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Z CBL's > Medicine C > Flashcards

Medicine C Flashcards

1
Q

Criteria for diagnosing an AKI

A
  • Rise in creatinine of 26µmol/L or more in 48 hours
    OR
    > 50% rise in creatinine over 7 days OR

Fall in urine output to< 0.5ml/kg/hourfor more than 6 hours in adults (8 hours in children).
OR
>25% fall in eGFR in children / young adults in 7 days.

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2
Q

Key features of delirium:

A
  • Acute cognitive impairment.
  • Fluctuates (more severe at some times than others).
  • Affects attention.
  • Affects alertness (hyperactive / hypoactive / mixed).
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3
Q

Hypoactive delirium

A

Acute onset of fatigue, sleepiness and being more socially withdrawn.

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4
Q

Common causes of delirium:

A
  • D - Drugs and Alcohol (Anti-cholinergics, opiates, anti-convulsants, recreational)
  • E - Eyes, ears and emotional (sensory deficits)
  • L - Low Output state (MI, ARDS, PE, CHF, COPD)
  • I - Infection
  • R - Retention (of urine or stool)
  • I - Ictal
  • U - Under-hydration/Under-nutrition
  • M - Metabolic (Electrolyte imbalance, thyroid, wernickes
  • (S) - Subdural, Sleep deprivation
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5
Q

Screening tools for delirium

A

Two commonly used screening tools for delirium are the 4AT and the Confusion Assessment Method (CAM).

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6
Q

What makes up the 4AT?

A
  • Alertness
  • Abbreviated mental test-4 (age, dob, place, current year)
  • Attention - months backwards
  • Acute changes / fluctuation.
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7
Q

Delirium management

A

Management of delirium is predominantly to treat the underlying cause. Maintaining an environment with good lighting and frequent reassurance is helpful. In extremely agitated patients small doses of haloperidol or olanzapine may be considered.

Specialist MDT, lighting, glasses, hearing aids, avoid catheters and lines, visits from family, facilitate good sleep hygiene. Good nutrition.

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8
Q

Donepezil is what?

A

Acetylcholinesterase inhibitor for alzheimers.

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9
Q

Investigations for delirium:

A

Bloods: U&E’s, TFT’s, urinalysis, auditory and ophthalmology assessment, fluid status assessment. Confusion bloods.

DRE - constipation. Med review. MDT. Pain review.

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10
Q

What are confusion bloods?

A

Calcium, TFT’s, Glucose, B12.

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11
Q

What are the geriatric giants aka frailty syndromes?

A

Immobility
Incontinence
Impaired cognition
Instability (falls)

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12
Q

Severe life threatening injuries that arise from falls?

A

NOF
Brain injury
Spinal injury

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13
Q

Define orthostatic hypotension:

A

Fall of 20mmHg in systolic
or
Fall in 10mmHg in diastolic

within 3 minutes of standing

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14
Q

What most commonly causes orthostatic hypotension?

A

Iatrogenic - anti-hypertensives and diuretic use.

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15
Q

When should you screen for osteoporosis?

A
  • All women aged 65 and over.
  • All men aged 75 and over.
  • All women 50-64 and all men 50-74 who have osteoporosis risk factors or recurrent falls.
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16
Q

What do bloods in osteoporosis show?

A

Osteoporosis is commonly associated with normal blood test values (e.g. normal ALP, normal calcium, normal phosphate, normal PTH).

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17
Q

Following a fragility fracture in women ≥ 75 years, do what?

A

Following a fragility fracture in women ≥ 75 years, a DEXA scan is not necessary to diagnose osteoporosis and hence commence a bisphosphonate.

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18
Q

Risk factors assessed in the FRAX score:

A
  • History of glucocorticoid use
  • rheumatoid arthritis
  • alcohol excess
  • history of parental hip fracture
  • low body mass index
  • current smoking
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19
Q

Important potential causes of fragility fractures:

A

Metastatic bone disease
Multiple myeloma
Osteomalacia
Paget’s

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20
Q

Mobtiz type 1

A

long long drop

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21
Q

Mobtiz type 2

A

2:1 or 3:1 ratio P:QRS

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22
Q

How should mobitz type 2 be managed?

