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ACC > Pt w/ Collapse (including WARFARIN reversal) > Flashcards

Pt w/ Collapse (including WARFARIN reversal) Flashcards

1
Q

List some important question to ask in the history of a patient presenting with collapse

A 
BEFORE
How did they feel
- Palpitations, dizzy, chest pain, breathlessness, headache, nausea, pale and clammy, weakness
Any triggers 
-last time they ate or drank?
-any illegal drugs or alcohol
DURING THE COLLAPSE
- do they remember falling or did they black out before 
- did they hit their head 
- did anyone else see (collateral hx)
- did they seize/shake/twitch 
- how long were they unconscious for?
- did they bite their tongue?
- were they incontinent or urine or faeces
AFTER
- How did they feel after (sleepy, sick)
- How do they feel now?
- Any ongoing chest pain or breathlessness
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2
Q

When do symptoms of alcohol withdrawal commonly occur?

When will they peak?

A

Start around 6-8 hours

Peak around 10-30 hours and then will start to subside

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3
Q

What are some features of alcohol withdrawal? (signs and symptoms)

A

Symptoms of alcohol withdrawal

  • anxiety
  • headache
  • sweating
  • fever
  • restlessness/tremor
  • nausea and vomiting
  • seizures (within 24-48 hours)
  • visual and auditory hallucinations
  • problems sleeping

Signs

  • tachycardia
  • hypertension
  • hypereflexia
  • fever
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4
Q

What is delirium tremens?
When does it occur?
Why is it important?

A

DELIRIUM TREMENS

  • most severe form of alcohol withdrawal
  • usually occur 2-3 days after alcohol withdrawal. Will also last 2-3 days
  • important as can lead to death

PHYSICAL SIGNS:

  • GLOBAL CONFUSION
  • agitation
  • fever
  • seizures
  • hallucinations
  • sweating
  • AUTONOMIC HYPERACTIVITY (increased BP and HR)
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5
Q

What investigations are important in someone with alcohol withdrawal?

A

Investigationsalcohol withdrawal
Bloods: FBC, U&E, glucose, THIAMINE
ECG
ABG - for metabolic acidosis (can cause alcoholic ketosis)

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6
Q

Initial management for alcohol withdrawal

Treatment for delirium tremens?

A
  • the benzodiazepine CHLORDIAZEPOXIDE (10-30mg) is very useful in the treatment of alcohol withdrawal
  • PABRINEX Is a thiamine-corrective solution that should also be given
  • Atenolol or propanol for hypertension
  • Carbamazepine for seizures

-ORAL LORAZAPAM if DELERIUM TREMENS (agitation, confusion, paranoia, and visual and auditory hallucinations)

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7
Q

What is a common cardiac causes of collapse?

Explain what it is

A

COMPLETE HEART BLOCK

  • incomplete/ lack of conduction between the SAN and the AVN
  • heart cant beat properly>cardiac output drops
  • complete (or third degree is the most likely to cause collapse)
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8
Q

Why might there still be heart beat in someone with complete heart block? How will this appear on ECG

A

Sometimes there is some accessory pacemaker tissue that generates and conducts a signal - known as an ESCAPE RHYTHM

  • will cause NARROW QRS COMPLEXES
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9
Q

What are some others signs of complete heart block?

A

Complete heart block

  • COLLAPSE
  • Haemodynamic instability (hypotension and bradycardia)
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10
Q

Whats the most common cause of complete heart block?

A

CORONARY ISCHAEMIA

INFERIOR WALL MI are the ones that are most likely to disturb the AVN and therefore ruin conduction and lead to heart block

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11
Q

What are some relevant investigations for patients with heart block and what might you find?

A

Investigations heart block
Bloods: FBC, U&E (hypotension), Troponin

ECG:
-strange relationship between p waves +QRS complexes
1st degree: prolonged PR int. -bigger than 3-5 s. squares (0.12-0.20)
2nd degree type 1/wenkeback: increasing then drop QRS
2nd degree type 2: fine, then drop QRS (ratio 2:1 or 3:1)
3rd degree: atria + ventricles indépendant

Also look for LBBB as evidence of old MI

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12
Q

Management of complete heart block?

A

Management

  • Identify causes where possible
  • Refer for pacemaker if idiopathic CHB
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13
Q

How does DKA typically present?

A

ALWAYS CONSIDER THIS IS THE COLLAPSED YOUNG PERSON
Can present in a large variety of ways that can be quite non specific (think about that boy in Bradford)

GI: nausea and vomiting, abdominal pain
Resp: Kussmauls breathing to blow off CO2 from met acid
-thirst (polydipsia) 
-going toilet more (polyuria) 
-sweet smelling breath 
-confusion 
-recent weight loss and fatigue 
-dehydration (decreased skin turgor, dry membranes increased CRT)
-shock: hypotension and tachycardia
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14
Q

Causes of DKA (explanation of symptoms)

Mechanism of DKA?

