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5th (Final year) > General Medicine #2 > Flashcards

General Medicine #2 Flashcards

1
Q

Causes of Mitral Regurgitation?

A

Leaflet:

  • Congenital
  • Endocarditis
  • Degenerative

Papillary muscle (MI/Marphans)

Dilatation

  • Cardiomyopathy
  • IHD
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2
Q

Signs of Mitral regurg?

A

Displaced apex beat (volume overload)

Quiet first heart sound

Pansystolic murmur - radiates to axilla

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3
Q

Two common valvular disorders secondary to rheumatic heart disease?

A

Aortic regurgitation

Mitral stenosis

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4
Q

Coarse of disease in Rheumatic Heart Disease?

A

Group A strep throat infection

2/4 weeks later = Acute Rheumatic Fever

Over 10-20 years there is repeated sub-clinical episodes, and/or autoimmune processes

then you get chronic rheumatic HD leading to leaflet thickening and fusion of commissures

  • Mitral stenosis
  • Aortic regurg
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5
Q

Features of mitral stenosis

A

Mid diastolic murmur

Loud first heart sound
- As blood is not freely flowing from left atrium the high pressures keep the valve open and then systole slams it shut = loud sound

Opening snap

Malar flush

AF

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6
Q

What’s the course of disease that results in Right heart failure in mitral stenosis?

A

High Left atrial pressure leads to…

high pulmonary pressure, which leads to…

Right ventricular hypertrophy…

Tricuspid regurgitation…

Right heart failure.

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7
Q

Causes of Aortic regurg (REALM)?

A

Rheumatic heart disease

Endocarditis

Ankylosing spondylitis

Leutic HD (tertiary syphilis)

Marphans

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8
Q

Is the apex displaced in Aortic regurg?

A

Yes - Volume overload

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9
Q

Features needed for ACS diagnosis?

A

Cardiac chest pain

Troponin

ECG changes

  • T wave inversion
  • ST elevation/Depression
  • Q waves
  • New LBBB
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10
Q

Investigations in cardiac ischaemia, and justification?

A

BOXES

Bloods
- FBC - anaemia can cause ischaemia
- U&Es - Impaired renal function - false positive trop. Hypo and Hyperkalaemia.
- Glucose - diabetic - aim for 4-11
- LFTs, baseline prior to statins
- Lipids
Serial trops

CXR

ECG

??Angiography/PCI

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11
Q

What is a good way to think of STEMI management (Dr Clarke)?

A

Immediate management - MONA

  • Morphine (& metoclopramide)
  • O2 if <94%
  • Nitrates (GTN sublingual)
  • Aspirin 300mg stat

Cardiology

  • PCI (or if >12hrs Alteplase)
  • Ticagrelor or clopidogrel loading dose (also IV hep or LMWH)
  • Angioplasty and stenting

Further preventative management (ABCDE)

  • ACE I
  • B-Blocker
  • Cholesterol lowering statin
  • Dual antiplatelets
  • Echo to assess left ventricular function
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12
Q

Maintenance antiplatelet regime following STEMI?

A

Clopidogrel 75mg daily OR Ticagrelor 90mg for 1 year

Aspirin 75mg daily indefinitely

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13
Q

Apart from ST elevation what other 2 sets of changes on the ECG are treated in the same way?

A

New LBBB

Posterior infarct (ST depression & R waves in V1 and V2)

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14
Q

Good way to think of NSTEMI/Unstable angina management?

A

Immediate (MONA)

  • Morphine (& metoclopramide)
  • O2 is sats <94
  • Nitrates sublingual
  • Aspirin 300mg stat

All patients (three things)

  • Aspirin 300mg
  • Nitrates or morphine to relieve chest pain if required
  • Clopidogrel 300mg

Then three things to consider:

  1. Coronary angiography
    - should be considered within 96 hours of first admission to hospital to patients who have a predicted 6-month mortality above 3.0%. It should also be performed as soon as possible in patients who are clinically unstable.

2 .Antithrombin treatment.
- Fondaparinux should be offered to patients who are not at a high risk of bleeding and who are not having angiography within the next 24 hours. If angiography is likely within 24 hours or a patient’s creatinine is > 265 µmol/l unfractionated heparin should be given.

  1. Intravenous glycoprotein IIb/IIIa receptor antagonists
    - (eptifibatide or tirofiban) should be given to patients who have an intermediate or higher risk of adverse cardiovascular events (predicted 6-month mortality above 3.0%), and who are scheduled to undergo angiography within 96 hours of hospital admission.
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15
Q

Presentation of patient in Acute LVF?

A

Inspection

  • Looks acutely unwell
  • Cold, clammy peripheries
  • Frothy blood stained sputum
  • Orthopnoeic, using accessory muscles
  • ?Wheeze

Obs

  • Tachycardia
  • Hypotension

Examination

  • Cardiomegaly - displaced beat, valve disease
  • 3rd and 4th Heart sounds
  • Right sided or bilateral pleural effusions
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16
Q

Radiographic changes in acute LVF?

A
  • Cardiomegaly
  • Upper lobe diversion
  • Diffuse mottling of lung fields
  • Prominent hilar shadows (bat wing appearance)
  • Pleural effusions
    Fluid in fissures
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17
Q

Investigations in acute Left ventricular failure?

A

BOXES

Bloods

  • FBC - exclude anaemia
  • U&Es - monitor renal function (with view to using diuretics)
  • Blood glucose - diabetes
  • BNP - SINGLE MEASUREMENT RAISED CONFIRMS DIAGNOSIS
  • ABG
  • Trop

Orifices
- NA

XRAY
- CXR

ECG

Special
- Echo

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18
Q

Causes of acute Left ventricular failure?

A

CHAMP

Coronary syndrome

Hypotensive emergency

Arrhythmia

Mechanical

  • Valve
  • VSD
  • LV aneurysm

PE

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19
Q

Acute management of acute LVF?

