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Year 3 > Medicine > Flashcards

Medicine Flashcards

1
Q

Chest Pain - ix

A

bedside: ECG, CBG
blood: FBC, U&Es, Trops, lipids
imaging: CXR, Echocardiogram, CTA, CTPA

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2
Q

Chest Pain - differentials

A

Cardiac- ACS, stable angina, cardiac tamponade
Resp- pleural effusion, pneumonia, PE, pulmonary oedema
MSK- costochondritis, muscle strain [e.g. after coughing]
Psych- anxiety
GI- GORD, gastritis

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3
Q

Palpitations - ix

A

bedside: ECG
bloods: FBC, U&Es, Trops, lipid
imaging: ?

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4
Q

Palpitations - differential diagnosis

A

AF, cardiomyopathy, MI, HF, valvular disease, anaemia

other causes: alcohol, caffeine, medication s/e, ectopic beats, hormone changes [pregnancy or menopause], anxiety/stress, thyroid problems [hyperthyroidism], intense exercise, recreational drug use, smoking

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5
Q

Limb pain [and swelling] - ix

A

bed: examination [peripheral vascular exam], CBG
blood: FBC, U&Es, D-dimer
imaging: CXR, CTPA, X-ray of limb/joint in pain
special: Wells’ score

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6
Q

Limb pain [and swelling] - differential diagnosis

A

DVT/PE; fracture; arthritis; diabetic neuropathy

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7
Q

Syncope/presyncope - ix

A

bed: ECG, CBG, BP
blood: FBC, U&Es, CBG, CRP
imaging: Echocardiogram, X-ray[?], CT [?]

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8
Q

Syncope/presyncope - differential diagnosis

A

reflex syncope [vasovagal], orthostatic hypotension, arrhythmias, structural cardiopulmonary disease, seizures, intoxication, metabolic disturbances

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9
Q

Arrhythmias - definition

A

abnormal heart rhythms
result from interruption to normal electrical signals that co-ordinate contraction of the heart muscle

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10
Q

Arrhythmias - types

A

bradycardia
sinus tachycardia
atrial fibrillation and flutter
supraventricular tachycardia
ventricular tachycardia [shockable cardiac arrest rhythm]
ventricular fibrillation [shockable cardiac arrest rhythm]
pulseless electrical activity [non-shockable cardia arrest rhythm]
asystole [non-shockable cardia arrest rhythm]

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11
Q

Bradyarrhythmia’s - defintion

A

slow heart rhythms <60bpm
sinus brady, sinoatrial node disease, 1 HB, 2 HB [Mobitz T1 and T2], complete heart block, asystole

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12
Q

Supraventricular tachycardias - defintion

A

fast rhythms characterised by narrow QRS complexes, arrhythmogenic focus is supraventricular [atrial]
>100bpm
sinus tachy, atrial tachy, atrial flutter, atrial fibrillation

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13
Q

Atrial Flutter - electrical activity

A

Typically electric signal passes from atria, stimulating contraction, then disappears through the AVN and into ventricles. In Atrial Flutter, there is a re-entrant rhythm in either atrium. Electrical signal re-circulates in a self-perpetuating loop due to extra electrical pathway in the atria. Goes round and round the atrium without interruption. Typically atrial rate is 300bpm

Signal doesn’t enter the ventricles on every lap due to long refractory period of the AVN. Often results in two atrial contractions for every single ventricular contraction [2:1]

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14
Q

Atrial Flutter - ECG characteristics

A

Sawtooth appearance on ECG, repeated P waves occurring at around 300/min with narrow complex tachycardia

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15
Q

Atrial Flutter - causes

A

Structural heart disease, pulmonary disease, toxins [alcohol, caffeine]

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16
Q

Atrial Flutter - ix

A

ECG will reveal sawtooth appearance, diagnosing AFlutter
If unclear then can give AV nodal blocking manoeuvres to reveal repeated P waves

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17
Q

Atrial Flutter - mx

A

cardioversion is the best treatment - direct current cardioversion using a synchronised shock with rapidly and safely restore sinus rhythm

anticoagulation is recommended before cardioversion

Class Ia [flecainide], Ic [propafenone] or III [amiodarone] drugs may be used

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18
Q

Atrial Fibrillation - electrical activity

A

Disorganised random electrical activity in the atria, only intermittently conducted by AVN causing the irregularly irregular ventricular beat

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19
Q

Atrial Fibrillation - ECG characteristics

A

absent P waves and irregular baseline with a variable [irregularly irregular] ventricular response rate
range from 90-170bpm but can be faster/slower

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20
Q

Atrial Fibrillation - causes

A

Ischaemic heart disease, valvular heart disease, hypertension, pulmonary disease, sepsis/infection, thyrotoxicosis, alcohol excess

SMITH mnemonic:
Sepsis
Mitral valve pathology
Ischaemic heart disease
Thyrotoxicosis
Hypertension

can be paroxysmal [transient], persistent [lasts longer than a week], or permanent

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21
Q

Atrial Fibrillation - s/s

A

Often asymptomatic, but may be diagnosed after a stroke
May also present with palpitations, sob, dizziness or syncope, symptoms of associated conditions [sepsis, thyrotoxicosis]

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22
Q

Atrial Fibrillation - mx

A

Restoration of sinus rhythm - pharmacological cardioversion [B-blocker, propranolol]; DC cardioversion

Antiarrhythmic drugs - amiodarone, digoxin

Rate control - b-blocker or verapamil

DOAC for anticoagulation to prevent/minimise stroke risk - apixaban, rivaroxaban

most people will end up on bisoprolol and a DOAC [apixaban]

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23
Q

How to calculate a CHA2DS2-VASc score

A

Congestive Heart Failure hx - 1p
Hypertension hx - 1p
Age >=75 - 2p
Diabetes hx - 1p
Stroke/TIA/thromboembolism hx - 2p
Vascular disease hx - 1p
Age 65-74 - 1p
Sex category [female] - 1p

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24
Q

What to do with a CHA2DS2-VASc score?

A

NICE recommends:
0- no anticoagulation
1- consider anticoagulation in men
2+- offer anticoagulation

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25
Q

Stable Angina - definition/pathophysiology

A

Caused by atherosclerosis affecting coronary arteries, narrowing lumen and reducing blood flow to myocardium
During times of high demand, insufficient supply of blood to meet demand
“Stable” when symptoms only come on with exertion and are always relieved by rest of glyceryl trinitrate

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26
Q

Stable Angina - s/s

A

3 main features:
Constricting pain expe4rienced in the chest +/- typical radiation to the arm/neck/jaw
Precipitated by physical exertion
Relieved by rest or GTN within 5m

other features:
dyspnoea, palpitations, syncope

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27
Q

Stable Angina - ix

A

bed: physical examination [cardiovascular], ECG
blood: FBC, U&Es, LFTs, Lipid profile, TFTs, HbA1C and fasting glucose
imaging: CTCA [CT coronary angiogram], invasive coronary angiography
special: cardiac stress testing

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28
Q

Stable Angina - dd

A

Unstable Angina/ACS
claudication

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29
Q

Stable Angina - mx

A

Medical management: immediate symptomatic relief [GTN spray], long-term symptomatic relief [bisoprolol, verapamil]
secondary prevention of cvd - four A’s - aspirin 75mg OD; atorvastatin 80mg OD; ACE inhibitor; Already on a b-blocker

Surgical management: PCI or CABG

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30
Q

ACS - definition/pathophysiology

A

As a result of a thrombus from an atherosclerotic plaque blocking a coronary artery
3 types: Unstable angina, STEMI/N-STEMI

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31
Q

ACS - s/s

A

central, constricting, crushing chest pain
radiates to the jaw/arms; nausea/vomiting; sweating/clamminess; a feeling of impending doom; sob; palpitations

symptoms continue at rest for >15m

silent MI is when a pt doesn’t experience typical pain during ACS; pt w/ diabetes are at risk of silent MIs due to neuropathy

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32
Q

ACS - ECG changes

A

STEMI: ST-segment elevation; new left bundle branch block

N-STEMI: ST depression, T wave inversion

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33
Q

ECG leads and arteries and heart area affected

A

I, aVL, V3-6: left coronary artery: anterolateral

V1-4: Left anterior descending: anterior

I, aVL, V5-6: circumflex artery: lateral

II, III, aVF: right coronary artery: inferior

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34
Q

ACS - ix

A

bed: ECG
bloods: FBC, U&Es, LFT, lipid profile, glucose, troponins
imaging: CXR, echocardiogram [once stable to assess functionality]

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35
Q

Classification of ACS

A

STEMI: ST elevation and new left bundle branch block

N-STEMI: raised troponin with either normal ECG or other ECG changes [ST depression/ T wave inverison]

Unstable angina: symptoms suggest ACS, normal troponin, normal ECG or other ECG changes [ST depression/T wave inversion]

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36
Q

ACS - initial mx

A

CPAIN
Call ambulance
Perform ECG
Aspirin 300mg
Intravenous morphine if required [and antiemetic]
Nitrate [GTN spray]

ROMAN
Reassure
Oxygen if required
Morphine
Aspirin 300mg
Nitrate [GTN spray]

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37
Q

ACS - surgical mx

A

STEMI within 12hrs
Percutaneous coronary intervention PCI if available within 2hr of presenting [angiography and angioplasty with stenting]
Thrombolysis if PCI is not available within 2hr [streptokinase, alteplase, tenecteplase]

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38
Q

ACS - ongoing mx

A

Echocardiogram once stable to assess functional damage
Cardiac rehabilitation
Secondary prevention

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39
Q

ACS - secondary prevention 6 A’s mnemonic

A

Aspirin 75mg OD
Another Antiplatelet clopidogrel for 12/12
Atorvastatin 80mg OD
ACE inhibitor [Ramipril]
Atenolol [or bisoprolol]
Aldosterone antagonist for those with HF

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40
Q

ACS - complications

A

DREAD
Death
Rupture of heart or papillary muscles
oEdema [heart failure]
Arrhythmia and Aneurysm
Dressler’s syndrome

