15. Acute Medicine Flashcards
What happens to the NDMA receptors and GABA receptors in acute and chronic alcohol consumption?
GABA, inhibitory receptors are increased and alcohol reduces NDMA receptor action.
In chronic, the body upregulates NDMA receptors (excitatory) and downregulates GABA.
Therefore, if you withdraw then the NMDA receptor increase is suddenly not dampened so the body goes into overdrive.
Risk factors for alcohol withdrawal?
Alcohol use disorder
History of alcohol withdrawal
Acute illness
Poor physical health (poor nutrition -> thiamine deficiency -> wernicke’s)
What are the signs of chronic or decompensated liver disease?
Encephalopathy Ascites Peripheral oedema Jaundice Bruising
AABB - Ammonia, Albumin, Bilirubin, Blood factors
What are the signs of wernicke’s encephalopathy?
Caused by thiamine - B1 deficiency Triad of Confusion Ataxia Nystagmus
CAN
How does alcohol withdrawal present?
- 6hours after - minor withdrawal - anxiety, agitation, palpitations, GI upset, sweating/tremor
- 12 hours - alcoholic hallucinosis
- 24 hours - withdrawal generalised tonic-clonic seizures
- 48 hours - withdrawal delirium - delirium tremens, severe tremor, fever, high BP and HR
spreading from the SNS, to mind, body and then systemic
How do we investigate alcohol withdrawal?
Screen with CADE or AUDIT-C ECG for arrhythmias ABG for resp alkalosis or met acidosis Glucose, FBC, U&E, LFTs, coagulation CT head for falls CXR - pneumonia or aspiration
Treatment for alcohol withdrawal?
Urgent!
- Benzos IV
- CT head urgent for seizures and head injury
- Detect and treat co-existing illnesses
Supportive.
- Rehydrate with IV fluid
- Pabrinex (vit B) for wernicke’s
- Glucose as often hypoglycaemic after thiamine!!
- Electrolytes imbalances
Always refer to alc management team
What are hives called in proper terms
Urticarial rash seen in anaphylaxis
What is angiodema?
Swelling around the face from anaphylaxis
How do we manage anaphylaxis?
Acute
- Call for help
- Remove the trigger e.g. IV antibiotics
- Lie the patient flat, legs elevated
- Adrenaline, 500 micrograms IM
- Reassess airway
Then,
- High-flow oxygen with 15L via non-rebreathe
- Monitor
- IV fluid challenge
- IM or slow IV chlorphenamine (the hives) and hydrocortisone
What do we do post-management for anaphylaxis?
Observe the patient
Safety netting with advice
Epipen on discharge with education
Refer to allergy service
What is anaphylaxis?
A sudden, life-threatening, systemic hypersensitive reaction characterised by sudden onset of airway and/or breathing and/or circulation problems after a trigger.
What does histamine cause to create anaphylaxis?
- Vessel dilation
- Leaky vessels
- Bronchospasm
What is different between asthma and anaphylaxis in bloods?
Anaphylaxis has tryptase
IV or IM adrenaline?
Always IM.
How does aspirin OD present?
Tinnitis, deafness, dizziness
Tachypnoea
Hyperthermia
N&V
Late -
Low BP and heart block
Pulmonary oedema
Low GCS and seizures
How do we treat aspirin overdose?
No antidote, mainly supportive
Consider ICU
How do we investigate aspirin OD?
ECG, ABG etc. for complications to assess
Plasma salicylate concentration!
Plasma paracetamol conc for mixed OD
How might paracetamol OD present?
Often asymptomatic Mild N&V and lethargy RUG pain Hepatomegaly Acute liver failure - jaundice
How do we investigate paracetamol OD?
ABG - lactic acidosis is a bad sign Urinalysis for kidney failure Serum paracetamol to stratifying liver injury LFTs, PT, INR Blood glucose U&Es FBC
How do we manage paracetamol OD?
IV N-acetylcysteine
Liver transplant
What are opiates vs opioids?
Opiate - naturally occuring e.g. codeine
Opioid - synthetic e.g. fentanyl
How do opiate ODs present
Triad -
Reduced consciousness
Respiratory depression (bradypnoea)
Miosis
Coma
How do we investigate opiate OD?
BM for low glucose differential
ABG for resp failure and acidosis
Plasma paracetamol for mixed OD
FBC, U&Es (renal impairment), LFTs, CT head for diff