A

A-E assessment
- Secure airway if needed, consider O2

Sit patient up

15L hi flo by non-rebreathe

Drugs

  • 40mg Furosemide IV
  • IV GTN/Isosorbide mononitrate (If systolic >90)
  • Consider inotropes (>90 systolic)
  • Consider ITU
  • Opiates if chest pain

Escalate - Cardio/ITU

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20
Q

4 Indications for a permanent pacemaker?

A

SA nodal disease (Sick Sinus Syndrome)

Symptomatic 2nd or 3rd degree Heart block

AF with slow Ventricular rate, or refractory AF

Cardiac resynchronisation in HF

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21
Q

Investigations of infective endocarditis?

A

BOXES

Bloods

  • FBC (WCC)
  • ESR/CRP
  • Blood cultures (3 sets)

Orifices
- Urine dip

X
- CXR

ECG

Special
- echocardiogram

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22
Q

Presentation of AKI, in terms of obs and bloods?

A

Rise of creatinine >= 50% within 7 days

<0.5mg/kg/hr (<30) urine output

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23
Q

Which drugs need to be stopped in AKI?

A

The DAAMN Drugs

Diuretics
ACEI
ARII
Metformin
NSAIDS
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24
Q

Causes of CKD?

A

HIDDEN

HTN
Infection
Diabetes
Drugs
Exotic stuff - SLE and Vasculitis
Nephritis - Glomerulonephritis
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25
Q

At what point do you start to treat Aortic Stenosis?

A

Symptoms and > ABOVE 40mmhg aortic valve gradient

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26
Q

What are the points on the CHA(2)DS(2)VASc(S) score

A 
Congestive HF - 1 point
Hypertension - 1 point
Age - 1 if above 65, 2 if above 75
Diabetes - 1 point
Stroke or TIA - 2 points
VASc - Prev. Vascular disease - 1 point
Sex - 1 point for female
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27
Q

Anaphylaxis immediate drug management?

A

500micrograms adrenaline 1 in 1000
200mg hydrocortisone
10mg chlorphenamine

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28
Q

What would papillary muscle rupture secondary to MI look like?

A

ARRHT

Acute Mitral regurg - Pansystolic murmur
Reduced volume pulse
Raised JVP
Hypotension
Tachycardia
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29
Q

Drug treatment for torsades des pointes?

A

Magnesium sulphate IV

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30
Q

What is the management of peri-arrest tachycardias?

A

Broad complex regular

  • Assume VT
  • DC cardioversion if haemodynamic instability
  • Amiodarone if not

Broad complex irregular

  • AF with BBB (treat as if AF)
  • Torsades Des Pointes (IV Mag sulf)

Narrow complex regular

  • SVT
  • vagal manoeuvres followed by IV adenosine

Narrow complex irregular

  • AF
  • Cardiovert if <48hrs, rate control if not
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31
Q

What is the most common congenital cardiac defect to be found in adulthood? How do they present?

A

ASD

Ejection systolic murmur (split S2)

Embolism may pass from venous side to cause a stroke

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32
Q

At what QRISK do you prescribe statins?

A

> 10%

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33
Q

What is a bisferiens pulse associated with?

A

Aortic valve disease

HOCM

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34
Q

How long is the QT normally?

A

10 small boxes (2 big squares)

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35
Q

Where are keloid scars most likely to form?

A

Sternum

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36
Q

What area of the skin do pemphigoid antibodies taret?

A

Desmosomes (the things that join the cells together)

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37
Q

What is erythroderma? What are the causes?

A

A rash that involves 95% of the skin

Causes:

  • eczema
  • psoriasis
  • drugs e.g. gold
  • lymphomas, leukaemias
  • idiopathic
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38
Q

Pharmacological treatment of scabies?

A

permethrin 5% is first-line
malathion 0.5% is second-line

Pruritus can persist for up to 6 weeks after treatment

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39
Q

Psoriasis management?

A
  • Regular emollients
    1. First-line: Potent corticosteroid applied OD plus vitamin D analogue applied OD (applied separately) for up to 4 weeks.
    2. Second-line: if no improvement after 8 weeks then offer a vitamin D analogue twice daily
    3. Third-line: if no improvement after 8-12 weeks then offer either: a potent corticosteroid applied twice daily for up to 4 weeks or a coal tar preparation applied once or twice daily
  • Short-acting dithranol can also be used
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40
Q

What is Leukoplakia?

A

Leukoplakia is a premalignant condition which presents as white, hard spots on the mucous membranes of the mouth. It is more common in smokers.

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41
Q

What is Lentigo Maligna? How does it present?

A

Lentigo maligna is a precursor to lentigo maligna melanoma. It begins as a suspicious flat freckle which can grow over 5-20 years to develop into melanoma.

Sun exposed skin.

Like a melanoma - key think is slow growth, like a melanoma.

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42
Q

What is Necrobiosis lipoidica diabeticorum, how does it present?

A
  • Shiny, painless areas of yellow/red skin typically on the shin of diabetics
  • Often associated with telangiectasia
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43
Q

What colour ca actinic keratoses be?

A

May be pink, red, brown or the same colour as the skin

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44
Q

What are curlings ulcers?

A

Stress ulcers in burns patients. Can bleed.

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45
Q

How can Acral lentiginous melanoma present?

A

Hutchinsons sign - nail bed

Enlarging discoloured skin patch on the palms, fingers, soles or toes with the characteristics of other flat forms of melanoma

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46
Q

Causes of acute addisonian crisis?

A
  1. Sepsis or surgery causing an acute exacerbation of chronic insufficiency (Addison’s, Hypopituitarism)
  2. Adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcemia)
  3. Steroid withdrawal
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47
Q

What is the bug in rheumatic fever?

A

Strep Pyogenes

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48
Q

Cardiac drug typically associated with angiodema?

A

ACEI

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49
Q

How long does a mouth ulcer have to be there to warrant a 2ww cancer pathway referral?

A

3 weeks

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50
Q

What is Ludwigs Angina? How does it present?

A

Cellulitis at the floor of the mouth, presents in patients with poor dentition who are immunocompromised (IVDU).