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41
Q

Aortic Stenosis - s/s

A

often symptomatic
can have a classic triad of symptoms: angina; dizziness; dyspnoea
Thrill in the aortic area on palpation; slow rising pulse; narrow pulse pressure; exertional syncope

Ejection-systolic, high-pitched murmur

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42
Q

Aortic Stenosis - causes

A

idiopathic age-related calcification [most common cause]
bicuspid aortic valve
rheumatic heart disease

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43
Q

Aortic Regurgitation - s/s

A

dyspnoea is the main presenting symptom [develops insidiously in chronic severe AR with LVF symptoms]
Thrill in the aortic area on palpation; collapsing pulse; wide pulse pressure; heart failure and pulmonary oedema

Early diastolic, soft murmur

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44
Q

Aortic Regurgitation - causes

A

idiopathic age-related weakness
bicuspid aortic valve
connective tissue disorders [Ehlers-Danlos syndrome; Marfan syndrome]

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45
Q

Mitral Stenosis - s/s

A

main presenting features are exertional dyspnoea and fatigue; can also have ankle swelling, palpitations, haemoptysis; chest pain

Tapping apex beat, malar flush, atrial fibrillation

Mid-diastolic, low-pitched ‘rumbling’ murmur

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46
Q

Mitral Stenosis - causes

A

Rheumatic heart disease
Infective endocarditis

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47
Q

Mitral Regurgitation - s/s

A

Thrill in mitral area on palpation, signs of HF and pulmonary oedema, AF, palpitations, fatigue and reduced exercise tolerance, dyspnoea

Pan-systolic, high-pitched ‘whistling’ murmur
Murmur radiates to the left axilla
Third heart sound may be heard

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48
Q

Mitral Regurgitation - causes

A

Idiopathic weakening of the valve with age
ischaemic heart disease
infective endocarditis
rheumatic heart disease
connective tissue disorders [Ehlers-Danlos, Marfan]

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49
Q

Tricuspid Regurgitation - s/s

A

Thrill in tricuspid area on palpation, raised JVP, pulsatile liver, peripheral oedema, ascites

Pan-systolic murmur with split second heart sound

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50
Q

Tricuspid Regurgitation - causes

A

Pressure due to LSHF or pulmonary hypertension
Infective endocarditis
Rheumatic heart disease
Carcinoid syndrome
Ebstein’s anomaly
Connective tissue disorders [Marfan syndrome]

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51
Q

Pulmonary Stenosis - s/s

A

Thrill in pulmonary area on palpation, raised JVP, peripheral oedema, ascites

Ejection systolic murmur; widely split second heart sound

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52
Q

Pulmonary Stenosis - causes

A

Usually congenital, may be associated with Noonan syndrome or Tetralogy of Fallot

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53
Q

Heart Failure - causes

A

Ischaemic heart disease; myocarditis/cardiomyopathy, hypertension, valvular heart disease, arrhythmias

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54
Q

Heart Failure - s/s

A

Symptoms- breathlessness, cough [pink/white frothy sputum], orthopnoea, paroxysmal nocturnal dyspnoea, peripheral oedema, fatigue

Signs, can include- tachycardia, tachypnoea, hypertension, murmurs on auscultation, 3rd heart sound, bilateral basal crackles, raised JVP, peripheral oedema

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55
Q

Heart Failure - ix

A

bed: obs, ECG
blood: BNP, U&Es, FBC, LFTs, TFTs, lipid profile, glucose, iron studies
imaging: CXR, echocardiogram

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56
Q

Heart Failure - New York Heart Association Classification

A

Class I: no limitation on activity
Class II: comfortable at rest; symptomatic with ordinary activities
Class III: comfortable at rest; symptomatic with any activity
Class IV: symptomatic at rest

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57
Q

Heart Failure - medical mx

A

ACE inhibitor [Ramipril] / ARB [candesartan] can be used if ACEi not tolerated
Beta blocker [Bisoprolol]
Aldosterone antagonist [Spironolactone]
Loop diuretics [Furosemide]

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58
Q

Cardiac Tamponade - definition/pathophysiology

A

Life-threatening condition caused by compression of the heart from the accumulation of fluid, blood, clots, or gas within the pericardial space
It prevents adequate filling and contraction of the heart

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59
Q

Cardiac Tamponade - causes

A

Any cause of pericardial effusion or haemorrhage into the pericardium can lead to cardiac tamponade

Common: pericarditis, tuberculosis, iatrogenic [post-invasive cardiac procedure], trauma, malignancy

Uncommon: connective tissue disease, radiation-induced, uraemia, post-MI, aortic dissection, bacterial infection

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60
Q

Cardiac Tamponade - s/s

A

Acute cardiac tamponade presents as hypotension due to cardiogenic shock
Symptoms- chest pain, dyspnoea, collapse, fatigue, peripheral oedema
Signs- [Beck’s triad: hypotension, elevated venous pressure and muffled heart sounds], tachycardia, pulsus paradoxus, pericardial rub, other features of shock [i.e. cool extremities, peripheral cyanosis, reduced urine output]

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61
Q

Cardiac Tamponade - ix

A

Diagnosed with urgent echocardiography
bed: obs, ECG
blood: ABG
imaging: urgent echo, CXR, CT or MRI

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62
Q

Cardiac Tamponade - mx

A

Urgent needle pericardiocentesis - urgent drainage of the pericardial fluid
may be done using anatomical landmarks, with echocardiography guidance or using fluoroscopy in a cardiac suite
cardiac surgery may be an option to drain effusions in some situations

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63
Q

Hypertension - definition

A

BP above 140/90 in clinical setting
confirmed with ambulatory or home readings above 135/85

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64
Q

Hypertension - causes

A

Essential HTN accounts for 90% - aka primary hypertension; developed on its own with no secondary cause

Secondary causes: ROPED mnemonic
Renal disease
Obesity
Pregnancy induced or Pre-eclampsia
Endocrine
Drugs [alcohol, steroids, NSAIDs, oestrogen]

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65
Q

Hypertension - complications

A

Ischaemic heart disease
Cerebrovascular accident
Vascular disease
Hypertensive retinopathy
Hypertensive nephropathy
Vascular dementia
Left ventricular hypertrophy
Heart failure

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66
Q

Hypertension - s/s

A

Typically asymptomatic however s/s may reflect underlying end organ damage
Symptoms- palpitations, angina, headaches, blurred vision, new neurology [limb weakness, paraesthesia]
Signs- new neurology [limb weakness, paraesthesia], retinopathy, cardiomegaly, arrhythmias, proteinuria

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67
Q

Hypertensive retinopathy - classification

A

Keith-Wagener Barker grades
Grade 1: generalised arteriolar narrowing [silver wiring]
Grade 2: focal narrowing and arteriovenous nipping
Grade 3: retinal haemorrhages, cotton wool spots
Grade 4: papilloedema

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68
Q

Hypertension - ix

A

bed: obs, bp, urinalysis, urinary protein creatinine ratio, ECG, direct ophthalmoscopy
blood: FBC, U&Es, fasting glucose, cholesterol, HbA1c
special: ambulatory bp monitoring, renal uss, endocrine tests [if indicated]

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69
Q

Hypertension - Staging

A

Stage 1: ABPM >135/85 or clinic bp 140/90
Stage 2: ABPM >150/95 or clinic bp >160/100
Stage 3: clinic bp >180/120

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70
Q

Hypertension - mx

A

Lifestyle- stop smoking, reduce alcohol, improve diet, exercise, decrease caffeine
Medical mx- T2DM or <55 start on ACEi/ARB, then add CCB or Thiazide like diuretic, then all 3 options if still not controlled
>55 or Black/Caribbean origin start on CCB, then add Thiazide like diuretic or ACEi/ARB, then all 3 options if still not controlled
4th option: spironolactone or alpha/beta-blocker depending on K+

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71
Q

Hypertensive emergencies - Malignant/Accelerated HTN

A

A BP >180/120 with signs of papilloedema and/or retinal haemorrhage
severe condition resulting in neurological, renal and cardiac damage, requiring admission and immediate management
Tx includes: IV Nitroprusside, labetalol and GTN infusions

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72
Q

Hyperlipidaemia - s/s

A

may only be seen in patients with very high levels of lipids
corneal arcus, tendon xanthoma, xanthelasma

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73
Q

Hyperlipidaemia - ix

A

Full lipid profile, HbA1c, assess for secondary causes of hyperlipidaemia, assess risk for anti-lipid therapy

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74
Q

Hyperlipidaemia - mx

A

Lifestyle modifications: dietary advice, physical activity, weight management, alcohol consumption, smoking cessation
Statin [HMG-CoA reductase inhibitor] - atorvastatin 80mg OD, at night
Fibrate - ezetimibe
Bempedoic acid [ACL inhibitor]
PCSK9 inhibitor - alirocumab

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75
Q

Peripheral Arterial Disease - defintion/pathophysiology

A

Refers to the narrowing of the arteries supplying the limbs and periphery, reducing blood supply. Usually affects lower limbs, resulting in claudication

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76
Q

Peripheral Arterial Disease - risk factors

A

Non-modifiable: older age, family history, male sex
Modifiable: smoking, alcohol consumption, poor diet, low exercise/sedentary lifestyle, obesity, poor sleep, stress

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77
Q

Peripheral Arterial Disease - medical co-morbidities

A

diabetes
htn
ckd
inflammatory conditions [rheumatoid arthritis, for example]
atypical antipsychotic medications

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78
Q

Intermittent Claudication - s/s

A

Crampy pain that predictably occurs after walking a certain distance
After stopping and resting, pain will ease

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79
Q

Critical Limb Ischaemia - s/s

A

6P’s
Pain
Pallor
Pulseless
Paralysis
Paraesthesia
Perishing cold

typically causes burning pain. Worse at night when leg is raise, as gravity no longer helps pull blood into foot