A

Causes

  • undiagnosed diabetes in young person
  • insufficient insulin (not enough/not taking)
  • infection or illness

Mechanism

  • Without insulin glucose is not drawn into cells
  • glucagon is produced
  • a) glycogenolysis b)gluconeogenesis (fatty acids>ketones)
  • very high levels of plasma glucose leads to diuretic osmosis and water and sodium are drawn OUT OF CELLS leading to the polyuria and polydipsia
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15
Q

Initial management of DKA

A

If the patient has altered mental state consider airway preservation and breathing support etc.

  1. FLUIDS IMPORTANT - 0.9% NaCl IV infusion over 1 Hr (next over 2 hrs, next over 2 hours, next over 4 hours)
  2. INSULIN INFUSION pump at 0.1 units/kg/hr
  3. POTASSIUM CORRECTION (insulin drives K into cells)
    - Consider monitoring urine output (?catheter)
  4. DEXTROSE
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16
Q

What condition occurs when blood glucose is high but there isn’t a considerable ketoacidosis?

A

HYPERGLYCAEMIC HYPEROSMOLAR STATE (HHS)

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17
Q

What are some clinical features of HHS?

A

HHS

  • Blood glucose >11.1mmol/L
  • LACK of urinary ketones
  • Increased blood osmolality leading to sx of polydipsia and polyuria
  • Weight loss and fatigue
  • Dehydration
  • Weakness
  • Leg cramps
  • Vision problems
  • Itchy skin
  • Poor kidney function
  • Altered consciousness
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18
Q

What causes HHS?

A
  • Can just happen with inter-current illness
  • Can happen in someone who had diabetes that is poorly controlled
  • Can occur in dehydration
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19
Q

What investigations are relevant in HHS?

A

HHS investigations

  • Blood glucose
  • FBC, U+Es (can effect renal function), CRP (to look for infection)
  • ECG
  • CXR (to look for infection)
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20
Q

What is the management of HHS?

A

VERY SIMILAR TO DKA

  • Insulin infusion 0.1U/kg/hr
  • Monitor potassium
  • Keep hydrated with salt boosts - NaCl 0.9%
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21
Q

What is classed as high blood glucose and what are some general symptoms?

A

BM >11.1mmmol
Classic triad of sx: polyphagia, polyuria and polydipsia

Sx of CHRONIC POOR GLUCOSE CONTROL:
- ED, blurred vision, poor kidney function, weight loss, restlessness, fatigue, poor wound healing, dry mouth, itchy skin

22
Q

What factors in the history are important to ascertain in someone presenting with seizures?

A

BEFORE
- any aura (visual, auditory, gustatory, olfactory, tactile), -headaches, feeling unwell - familiar to pt?
DURING
- were the jerking/twitching (tonic clonic)
-were they unconscious/how long for,?
-did they bite their tongue
-were they incontinent?
AFTER
- are they sleep/confused/drowsy and how long for
- Do they have headache

23
Q

Explain partial seizures

A

PARTIAL

  • SIMPLE PARTIAL - they are aware. focal motor and sensory /autonomic symptoms
  • COMPLEX PARTIAL
  • awareness is impaired. Usually temporal lobe. Post-ictal confusion is common but fast to resolve
  • parietal=strange feelings
  • PARTIAL WITH 2RY GENERALISATION - seizure starts with focal motor or sensory deficits and then will become convulsions (2/3 of pt with partial seizures)
24
Q

Explain generalised seizures

A

GENERALISED

  • ABSENCE SEIZURES: more common in children - unresponsive for several seconds
  • TONIC-CLONIC SEIZURES: classical jerking seizures, pt will collapse. Post ictal period is considerable with dizziness and confusion
  • MYOCLONIC - sudden jerking of a limb or trunk may cause patient to fall to ground
  • ATONIC SEIZURES - pt goes completely floppy
25
Q

What is status epileptics?

Management of status epileptics?

A

Status epileptics >5 mins OR 3+ seizures in 1 hour

Management status epileptics

  • ABCDEG approach and call senior (maintain airway-nasopharyngeal airway)
  • Recovery position
  • Start timing
  • Oxygen 15L/non-rebreathe mask
  • Check GLUCOSE – if <3.5 → 100ml of 20% glucose STAT

CALL FOR HELP!!!
STEP 1 AT 5 MINS
-IV lorazepam 0.1mg/kg (max 4mg)

STEP 2 REPEAT AFTER 10 MINS

STEP 3 AT 20 MINS

  • IV Phenytoin loading dose (20mg/kg max dose 2g)
  • If they already take phenytoin give IV phenobarbital infusion
  • use separate IV line

STEP 4 INTUBATE (ICU and rapid sequence induction)

  • Thiopentone or propofol on ICU/HDU
  • Transfer to ICU
26
Q

Status Epilipticus
What do you do if you cannot get IV ?