Pts get malaise, fever and dysphagia progressing to airway obstruction.

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51
Q

What is Sialolithiasis and Sialadenitis?

A

Sialolithiasis

  • Stones in Whartons duct
  • Pts get facial pain, and swelling of the submandibular gland

Sialadenitis

  • Post-staph aureus infection
  • May see pus
  • Can get submandibular abscess
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52
Q

What are stensens duct and whartons duct?

A

Stensen’s duct is in the Parotid

Wharton’s is the submandibular, W = Lower down

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53
Q

Management of sudden onset sensorineural hearing loss?

A

Urgent ENT referral and High dose steroids

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54
Q

What cardiac abnormality is acromegaly associated with?

A

Cardiomegaly

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55
Q

What is Acute Necrotizing Ulcerative Gingivitis (ANUG)? Management?

A

On a spectrum of disease from simple Halitosis to ANUG.

Painful bleeding gums with halitosis and punched-out ulcers on the gums

Management:

  • Paracetamol
  • Chlorhexidine mouthwash
  • Metronidazole
  • Refer to dentist
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56
Q

Management of a pituitary adenoma

A

Depends on type

Prolactinoma
- Bromocriptine

Micro/Macro

  • Definitive is neurosurgery
  • Micro has better success rates
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57
Q

What is a Sistrunk’s procedure for?

A

Thyroglossal cyst.

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58
Q

How does MODY (diabetes) present? Management?

A

T2DM in those <25 y/o, FH.

Manage with Sulphonylureas.

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59
Q

Causes of a raised prolactin?

A 
Pregnancy
Prolactinoma
Physiological
Polycystic ovarian syndrome
Primary hypothyroidism
Phenothiazines, metocloPramide, domPeridone
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60
Q

What is C peptide, how does it normally react to exogenous insulin? If this is abnormal, likely diagnosis? What is it like in T1 and T2 DM?

A

C peptide is produced when insulin is produced, so when exogenous insulin is given it should fall.

If it does not fall - insulinoma

It is low in T1DM
It is normal/high in T2DM

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61
Q

What is Whipples triad for insulinoma?

A

Symptoms and signs of hypoglycemia

Plasma glucose < 2.5 mmol/L

Reversibility of symptoms on the administration of glucose

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62
Q

Causes of gingival hyperplasia?

A

Phenytoin
Ciclosporin
Calcium channel blockers

AML

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63
Q

Palpable abdominal mass in child (<15 y/o) warrants what management option?

A

48 hour referral to secondary care to exclude wilms tumour of nephroblastoma

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64
Q

Management of addisonian crisis?

A

Hydrocortisone 100mg IV/IM

1L N Saline over 60 mins (w/ dextrose if hypoglycaemic)

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65
Q

If a postmenopausal woman has suffered a fracture, what is the management plan?

A

Treat as osteoporosis

- Risendronate and calcium supplementation

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66
Q

What is erythrasma? Treatment?

A

Erythrasma is a generally asymptomatic, flat, slightly scaly, pink or brown rash usually found in the groin or axillae.

Topical miconazole/antibacterial

Or ORAL erythromycin (if extensive)

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67
Q

Orlistat mechanism of action?

A

Pancreatic lipase inhibitor

lose weight

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68
Q

Management of actinic keratoses?

A
  1. Prevention of further risk: e.g. sun avoidance, sun cream
  2. Fluorouracil cream: typically a 2 to 3 week course. The skin will become red and inflamed - sometimes topical hydrocortisone is given following fluorouracil to help settle the inflammation
  3. Topical diclofenac: may be used for mild AKs. Moderate efficacy but much fewer side-effects
  4. Topical imiquimod: trials have shown good efficacy
    cryotherapy
  5. curettage and cautery
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69
Q

How many skin types are there?

A

1-6

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70
Q

How do you differentiate between a Cystic hygroma and a Branchial cyst?

A

Cystic Hygroma

  • Present at birth
  • Transilluminates better than branchial
  • POSTERIOR triangle, multilobulated

Branchial cyst

  • Fluid has Cholesterol
  • Usually transilluminates
  • Teens/young adults
  • Anterior triangle, at level of the hyoid.
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71
Q

PE typically causes what pattern on ABG?

A

Respiratory alkalosis (hyperventilation)

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72
Q

What syndrome is associated with coarctation of the aorta?

A

Turners

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73
Q

ECG changes in hypothermia?

A 
bradycardia
'J' wave - small hump at the end of the QRS complex
first degree heart block
long QT interval
atrial and ventricular arrhythmias
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74
Q

Management of acute and prophylaxis of variceal haemorrhage?

A

Propranolol for prophylaxis

Acute - terlipressin

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75
Q

Presentation of villous adenoma?

A

Non-specific lower gastrointestinal symptoms

Secretory diarrhoea may occur

Microcytic anaemia

Hypokalaemia

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76
Q

What is Plummer-Vinson Syndrome? Triad?

A

Rare disease, unknown cause

Triad of:

  • Dysphagia (secondary to oesophageal webs)
  • Glossitis
  • Iron-deficiency anaemia
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77
Q

Treatment in acute pheochromocytoma?

A

Phenoxybenzamine

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78
Q

How do you treat VT?

A

Haemodynamically unstable
- Synchronised DC cardioversion

Haemodynamically stable
- IV amiodarone

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79
Q

What is the starting regime for newly diagnosed Type 1 diabetics?

A

basal–bolus using twice‑daily insulin detemir

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80
Q

What murmurs are a VSD, ASD and Tetralogy of Fallot associated with?

A

VSD
- Pansystolic

ASD
- Ejection systolic, split s2, heard at the back

Tetralogy of fallot
- Ejection systolic

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81
Q

What diabetic medication increases risk of osteoporosis?

A

Thiazolidinediones

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82
Q

Management of acne rosacea?

A

mild/moderate: topical metronidazole

severe/resistant: oral tetracycline

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83
Q

In arteriovenous fistula which vein is usually connected to he radial artery?