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80
Q

Peripheral Arterial Disease - s/s

A

signs of risk factors: tar staining, xanthomata
signs of cvd: missing limbs/digits, midline sternotomy scar, inner calf scarring for saphenous vein harvesting, focal weakness suggestive of previous stroke
weak peripheral pulses on palpation
pallor, cyanosis, dependent rubor, muscle wasting, hair loss, ulcers, poor wound healing, gangrene
reduced skin temperature, reduced sensation, prolonged capillary refill time, changes during Buerger’s test

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81
Q

Arterial Ulcers - description

A

Caused by ischaemia secondary to inadequate blood supply
smaller than venous
deeper than venous
well defined borders
‘punched-out’ ppearance
occur peripherally [on toes]
reduced bleeding
painful

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82
Q

Venous Ulcers - description

A

Caused by impaired drainage and pooling of blood in legs
occur after minor injury to leg
larger than arterial
more superficial than arterial
irregular, gently sloping borders
affect the gaiter area [mid-calf to ankle]
less painful than arterial
occur with other signs of chronic venous insufficiency [haemosiderin staining, venous eczema]

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83
Q

Peripheral Arterial Disease - ix

A

ABPI
Duplex ultrasound
Angiography- CT or MR- using contrast to highlight arterial circulation

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84
Q

ABPI - result interpretation

A

0.9-1.3 normal
0.6-0.9 mild peripheral arterial disease
0.3-0.6 moderate to severe peripheral disease
0.3 severe disease to critical ischaemia

> 1.3 can indicate calcification of arteries, this is more common in diabetic pts

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85
Q

Intermittent Claudication - mx

A

Lifestyle changes
Exercise training - structured, supervised program of regularly walking to the point of near-maximal claudication and pain, then resting and repeating
Medical mx- atorvastatin 80mg OD; clopidogrel 75mg OD; Naftidrofuryl oxalate [5HT2 receptor antagonist; peripheral vasodilator]
Surgical mx- endovascular angioplasty and stenting; endarterectomy; bypass surgery

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86
Q

Critical Limb Ischaemia - mx

A

Urgent referral to vascular team and analgesia for pain
Urgent revascularisation: endovascular angioplasty and stenting; endarterectomy; bypass surgery; amputation if it is not possible to restore blood flow

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87
Q

Acute Limb Ischaemia - mx

A

Urgent referral to on-call vascular team for assessment
options include: endovascular thrombolysis; endovascular thrombectomy; surgical thrombectomy; endarterectomy; bypass surgery; amputation if it is not possible to restore blood flow

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88
Q

Who is best managed on Coronary Care Unit [CCU]?

A

MI, ACS, HF, other cardiac problems
AF, AFlutter, other arrhythmias
Acute cardiac problems

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89
Q

Name some CVD risk factors

A

Hypertension
Smoking
High cholesterol
Diabetes
Inactivity/Sedentary lifestyle
Overweight/obesity
Family history of CVD
Ethnicity [south asian or black african or african caribbean - ++risk of cvd]
Increased age
Male sex
Poor diet
Excessive alcohol consumption

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90
Q

How to combat CVD risk factors

A

Stop smoking
Have a balanced diet
Exercise regularly
Maintain a healthy weight
Cut down on alcohol
Take medications prescribed to you by doctors
Manage/control other chronic conditions

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91
Q

Diabetes Mellitus Type I - s/s

A

4 T’s
tired, thirsty, toilet [polyuria], thin [weight loss]

vomiting, mild-moderate dehydration, BMI <25

some patients can present with DKA as their first s/s of DMTI

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92
Q

Diabetes Mellitus Type I - pathophysiology

A

Destruction of beta-cells in the pancreas leads to the progressive reduction in insulin secretion
Leads to impaired ability to maintain normal blood glucose levels and results in hyperglycaemia

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93
Q

Diabetes Mellitus Type I - differentials

A

Type II DM
Diabetes insipidus
Steroid therapy
Psychogenic polydipsia
MODY-DM

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94
Q

Diabetes Mellitus Type I - ix

A

diagnosed when classical clinical features are found in the presence of a raised random blood glucose level
Majority of patients will be children/adolescents, but don’t discount in adults [LADA]

Further investigations if required:
*autoantibodies
*investigations for pancreatic cancer

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95
Q

Diabetes Mellitus Type I - mx

A

Life-long exogenous insulin to prevent acute complications [DKA] and long-term complications [CKD, IHD, retinopathy]
Some oral hypoglycaemics can be used too

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96
Q

Insulin regimes for TIDM

A

Basal-bolus: typically involves a rapid/short acting insulin before meals and a long acting insulin for basal requirements. This is the standard approach for patients newly diagnosed with TIDM
one/two/three injections per day: uses both short and intermediate acting insulin
continuous insulin infusion via a pump: uses short/rapid acting insulin. Used in patients who are experiencing troubling hypoglycaemic episodes with multiple daily injections

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97
Q

Blood glucose monitoring in TIDM

A

All patients with TIDM should be offered continuous blood glucose monitoring known as CGM. There are two types:
real-time continuous CGM: automatically recorded BGs and shown on a handheld device
intermittently scanned CGM: BG measured only when you scan a device over a sensor

Patients don’t have to use CGM, they can instead opt for a capillary blood glucose monitor

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98
Q

Blood glucose targets in TIDM

A

On waking- 5-7mmol/L
Before meals- 4-7mmol/L
Post meals: test 90m after food, 5-9mmol/L

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99
Q

Treatment targets in TIDM

A

Long-term control is monitored with HbA1c - should be assessed/repeated every 3-6months to assess glycaemic control
Patients and clinicians should target a HbA1c <48mmol/L

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100
Q

Monitoring for complications of TIDM

A

regular diabetic assessment is essential for all patients to improve morbidity and mortality

annual basis [or more frequently if required], pts should receive a diabetic review. includes assessment of injection site problems, retinopathy, nephropathy, diabetic foot problems, cardiovascular risk factors and thyroid disease

retinopathy- annual screening
nephropathy- renal function [eGFR] and albumin:creatinine ratio
diabetic foot problems- full examination including footwear, monofilament assessment of neuropathy, vascular assessment +/- dopplers
cardiovascular- primary/secondary prevention strategy with optimisation of bp, lipids, weight, smoking and others
thyroid- tfts
dental disease- advise regular oral health review

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101
Q

How to safely prescribe insulin

A

Use a special insulin prescribing chart
MUST write Units, not U
Specify the brand name and indicate the device the patient uses [vial, pen, pen cartridge, pump]
Write pre-breakfast/lunch/dinner instead of times if insulin must be taken before meals
Ensure you confirm with their prescription if unsure of the dose - never estimate

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102
Q

Diabetes Mellitus Type II - s/s

A

May be asymptomatic

May have: lethargy, polyuria, polydipsia, weight loss, recurrent infections [thrush, balanitis]

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103
Q

Diabetes Mellitus Type II - ix

A

major diagnostic tool is the measurement of glycated haemoglobin HbA1c
Symptomatic and elevated HbA1c = diagnosis
Asymptomatic and elevated HbA1c = repeat HbA1c, if that’s elevated then a diagnosis can be made

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104
Q

Diabetes Mellitus Type II - mx

A
  1. lifestyle advice
  2. antidiabetic drugs
  3. insulin use in tiidm
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105
Q

Diabetes Mellitus Type II - lifestyle advice

A

dietary changes - healthy and balanced, plenty of fibre, low-index carbohydrate and controlling intake of high-fat foods; weight loss may be appropriate
exercise and physical activity - can help lower blood glucose; at least 150 minutes of moderate intensity activity over a weekly period
alcohol consumption - increases weight and may exacerbate or prolong hypoglycaemia induced by oral hypoglycaemic
smoking cessation - should be available and offered to all patients

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106
Q

Antidiabetic drugs - metformin

A

Metformin is one of most common medications in TIIDM - biguanide; lowers BG through inhibiting hepatic gluconeogenesis and increasing peripheral insulin sensitivity; first line unless contra-indicated [poorly tolerated, CKD, risk of lactic acidosis]

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107
Q

Antidiabetic drugs - sulfonylureas

A

exs- Gliclazide, glipizide, glimepiride, tolbutamide
moa- Stimulate the pancreas to produce more insulin
c/i- porphyria; ketoacidosis; renal impairment; hepatic impairment
s/e- abdo pain/n/v/d/c, hepatic impairment, weight gain, rash, pruritus, angioedema, erythema, hypoglycaemia, hyponatraemia, dizziness/tremor/drowsiness
d/i- beta-blockers, other antidiabetic drugs, alcohol, steroids, some abx, phenytoin

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108
Q

Antidiabetic drugs - DPP-4 inhibitors

A

exs- sitagliptin, saxagliptin, alogliptin
moa- blocks DPP-4 enzyme; increases levels of incretins to inhibit glucagon release and increase insulin secretion
c/i- ketoacidosis, hepatic impairment, heart failure, pancreatitis, elderly
s/e- c/v/n/d, gord, gastritis, pancreatitis, headache, dizziness, tremor, back pain, arthralgia, increased risk of infections
d/i- b-blocker, acei, digoxin, rifampicin, other antidiabetics, alcohol, steroids

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109
Q

Antidiabetic drugs - glitazones

A

exs- pioglitazone
moa- activate ppar[gamma]; enhances tissue sensitivity to insulin and reduces hepatic gluconeogenesis
c/i- HF, bladder cancer, hepatic impairment, elderly, insulin, rf for bone fracture, bladder cancer, hf
s/e- ++fractures, ++infection, bladder cancer, hepatic impairment, numbness, visual impairment, weight gain, insomnia
d/i- b-blockers, nsaids, other antidiabetic drugs

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110
Q

Antidiabetic drugs - SGLT-2 inhibitors

A

exs- empagliflozin, dapagliflozin
moa- blocks sglt2 transporter in proximal convoluted tubule, stopping reabsorption of glucose
c/i- dka, renal impairment, increasing age, active foot disease, hepatic impairment
s/e- uti, urosepsis, vulvovaginitis, balanoposthitis, fournier’s gangrene, constipation/nausea, thirst, dyslipidaemia, lower limb amputation, renal impairment
d/i- thiazides and loops diuretics, insulin, digoxin, lithium