What should you give if alcoholism suspected?

A

NO IV ACCESS IN STATUS EPILIPTICUS
-buccal midazolam or rectal diazepam

*In an alcohol related seizure, give 200mg IV pabrinex(thiamine) 2 PAIRS IV

27
Q

What are the brain 2 initial blood supplies and what do these feed into?
- Where are strokes more common?

A 
Internal carotids (supply the anterior and middle cerebral arteries)
Basilar arteries (supply the posterior cerebral arteries)
  • Strokes more common in the anterior circulation
28
Q

What are the two main types of stroke and what are the proportions of their occurrence?

A

Ischaemia (80-85%) and haemorrhage (15-20%)

29
Q

What are the symptoms of anterior circulation stroke?

A
  • Unilateral weakness (limb and facial droop)
  • Difficult speaking
  • Numbness and loss of sensation
  • Cognitive impairment
30
Q

What are some symptoms of posterior circulation strokes?

A

Posterior stroke symptoms
Same plus:
-vertigo/dizzyness
-nausea

CEREBELLAR SYMPTOMS (DANISH)

  • Dysdiadokinesia
  • Ataxia (Rombergs sign-close eyes lose balance)
  • Nystagmus (H test)
  • Intention tremor (nose to finger)
  • Slurred staccato speech
  • Hypotonia
31
Q

Causes of stroke / TIA

A
  • Most common is atherosclerotic plaque aetiology
  • Haemorrhage: aneurysm rupture, SAH,HTN
  • Carotid artery dissection (most common cause of ischimic stroke in young people)
  • Cerebral embolism (from AF, endocarditis, MI)
32
Q

Investigations for stroke/TIA

A

ABCDEG assessment (CHECK GLUCOSE)
FAST screen
ROSIER to confirm stroke diagnosis
URGENT CT WITHIN 1 HOUR

33
Q

Initial management of ischemic stroke

A

IF WITHIN 4.5 HOURS

  • Give ALTEPLASE thrombolysis once haemorrhage is excluded by CT (ischemia will look dark on CT). (0.9mg/kg max 90mg, 10% as a bolus)
  • Control BP (<180/110)
  • do CT 24 hours after to look for bleeds
  • Then give 300mg aspirin within 24 hours

IF AFTER 4.5 HOURS

  • Give aspirin 300mg for 2 weeks
  • May need thrombectomy if within 6 hours
  • FIND CAUSE: carotid USS, echo and angiogram (might need thrombectomy if PCA and within 24 hours)
  • TREAT COMPLICATIONS (aspiration pneumonia-chest X ray)
  • ADMIT to stroke ward- NBM
34
Q

What are some symptoms of SAH?

What is a really important thing to examine for in SAH presentation

A

THUNDERCLAP HEADACHE

  • collapse LOC
  • vomiting
  • neck stiffness (kernings sign)
  • photophobia
  • dizzyness and confusion
  • fits
  • EXAMINE FOR THIRD NERVE PALSY (down and out) posterior communicating artery aneurysm
35
Q

What is the cause of SAH?

A

Most commonly is ruptured berry aneurysm on the circle of willis
- ask about FH because these are familial (also polycystic kidney disease)

36
Q

What investigations are important in SAH

A

Investigations SAH

  • ABCDEG assessment
  • OBSERVATIONS (raised ICP can cause Cushings triad (hypertension, bradycardia and irregular breathing)
  • CRANIAL NERVE EXAM (CN3 palsy)
  • URGENT CT head within 6 hours - starfish shaped hyperdensity
  • ECG
  • LP - if CT head NEGETIVE but history is suggestive, yellow CSF due to bilirubinxanthochromia (wait 12 hours)
  • ANGIOGRAPHY - to identify aneurysms
  • Do HUNT AND HESS scoreto asses severity
37
Q

Specific management of SAH

A
  1. Analgesia and anti-emetic (codeine)
  2. If there are evidence of ICP increase can give MANNITOL 200mL 10%
  3. Prevent vasospasm - calcium channel blockers - NIMODIPINE
  4. Prevent rebleeding- REFER to NEUROSURGERY (clipping and coiling (form clot to stop)
38
Q

What is mannitol?

A

-osmotic diuretic that forces protein out of the blood causes a drop in pressure - it temporarily decreases ICP until more definitive measures can be found

39
Q

What is the typical history of a VASOVAGAL SYNCOPE?

