litre/hour OR bicarbonate should rise by at least 3 mmol/L/hour and blood glucose concentration should fall by at least 3 mmol/litre/hour.
76
When should the insulin infusion be continued in dka?
Until blood ketone concentration is below 0.6 mmol/litre, blood pH is above 7.3 and/or venous bicarbonate is over 18 mmol/L.
77
What are the criteria for moderate severity in asthma?
Increasing symptoms PEFR > 50 - 75% of best or predicted No features of acute severe asthma
78
What are the criteria for severe asthma?
Any one of: PEFR 33 - 50% of best or predicted Respiratory rate ≥ 25 breaths/minute Heart rate ≥ 110 beats/minute Inability to complete sentences in one breath
79
What are the criteria for life-threatening asthma?
Any one of the following in a patient with severe asthma: Clinical signs Altered conscious level Exhaustion Arrhythmia Hypotension Cyanosis Silent chest Poor respiratory effort Measurements PEFR < 33% of best or predicted Oxygen saturations < 92% PaO2 < 8 kPa Normal PaCO2 (4.6 - 6.0 kPa)
80
What indicates a near-fatal asthma condition?
Raised PaCO2 and/or requiring mechanical ventilation with raised inflation pressures
81
Wells score for PE
82
Maintenance fluids in children calculation
83
What does the Mental Health Act (2007) allow?
Compulsory admission of people who have a mental disorder that warrants assessment or treatment in hospital and need to be admitted for their own health or safety, or for the protection of others.
84
What is Section 2 of the Mental Health Act?
Allows compulsory admission for up to 28 days for assessment.
85
What is Section 3 of the Mental Health Act?
Allows compulsory admission for up to 6 months for treatment.
86
What is required for admission under Sections 2 and 3?
An application from an approved mental health professional (AMHP) or the person's nearest relative, and written recommendations from two doctors, one of whom must be section 12 approved.
87
What happens if there is no obvious second medical recommendation for Section 2?
Another section 12-approved doctor is usually asked to assess the individual, but if impractical, any registered medical practitioner may provide the second recommendation without conflicts of interest.
88
What is Section 4 of the Mental Health Act?
Used in exceptional cases to permit compulsory admission for up to 72 hours if there is urgent necessity.
89
What is required for admission under Section 4?
An application from an AMHP or the person's nearest relative and just one medical recommendation.
90
What happens after a compulsory admission under Section 4?
This section is usually converted to a Section 2, requiring further involvement of the GP.
91
What is Section 5 of the Mental Health Act?
Permits emergency holding powers for admitted patients to provide temporary restraint while awaiting assessment by a psychiatrist.
92
What are the holding powers under Section 5?
Section 5 (2) allows a doctor holding power for 72 hours, and Section 5 (4) allows a registered mental health nurse holding power for 6 hours.
93
What is Section 136 of the Mental Health Act?
Allows police to take people from a public place to a place of safety for examination by a registered medical practitioner and interview by an AMHP.
94
What is the rule for young people aged 16 or 17 regarding hospital admission?
They cannot be admitted or kept in hospital for treatment for a mental disorder based on their parents' consent if they have the capacity to consent but refuse.
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