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111
Q

Antidiabetic drugs - GLP-1 receptor agonists

A

exs- exanatide, dulaglutide, semaglutide [administered as a sc injection]
moa- activates GLP-1 receptor; increases insulin secretion and decreases glucagon secretion ; slows gastric emptying and decreases food intake
c/i- ketoacidosis, pancreatitis, renal impairment, hepatic impairment, gi disease
s/e- acute pancreatitis, n/v/d, gord, gallbladder disorders/cholecystitis/cholelithiasis, headache, drowsiness, dizziness, renal impairment, sinus tachy, skin reactions
d/i- b-blockers, paracetamol, warfarin, other antidiabetic drugs

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112
Q

Insulin-based regimes for TIIDM

A

should be considered in patients with poor glycaemic control despite dual antidiabetic with metformin and another agent
regimes include:
1. once/twice daily intermediate acting insulin
2. intermediate insulin along a short acting as separate injections or a premixed formula
3. once daily long acting insulin therapy
4. basal/bolus regimes

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113
Q

Treatment targets for TIIDM

A

largely based on serial measurements of HbA1c
mx with lifestyle: <48mmol/L
mx with lifestyle and single antidiabetic agent: <48mmol/L
mx with drug associated with hypoglycaemia: <53mmol/L
mx with higher intensification regimes: <53mmol/L

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114
Q

DKA - pathophysiology

A

Inability to utilise glucose leads to an accumulation of glucose within the blood
As glucose can’t be utilised, glycogen stores are broken down [glycogenolysis] and there’s an increased formation of glucose from other substrates [gluconeogenesis]
Lack of use of glucoes leads to the breakdown of fats [lipolysis] to increase fatty acids; these are used in ketogenesis
Ketone bodies [acetone, beta-hydroxybutyrate and acetoacetate] are increased in the blood - leading to ketonaemia; they are weak acids, leads to significant acidosis and severe illness in increasing quantities

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115
Q

DKA - s/s

A

Symptoms- nausea, vomiting, polyuria, polydipsia, abdominal pain, leg cramps, headache
Signs- abdominal tenderness, dehydration, hypotension, Kussmaul breathing, reduced consciousness, coma

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116
Q

DKA - diagnosis criteria

A

Diagnosis is made on identification of biochemical triad of hyperglycaemia, acidaemia, ketonaemia/ketonuria

Lab glucose: >11.0mmol/L
VBG/ABG: <7.3 or bicarb <15mmol/L
Ketone: cap. >=3mmol/L or urinary +++ or above

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117
Q

DKA - ix

A

bed: ECG, urinalysis +/-MSU, beta hcg
blood: FBC, U&Es, CRP, LFTs, cultures, troponin
imaging: CXR

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118
Q

DKA - main goals of management

A

*restore circulating volume and tissue perfusion
*clear serum/urinary ketones and halt ketogenesis
*decrease serum glucose towards a normal level
*correct electrolyte derangements
*identify and treat underlying precipitant

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119
Q

DKA - referral to high dependency unit [level 2 care]

A

One or more of the following
*blood ketone >6mmol/L
*bicarbonate level <5mmol/L
*pH <7.0
*GCS <=12
*Systolic BP <90mmHg
*Hypokalaemia on admission <3.5mmol/L

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120
Q

DKA - circulating volume mx

A

Fluid of choice is usually 0.9% NaCl
1L over 1hr, then 2Ls each over 2hrs, then 2Ls each over 4hrs

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121
Q

DKA - potassium replacement

A

IV insulin regime reduces K+ so potassium should be monitored closely and potassium should be added to the fluids when necessary/indicated

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122
Q

DKA - insulin therapy

A

patients are started on a fixed rate IV infusion
0.1units/kg/hour
infusion is set up using 50units of short acting insulin with 50mls of 0.9% saline
When blood glucose drops <14mmol/L, IV 10% dextrose should be administered at 125ml/hr
continue with patients long-acting insulin

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123
Q

DKA - monitoring during treatment

A

Each hour blood ketones and glucose should be checked
VBG should be used at 1hr, 2hrs and then 2hrs thereafter
K+ checked every 4hrs minimum within first 24hrs
consider cardiac and saturation monitoring
fluid input/output chart should be kept

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124
Q

DKA - treatment targets

A

blood ketones: fall by >=0.5mmol/L/hr
bicarbonate: rise by >=3.0mmol/L/hr
blood glucose: fall by >=3.0mmol/L/hr
poatssium: maintain between 4-5.5mmol/L

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125
Q

Hyperglycaemic hyperosmolar state [HHS] - pathophysiology

A

Relative lack of insulin coupled with a rise in counter-regulatory hormones [cortisol, growth hormone, glucagon] that leads to a profound rise in glucose

reduced glucose utilisation, increased gluconeogenesis and glycogenolysis leads to hyperglycaemia and osmotic diuresis [increased urination due to increased glucose in the urine]

as water is lost, there is profound dehydration and reduced circulating volume - results in hyperosmolarity and hyperglycaemia

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126
Q

Hyperglycaemic hyperosmolar state [HHS] - s/s

A

Usually insidious onset, with development of increased renal water loss and dehydration over days-weeks

Symptoms- polydipsia, polyuria, nausea, vomiting, muscle cramps, weakness, altered mental status, seizures, coma
Signs- dehydration, hypotension, decreased urine output, decreased conscious level, coma, focal neurology signs, features of a precipitating cause

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127
Q

Hyperglycaemic hyperosmolar state [HHS] - diagnosis

A

based on identification of characteristic features:
lab glucose: >30mmol/L
serum osmolality: >320mOsm/kg [2NA + urea + glucose]
ketones: urine 1+, trace, negative OR blood <3mmol/L

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128
Q

Hyperglycaemic hyperosmolar state [HHS] - ix

A

bed: ECG, urinalysis +/- MSU, beta hcg
blood: FBC, U&Es, CRP, LFTs, blood cultures, troponin, amylase, CK
imaging: CXR, CT head [if reduced GCS or focal neurology]

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129
Q

Hyperglycaemic hyperosmolar state [HHS] - management principles

A

*normalise osmolality
*normalise blood glucose
*replace fluid and electrolytes
*prevention of arterial/venous thrombosis
*prevention of complications and foot ulceration

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130
Q

Hyperglycaemic hyperosmolar state [HHS] - referral to HDU

A

*osmolality >350mOsm/kg
*sodium >160mmol/L
*pH <7.1
*GCS <12
*systolic BP <90mmHg
*serum creatinine >200μmol/L
*macrovascular event [mi, cva]
*severe electrolyte abnormalities [hyper/hypokalaemia]

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131
Q

Hyperglycaemic hyperosmolar state [HHS] - IV fluids

A

0.9% normal saline; at least 1L should be given over an hour
further fluids can be given, aiming for a positive fluid balance based on hourly measurement of urine output

rapid correction of fluid deficit is not advisable as it can precipitate osmolar shifts leading to cerebral oedema - aim for 4L positive within the first 24hrs

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132
Q

Hyperglycaemic hyperosmolar state [HHS] - insulin therapy

A

should only be commenced if there’s evidence of significant ketonaemia
should be given as a fixed rate iv insulin infusion at 0.05units/kg/hr

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133
Q

Hyperglycaemic hyperosmolar state [HHS] - electrolyte replacement

A

sodium, potassium, phosphate and magnesium should be monitored regularly [4hrly min.] and replaced as necessary

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134
Q

Hyperglycaemic hyperosmolar state [HHS] - monitoring

A

should be on cardiac monitoring and assessed at regular intervals
every hour- blood glucose, urea and electrolytes and lab/calculated osmolality should be completed for the first 6hr
satisfactory fall in osmolality [3-8mOsm/kg/hr] and glucose [5mmol/L/hr] then bloods reduced to two hourly

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135
Q

Diabetic Foot Ulcer - s/s

A

often painless
drainage/pus from the foot; unusual swelling; irritation; erythema; odour
partial/complete gangrene can appear around the ulcer depending on severity - odours, discharge, pain and numbness can occur alongside

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136
Q

Diabetic Foot Ulcer - management

A

X-rays; MRI; bone scans

non-surgical: shoe modification; wound care; total contact casting
surgical: surgical debridement, abx, contact casting; ostectomy; partial calcanectomy; amputation

better management of diabetes or glycaemic control

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137
Q

Retinopathy - s/s

A

on viewing the retina:
dot and blot haemorrhages, hard exudates, cotton wool spots
intraretinal microvascular abnormalities, venous beading
new vessels at the disc and elsewhere, fibrosis, traction retinal detachment
exudates, oedema

persistent damage to the retina leads to areas of ischaemia and release of angiogenetic factors [e.g. vascular endothelial growth factor]; this promotes new formation of vessels that are weak and friable and consequently leads to complications such as haemorrhage, fibrosis, and retinal detachment

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138
Q

Retinopathy - mx

A

Good glycaemic control and regular screening to assess early changes are key to preventing and managing disease
photocoagulation is used to manage proliferative disease - aim is to burn holes within the ischaemic retina to prevent release of angiogenesis factors

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139
Q

Nephropathy - s/s

A

Earliest sign is presence of microalbuminuria, is assessed with an albumin:creatinine ratio
Microalbuminuria is a marker of systemic microvascular damage

CKD in diabetes is evidence by a persistently low eGFR <60mmol/L and/or AC persistently >3mg/mmol/L

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140
Q

Nephropathy - mx

A

Patients should be treated with an ACE inhibitor or ARB, even in the presence of normotension

TIIDM and CKD: consider SGLT2 inhibitor

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141
Q

Neuropathy - s/s

A

Peripheral neuropathy occurs in leg secondary to loss of vibration, pain, temperature sensation - symmetrical polyneuropathy

damage to a single cranial or peripheral nerve - mononeuropathy

symmetrical pain, weakness, wasting of proximal muscles of the leg [as a result of disease affecting the lumbosacral plexus] - diabetic amyotrophy

postural hypotension, gastroparesis, diarrhoea, bladder dysfunction, erectile dysfunction - autonomic neuropathy [requires MDC]

