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1
Q

What are serious symptoms in the context of dizziness

A

Neurological deficit
Persisting or worsening course
Red flags in background (Known Ca, Previous neurological diseases, ENT issues
History of trauma

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2
Q

Acute investigations for dizziness

A

Bloods including clotting, G+S
ECG
CTH
Inform Reg
MRI when able

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3
Q

Treatment for strokes

A

300mg Aspirin
Thrombolysis if <4.5h
Thrombectomy if <12h
BP control for bleeds (130/80)
Long term would need to consider prevention (BP control, Antiplatelets, Statins, Anticoagulation for AF, Carotid endoartectmy in carotid stenosis)

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4
Q

How are stroke services structured

A
  • Not always at every hospital
  • Often agreements between hospitals are done
  • Priority is for transfer to urgent centers prior to investigations
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5
Q

What are long term goals for NHS stroke services

A

90% stroke patients to be on specialist stroke unit
10% thrombectomy expansion
Expanding tech to ensure CT perfusion scans are used, expanding telehealth interpretation, expansion of hyperacute pathways use of AI in CT/MRI Scans
Improvement to post-stroke rehab
2025 aim to have best performance in europe for thrombolysis

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6
Q

Causes for seizures

A

Infection
Hypoglycaemia
Medication toxcicity
electrolytes
Intracranial pathology

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7
Q

Post pneumothorax discharge plans

A

If primary pneumothorax has been sucessfully aspirated with resolution of symptoms they can be discharged

Ensure to safety net

Needs follow up and repeat XR in 2-4 weeks in respiratory clinic/ambulatory care

Avoid diving permanently (unless had pleurectomy, no air travel for 4 weeks, avoid strenuous activity

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8
Q

Invetigations for medication overdose

A

EXG
Tox screen
Bloosds + coag incl paracetamol/salicylate/ethanol levels + VBG

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9
Q

General management of overdose

A

Charcoal if 1-2 post ingestion
Tox base
MHLT input
Toxicology if required
Escalation if necessary

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10
Q

Explain the mechanism of paracetamol overdose

A

Paracetamol is partially metabolised by CYP450 to a toxic metabolite NAPQI. In healthy metabolism this is conjugated by glutathione to a non-toxic compound and excreted into the urine. In overdose glutathione is saturated and NAPQI accumulates

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11
Q

How does N-Acetyl Cysteine work

A

Glutathione donator to conjugate excessive NAPQI1

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12
Q

What timeframe is NAC most effective in

A

within 8 hours

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13
Q

Differentials for unilateral weakness

A

SOL
Dissection
CNS infection
Delirium

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14
Q

BP target for ischaemic strokes

A

Not usually a target
If considering thrombolysis aim <185/115

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15
Q

Safe timeframe for initiation of DOAC for AF in context of acute ischaemic stroke

A

> 2 weeks from event

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16
Q

Name a stroke classification and its criteria

A

Bamford/Oxford criteria

TAC - 3/3 (Weakness/Hemianopia/Cognitive)

PAC - 2/3 (Weakness/Hemianopia/Cognitive)

POCS - Posterior or cerebellar signs

LACS - Pure motor/Sensory

NIHSS may also be used but this is usually used for severity

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17
Q

Recommendations for antihypertensive treatment in acute ischaemic stroke

A

only recommended with hypertensive emergencies

Discuss with stroke team

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18
Q

Recommendations for BP control in acute haemorrhagic strokes

A

Aim <140mmg with magnitude drop <60mmHg within the first hour

Can be done via labetalol or GTN infusions

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19
Q

Differentials for acutely swollen joint

A

Septic arthritis
Cellulitis
Trauma
Gout/Pseudogout
Inflammatory arthropathy
DVT

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20
Q

How do gout crystals appear on polarised light microscopy

A

Negatively bifringent needles

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21
Q

How do pseudogout crystals appear on polarised light microscopy

A

Positively bifringent rhomboid shaped crystals

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22
Q

Risks factors for septic arthritis

A

> 80
IVDU
RA
Immunosuppression
Diabetes
Joint replacement

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23
Q

Common causative organisms for septic arthritis

A

Staph aureus
Neisseria in young/sexually active
Tb/Fungal/Viral cases (rare)