A

Definitive management is with a permanent pacemaker as thesepatients are at risk of risk of complete heart blockand becoming haemodynamically unstable.

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23
Q

Definitive management of 3rd degree heartblock

A

Permanent pacemaker due to the risk of sudden death.

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24
Q

Stroke + AF start what?

A

DOAC

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25
Q

When do use warfarin in post stroke management?

A

Warfarin used over DOAC’s in valvular AF e.g prosthetic valves.

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26
Q

Acute stroke management within 4.5hrs of onset?

A

Alteplase (tissue plasminogen activator) is indicated in patients presenting within4.5 hours of symptom onset

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27
Q

When can mechanical thrombectomy be performed?

A

Mechanical Thrombectomy can be performed in patients with anterior circulation strokes within 6 hours of symptom onset, provided that they have a good baseline functional status and lack of significant early infarction on initial CT scan. Mechanical Thrombectomy can also be performed in posterior circulation strokes up to 12 hours after onset.

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28
Q

Secondary stroke prevention: HALTSS

A
  • Hypertension: studies show there is no benefit in lowering the blood pressure acutely (as this may impair cerebral perfusion) unless there is malignant hypertension (systolic blood pressure >180 mmHg). Anti-hypertensive therapy should, however, be initiated 2 weeks post-stroke.
  • Antiplatelet therapy: patients should be administered Clopidogrel 75 mg once daily for long-term antiplatelet therapy. In patients with ischaemic stroke secondary to atrial fibrillation, however, warfarin (target INR 2-3. or a direct oral anticoagulant (such as Rivaroxaban or Apixiban) is initiated 2 weeks post-stroke.
  • Lipid-lowering therapy: patients should be prescribed high dose atorvastatin 20-80 mg once nightly (irrespective of cholesterol level this lowers the risk of repeat stroke).
  • Tobacco: offer smoking cessation support.
  • Sugar: patients should be screened for diabetes and managed appropriately.
  • Surgery: patients with ipsilateral carotid artery stenosis more than 50% should be referred for carotid endarterectomy.
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29
Q

Fluent aphasia or receptive aphasia. Speech remains fluent but makes little sense and commonly includes nonsense or irrelevant words. Interestingly, the person does not realise they are using incorrect words.

A

Wernicke’s aphasia - seen in house

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30
Q

What is Broaca’s aphasia?

A

This is classically caused by lesions affecting the frontal lobe and is called non-fluent or expressive aphasia. Patients have difficulty speaking fluently, and their speech may be limited to a few words at a time. Speech is halting or effortful. Generally, there are able to understand speech well and` maintain the ability to read.

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31
Q

What scoring system is used to assess for stroke?

A

Rosier scoring system

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32
Q

How does an ischaemic stroke present on CT?

A
  • May show areas of low density in the grey and white matter of the territory. These changes may take time to develop.
  • Other signs include the ‘hyperdense artery’ sign corresponding with the responsible arterial clot - this tends to visible immediately.
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33
Q

Dysarthria

A

Slurred speech

34
Q

Dysphagia

A

Difficulty producing speech

35
Q

Stroke mimics

A

MS
Migraine
Malignancy
Subdural / other bleed

36
Q

Management of AF

A
  • Conservative - Lifestyle, smoking cessation
  • Anticoagulation(based on CHA₂DS₂-VASc score) - direct-acting oral anticoagulants (DOACs) or warfarin
  • Rhythm control(if new onset, reversible, haemodynamically unstable, younger) - synchronised DC cardioversion, or pharmacological cardioversion (e.g. flecainide or amiodarone).
  • Rate control- beta-blocker (e.g bisoprolol), rate-limiting calcium channel blocker (e.g. verapamil, diltiazem), digoxin
  • Surgery- left atrial ablation, pace and ablate.

Address any underlying cause!

37
Q

When should you stop a DOAC before surgery?

A

24-48hrs before surgery dependent on risk.

38
Q

When to rhythm control AF?

A

Onset less than 48hrs or anti-coagulated for 3 weeks.

39
Q

SVT Management:

A
  1. Vagal manoeuvres:
    • Valsalva manoeuvre: e.g. trying to blow into an empty plastic syringe
    • carotid sinus massage
  2. Intravenous adenosine
    • rapid IV bolusof6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg
  3. Electrical cardioversion.
40
Q

When would you not give adenosine?