A

The cephalic vein

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84
Q

Why do long term dialysis patients need a AV fistula?

A

Easy access to high flow, high pressure arterial blood

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85
Q

Apart from an AV fistula what two other methods could you use for dialysis?

Drawbacks?

A

Dual-lumen tunneled catheter, centrally placed (for AKI mostly)
- Drawback is a high recirculation rate

Peritoneal dialysis
- Risk of infection

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86
Q

What questions can you ask to assess someone’s CKD symptoms?

A
  1. What are your energy levels like?
  2. Do you get breathless?
  3. Do you suffer from itching? (pruritis)
  4. Bone pain, or gout?
  5. Numb or tingling feeling? (parasthesia)
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87
Q

Three common causes of tiredness (Dr Clarke)?

A

Anaemia
Solute retention (CKD)
Psychosocial

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88
Q

Three common causes of breathlessness (Dr Clarke)

A

Anaemia
Fluid overload (e.g.CKD)
heart failure

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89
Q

Why does CKD lead to peripheral neuropathy?

A

Retention of beta-2-microglobulin

Diabetes is a common cause of CKD

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90
Q

Features of CKD (mnemonic)?

A

BIG BEAN

Breathlessness
Itching
Gout

Bone pain
Energy low
Ankle swelling
Neuropathy

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91
Q

Features of Nephrotic syndrome?

A

Proteinuria (>3g in 24hrs)

Hypoalbuminaemia (<30g/dl)

Oedema (loss of protein oncotic pressure allows salt and water into ECF)

Hypercholesterolaemia (liver synthesised more cholesterol)

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92
Q

Main cause of nephrotic syndrome in children?

A

Minimal change disease often Idiopathic (steroid responsive)

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93
Q

Main cause of nephrotic syndrome in adults?

A

Glomerulosclerosis - especially due to diabetes

Membranous glomerulonephritis (usually idiopathic)

Amyloidosis

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94
Q

Treatment of nephrotic syndrome?

A

Diuretics and salt restriction for oedema

Minimal change - Steroids +/- cyclophosphamide

ACEI (reduced protein excretion)

Anticoagulation (there is hypercoagulation)

Statins

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95
Q

Features of acute nephritis/Acute nephritic syndrome?

A

Abnormal HOST response?

Hypertension
Oliguria
Smoky brown haematuria with casts
Trace of oedema

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96
Q

Causes of acute nephritic syndrome?

A

Post strep
IgA nephritis
Vasculitis - SLE

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97
Q

Special investigations in acute nephritis?

A

Throat swab
ASO titre
24hr urinary protein

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98
Q

Treatment of acute nephritis?

A

Penicillin in Streptococci present

Salt restriction and anti-hypertensive drugs

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99
Q

What is glomerulonephritis, what is it made up of roughly?

A

Basically any condition that leads to inflammation of the glomerulus or the nephrons

Divided up into roughly nephrotic presentation or nephritic presentation.

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100
Q

What is haemolytic uraemic syndrome? Presentation? management?

A

Triad of:

  • acute renal failure
  • microangiopathic haemolytic anaemia
  • thrombocytopenia

Occurs commonly in young children, after dysentry

Management is supportive

101
Q

Features of Dominant PCKD?

A 
Hypertension
Recurrent UTIs
Abdominal pain
Renal stones
Haematuria
CKD

Has extra-renal manifestations causing

  • Berry aneurysms - SAH
  • Liver cysts (also pancreas, spleen)
102
Q

What are the main causes of a normal anion gap metabolic acidosis?

A

Dehydration
Addisons
Renal tubular acidosis

103
Q

What is goodpasture’s syndrome?

A

Anti-glomerular basement membrane antibodies against type IV collagen. More common in men.

Presents with:

  • Pulmonary haemorrhage
  • Followed by rapidly progressive glomerulonephritis
104
Q

Differences in presentation of IgA nephritis and Post-strep glomerlulonephritis

A

IgA

  • 1-2 days after URTI
  • Large macroscopic Haematuria

Post-strep

  • 1-2 weeks after
  • Proteinuria

Both can be associated with haematuria

105
Q

How does Recessive PCKD present?

A

Normally in very young children or within the womb. Newborn children may have potter’s syndrome (due to oligohydramnios)

106
Q

What is the mode of inheritance of alports syndrome, how does it present?

A

X linked dominant

  1. microscopic haematuria
  2. progressive renal failure
  3. bilateral sensorineural deafness
  4. retinitis pigmentosa
  5. lenticonus: protrusion of the lens surface into the anterior chamber

Renal biopsy: splitting of lamina densa seen on electron microscopy

107
Q

What is Renal papillary necrosis?

How does it present?

What are it’s causes?

A

Renal papillary necrosis describes the coagulative necrosis of the renal papillae due to a variety of causes.

Presentation:

  • visible haematuria
  • loin pain
  • proteinuria

Causes

  • pyelonephritis
  • diabetic nephropathy
  • obstructive nephropathy
  • analgesic nephropathy
  • sickle cell anaemia
  • Acute interstitial nephritis
108
Q

What are the differences between the two types of autosomal dominant polycystic kidney disease?

A

Type 1

  • Chromosome 16
  • More common (85%)
  • Presents earlier

Type 2

  • Chromosome 4
  • 15% of cases
109
Q

What does fanconi syndrome result in?

A

Type 2 (proximal) renal tubular acidosis,
Rickets/osteomalacia
Polyuria

110
Q

What is Membranoproliferative glomerulonephritis (IgA)? Overview?

A

Also known as mesangiocapillary glomerulonephritis or IgA nephropathy

May present as nephrotic syndrome, haematuria or proteinuria.

Associated with subcut tissue loss from face

Poor prognosis

111
Q

First option for renal replacement in independent patients?

A

First option is peritoneal dialysis, if not contraindicated (abdo pathology)

112
Q

Mainstay treatment in rhabdomyolysis?

A

IV fluid resus (normal saline)

113
Q

What is Dialysis disequilibrium syndrome?

