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IMT Interview > IMT Interviews > Flashcards

IMT Interviews Flashcards

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
Q

Abdominal pain important differentials

A

Pyelonephritis
Acute Cholecystitis
Ectopic
DKA
Gastroenteritis
Bowel obstruction
lower LRTI
Acute pancreatitis
Acute hepatitis
Decompensated CLD

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26
Q

How many deaths worldwide are associated with antimicrobial resistance

A

5 million in 2019

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27
Q

Who kinds of countries are affected more by antimicrobial resistance

A

developing countries

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28
Q

Differentials for TIA

A

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

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29
Q

Management for TIA

A

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

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30
Q

What are the rules for TIA w driving

A

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

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31
Q

Apart from obvious in history what are some key points to ask about in history for SOB

A

Tb exposure, COVID + Vaccines
FH of cardiac problems, CF, alpha-1 antitrypsin

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32
Q

Clinic investigations for SOB

A

Sputum samples
ECG
FBC - (Thrombocytosis), UE, CRP
CXR
Spirometry + Peak flow
CT Chest if needed

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33
Q

PR Bleeds causes

A

Mesentric ischaemia
IBD
Infective gastroenteritis
Malignancy
Diverticulitis
Haemorrhoids/Tears

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34
Q

D dimer sensitivity

A

45%

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35
Q

What should be used in conjunction with D -dimer in assesment of VTE

A

Wells score

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36
Q

Definition for sepsis

A

life threatening organ dysfunction due to a dysregulated host response to infection

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37
Q

Definition for septic shock

A

Underlying circulatory and cellular/metabolic abnormalities that are profound enough to substantially increase mortality

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38
Q

Clinical indicators for septic shock

A

persistent hypotension requiring vasopressors to maintain MAP greater than or to 65mmHg, Lactate >2

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39
Q

Where did the sepsis 6 come from

A

Designed via the surviving sepsis campaign bundle

Bundle of therapies designed to reduce the mortality of patients with sepsis

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40
Q

Risk factors for sepsis

A

Malignancy
Age
Older than 65 years
Immunocompromise
Haemodialysis
Alcoholism
Diabetes

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41
Q

Overall mortality for sepsis

A

36%

42
Q

Differentials for unconciousness

A

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
Q

Common causes for hypoglycaemia

A

Alcohol
Insulin, SUs, Beta blockers, Salicylates, Quinines Pentamidine
Organ failure
Infection
Adrenal failure
Myxodema
Hypopituitarism
Insulinomas

44
Q

Driving rules with diabetes

A

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
Q

Differentials for headache

A

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
Q

What blood test is needed prior to LP

A

Clotting

47
Q

Symptoms for meningitis

A

Headache, neck stiffness and fever
Rash - meingoccoal usually
Confusion/Altered conciousness - may be the only symptoms
Focal neurological signs
Seizures

48
Q

How many patients are the classic symptoms of meningitis missing in

A

18%

49
Q

How many patient are seizures a presenting feature in

A

30%

50
Q

What should be done if someone has focal neurological deficit in the context of meningitis?

A

neuroimaging as there may be a abscess/encephalitis

51
Q

Commom bacterial causes meningitis

A

Neisseria meningitides
Step pneumonia
Listeria/GNB if immunocompromised or elderly

52
Q

Treatment for meningitis

A

Benpen if rash present
if no rash cefotaxime or ceftriaxone

53
Q

What should be done if pen allergic and needing treatment for meningitis

A

Urgent discussion with microbiology
may need vancomycin and chloramphenicol

54
Q

Guidelines for LPs in patients without a CT

A

only advised if:
- No septicaemia
- No focal neurological signs
- No decrease in conciousness

55
Q

CSF appearance in Viral vs Bacterial meningitis

A

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
Q

Who needs to be contacted if a case of meningitis is diagnosed

A

Public health England - advice on vaccination and will assist in contact tracing

Relatives/Close contacts - may need contact tracing

Local microbiology team

57
Q

Differnetials for purpuric rash and fever

A

Gonnoccaemia
Bacterial septicaemia with DIC
Haemotogical malignancy with septicaemia
HSP
Viral haemorrhagic fevers

58
Q

SVT causes

A

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
Q

How does adenosine work

A

Works on AV node by blocking conduction - causes transient heart block. Mediated by A1 receptor

60
Q

CI for adenosine

A

2nd or 3rd degree heart block without a pacemaker

Long QT

Decompensated HF

Asthma

61
Q

Symptoms of adenosine

A

Flushing
Light headedness
Sense of impending doom

62
Q

Dose for adenosine

A

6mg then 12mg if no effect

63
Q

What does it mean if adenosine doesn’t work

A

Nodal tachycardia ruled out
May be atrial instead

64
Q

Aside from adenosine what are therapies for SVT

A

TREAT UNDERLYING CAUSE

Beta blocker

Calcium channel blockers

if broad complex consider amiodarone

65
Q

How can SVTs be classified

A

site of origin (atrial/Nodal)
Rhythm regularity (regular/irregular)

66
Q

Time frame to give medication in a seizure

A

5 min

67
Q

How to treat seizures despite benzodiazepines

A

Call ITU may need admission for status

Consider phenytoim (needs cardiac monitor)