A
  • Sudden, transient loss of consciousness/collapse <2 mins with a quick recovery
  • Other vasovagal symptoms such as sweating, flushing, paler, dizziness, feeling sick and visual/ hearing changes
40
Q

Causes of vasovagal syncope?

Whats a syndrome that can cause transient arrythmias and syncope?

A
  • Due to neurological increase in vagal tone which causes a drop in BP (bradiacardia and vasodilation) and hence collapse
  • Provoked by emotion, pain, standing for too long, overwarm environment
  • Can often happen in a situation - situation syncope, cough, exercise or urination
  • Stokes Adams syndrome - transient arrhythmias lead to decreased CO and LOC
41
Q

Important investigations in someone with vasovagal syncope

A

Lying and standing BP (low BP can be a cause)

  • Rule out other causes: ECG and Bloods:
  • Blood glucose
  • FBC, U+Es
42
Q

Contraindications for Alteplase?

A

Contraindications for Alteplase
ABSOLUTE
•Current or previous haemorrhage
•Neurosurgery/head trauma/stroke last 3 months
• Systolic BP >185(treat with labetalol)
• Aneurysmor intracranial cancer
• Known clotting disorder(inc anticoagulants or INR>1.7
• Hypo or hyperglycaemic(<3 or >22)

RELATIVE
•Rapidly improving/minor symptoms
•Recent surgery or non head trauma (2 weeks)
• Seizure at onset of stroke
•Post MI pericarditis 
•Pregnancy
• Recent LP
43
Q

What are your differentials for collapse?

A

REFLEX SYNCOPE

  • Vasovagal
  • Situational (cough)
  • Carotid sinus syncope

ORTHOSTATIC HYPOTENSION

  • Primary autonomic failure
  • Secondary autonomic failure (diabetes, uraemia)
  • Drug induced (inc alcohol)
  • Volume depletion (haemorrhage/vomiting)

CARDIAC SYNCOPE (worse prognosis)

  • Arrythmias
  • Structural heart disease
other causes 
Vascular: Stroke/AAA/vasovagal/ ACS/aortic dissection
Resp: PE 
Neuro: Epilepsy/brain injury  
Cardiac: Heart block
Metabolic: DKA, ectopic pregnancy
Neoplasm:
Trauma:

Rule of 15%:
PE/aortic dissection/ACS/ectopic pregnany/ruptured AAA/SAH

44
Q

How will CT heads appear for patients with ischaemic and haemorrhagic strokes?

A

Ischaemic - large darkened patch

Haemorrhagic - large bright, white patch with possible midline shift and compression/disappearance of ventricles.

45
Q

What is the NIHSS score

A

severity of stroke

46
Q

Secondary prevention of ischemic stroke?

What happens if caused by AF?

A

ISCHEMIC STROKE- PREVENT FURTHER DISEASE
1. 300mg Aspirin for 2 weeks/until discharge (or 600mg rectal if no swallow)

  1. Aspirin and clopidogrol 75mg (1-3 months)
  2. Lifelong clopidogrel 75mg

IF CAUSED BY AF: give anticoagulation DOAC/warfarin if AF (start 2 weeks post stroke to prevent secondary haemorrhage)

47
Q

What do you do if someone is on warfarin with an MAJOR BLEED?

A

Warfarin and ACTIVE MAJOR BLEEDS (inc subdura,ocular)

  • STOP warfarin
  • IV Vitamin K 5mg
  • Prothrombin complex e.g. Beriplex, Octiplex
  • Re-check INR 24hrs
48
Q

What do you do about warfarin if MINOR bleed? (INR 5-8 vs INR >8)

A

Warfarin in minor bleeds

  • stop warfarin
  • IV vitamine K 1-3mg (if IRN>8 you can give another dose in 24 hours if not helped)
  • Continue when INR <5
49
Q

What do you do about raised INR for someone who is NOT bleeding? (INR 5-8 vs INR >8)

A

Warfarin for non bleeds
INR 5-8
-hold warfarin 2 days
-reduce next maintenance dose

INR >8
-stop warfarin
PO vitamin K 1-5mg
Restart when INR < 5.0

50
Q

Name some important causes of seizures?

A

EPILEPSY (do EEG, nerve exams, prolactin)
Vascular-Strokes/TIAs/SAH, Arrhythmias (check ECG)
Infection- FBC, lumbar puncture and cultures
Trauma-head injury (do MRI if focal)
Autoimmune
Metabolic- hypoglycaemia (check glucose). Electrolytes (UsEs)
Idiopathic-drugs/alcohol (toxicology screen)
Neoplastic (MRI if focal)
Pregnancy (pregnancy test)

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