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24
Q

How does septic arthritis spread

A

usually haematogenous but can spread via local invasion

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25
Abdominal pain important differentials
Pyelonephritis Acute Cholecystitis Ectopic DKA Gastroenteritis Bowel obstruction lower LRTI Acute pancreatitis Acute hepatitis Decompensated CLD
26
How many deaths worldwide are associated with antimicrobial resistance
5 million in 2019
27
Who kinds of countries are affected more by antimicrobial resistance
developing countries
28
Differentials for TIA
Metabolic - Hypoglycaemic, Drugs, Alcohol Dizziness - BPPV, Menieres, Labyrinthitis Neurological - seizure, hemiplegic migraines, MS, LMN neuropathy Trauma Infective - Encephalitis, Abscesses Encephalopathies - Wernickes SOL Acute confusional states
29
Management for TIA
Lifestyle - lose weight, exercise, stop smoking/drinking, low salt diet Manage risk factors - diabetes, hypertension (<130mmHg unless has severe bilateral carotid stenosis) Medications - Antihypertensives if required Statins, Antiplatelets ECG, USS Doppler carotid (DOAC if AF - needs neuroimaging prior) MRI Leaflets and safety net for signs of stroke/TIA in future
30
What are the rules for TIA w driving
Not drive for 1/12 Do not need to inform DVLA - if there is a futher TIA they must not drive for 3 months and inform DVLA at this point
31
Apart from obvious in history what are some key points to ask about in history for SOB
Tb exposure, COVID + Vaccines FH of cardiac problems, CF, alpha-1 antitrypsin
32
Clinic investigations for SOB
Sputum samples ECG FBC - (Thrombocytosis), UE, CRP CXR Spirometry + Peak flow CT Chest if needed
33
PR Bleeds causes
Mesentric ischaemia IBD Infective gastroenteritis Malignancy Diverticulitis Haemorrhoids/Tears
34
D dimer sensitivity
45%
35
What should be used in conjunction with D -dimer in assesment of VTE
Wells score
36
Definition for sepsis
life threatening organ dysfunction due to a dysregulated host response to infection
37
Definition for septic shock
Underlying circulatory and cellular/metabolic abnormalities that are profound enough to substantially increase mortality
38
Clinical indicators for septic shock
persistent hypotension requiring vasopressors to maintain MAP greater than or to 65mmHg, Lactate >2
39
Where did the sepsis 6 come from
Designed via the surviving sepsis campaign bundle Bundle of therapies designed to reduce the mortality of patients with sepsis
40
Risk factors for sepsis
Malignancy Age Older than 65 years Immunocompromise Haemodialysis Alcoholism Diabetes
41
Overall mortality for sepsis
36%
42
Differentials for unconciousness
Toxic causes (opiates, alcohol, anxiolytics, antidepressants) Metabolic disturbances - hypoglycaemia, electrolyte disturbances Trauma - head injury Vascular event - ICH, Infarct Infective - encephalitis, meningitis Neurological causes - could be post-ictal
43
Common causes for hypoglycaemia
Alcohol Insulin, SUs, Beta blockers, Salicylates, Quinines Pentamidine Organ failure Infection Adrenal failure Myxodema Hypopituitarism Insulinomas
44
Driving rules with diabetes
Inform DVLA if taking insulin or SU Check BG before driving Take regular breaks to test blood <5 - dont drive if they have a hypo they should treat and not drive for 45 minutes until BM >5
45
Differentials for headache
VIVID V - Vascular (SAH, subdural, CVST) I - Meningitis, Encephalitis V - Vision threatening (TA, cavernous sinus thrombosis) I - Intracranial-Pressure (SOL, hydrocephalus, cerebral oedema) D - Dissection
46
What blood test is needed prior to LP
Clotting
47
Symptoms for meningitis
Headache, neck stiffness and fever Rash - meingoccoal usually Confusion/Altered conciousness - may be the only symptoms Focal neurological signs Seizures
48
How many patients are the classic symptoms of meningitis missing in
18%
49
How many patient are seizures a presenting feature in
30%
50
What should be done if someone has focal neurological deficit in the context of meningitis?
neuroimaging as there may be a abscess/encephalitis
51
Commom bacterial causes meningitis
Neisseria meningitides Step pneumonia Listeria/GNB if immunocompromised or elderly
52
Treatment for meningitis
Benpen if rash present if no rash cefotaxime or ceftriaxone
53