A

Contraindicated in asthmatics - verapamil is a preferable option.

41
Q

How to prevent future episodes of SVT?

A
  • Beta-blockers
  • Radio-frequency ablation (AV node re-entry tachycardia).
42
Q

Management of AMD?

A
  1. Vitamin supplementation A, C ,E + zinc
  2. Anti-VEGF (vaso endothelial growth factor)
  3. Laser photocoagulation for wet AMD
43
Q

Investigations for AMD?

A
  1. Slit lamp microscopy - shows any pigment, exudative, haemorrhagic changes.
  2. Ocular coherence tomography is used to visualise the retina in three dimensions.
  3. Amsler grid testing and visual fields assessment
  4. Funduscopy
44
Q

What is the management of an ischaemic stroke if the patient has a BP 185/110?

A

185/110 is a contraindication for thrombolysis. Need to give IV labetalol in boluses to reduce the BP first.

45
Q

Secondary prevention stroke management for anticoagulation?

A
  1. 300mg aspirin for 2 weeks after.

2a. Clopidogrel 75mg lifelong if non AF
2b. DOAC if in AF.

46
Q

What do the DVLA say about a patient who has had a stroke?

A
  1. Must not drive for 4 weeks.
  2. If reduced visual acuity may need referral for a driving assessment and ophthalmology review.
47
Q

Non-pitting oedema

A

High protein and salt content. Associated with conditions affecting the thyroid and lymphatic system.

48
Q

What is the triad of nephrotic syndrome?

A
  1. High proteinuria (>3.5g)
  2. Hypoalbuminaemia
  3. Peripheral oedema
49
Q

How to investigate nephrotic syndrome

A

Kidney biopsy generally required.

50
Q

What typically causes minimal change disease?

A

Idiopathic
NSAID use
Hodgkin’s lymphoma

51
Q

What is classed as hypoalbuminaemia

A

<30g/L

52
Q

What are the complications of nephrotic syndrome?

A
  1. Thrombotic disease - pts need to be started on LMWH.
  2. Hyperlipidaemia.
  3. Increased risk of infection (due to immunoglobulins being lost in the urine).
53
Q

Why do patients with nephrotic syndrome become in a hypercoagulable state?

A

Loss of inhibitory coagulation factors in the urine, and increased synthesis of procoagulatory factors by the liver.

54
Q

What is seen on kidney biopsy in minimal change disease?

A

Foot effacement of the podocytes

55
Q

How is minimal change disease managed?

A
  1. Steroids (highly responsive)
  2. Cyclophosphamide used in steroid-resistant cases.
56
Q

Causes of nephrotic syndrome:

A

Minimal change disease
FSGS
Minimal change nephropathy
Membranous nephropathy
Diabetic nephropathy

57
Q

What are the features of nephritic syndrome?

A
  1. Haematuria
  2. Hypertension
  3. Oliguria
  4. Fluid retention/Oedema
  5. Usually associated with reduced renal function.
58
Q

Pathology of nephrotic vs nephritic

A

Damage to the podocytes causes (heavy) proteinuria (nephrotic).

Glomerular injury caused by Autoantibodies or Immune complex deposition usually causes haematuria +/- mild to moderate proteinuria (nephritic).

59
Q

Management of diabetic nephropathy

A
  • Dietary protein restriction
  • Tight glycaemic control
  • BP control: aim for< 130/80 mmHg
  • ACE inhibitor or angiotensin-II receptor antagonist
    • should be start if urinary ACR of 3 mg/mmol or more
    • dual therapy with ACE inhibitors and angiotensin-II receptor antagonist should not be started
  • Control dyslipidaemia e.g. Statins
60
Q

Investigation for FSGS:

A
  • Renal biopsy
    • Focal and segmental sclerosis and hyalinosis on light microscopy
    • Effacement of foot processes on electron microscopy
61
Q

Management of FSGS:

A
  • Steroids +/- immunosuppressants
62
Q

Whats the most common cause of nephrotic syndrome in older people?

A

Membranous nephropathy

63
Q

How to distinguish between post-streptococcal glomerulonephritis and IgA nephropathy?