68
Q

Status epilepticus definition

A

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
Q

What is the definition of refractory seizures and their treatment

A

> 60mins

ITU admission for GA

70
Q

Complications of TC seizures

A

Hyperthermia
Rhabdomylosis
Lactic acidosis
Respiratory failure
Aspiration
Hypotension

71
Q

Rules for driviing with epilepsy

A

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
Q

When do you treat seizures

A

not until second epileptic seizure unless structural abnormality is discovered or EEG shows unoquivocal epileptic activity

73
Q

Causes for decompensation of HF

A

Intercurrent illness
MI
Cardiac arrythmias
HTN
Inadequate fluid restriction
Diet
Lack of compliance with medications

74
Q

ITU referral criteria in DKA

A

pH <7.1
‘Severe DKA’ - >6mmol, Bicarb <5
Hypokalaemia on admission below 3.5
GCS 12
Systolic <90
Significant comorbidity
pregnant

75
Q

Risk factors for delirium

A

Age >65
Dementia
Multiple comorbidities
Visual and hearing impairment
REcent surgery
Polypharmacy
Drugs and alcohol dependence

76
Q

Secondary causes of dementia

A

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
Q

Medications for alzhimers

A

Donepezil (acetylcholinesterases)
Memantine (NMDA antagonist) in severe disease (MMSE 3-14)

78
Q

Common triggers for addinsonian crisis

A

Infection
Surgery
Anaesthesia
Trauma
Exogenois steroid withdrawl

79
Q

Other autoimmune diseases assoicated with addisons

A

vitiligo, alopecia, coeliac, TDM, premature ovarian faillure, AI thyroid disease

Called autoimmune polyendocrine syndrome

80
Q

complication of rapid correction of hyponatraemia

A

cerebral pontine myelinosis

Osmotic demyelination of nerves

81
Q

Life threatening features of anaphylaxis

A

Airway - Swelling, hoarse voice, Stridor
Breathing - Wheeze, Shortness of breath, Respiratory arrest
Circulation: Pale, Clammy Tachycardia, Cardiac arrest, Shock

82
Q

Common causes for anaphylaxis

A

Drugs/Iv infusions (abx, contrast, IV immunoglobins, blood products)
Insect bites
Food
Other causes - latex, Hair dye

83
Q

What should you do in a patient with anaphyaxis with threatened airway and inability to intubate

A

Emergency cricothyroidectomy

14G needle - 100%

84
Q

Diarrhoea causes

A

Infective
IBS
Anxiety
Inflammatory bowel disease
Hyerthyroidism
Malabsorption - pancreatic insufficiency, coeliac

85
Q

Systemic signs of IBD

A

Aphthous ulcers
Erythema nodosum
Pyoderma gengrenosum
Peripheral arthropathy
Sacroiliitis
Ank Spond
Eye complications - uveitis

86
Q

Signs of severe attack for IBD

A

> 6 bloody stools/day
Systemically unwell (pyrexial, tachycardic)
Hb <10
Albumin <30
Toxic dilatation

87
Q

Appearance of crohns on colonoscopy

A

Cobblestone
Skip lesions/small bowel or upper GI disease

US is colon only

88
Q

Surgical management in crohns vs UC

A

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
Q

Important history points in Jaundice

A

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
Q

Signs of cirrhosis on clinical exam

A

Palmar erythema
Clubbing
Jaundice
ecchymosis
Track marks
Gynecomastia
Testicular atrophy
Hepatomegaly
Caput meduase
Spider naevi
abdominal distension

91
Q

Causes for cirrhosis

A

Alcohol
NAFLD
AI hepatitis
Hep B/C
Wilsons
Haemachromatosis
PV thrombosis
Budd Chiari
PBC/PSC
CF
Alpha1 antirypsin
Isoniazid, Methotrexate, Amiodarone

92
Q

Causes for decompensated cirrhosis

A

Intercurrent infection (SBP, Pneumonia)
Acute GI hemorrhage
Hepatotoxic insult (alcohol, paracetamol, acute hepatitis)
Drugs (diuretics, Sedatives, narcotics)
Metabolic derrangements - Hypoglycaemia, electrolyte disturbance

93
Q

Encephalopathy Grading

A

Grade 1 – Insomnia/reversal of day/night sleep pattern

Grade 2 – Lethargy/disorientation

Grade 3 – Confusion

Grade 4 - Coma

94
Q

Managing Chronic cirrhosis

A

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
Q

Important factors ive missed for asthma exacerbation

A
  • Abx if infected!
  • Discharge to GP and review in 48 hours for exacerbations
  • Check technique/remove exacerbating factors
  • Smoking cessation!
96
Q

Causes for UGI Bleeds

A
  • Mallory-weiss
  • AVMs
  • Gastritis
  • ingested blood
97
Q

Additions in therapy for variceal bleeds

A

Terlipressin
Antibiotics
IV PPI
Consider ITU (SB tube, CVC)

98
Q

CI for terlipressin

A

IHD

99
Q

Sepsis + Ra = ?

A

assess for neutropenic sepsis

100
Q

Management of neutropenic sepsis in context of methotrexate/other immunosuppressants

A

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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