What should be done if pen allergic and needing treatment for meningitis
Urgent discussion with microbiology may need vancomycin and chloramphenicol
54
Guidelines for LPs in patients without a CT
only advised if: - No septicaemia - No focal neurological signs - No decrease in conciousness
55
CSF appearance in Viral vs Bacterial meningitis
Bacterial: Cloudy/turbid fluid Elevated WCC - neutrophils Low glucose Elevated protein 15% have positive negative culture Viral: Clear fluid Raised WCC at lower levels Lymphocytic Normal glucose Protein slightly raised
56
Who needs to be contacted if a case of meningitis is diagnosed
Public health England - advice on vaccination and will assist in contact tracing Relatives/Close contacts - may need contact tracing Local microbiology team
57
Differnetials for purpuric rash and fever
Gonnoccaemia Bacterial septicaemia with DIC Haemotogical malignancy with septicaemia HSP Viral haemorrhagic fevers
58
SVT causes
Cardiac - structural/HF/Cardiomyopathy Resp - PE Infection Hyperthyroidism Volume loss Electrolyte imbalance (low K, low Mg) Drugs/alcohol - caffeine, alcohol, salbutamol, amphetamines Pain/Stress
59
How does adenosine work
Works on AV node by blocking conduction - causes transient heart block. Mediated by A1 receptor
60
CI for adenosine
2nd or 3rd degree heart block without a pacemaker Long QT Decompensated HF Asthma
61
Symptoms of adenosine
Flushing Light headedness Sense of impending doom
62
Dose for adenosine
6mg then 12mg if no effect
63
What does it mean if adenosine doesn't work
Nodal tachycardia ruled out May be atrial instead
64
Aside from adenosine what are therapies for SVT
TREAT UNDERLYING CAUSE Beta blocker Calcium channel blockers if broad complex consider amiodarone
65
How can SVTs be classified
site of origin (atrial/Nodal) Rhythm regularity (regular/irregular)
66
Time frame to give medication in a seizure
5 min
67
How to treat seizures despite benzodiazepines
Call ITU may need admission for status Consider phenytoim (needs cardiac monitor)
68
Status epilepticus definition
seizure lasting >5 mins, or 2 or more seizures within a 5 minute period without return to normal Can be convulsive or non convultive
69
What is the definition of refractory seizures and their treatment
>60mins ITU admission for GA
70
Complications of TC seizures
Hyperthermia Rhabdomylosis Lactic acidosis Respiratory failure Aspiration Hypotension
71
Rules for driviing with epilepsy
Stop driving + inform DBLA private car/motorcycle - 6 months initially LGV for 5 years + return once had an assessment from neurologist and has no clinical factors or investigation results (EEG/MRI) than show there is a risk for further seizures >2% per anum
72
When do you treat seizures
not until second epileptic seizure unless structural abnormality is discovered or EEG shows unoquivocal epileptic activity
73
Causes for decompensation of HF
Intercurrent illness MI Cardiac arrythmias HTN Inadequate fluid restriction Diet Lack of compliance with medications
74
ITU referral criteria in DKA
pH <7.1 'Severe DKA' - >6mmol, Bicarb <5 Hypokalaemia on admission below 3.5 GCS 12 Systolic <90 Significant comorbidity pregnant
75
Risk factors for delirium
Age >65 Dementia Multiple comorbidities Visual and hearing impairment REcent surgery Polypharmacy Drugs and alcohol dependence
76
Secondary causes of dementia
Metabolic (B12/Folate/Thiamine deficiency, Hypohyroid, Cushings, wilsons Vascular Cerebrovascular disease, subdural haematoma, Neoplastic Inflammatory Infections: Syphilis, HIV Drugs and toxins: heavy metal exposure
77
Medications for alzhimers
Donepezil (acetylcholinesterases) Memantine (NMDA antagonist) in severe disease (MMSE 3-14)
78
Common triggers for addinsonian crisis
Infection Surgery Anaesthesia Trauma Exogenois steroid withdrawl
79
Other autoimmune diseases assoicated with addisons
vitiligo, alopecia, coeliac, TDM, premature ovarian faillure, AI thyroid disease Called autoimmune polyendocrine syndrome
80
complication of rapid correction of hyponatraemia
cerebral pontine myelinosis Osmotic demyelination of nerves
81
Life threatening features of anaphylaxis
Airway - Swelling, hoarse voice, Stridor Breathing - Wheeze, Shortness of breath, Respiratory arrest Circulation: Pale, Clammy Tachycardia, Cardiac arrest, Shock
82
Common causes for anaphylaxis