A

The key distinguishing factor is that post-streptococcal glomerulonephritis typically presents 3-4 weeks after a sore throat/skin infection whereas IgA nephropathy typically presents 3-4 days after a mild URTI.

64
Q

Causes of nephritic syndrome?

A

SHARP AIM

S - SLE
H - Henloch schonlein purpura
A - Anti-GBM (goodpastures)
R - Rapidly progressive glomerulonephrtitis
P - Post-streptococcal GN
A - Alport’s syndrome - sensorineural hearing loss. X-linked dominant.
I - IgA nephropathy (AKA Berger’s disease)
M - Membranoproliferative GN

65
Q

Management of nephrotic syndrome:

A
  1. Treat underlying cause.
  2. Symptomatic improvement - dietary sodium restriction + loop diuretic.
  3. ACE / ARB indicated due to anti-proteinuric properties (monitor BP and renal function).
  4. Normal protein intake.
  5. Avoid bed rest, LMWH due to hypercoagulable state.
  6. Vaccination needed in long-standing nephrotic syndrome (due to Ig loss in urine).
  7. Statin if long-standing hyperlipidaemia.
66
Q

What consideration is needed when giving patients with nephrotic syndrome a diuretic?

A

May need IV diuretics due to malabsoprtion due to gut mucosal oedema.

67
Q

HMG-CoA reductase inhibitor =

A

statin

68
Q

Polarised light microscopy shows what for what?

A

Gout - Negatively birefringent needle shaped crystals
Pseudogout - positively birefringent rhomboid crystals

69
Q

How is staph a described on gram stain?

A

Gram positive cocci in clusters

70
Q

Investigations for the hot joint:

A
  • Joint aspiration before any antibiotics are given. Joint aspirate shows WCC over 50,000 in SA.
  • Bloods: CRP / ESR / FBC /LFT / U&E’s / urate levels / CCP or RF
  • Renal profile - sepsis related AKI.
  • Blood Cultures to check for SA!
  • X-ray (can show chondrocalcinosis pg / trauma)
  • Urinalysis
  • MRI - osteomyelitis - Highly sensitive but also highly resource intensive.
  • Genital swabs - gonorrhoea / chlamydia.
71
Q

What criteria is used for SA?

A

Kocher’s criteria:
Fever >38.5
ESR >40
WCC >12
Non-weight bearing

72
Q

Risk factors for SA to ask about in an OSCE:

A
  1. Predisposition to infection (immunosuppression / alcohol)
  2. Damaged joints - RA / OA / Joint replacement
  3. Opportunistic infections: Skin wound / IVDU / IA steroid injections.
73
Q

What is anti-gbm?

A

Anti-glomerular basement membrane (GBM) disease (previously known as Goodpasture’s syndrome) is a rare type of small-vessel vasculitis associated with both pulmonary haemorrhage and rapidly progressive glomerulonephritis

74
Q

What is anti-gbm?

A

Anti-glomerular basement membrane (GBM) disease (previously known as Goodpasture’s syndrome) is a rare type of small-vessel vasculitis associated with both pulmonary haemorrhage and rapidly progressive glomerulonephritis

75
Q

Features of anti-gbm?

A
  • Pulmonary haemorrhage
  • Rapidly progressive glomerulonephritis
    • this typically results in a rapid onset acute kidney injury
    • nephritis → proteinuria + haematuria
76
Q

Investigations for anti-gbm?

A
  • Renal biopsy: linear IgG deposits along the basement membrane
  • Raised transfer factor secondary to pulmonary haemorrhages
77
Q

Management of anti-gbm aka goodpastures?

A
  • plasma exchange (plasmapheresis)
  • steroids
  • cyclophosphamide
78
Q

What scale is used to measure disability post stroke?

A

Modified Rankin scale (mRS)

79
Q

What type of stroke has the worst prognosis in terms of mortality?

A

TACS

80
Q

Scale used to assess for stroke in ED?

A

ROSIER Scale

81
Q

Follow up managment for a stroke patient:

A

HALTSS + echo + DVLA (1 month off driving if good functional recovery).

82
Q

TIA investigations:

A

Doppler, echo, ECG (24hour), MRI

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