A

Dialysis disequilibrium syndrome is a rare complication and usually affects those who have recently started renal replacement therapy. It is caused by cerebral oedema,

114
Q

WHat type of syndrome does proliferative and non-proliferative glomerulonephritis cause?

A

Generally proliferative glomerulonephritis causes nephritic syndrome and non-proliferative glomerulonephritis causes nephrotic syndrome

115
Q

How do you calculate the anion gap?

A

([Na+] + [K+]) - ([Cl] + [HCO3]) Normal is 8-14

116
Q

What type of AKI causes proteinuria?

A

Intrinsic only

117
Q

Normal range for anion gap?

118
Q

What rise in Creatinine and Fall in eGFR is acceptable following CKD treatment with ACEI?

A

NICE suggest that a decrease in eGFR of up to 25% or a rise in creatinine of up to 30% is acceptable

119
Q

How do you screen for diabetic nephropathy?

A

all patients should be screened annually
albumin:creatinine ratio (ACR) in early morning specimen
ACR > 2.5 = microalbuminuria

120
Q

Diabetes insipidus gives what result on the plasma and sodium osmolality?

A

Diabetes insipidus is characterised by a high plasma osmolality and a low urine osmolality

Not enough ADH/not responding

SO can’t concentrate the urine to shift the concentrated Na+ in the plasma.

Aquaporins are there to draw the water out na concentrate the urine so that plasma osmolality can be reduced

121
Q

Presentation of renal cell carcinoma?

A

Classical triad: haematuria, loin pain, abdominal mass

Can also get pyrexia and left varicocele

122
Q

Common cause of bacterial otitis media?

A

Haemophilus influenzae

123
Q

In dehydration the rise in urea or creatinine is higher?

A

Urea is much higher

Creatinine is high in AKI

124
Q

Complications of nephrotic syndrome?

A
  1. Increased risk of infection due to urinary immunoglobulin loss
  2. Increased risk of thromboembolism related to loss of antithrombin III and plasminogen in the urine. This may result in a renal vein thrombosis, resulting in a sudden deterioration in renal function.
  3. Hyperlipidaemia
  4. Hypocalcaemia (vitamin D and binding protein lost in urine)
  5. AKI
125
Q

If the GFR is lowered to stage 1/2 levels can you diagnose CKD on this alone?

A

No, you also need symptoms or signs of disease.

126
Q

What is the glucose requirement for patients, when prescribing fluids?

A

When prescribing fluids, the glucose requirement is 50-100 g/day irrespective of the patient’s weight

127
Q

What type of renal dysfunction does rhabdomyolysis cause?

A

Renal tubular necrosis

128
Q

What stage of pregnancy can pre-eclampsia occur?

A

> 20 weeks

129
Q

At what rate should you prescribe fluids?

A

30 ml/kg/24hr.

130
Q

Tiredness on CKD is commonly caused by what?

131
Q

What conditions cause enlarged kidneys on USS?

A

HIV associated nephropathy
Autosomal dominant polycystic kidney disease
Diabetic nephropathy
Amyloidosis

132
Q

How does amyloidosis typically present?

A

Typically 50-65 yrs, with breathlessness and weakness.

Can affect any organ in the body, commonly renal failure, with organomegaly.

133
Q

What are the intrarenal causes of AKI?

A

Main ones:

  1. Acute tubular necrosis
  2. Interstitial nephritis
  3. Acute Glomerulonephritis
134
Q

How can you use a urine dip to differentiate the causes of AKI?

A

(May be incomplete)

Nitrites - infection

Protein - Intra-renal cause

Blood - High in Nephritic syndrome (GN)

Leukocytes - high in infection, or in interstitial nephritis

135
Q

What are the 4 phases of sub acute (de quervain’s) thyroiditis?

A

phase 1 (lasts 3-6 weeks): hyperthyroidism, painful goitre, raised ESR

phase 2 (1-3 weeks): euthyroid

phase 3 (weeks - months): hypothyroidism

phase 4: thyroid structure and function goes back to normal

136
Q

What medications do you usually have to give to kids with turner’s syndrome?

A

Growth Hormone

137
Q

What is acute tubular necrosis?

  • Presentation
  • Causes
A

Most common cause of intra-renal AKI.

Presents as:

  • AKI
  • Muddy brown casts
  • Proteinuria on dipstick

Most commonly caused by :

  • Renal ischaemia e.g. shock, sepsis
  • Toxins: aminoglycosides, rhabdomyolysis, tumour lysis, heavy metals
138
Q

What is Interstitial nephritis?

  • Presentation
  • Causes
  • Complications
A

One of the causes of AKI (can also cause other renal pathology)

Presents as intra-renal AKI, also:

  • Fever, rash, arthralgia
  • Hypertension
  • Eosinophiluria (immune reaction)

Caused by immune reaction to drugs, such as:
- NSAIDS

Can lead to renal papillary necrosis

  • Haematuria
  • Flank pain
139
Q

What is acute glomerulonephritis? Presentation?

A

Presentation:

  • Haematuria
  • Proteinuria
  • Oedema
  • Hypertension
  • Can present as AKI
  • Can present as nephritic syndrome
140
Q

What is glomerulosclerosis? Presentation?

A

Sclerosis of glomeruli, caused by a dew different conditions

Commonly diabetes and hypertension

141
Q

What is minimal change disease Presentation?

A

Type of Glomerulonephritis

- presents as nephrotic syndrome.

142
Q

In post renal AKI, what are the causes of obstruction?

A

Ureters

  • Malignancy
  • Stone
  • Stricture

Bladder

  • Malignancy
  • Stone
  • Neuropathic

Urethral

  • Malignancy
  • Stone
  • BPH
  • Stricture
  • Infection
  • trauma

Catheter

  • Sediment
  • Clots
143
Q

In post renal AKI, what are the causes of obstruction?