Drugs/Iv infusions (abx, contrast, IV immunoglobins, blood products) Insect bites Food Other causes - latex, Hair dye
83
What should you do in a patient with anaphyaxis with threatened airway and inability to intubate
Emergency cricothyroidectomy 14G needle - 100%
84
Diarrhoea causes
Infective IBS Anxiety Inflammatory bowel disease Hyerthyroidism Malabsorption - pancreatic insufficiency, coeliac
85
Systemic signs of IBD
Aphthous ulcers Erythema nodosum Pyoderma gengrenosum Peripheral arthropathy Sacroiliitis Ank Spond Eye complications - uveitis
86
Signs of severe attack for IBD
>6 bloody stools/day Systemically unwell (pyrexial, tachycardic) Hb <10 Albumin <30 Toxic dilatation
87
Appearance of crohns on colonoscopy
Cobblestone Skip lesions/small bowel or upper GI disease US is colon only
88
Surgical management in crohns vs UC
30% UC patients require colectomy Urgency indications: colonic perforations, bleeding, toxic megacolon, fulminating disease (oxford criteria on Day 3) Crohns is not curative and only indicated for perforation, obstruction, abscess formation and fistulae High recurrence rate after surger
89
Important history points in Jaundice
PMH: Gallstones previous liver history, Diabets, recent blood transfusion FH: Gilberts, Wilsons, Haemachromatosis, Sickle cell, Spherocytotosis SH: IVDU, Tattoos, Vaccination history, alcohol, travel history (for malaria/dengue/thyphoid)
90
Signs of cirrhosis on clinical exam
Palmar erythema Clubbing Jaundice ecchymosis Track marks Gynecomastia Testicular atrophy Hepatomegaly Caput meduase Spider naevi abdominal distension
91
Causes for cirrhosis
Alcohol NAFLD AI hepatitis Hep B/C Wilsons Haemachromatosis PV thrombosis Budd Chiari PBC/PSC CF Alpha1 antirypsin Isoniazid, Methotrexate, Amiodarone
92
Causes for decompensated cirrhosis
Intercurrent infection (SBP, Pneumonia) Acute GI hemorrhage Hepatotoxic insult (alcohol, paracetamol, acute hepatitis) Drugs (diuretics, Sedatives, narcotics) Metabolic derrangements - Hypoglycaemia, electrolyte disturbance
93
Encephalopathy Grading
Grade 1 – Insomnia/reversal of day/night sleep pattern Grade 2 – Lethargy/disorientation Grade 3 – Confusion Grade 4 - Coma
94
Managing Chronic cirrhosis
Treat underlying disease (stop alcohol, Antivirals, immunosuppression in AI hepatitis) Abstinence from alcohol helps non ARCLD Screen complications (regular endoscopy, abdo US, AFP) Prophylactic abx for SBP diuretics/paracentesis for chronic abdominal distension + symptoms
95
Important factors ive missed for asthma exacerbation
- Abx if infected! - Discharge to GP and review in 48 hours for exacerbations - Check technique/remove exacerbating factors - Smoking cessation!
96
Causes for UGI Bleeds
- Mallory-weiss - AVMs - Gastritis - ingested blood
97
Additions in therapy for variceal bleeds
Terlipressin Antibiotics IV PPI Consider ITU (SB tube, CVC)
98
CI for terlipressin
IHD
99
Sepsis + Ra = ?
assess for neutropenic sepsis
100
Management of neutropenic sepsis in context of methotrexate/other immunosuppressants
The main cause of a sudden deterioration in patients taking methotrexate, who have previously been stable, is secondary to drug interactions and anything that might affect the excretion of methotrexate resulting in elevated drug levels. This is the likely cause of this presentation given the new AKI. The most common drug interaction which can lead to methotrexate toxicity is with NSAIDs which are commonly used in rheumatoid arthritis to manage flares of pain, inflammation and swelling. NSAIDs and methotrexate in combination can result in nephrotoxicity which reduces the excretion of methotrexate, leading to toxicity. Other common medications that would be important to ask about in the drug history would include recent penicillin use or proton pump inhibitor use. Additionally, I would like to know if the patient has been taking folic acid regularly. Folic acid is given in combination with methotrexate to reduce the toxic effects of methotrexate. Methotrexate inhibits the enzyme which converts folic acid into its active form, which is necessary for the synthesis of both DNA and RNA. If the patient has recently stopped taking folic acid, this may be a reason for the onset of myelosuppression for someone who has previously been stable.

IMT Interview (1 decks)

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