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142
Q

Neuropathy - mx

A

medications for nausea/vomiting, analgesia
maintaining good glycaemic control, cholesterol monitoring, bp monitoring +/- tx

cannot reverse disease, can only manage symptoms and prevent symptoms from getting worse

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143
Q

Hyperglycaemia - s/s

A

Polyuria; polydipsia; lethargy; thrush/other recurring bladder/skin infections; headaches; blurred vision; weight loss; nausea

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144
Q

Hyperglycaemia - causes

A

Increased blood sugar in people with diabetes can be caused by stress, illness, eating too much, lack of exercise, dehydration, missing/taking an incorrect dose of medication, over-treating an episode of hypoglycaemia, taking steroids or other medications

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145
Q

Hyperglycaemia - ix

A

bed: CBG, ECG, beta hcg, urine dip
blood: fbc, u&es, lfts, tfts, VBG/ABG
imaging: -
special: -

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146
Q

Hyperglycaemia - mx

A

Lifestyle: improve diet, drink plenty of fluids, exercise more often
Medical: adjust insulin or other antidiabetic medications

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147
Q

Hypoglycaemia - s/s

A

feeling hungry, trembling/shakiness, sweating
in more severe cases- confusion, difficulty concentrating
very severe cases- loss of consciousness

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148
Q

Hypoglycaemia - ix

A

bed: CBG
blood: fbc, u&es, tfts, VBG/ABG
imaging: -
special: -

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149
Q

Hypoglycaemia - mx

A

Lift juice, dextrose tablets, something high in sugar
Glucogel
Glucose infusion
Glucagon IM injection

then assess medications and insulin regime - ensure that it’s not too much for the patient

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150
Q

Hypoglycaemia - causes

A

overdose of diabetes medication
exercise, food, alcohol
fasting/malnutrition
reactive hypoglycaemia - pancreas produces too much insulin after a large carbohydrate-based meal
Addison’s disease
some medications- propranolol, malaria medication
severe illness affecting liver, kidneys or thyroid

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151
Q

Hypernatraemia - s/s

A

Symptoms- thirst, dehydration, lethargy, fever, n/v/d, confusion, abnormal speech
Signs- dry mucous membranes, postural hypotension, tachycardia, hypotension, altered mental status, oliguria, polyuria

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152
Q

Hypernatraemia - ix

A

Diagnosis is made on lab sample of plasma sodium >145mmol/L
Urine electrolytes and osmolality can help identify a cause
bloods: FBC, U&Es, LFTs, bone profile, blood glucose, plasma omsolality, CRP/ESR, CK

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153
Q

Hypernatraemia- mx

A

Restoration of total body water and treating the underlying cause
usually a combination of crystalloids are used to help restore water depletion while not overcorrecting the serum sodium
vital to recheck sodium regularly and fluid balance assessed

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154
Q

Hyponatraemia - s/s

A

Often asymptomatic, if symptoms present then typically vague and non-specific
Headache, confusion, n/v, lethargy, irritability, seizures, LOC, coma
s/s may also reflect the underlying cause [HF, pancreatitis]

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155
Q

Hyponatraemia - ix

A

urine: omsolality and sodium
blood: U&Es, glucose, lipids, TFTs, LFTs, early morning cortisol

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156
Q

Acute hyponatraemia - mx

A

Should be managed in a HDU especially if neurological symptoms present

mild/moderate neurological symptoms- treat underlying cause, medication review, non-essential fluids to be stopped

moderate/severe neurological symptoms- rapid correction of serum sodium using hypertonic saline [1.8-3% saline]

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157
Q

Chronic hyponatraemia - mx

A

mx is based on underlying cause

hypovolaemic- iv fluid replacement with normal saline, medication review

euvolaemic- fluid restriction as it is typically SIADH; demeclocycline [ADH inhibitor] or vaptan [vasopressin receptor antagonist]

hypervolaemic- treat underlying cause, fluid and salt restriction and use diuretics

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158
Q

Hyponatraemia - complications

A

cerebral oedema
osmotic demyelination syndrome

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159
Q

Hyperkalaemia - s/s

A

Frequently asymptomatic and difficult to diagnose without a lab sample

Symptoms- fatigue, generalised weakness, chest pain, palpitations
Signs- arrhythmias, reduced power, reduced reflexes, signs of the underlying cause

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160
Q

Hyperkalaemia - ix

A

Lab sample of plasma potassium of >=5.5mmol/L; usually achieved by A/VBG
other ix to consider:
urinalysis, ECG, FBC, U&Es, bone profile, CRP, blood cultures, CK

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161
Q

Hyperkalaemia - ECG changes

A

peaked/tall tented T waves
prolonged PR interval
widening QRS interval
small/absent P waves
AV dissociation
sine wave pattern
asystole

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162
Q

Hyperkalaemia - mx

A

Medical emergency - ABCDE assessment
ECG, cardiac monitoring, stop any K-containing fluid or medication
Protect myocardium- 30ml of 10% calcium gluconate over 10minutes
Drive potassium intracellularly- insulin infusion 10units of short acting insulin alongside dextrose [50ml 50%] over 30minutes
Eliminate potassium from the body- loop diuretics, potassium-binding resins, haemodialysis

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163
Q

Hypokalaemia - s/s

A

Symptoms- fatigue, generalised weakness, muscle cramps and pain, palpitations, constipation
Signs- arrhythmias, muscle paralysis and rhabdomyolysis

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164
Q

Hypokalaemia - ix

A

Diagnosis is based on plasma potassium <3.5mmol/L

other ix to consider:
ECG, urine osmolality and electrolytes, FBC, U&Es, bone profile, magnessium, A/VBG, CK

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165
Q

Hypokalaemia - ECG changes

A

flat T waves
ST depression
U waves
prolonged PR

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166
Q

Hypokalaemia - mx

A

mild to moderate - oral replacement route, SANDO-K for example
severe or symptomatic - IV replacement, 40mmol of KCL in 1L of normal saline; if higher K required then should be done in HDU/ITU setting

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167
Q

Hypercalcaemia - s/s

A

Bones- fragility fractures, bone pain
Stones- renal calculi
Thrones- polyuria, constipation
Abdominal groans- abdo pain, n/v, pancreatitis
Psychic moans- mood disturbance, depression, fatigue, psychosis

other features: myalgia, insomnia, dehydration, hypertension, cardiac arrhythmias

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168
Q

Hypercalcaemia - ix

A

Confirm hypercalcaemia with a bone profile
PTH levels - helps identify a cause

other ix to consider:
FBC, U&Es, LFT, CRP/ESR, TFTs, Vit D levels, malignancy screen, urine calcium levels, general imaging [CXR, CT chest abdo pelvis if malignancy suspected], parathyroid imaging

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169
Q

Hypercalcaemia - mx

A

Mild and asymptomatic/mild symptoms- increase oral fluids and avoid precipitants

Moderate- acute rise requires inpatient admission for IV fluids

Severe- all patients require urgent admission to hospital and treatment; aggressive iv fluids and consideration of bisphosphonates, particularly if malignancy is suspected

alternative therapies: corticorsteroids; surgery [1` hyperparathyroidism]; cinacalcet; dialysis

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170
Q

Hypocalcaemia - s/s

A

Symptoms- paraesthesia, muscle cramps, wheezing, voice changes, CNS disturbances, chest pain, palpitations
Signs- Trousseau’s sign; Chvostek’s sign

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171
Q

Hypocalcaemia - ix

A

Serum corrected calcium <2.2mmol/L for a diagnosis
consider: bone profile, U&Es, Vit D, parathyroid hormone, magnesium, ECG [can cause prolonged QT interval and arrhythmias]

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172
Q

Hypocalcaemia - mx

A

Acute severe [<1.9mmol/L] is medical emergency
IV calcium gluconate 10-20ml of 10% calcium gluconate over 10min
Follow up infusion of 100ml 10% in 1L of dextrose 5% or NaCl 0.9%
Treat co-existing pathology- vit d or magnesium
Calcium monitoring

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173
Q

Diabetes Insipidus - patho

A

results from a deficiency of, or resistance to, anti-diuretic hormone
ADH usually acts on DCT and collecting duct to increase water reabsorption independent of sodium. Stimulates arginine vasopressin receptor 2 leading to insertion of aquaporin-2 channels onto membrane, allowing free entry of water
ADH also causes vasoconstriction of arterioles

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174
Q

Diabetes Insipidus - causes

A

central - reduced release of ADH:
*idiopathic
*neurosurgery
*trauma
*familial/genetic DI
*infection- TB, abscess, meningitis
*tumours
*infiltrative disease - sarcoidosis
*other- post-radiotherapy, vascular

nephrogenic - normal ADH but impaired response from kidneys:
*arginine vasopressin receptor 2 mutation
*aquaporin 2 mutation

acquired - impair the ability to concentrate urine:
*medications
*electrolyte imbalances
*renal disease

175
Q

Diabetes Insipidus - s/s

A

characteristic features are polyuria, polydipsia, nocturia
polyuria can reach 10-15L/day
may be signs of dehydration
may be signs of underlying pathology

176
Q

Diabetes Insipidus - ix

A

Water deprivation test can be used to diagnose

blood: FBC, renal function, plasma glucose and osmolality, HbA1c, bone profile
urine: 24hr urine collection, urine specific gravity, urine osmolality
further testing may be indicated depending on the suspected underlying cause

177
Q

Diabetes Insipidus - mx

A

Central may be treated with synthetic ADH [desmopressin]
-risk of water retention and subsequent hyponatraemia
-if underlying cause is identified, treat appropriately

Nephrogenic is more complicated
-orla hydration may be sufficient
-diuretics may be used [Bendroflumethiazide]
-Desmopressin may be used, supraphysiological levels may overcome the relative resistance to it

178
Q

Syndrome of Inappropriate Anti-Diuretic Hormone [SIADH] - patho

A

results from excess ADH secretion
abnormal release leads to the kidney retaining more water, leading to an increase in total body water - subsequent dilutional hyponatraemia
increase in TBW causes an increase in extracellular fluid that results in increased sodium excretion
results in: hypotonic hyponatraemia, concentrated urine, euvolaemic state