A

Ureters

  • Malignancy
  • Stone
  • Stricture

Bladder

  • Malignancy
  • Stone
  • Neuropathic

Urethral

  • Malignancy
  • Stone
  • BPH
  • Stricture
  • Infection
  • trauma

Catheter

  • Sediment
  • Clots
144
Q

Complications of AKI?

A

Hyperkalaemia

Pulmonary oedema

Acidosis

Uraemia

145
Q

Indications for dialysis?

A

Hyperkalaemia >7 - resistant to treatment

Pulmonary oedema - resistant to treatment

Metabolic acidosis - pH <7.2

Uraemia - pericarditis, encephalopathy

146
Q

General management strategy for AKI?

A

Correct fluid balance
Stop nephrotoxic drugs

Treat cause

Manage complications

147
Q

What are the types of glomerulonephritis?

A

Minimal change.
Diffuse: affecting all glomeruli
Focal: affecting only some of the glomeruli.
Segmental: only affecting parts of an affected glomerulus

148
Q

Treatment of choice for trigeminal neuralgia?

A

Carbemazepine

149
Q

What are the findings of lateral medullary syndrome?

A

Wallenberg’s syndrome - Inferior posterior cerebellar artery infarct

Ipsilateral

  • ataxia,
  • nystagmus
  • dysphagia
  • facial numbness
  • cranial nerve palsy e.g. Horner’s

Contralateral
- limb sensory loss

150
Q

What are the findings of Weber’s syndrome?

A

Brainstem infarct:

  1. ipsilateral III palsy
  2. contralateral weakness
151
Q

How do you classify strokes?

A

Use the three main criteria for anterior circulation.

  1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
  2. homonymous hemianopia
  3. higher cognitive dysfunction e.g. dysphasia

Total anterior circulation (middle and anterior cerebral arteries)
- All three present

Partial anterior circulation (a division of the anterior/middle arteries)
- 2 of the criteria

Posterior circulation stroke, 1 of the following

  1. cerebellar or brainstem syndromes
  2. loss of consciousness
  3. isolated homonymous hemianopia

Lacunar infarct (basal ganglia):

  1. unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
  2. pure sensory stroke.
  3. ataxic hemiparesis

Then the odd syndromes

  • Lateral medullary
  • Webers (brainstem)
152
Q

What is a quick and easy bedside test to perform to confirm that fluid is CSF?

A

Check glucose

not present in mucous

153
Q

What is a colles fracture, what structure is commonly damaged?

A

Fall on outstretched hands, fractures radius

Damages MEDIAN nerve.

154
Q

Basically what does pyramidal and extrapyramidal refer to? (Dr clarke)

A

Both refer to movement

Extrapyramidal essentially refers to the basal ganglia’s role in movement, and their tracts

  • Initiation (Direct/indirect)
  • Postural reflexes

Pyramidal refers to UMN tracts (corticospinal)

155
Q

Difference in clasped knife and lead pipe rigidity?

A

Clasped pipe give way

Lead pipe has rigidity the whole way

156
Q

What abnormalities of tone might you find on neurological examination?

A

Clasped pipe rigidity, lead pipe rigidity, cogwheel rigidity

157
Q

Causes of peripheral neuropathy?

A 
Alcohol
B12 deficiency
CKD 
Diabetes and drugs
Every vasculitis

Plus

  • Cancer (paraneoplastic)
  • Lyme disease
  • CHarcot marie tooth
158
Q

What are the cerebellar signs, mnemonic?

A

DANISH

Dysdiadokinesis
Ataxia 
Nystagmus 
Intention tremor 
Staccato speech - west register street, baby hippopotamus, british constitution.
Hypotonia
159
Q

What do you do to test hand function on examination? (Dr Clarke)

A

Grip
Pincer grip
Prayer sign
FIne movement (play the piano with your fingers)

160
Q

What muscle is pincer grip testing, what does an abnormal (froments) sign look like?

A

Adductor policis brevis

frOments (like an O)

161
Q

Why do you do thrombolysis in stroke?

A

To salvage the ischaemic penumbra

162
Q

SIgns of an ulnar nerve palsy?

A

Sensory loss over fifth finger and ulnar half of the fourth finger

Weakness and wasting of first dorsal interosseus

163
Q

Weakness in what causes a claw hand?

A

Weakness of the lumbricals

164
Q

Signs of optic neuropathy?

A 
Pale disc - due to optic atrophy (after optic neuritis)
Loss of visual acuity
Loss of red colour vision
Central scotoma
Afferent pupillary defect
165
Q

Causes of optic neuropathy?

A

Demyelination
Trauma
Compression (pit tumours)
Ischaemic - diabetes

166
Q

Why do you get sparing of the upper face in UMN lesion?

A

Bilateral cortical representation

167
Q

Management of bells palsy?

A

High dose steroids (if within 72hrs)

Eye drops during day
Tape to close eye at night

168
Q

Early parkinsons management?

A

L dopa

DA agonist if less disabled
- Ropinirole

169
Q

Late PD management?

A

DA agonists
- Ropinirole

COMT inhibitors
- Entacapone

MAOB inhibitors
- selegiline

170
Q

Sever PD management?

A

Apomorphine (Non selective DA agonist)

Deep brain stim

171
Q

Treatment of an acute MS attack?

A

IV methylpred 3 days

172
Q

Signs of a complete occulomotor palsy?

A

Pupil down and out

Partial ptosis

173
Q

Causes of a complete occulomotor palsy

A

Diabetes

Posterior communicating artery aneurysm

  • usually painful
  • if painful RULE THIS OUT

Raised ICP

174
Q

What signs do you get on horners syndrome?

A

Lack of parasympathetic

Constricted pupil
Slight ptosis
Reduced sweating over forehead

175
Q

SIgns and causes of a sixth nerve palsy?

A

Failure of abduction (LR6)

Eye is adducted inwards

Can be many things

  • Diabetes
  • Trauma
  • Raised ICP
  • MS
  • Idiopathic
176
Q

What is myotonic dystrophy? Presentation?

A

Myotonic dystrophy is an inherited myopathy with features developing at around 20-30 years old.

Autosomal dominant.

Frontal balding
Bilateral ptosis
Cataracts
Dysarthria

177
Q

What is huntington’s disease? Presentation and such

A

Autosomal dominant

Chorea

Personality changes (e.g. irritability, apathy, depression) and intellectual impairment

Dystonia

saccadic eye movements

178
Q

What is Neuroleptic malignant syndrome

  • causes
  • features
A

Caused by antipsychotics. Carries 10% mortality rate.

  1. pyrexia
  2. rigidity
  3. tachycardia
179
Q

Treatment of neuroleptic malignant syndrome?

A

IV fluids, stop drug

Dantrolene (muscle relaxant) or bromocriptine (DA antag)

180
Q

Medications first line for focal and for generalized seizures?

A

Valproate - generalised

Carbamazepine - focal

181
Q

Treatment for ALS?

A

Riluzole:

  1. Prevents stimulation of glutamate receptors
  2. Used mainly in amyotrophic lateral sclerosis
  3. Prolongs life by about 3 months

Respiratory care

  • non-invasive ventilation (usually BIPAP) is used at night
  • studies have shown a survival benefit of around 7 months
182
Q

What is Friedreich’s ataxia?

A

Teenage onset hereditary ataxia. autosomal recessive.

  1. absent ankle jerks/extensor plantars
  2. cerebellar ataxia
  3. optic atrophy
  4. spinocerebellar tract degeneration
183
Q

What is astereognosis, what lobe would cause it?

A

Tactile agnosia - cannot recognise objects from their feel

Parietal lobe

184
Q

What are the two main dystrophinopathies, how are they different?

A

Duchenne muscular dystrophy

  • <5 years
  • Learning disability

Becker muscular dystrophy

  • > 10 years old
  • No learning difficulty
185
Q

What is the ischaemic stroke thrombolysis window?

A

4.5 hours (when CT scan has excluded haemorrhage)

186
Q

What are the four types of motor neurone disease?

What has the best, and what has the worst prognosis?

A

ALS (50%)
- LMN signs in arms and UMN in legs

Primary lateral sclerosis
- UMN only

Progressive muscular atrophy

  • LMN signs only
  • Best prognosis

Progressive bulbar palsy

  • Palsy of tongue
  • Worst prognosis
187
Q

Features of restless leg syndrome?

A
  • Uncontrollable urge to move legs (akathisia). Symptoms initially occur at night but as condition progresses may occur during the day. Symptoms are worse at rest
    paraesthesias e.g. ‘crawling’ or ‘throbbing’ sensations
    movements during sleep may be noted by the partner - periodic limb movements of sleeps (PLMS)
188
Q

Treatment for restless leg syndrome?

A

Ropinirole

189
Q

What is ataxic telangiectasia?

A

Ataxic telangiectasia is an autosomal recessive disorder caused by a defect in the ATM gene which encodes for DNA repair enzymes.

One of the inherited combined immunodeficiency disorders. Other is friedreichs ataxia.

190
Q

Main difference/esiest to differentiate between friedreichs ataxia and ataxic telangiectasia?

A

Ataxic telangiectasia presents earlier (1-2 years)

191
Q

What is the aetiology of myasthenia gravis?

A

Myasthenia gravis is an autoimmune disorder resulting in insufficient functioning acetylcholine receptors.

192
Q

What is charcot marie tooth? features?

A

Hereditary sensorimotor neuropathy

Autosomal dominant

  • Features start at puberty
  • Distal muscle wasting, pes cavus, clawed toes
  • Foot drop, leg weakness often first features
193
Q

What do the lesions of the cerebellar vermis and hemisphere present with?

A

Vermis presents with ataxic gait

Hemisphere presents with finger-nose ataxia

194
Q

When do you particularly need a CT before LP?

A

Any evidence of a raised ICP. Need to rule out SOL, if there was a SOL then there is a risk the brain herniates through the foramen magnum.

195
Q

Features of frontotemporal dementia?

A

Includes Picks disease

Insidious onset
>65 Y/o
Preserved memory and Visuospatial skills
Personality change and conduct problems

196
Q

Radial nerve palsy ‘saturday night palsy’ presentation?

A

Wrist drop

Sensory loss to small area between the dorsal aspect of the 1st and 2nd metacarpals

197
Q

Visual hallucinations with dementia most likely diagnosis/

A

Lewy body Dementia

198
Q

Features of Venous sinus thrombosis?

A

Headache (may be sudden - but not as much as SAH)

Nausea and vomiting is common in all sinuses

Cavernous sinus

  • Periorbital oedema
  • Opthalmoplegia

Sagittal sinus
- Seizures

Lateral sinus (transverse)

  • 6th nerve palsy
  • 7th nerve palsy
199
Q

Dietary intervention in childhood epilepsy?

A

Ketogenic diet.

200
Q

What are the steps in treating paediatric status epilepticus?

A

1 Buccal midazolam/ IV lorazepam

2 IV lorazepam

3 IV phenytoin (phenobarbital if already on regular phenytoin)

4 Rapid sequence induction of anaesthesia using thiopental sodium

201
Q

What nerve supplies the extensor campartment of the upper limb?

A

The radial nerve

202
Q

What nerve provides innervation to the flexor muscles of the upper arm?

A

Musculocutaneous

  • Coracobracialis
  • Brachialis
  • Biceps brachii
203
Q

What features do you get on a musculocutaneous nerve injury?

A

Weakness of elbow flexion

Cutaneous sensory loss to the lateral portion of the forearm

204
Q

What does the ulnar nerve innervate (motor)

A

Flexor carpi ulnaris

(1/2 of flexor digitorum profundus)

Hypothenar eminence

205
Q

What nerves innervate the intrinsic muscles of the hand?

A

The ulnar nerve does all except:

Thenar and first two lumbricals - Median

206
Q

What nerves innervate the flexor compartment of the arm?

A

The median nerve, apart from

Flexor carpi ulnaris
1/2 of flexor digitorum profundus

207
Q

DVLA driving rules for diagnosed epilepsy, for normal vehicles and for private (group 2) vehicles?