179
Q

Syndrome of Inappropriate Anti-Diuretic Hormone [SIADH] - causes

A

CNS: stroke, subarachnoid haemorrhage, trauma, psychosis
neoplasia: small cell lung cancer, other lung cancers, neuroblastoma
infective: HIV, pneumonia
drugs: carbamazepine, cyclophosphamide, SSRIs, MDMA
hormonal: hypothyroidism, hypopituitarism
surgery: trans sphenoidal pituitary surgery is a procedure with a high-risk of SIADH

180
Q

Syndrome of Inappropriate Anti-Diuretic Hormone [SIADH] - s/s

A

Large proportion will be asymptomatic
Symptoms- headache, confusion, lethargy, anorexia
Signs- seizures, reduced GCS, coma, myoclonus, ataxia, hyporeflexia, asterixis

features of underlying pathology may be present

181
Q

Syndrome of Inappropriate Anti-Diuretic Hormone [SIADH] - ix

A

blood: renal function, serum osmolality
urine: urinary osmolality, urine sodium

182
Q

Syndrome of Inappropriate Anti-Diuretic Hormone [SIADH] - mx

A

Fluid restriction: typically 500ml-1000ml/24hrs
Pharmacological: demeclocycline, though vaptans are typically used now
Hyponatraemia: severe hyponatraemia requires intensive care due to risk of neurological damage as a result of cerebral oedema
Long-term: many cases it is self-limiting or reversible; other times it may persist for longer and require fluid restriction and oral salt

183
Q

Hypoparathyroidism - s/s

A

Symptoms occur due to low calcium
tingling/numbness in fingers, muscle cramps, wheezing, voice changes, CNS disturbances, chest pain, palpitations
Trousseau’s sign and Chvostek’s sign

184
Q

Hypoparathyroidism- ix

A

blood: calcium, thyroid functions, kidney function, LFTs, bone profile, vitamin D
imaging: bone scan, kidney scan
urine: 24hr urine collection

185
Q

Hypoparathyroidism - mx

A

calcium medications and a vitamin d analogue

186
Q

Hyperparathyroidism - patho

A

++PTH lead to increased kidney calcium reabsorption, increased intestinal absorption of calcium and increased osteoclast activity and ++ calcium absorption from bone
all of these increase serum calcium
so ++PTH leads to hypercalcaemia

187
Q

Hyperparathyroidism - s/s

A

Kidney stones
Painful bones, fragility fractures
Constipation, n/v
fatigue, depression, psychosis

188
Q

Hyperparathyroidism - types

A

1- uncontrolled PTH due to a tumour of the parathyroid glands 2- low vit d or CKD reduces calcium reabsorption, so PTH is excreted, but calcium will remain low and PTH will be high
3- when 2 continues for an extended period after the underlying cause has been treated; hyperplasia of PTglands as a result of increased PTH requirements, then when underlying cause has gone, there’s still a high level of PTH

189
Q

Hyperparathyroidism - mx

A

1- remove the tumour surgically 2- treat underlying vitamin D deficiency or CKD [transplant]
3`- surgically remove part of the parathyroid tissue to return the parathyroid hormone to an appropriate level

190
Q

Adrenal insufficiency - patho

A

When adrenal glands don’t produce enough steroid hormones, particularly cortisol and aldosterone
Addison’s disease is when adrenal glands have been damaged, reducing cortisol and aldosterone- primary adrenal insufficiency - commonly autoimmune

191
Q

Adrenal insufficiency - types

A

1- autoimmune typically, Addison's disease 2- inadequate ACTH and lack of stimulation of adrenal glands, subsequently low cortisol- as a result of loss or damage to pituitary gland- tumours, surgery, radiotherapy, trauma
3`- inadequate CRH from hypothalamus, usually from pt taking long-term oral steroids causing suppression of hypothalamus

192
Q

Adrenal insufficiency - s/s

A

Symptoms- fatigue, muscle weakness and cramps, dizziness and fainting, thirst and craving salt, weight loss, abdominal pain, depression, reduced libido
Signs- bronze hyperpigmentation [particularly in creases, as a result of ACTH stimulating melanocytes to produce melanin], hypotension

193
Q

Adrenal insufficiency - ix

A

U&Es [hyponatraemia, hyperkalaemia, hypoglycaemia, raised U+C, hypercalcaemia]
early morning cortisol
short Synacthen test
ACTH levels in blood
Autoantibodies
CT/MRI of adrenal glands - not routinely required
MRI of pituitary gland

194
Q

Adrenal insufficiency - short Synacthen test

A

aka ACTH stimulation test
Provide a dose of synthetic ACTH, and cortisol is checked before, 30 and 60 min after the dose
Would usually stimulate adrenal glands to produce cortisol, it should be at least double
Failure to double indicates: primary adrenal insufficiency or very significant adrenal atrophy after prolonged ACTH absence in 21 adrenal insufficiency

195
Q

Adrenal insufficiency - mx

A

Hydrocortisone [glucocorticoid] to replace cortisol
Fludrocortisone [mineralocorticoid] to replace aldosterone if it is also insufficient
Pts are given a steroid card, ID tag and emergency letter to alert emergency services that they depend on steroids
Double doses are given during acute illness to match normal steroid response
Pts and close contacts are taught to give IM hydrocortisone in an emergecny

196
Q

Adrenal crisis - patho

A

Acute presentation of severe adrenal insufficiency
may be the initial presentation of adrenal insufficiency or triggered by infection, trauma, other acute illness
Don’t wait to perform investigations to establish diagnosis before starting treatment

197
Q

Adrenal crisis - s/s

A

reduced consciousness
hypotension
hypoglycaemia
hyponatraemia and hyperkalaemia

198
Q

Adrenal crisis - mx

A

ABCDE approach
IM or IV hydrocortisone [100mg initially, followed by an infusion or 6hrly doses until recovered]
IV fluids
correct hypoglycaemia [IV dextrose, for example]
monitor electrolytes and fluid balance

199
Q

Cushing’s Syndrome - patho

A

Caused by prolonged exposure to an excess of glucocorticoids
can be exogenous or endogenous [external or internal cortisol]
defined based on whether the cortisol excess is ACTH dependent [cortisol excess is driven by PTH, from pituitary or ectopic sources] or independent [cortisol excess isn’t related to ACTH, can be consumption of cortisol or adrenal lesions]

200
Q

Cushing’s Syndrome - causes

A

ACTH dependent: Cushing’s Disease [pituitary adenoma]; ectopic ACTH producing tumour [bronchial carcinoma]

ACTH independent: endogenous administration [prolonged glucocorticoid intake, results in suppression of crh and acth]; primary adrenal lesion [adenomas, carcinomas, hyperplasia]

201
Q

Cushing’s Syndrome - s/s

A

Symptoms- tiredness, depression, weight gain, easy bruising, amenorrhoea, reduced libido, striae
Signs- acne, moon face, facial plethora [excessive blood flow to the face], buffalo hump, hypertension, proximal muscle weakness, hyperpigmentation [in ACTH dependent causes]

202
Q

Cushing’s Syndrome - mx

A

24-hr urinary cortisol - levels 3-4x higher than normal are highly suggestive of Cushing’s syndrome
midnight cortisol - demonstrates loss of normal circadian pattern
low-dose dexamethasone suppression - 1mg of dex given at 11pm, cortisol measured at 8am. cortisol should be reduced however it isn’t in cushing’s

ACTH measured in plasma - suppressed ACTH indicates ACTH independent cause; raised suggests ACTH dependent cause

then further investigate for causes of each cause of in/dependent

203
Q

Cushing’s Syndrome - mx

A

Exogenous Cushing’s - withdraw glucocorticoid medications, but should not stop suddenly - this can cause Addisonian crisis

Cushing’s Disease - remove adenoma with transsphenoidal surgery [gold standard]

Medical mx - medical therapy is used to bridge the gap between definitive mx or when surgery isn’t possible; metyrapone can be used to reduce cortisol synthesis

Pituitary irradtion - used in children/young people/surgical option hasn’t worked; takes 6-12m to work

Adrenalectomy - all other therapies have failed, last resort option, is to take both adrenal glands out [bilateral adrenalectomy]; but will have to take lifelong glucocorticoid and mineralocorticoid replacement

204
Q

Cushing’s Syndrome - mx

A

Exogenous Cushing’s - withdraw glucocorticoid medications, but should not stop suddenly - this can cause Addisonian crisis

Cushing’s Disease - remove adenoma with transsphenoidal surgery [gold standard]

Medical mx - medical therapy is used to bridge the gap between definitive mx or when surgery isn’t possible; metyrapone can be used to reduce cortisol synthesis

Pituitary irradiation - used in children/young people/surgical option hasn’t worked; takes 6-12m to work

Adrenalectomy - all other therapies have failed, last resort option, is to take both adrenal glands out [bilateral adrenalectomy]; but will have to take lifelong glucocorticoid and mineralocorticoid replacement

205
Q

Hyperthyroidism - patho

A

1 hyperthyroidism- thyroid pathology, produces too much thyroid hormone 2 hyperthyroidism- pathology of hypothalamus or pituitary gland; too much TSH stimulates T3 and T4 production
Graves’ disease- autoimmune condition where TSH receptor antibodies cause primary hyperthyroidism; TSH receptor antibodies stimulate TSH receptors on thyroid, causing hyperthyroidism
Toxic multinodular goitre- nodules on thyroid are unregulated by the thyroid axis, continuously producing excessive thyroid hormones

206
Q

Hyperthyroidism - causes

A

GIST
G- Graves’ disease
I- Inflammation [thyroiditis]
S- Solitary toxic thyroid nodule
T- Toxic multinodular goitre

207
Q

Hyperthyroidism - s/s

A

anxiety and irritability, sweating and heat intolerance, tachycardia, weight loss, fatigue, insomnia, frequent loose stools, sexual dysfunction, brisk reflexes on examination