A

Normal
- Need to be seizure free for 12 months

Group 2 (busses, lorries)
- Need to be seizure free for 10 years
208
Q

How long off driving for unprovoked/isolated seizure?

A

6 months seizure free

209
Q

DVLA rules for driving in syncope?

A

simple faint: no restriction
single episode, explained and treated: 4 weeks off
single episode, unexplained: 6 months off
two or more episodes: 12 months off

210
Q

Stroke or TIA DVLA driving rules?

A

4 weeks off

If multiple TIAs then it’s three months

211
Q

Weakness (e.g. face and arms) in post ictal state, most likely represents what type of epilepsy?

A

Focal-onset epilepsy

212
Q

Classic signs the diagnosis is MND?

A

Fasciculations
Mix of UMN and LMN signs
NO sensory signs

213
Q

When starting a phenytoin infusion, what do you need to monitor?

A

Cardiac monitoring needs to be initiated

214
Q

Features of common peroneal nerve injury?

A
  1. Weakness of foot dorsiflexion
  2. weakness of foot eversion
  3. weakness of extensor hallucis longus
  4. sensory loss over the dorsum of the foot and the lower lateral part of the leg
  5. wasting of the anterior tibial and peroneal muscles
215
Q

Important risk factors for MS?

A

Smoking
Prev. Infectious mononucleosis
Vit D deficiency
FH

216
Q

What is hoffman’s sign, what pathology does it illicit?

A

Flick distal phalanx of middle finger, if positive there is exaggerated flexion of distal phalanx of thumb.

Test for UMN pathology in upper limb

  • DCM
  • MS
217
Q

When can you stop anti-epileptic drugs?

A

Can be considered if seizure free >2 years, and you stop them over 2-3 months

218
Q

Trans tentorial (uncle) herniation typically causes what palsy?

A

Third nerve palsy

219
Q

What is internuclear opthalmoplegia?

Features?

A

A cause of horizontal disconjugate eye movement
due to a lesion in the medial longitudinal fasciculus, which connects the IIIrd, IVth and VIth cranial nuclei.

Features:

  1. Impaired adduction of the eye on the same side as the lesion
  2. Horizontal nystagmus of the abducting eye on the contralateral side

MS, vascular disease

220
Q

Supranuclear palsy (Parkinsons plus) cardinal features?

A

Dysarthria and reduced vertical eye movements

221
Q

Bug often associated with Guillian Barre?

A

Campylobacter

222
Q

Features of multiple systems atrophy?

A
  1. Parkinsonism
  2. Autonomic disturbance (atonic bladder, postural hypotension, erectile dysfunction)
  3. Cerebellar signs
223
Q

Classic presentation of idiopathic cranial hypertension?

A

Obese, young female with headaches / blurred vision

224
Q

In MS what do you use for spasticity, (inc involuntary movements of the leg)?

A

Baclofen or gabapentin

225
Q

In MS what do you use to treat a relapse?

A

High dose steroids oral or Iv methylpred

226
Q

What drugs do you use as disease modifying agents in MS?

A

Beta interferon - if criteria met

Others include

  • Glatiramir
  • natalizumab
  • fingolimod
227
Q

If someone is in status epilepticus what is the first line management?

A

If you have IV access
- IV Lorazepam

If you don’t
- Rectal Diazepam

228
Q

Erbs palsy presents how?

A

Clinically his arm is hanging loose on the side. It is pronated and medially rotated.

Trauma hx

229
Q

Klumpke’s paralysis, what trunks, what presentation?

A

C8-T1

Horners
Loss of intrinsic muscles of hands

230
Q

What dementia is associated with MND?

A

Frontotemporal dementia

231
Q

What blood test can be used to differentiate between a pseudo seizure and a true epileptic seizure?

A

Prolactin (raised after true seizure).

232
Q

Centor criteria for tonsillitis?

A

3 or more needed.

  1. Presence of tonsillar exudate
  2. Tender anterior cervical lymphadenopathy or Lymphadenitis
  3. History of fever
  4. Absence of cough
233
Q

Treatment course length and antibiotic for tonsillitis?

A

Phenoxymethylpenicillin for 10 days

234
Q

First line investigation in Conns syndrome?

A

Renin:aldosterone ratio

235
Q

How often are type 1 diabetics recommended to monitor blood sugars?

A

Type 1

- atl 4 times, inc before each meal and before bed

236
Q

What is a waterlow score used for?

A

Pressure ulcers

237
Q

First line treatment for long QT syndrome?

A

Beta blockers - propranolol

238
Q

What is the difference between pityriasis rosea and pityriasis versicolour?

A

Rosea

  • Herald patch, followed by scaly rash
  • HHV6/7

Versicolour

  • Melassezia yeast infection
  • Scaly skin round trunk, neck or arms
  • Men in hot humid conditions
239
Q

First line treatment for fungal nail infection?

A

Oral terbinafine

240
Q

Little’s area is on the anterior or posterior nasal septum?

A

The anterior

241
Q

What foods should those on warfarin avoid?

A

Foods high in Vit K - broccoli, kale, sprouts, spinach

242
Q

Characteristic features of Prerenal uraemia?

A

Low urine sodium

High urine osmolality

243
Q

Common causes of peritonitis on peritoneal dialysis?

A

Staph epidermidis most common, then staph aureus

244
Q

What thyroid dysfunction causes menorrhagia?

A

Hypothyroidism

245
Q

How do you treat Conns syndrome?

A

If it’s an adrenal adenoma - surgery

If its bilateral adrenocortical hyperplasia - spironolactone

246
Q

What is trousseau’s sign?

A

Hypocalcaemia

Carpal twitching after blood pressure

247
Q

What is Chvostek’s sign?

A

Tapping over parotid causes facial muscles to twitch

248
Q

Urinary findings in acute interstitial nephritis?

A

Raised white cells and eosinophils

249
Q

Most common type of thyroid cancer?

5th (Final year) (34 decks)

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