Graves’ disease specifically:
*diffuse goitre without nodules
*graves’ eye disease [inc. exophthalmos]
*pretibial myxoedema
*thyroid acropachy [hand swelling and finger clubbing]

208
Q

Thyroid Storm - summary

A

Thyrotoxic crisis
presents- fever, tachycardia, delirium, v/d, abdo pain
can be life-threatening and requires admission for monitoring
treated the same as any other thyrotoxicosis, although may also require fluid resus, anti-arrhythmic meds, b-blockers

209
Q

Hyperthyroidism - ix

A

bed: ECG, CBG
blood: FBC, U&Es, LFTs, TFTs, autoantibodies
imaging: ultrasonography, thyroid uptake scan

210
Q

Hyperthyroidism - mx

A

Pharmacological- carbimazole or propylthiouracil [pancreatitis risk]; b-blocker or ccb may be prescribed to treat symptoms
Radioactive iodine- uptake of radioactive idone caused destruction in the thyroid and reduces thyroid hormone release [c/i- pregnancy, falling pregnant, breastfeeding, fathering a child]
Thyroidectomy- removal of thyroid gland is definitive if malignancy is suspected or medications aren’t suitable

211
Q

Hypothyroidism - patho

A

Insufficient T3 and T4
1- thyroid behaves abnormally and doesn't produce enough T3/4; negative feedback is absent, resulting in ++TSH 2- pituitary behaves abnormally and produces inadequate TSH, under stimulating thyroid gland and insufficient T3/4 is produced

212
Q

Hypothyroidism - Hashimoto’s Thyroiditis

A

Hashimoto’s thyroiditis is most common cause of 1` hypothyroidism
Autoimmune condition causing inflammation of thyroid gland
Associated with anti-TPO antibodies and anti-Tg antibodies

213
Q

Hypothyroidism - Iodine deficiency

A

most common cause in the developing world

214
Q

Hypothyroidism - other causes of 1`

A

treatments for hyperthyroidism can cause hypothyroidism
*carbimazole
*propylthiouracil
*radioactive iodine
*thyroid surgery

lithium inhibits production of thyroid hormones and can cause goitre and hypothyroidism

amiodarone can cause hypothyroidism and thyrotoxicosis

215
Q

Hypothyroidism - causes of 2`

A

Often associated with a lack of other pituitary hormones [e.g. ACTH]
can be caused be:
*tumours
*surgery
*radiotherapy
*Sheehan’s syndrome
*trauma

216
Q

Hypothyroidism - s/s

A

Symptoms- tiredness, lethargy, weight gain, cold intolerance, menstrual irregularities, reduced libido, goitre
Signs- hair loss, dry skin, goitre, bradycardia, myxoedema, delayed relaxation phase of deep tendon reflexes

217
Q

Hypothyroidism - ix

A

Thyroid profile - measure TSH and T3/4
+TSH; -T3/4: primary hypothyroidism
-TSH; -T3/4: secondary hypothyroidism
Autoantibodies: anti-TPO and anti-Tg
Other blood: FBC, B12 and folate, serum lipids, HbA1c, coeliac serology

Suspicious of malignancy? ultrasonography and urgent 2ww

218
Q

Hypothyroidism - mx

A

Oral levothyroxine is main management option; synthetic T4 and metabolises to T3 in the body
Dose is titrated based on TSH level, usually every 4wks

if TSH is high, levothyroxine is too low so increase dose
if TSH is low, levothyroxine is too high so reduce dose

Liothyronine sodium is a synthetic T3 and is rarely used, only under specialist supervision, when levothyroxine is not tolerated

219
Q

Abdominal pain - causes

A

GORD, gastritis, PUD, perforated ulcer, perf AAA, hepatitis, cholecystitis, gallstones, IBD/IBS, gastroenteritis, diverticula disease, mesenteric ischaemia, colitis, bowel obstruction, testicular pathology, ovarian pathology, urinary retention, kidney stones, cancers, ectopic pregnancy, abnormal MI presentation, UTI

220
Q

Abdominal pain - ix

A

bed: ECG, beta-HCG, urine dip + MSU
blood: FBC, U&Es, LFTs, CRP, CK, Troponins
imaging: CT abdo pelvis with contrast, ultrasound of abdomen/urinary tract, erect CXR, abdominal XR
stool: culture and sensitivity, faecal calprotectin, occult test
surgery: exploratory laparotomy may be used; if testicular torsion is suspected surgery is required for diagnosis and treatment

221
Q

Abdominal pain - mx

A

ABCDE approach to guide management
pain relief, IV fluids if needed
pt NBM if surgery suspected

other management options are dependent on what hx, ex, ix show

222
Q

Haematemesis - causes

A

GORD, PUD, malignancy, Mallory-Weiss tears, Boerhaave syndrome, gastritis, oesophagitis

223
Q

Haematemesis - ix

A

bed: insert IV cannulas [two grey 16G large bore]
blood: FBC, U&Es, LFTs, CRP, ABG, crossmatch and G+S, coagulation screen
imaging: endoscopy

224
Q

Haematemesis - mx

A

ABCDE approach; emergency situation
if hypovolaemic; fluid resuscitate. Administer 500ml bolus of 0.9% NaCl over <15m; then reassess for fluid overload. Blood loss is typically replaced with blood however. So pt will probably require blood products
O- blood should be administered, reassess after each unit
Platelets may be required, especially in pts with liver pathology
FFP can be given if PT or APPT is 1.5x greater than normal
Prothrombin complex is offered to pts on warfarin to reverse effects of warfarin
Terlipressin causes vasoconstriction of splenic artery - good if suspecting varices
Prophylactic antibiotic therapy to pts with suspected/confirmed variceal bleeding - Ciprofloxacin 1g OD for 7/7
Endoscopy performed on all unstable pts urgently; all other pts within 24hrs - allows diagnosis and management

225
Q

Malaena - causes

A

GORD, PUD, malignancy, Mallory-Weiss tears, Boerhaave syndrome, gastritis, oesophagitis

226
Q

Malaena - ix

A

Same as for haematemesis

227
Q

Maleana - mx

A

Same as for haematemesis

228
Q

Lower GI bleeding - causes

A

diverticulosis, haemorrhoids, fissures, fistulas, ischaemic colitis, angiodysplasia, polyps, malignancy, IBD, infection

229
Q

Lower GI bleeding - ix

A

bedside: DRE, obs, BP, CBG, ECG, stool microscopy, culture and sensitivities, faecal calprotectin
bloods: FBC, U&Es, LFTs, haematinics, clotting, A/VBG, G+S/CM
imaging: erect CXR, CT abdo/pelvis with contrast, CT angiography
special: flex sig, colonoscopy, UGI endoscopy, angiographic transarterial embolisation

230
Q

Lower GI bleeding - mx

A

ABCDE approach; acute patient
Assess and resuscitate as necessary
Then calculate shock index
Stable? Unstable? Active bleed?

Stable: endoscopy
Unstable/Active: CT angiogram, treat with IR/endoscopy, surgery is an option

231
Q

Jaundice - causes

A

Yellow complexion occurs from elevated bilirubin
Pre-hepatic [excessive breakdown of RBCs]: sickle cell disease, hereditary spherocytosis, autoimmune haemolytic anaemia, iatrogenic

Hepatic and unconjugated: Gilbert’s syndrome, hyperthyroidism, antibiotics, anti-retroviral drugs

Hepatic and conjugated: hepatocellular injury [hepatitis, alcohol, fatty liver, hereditary haemochromatosis, medications], infiltrative disorders [sarcoidosis, amyloidosis, tuberculosis], malignancy

Post-hepatic [biliary obstruction]: primary sclerosing cholangitis, stricturing of bile ducts, choledocholelithasis [gallstones], malignancy [i.e. head of pancreas tumour] parasitic infections, Mirizzi’s syndrome

232
Q

Jaundice - ix

A

blood: FBC, U&Es, LFTs, coagulation, CRP, renal function, haemolysis screen
imaging: USS, CT abdo/pelvis, MRI liver, MRCP/ERCP

233
Q

Jaundice - mx

A

treat underlying cause
anti-histamines for pruritus
ERCP - removing obstruction of biliary tree, placing stents, taking biopsy for malignancy

234
Q

Diarrhoea - causes

A

malignancy, IBD/IBS, gastroenteritis, diet, hyperthyroidism, medication side-effects
may be normal for some patients

235
Q

Diarrhoea - ix

A

bed: DRE, faecal calprotectin, occult test, stool microscopy/sensitivity/cultures
blood: FBC, U&Es, LFTs, TFTs, CRP

236
Q

Diarrhoea - mx

A

Fluids
Antimotility medication- codeine phosphate, loperamide

237
Q

Nausea and Vomiting - causes

A

medication side effects, pregnancy, post-operative, bowel obstruction, infection, gastroenteritis, motion sickness, migraine, pain, indigestion, stress, alcohol

238
Q

Nausea and Vomiting - ix

A

bed: ECG, beta-HCG, CBG
blood: FBC, U&Es, LFTs, TFTs, CRP
imaging: AXR, CT abdo contrast, USS

239
Q

Nausea and Vomiting - mx

A

anti-emetics
fluids, especially if dehydrated
electrolyte monitoring and replacement if indicated
treatment for underlying pathology/disease

240
Q

Upper GI bleeding - causes

A

PUD, gastritis, oesophageal varices account for majority of cases

oesophagus: oesophagitis, varices, malignancy, GORD, MWT
stomach: PUD, MWT, gastric varices, gastritis, malignancy
duodenum: PUD, diverticulum, aortoduodenal fistula, duodenitis
other: swallowed blood, bleeding disorders, angiodysplasia

241
Q

Upper GI bleeding - s/s

A

Symptoms- haematemesis, dizziness, syncope, weakness, abdominal pain, dyspepsia, heartburn, melaena, haematochezia, weight loss
Signs- dehydration, pallor, confusion, tachycardia, hypotension, abdominal tenderness, melaena, haematochezia, stigmata or liver disease [spider naevi, ascites, hepatomegaly], telangiectasia

242
Q

Upper GI bleeding - ix

A

bed: obs, ECG, urine output, DRE
blood: FBC, A/VBG, U&Es, LFTs, coagulation screen, G+S/CM
imaging: CXR; upper GI endoscopy

243
Q

Upper GI bleeding - mx

A

Initially resuscitated with ABCDE approach
Endoscopy
Non-variceal bleeding: endoscopy [clips with adrenaline, or thermal coagulation with adrenaline] or medical [PPI]
Variceal bleeding: endoscopy [band ligation or endoscopic sclerotherapy]; pharmacological [terlipressin IV, prophylactic abx therapy]
Varices may re-bleed: in this case, Sengtaken-blakemore tube to tamponade bleeding; oesophageal stent; transjugular intrahepatic portosystemic shunt TIPS procedure

244
Q

Crohn’s Disease - s/s

A

Cobblestone appearance, rosethorn ulcers, obstruction, hyperplasia, narrowing, skip lesions

Symptoms- n/a, low grade fever, weight loss, abdo pain, diarrhoea, rectal bleeding, perianal disease
Signs- pyrexia, dehydration, angular stomatitis, aphthous ulcers, pallor, tachycardia, hypotension, abdominal tenderness/mass/distension

can have extra-intestinal manifestations - skin, eyes, joints, anaemia

245
Q

Crohn’s Disease - ix

A

bed: obs, ECG, urinalysis, stool microscopy/sensitivity/culture/parasites/c.diff toxin, faecal calprotectin
blood: FBC, LTFs, U&Es, CRP, magnesium, haematinics, bone profile, clotting
imaging: AXR, CT, MRI small bowel, Barium follow through, colonoscopy, upper gi endoscopy
special: examination under anaesthesia

246
Q

Crohn’s Disease - mx

A

Induce remission and then maintain

*diet management
*corticosteroids [budesonide/prednisolone]
*infliximab
*methotrexate
*azathioprine

Surgical options are available

247
Q

Ulcerative Colitis - s/s

A

Continuous mucosal inflammation, inflammatory polyps, goblet cell depletion, crypt abscesses, inflammatory infiltrate in lamina propria

Symptoms- weight loss, fatigue, abdominal pain, loose stools, rectal bleeding, tenesmus, urgency
Signs- febrile, pale, dehydrated, abdominal tenderness, abdominal distension/mass, tachycardic, hypotensive

248
Q

Toxic megacolon - s/s

A

fever
tachycardia
hypotension
dehydration
altered mental status
biochemical abnormalities
abdominal distension and tenderness

249
Q

Ulcerative Colitis - ix

A

bed: obs, ECG, urinalysis, urine MCS, C.diff toxin, faecal calprotectin
blood: FBC, LFTs, U&Es, CRP, A/VBG, haematinics, magnesium, clotting, autoantibodies
imaging: AXR
endoscopy: colonoscopy is diagnostic investigation of choice

250
Q

Ulcerative Colitis - mx

A

Induce and maintain remission

*aminosalicylates and/or steroids
*steroid enema
*azathioprine
*infliximab

Surgical intervention- proctocolectomy, with ileal pouch anal anastamosis or end ileostomy

251
Q

Paracetamol Overdose - s/s

A

Symptoms- n/v, anorexia, malaise, abdominal pain, altered mental status, confusion, scars [?previous self harm]
Signs- asterixis, bruising, jaundice, RUQ tenderness, oliguria/anuria, tachycardia, hypotension, coma

252
Q

Paracetamol Overdose - ix

A

blood: FBC, U&Es, LFTs, bone profile, A/VBG, blood glucse, paracetamol levels, salicylates levels, coag screen
special: Nomogram

253
Q

Paracetamol Overdose - mx

A

Principle treatment is N-acetylcysteine [NAC]
21 hr regime:
Over 1hr: 200ml 0.9% NaCl with 150mg/kg of NAC
Over 4 hrs: 500ml 0.9% NaCl with 50mg/kg of NAC
Over 16hrs: 1L 0.9% NaCl with 100mg/kg of NAC

within 8hrs of ingestion- activated charcoal can be given

stop tx when INR <=1.3 and ALT normal

referral to psychiatry should be considered

254
Q

Acute Liver Failure [ALF] - definition

A

A syndrome of acute liver dysfunction without underlying chronic liver disease
-coagulopathy of hepatic origin
-altered levels of consciousness due to hepatic encephalopathy

255
Q

ALF - primary causes

A

viruses [A, B, E]
paracetamol
non-paracetamol medications [statins, carbamazepine, ecstasy]
toxin-induced
Budd-Chiari syndrome
pregnancy-related
autoimmune hepatitis
Wilson’s disease

256
Q

ALF - secondary causes

A

ischaemic hepatitis
liver resection
severe infection
malignant infiltration
heat stroke
haemophagocytic syndromes

257
Q

ALF - s/s

A

Characterised by jaundice, confusion, coagulopathy

S/S- altered mental status, confusion, asterixis, jaundice, RUQ pain/tenderness, hepatomegaly, ascites, bruising, GI bleeding, hypotension, tachycardia, raised intracranial pressure

258
Q

ALF - ix

A

Early transfer to a transplant centre
urgent blood tests: FBC, LFTs, U&Es, bone profile, blood glucose, arterial ammonia, ABG, coagulation, lactate dehydrogenase, lipase/amylase, blood cultures
imaging: Doppler ultrasound, CT abdo/pelvis

259
Q

ALF - non-invasive liver screen

A

Toxicology screen
Paracetamol serum level
Autoimmune markers [ANA, autoantibodies, immunoglobulins, ANCA]
Viral screen [hep A through to E; CMV, EBV, HSV, VZV, Parvovirus]

260
Q

ALF - mx

A

CVS- fluid resus +/- inotropic agents
Resp- intubation + ventilation may be needed; chest physio
GI- nutrition [NG feed+/-TPN] gastric ulcer prophylaxis, pancreatitis risk assessment, manage GI bleeding if/when necessary
Metabolic- hypoglycaemia [maintain 8-11mmol/L]; hyponatraemia [140-145mmol/L]; acidosis and lactate; hypophosphatemia [suggests liver regeneration, good prognostic sign, needs correction]
Renal- AKI is common, monitor and treat when necessary
Coagulopathy- use blood products if bleeding
Sepsis- Early aggressive treatment of infection with broad spec abx
Neurological- may require ventilation + intubation; at risk of raised ICP, monitor
Liver- assessed and considered for urgent transplantation

261
Q

Chronic Liver Disease - patho

A

Repeated insults to the liver, which can result in inflammation, fibrosis, and ultimately cirrhosis

262
Q

Chronic Liver Disease - causes

A

alcohol
viral [hep a-e]
inherited [alpha-1-antitrypsin deficiency; wilson’s disease; hereditary haemochromatosis]
metabolic [non-alcohol fatty liver disease]
autoimmune [autoimmune hepatitis]
biliary [primary biliary cholangitis; primary sclerosing cholangitis]
vascular [ischaemic hepatitis; Budd-Chiari syndrome; congestive hepatopathy]
medication [drug-induced liver injury]
cryptogenic [no known cause]
other [many rare cases]

263
Q

Chronic Liver Disease - how to screen for different causes

A

alcohol- alcohol history
virus- sexual health history, food/diet history, travel history, iv drug use, tattoos
inherited- past family history
metabolic- diabetic, diet, exercise
autoimmune- other autoimmune conditions
biliary- IBD?
medication- drug hx

264
Q

Chronic Liver Disease - how to screen for inherited [+autoimmune] causes

A

Haemochromatosis- ‘golden skin’, endocrine abnormalities, thyroid problems, erectile dysfunction
Alpha-1-antitrypsin- COPD, liver cirrhosis, emphysema
Wilson’s- psychiatric changes, eye changes
Autoimmune- ‘period problems’, typically young women

265
Q

Chronic Liver Disease - s/s

A

stigmata of cld- caput medusa, splenomegaly, palmar erythema, dupuytren’s contracture, leukonychia, gynaecomastia, spider naevi

features of hepatic decompensation- encephalopathy, ascites, jaundice, GI bleeding, coagulopathy

266
Q

Chronic Liver Disease - ix

A

Liver biopsy is considered gold-standard diagnostic method for identifying cirrhosis
LFTs
Transient elastography
Imaging: USS, CT, MRI

267
Q

Chronic Liver Disease - mx

A

Treat underlying pathology, prevent progression and manage complications
hepatic encephalopathy- lactulose, long term abx [refaximin]
ascites- spironolactone, furosemide, paracentesis
gi bleeding- b-blockers if not bleeding; acute bleed needs ligation; after bleeding use surveillance and b-blockers
spontaneous bacterial peritonitis- abx as per local guidelines, albumin solution, long term prophylactic abx
hepatocellular carcinoma- high risk so 6monthly surveillance with uss +/- afp blood test
transplant is potentially life-saving treatment

268
Q

Causes of abnormal ALT

A

hepatitis, infection, cirrhosis, liver cancer, other liver diseases
may also be a lack of blood flow to the liver
medications or poisons

269
Q

Causes of abnormal AST

A

hepatitis, cirrhosis, mono, other lvier disease, heart problems, pancreatitis

270
Q

Causes of abnormal ALP

A

high- blockage of bile ducts, cirrhosis, hepatitis, mono, bone disorders, heart failure, hodgkin lymphoma, infection
low- zinc deficiency, malnutrition, pernicious anaemia, thyroid disease, Wilson’s disease

271
Q

Causes of abnormal GGT

A

high- hepatitis, cirrhosis, mono, other liver diseases, heart problems, pancreatitis

272
Q

Causes of abnormal bilirubin

A

Gilbert’s syndrome, gallstones, liver dysfunction, hpcc, hepatitis, bile duct inflammation, intrahepatic cholestasis of pregnancy, haemolytic anaemia

273
Q

Causes of abnormal albumin

A

low- cirrhosis, hepatitis, fatty liver disease, kidney disease, malnutrition, infection, digestive diseases, burns, thyroid dysfunction

high- dehydration, diarrhoea, medications

274
Q

Causes of abnormal lactate dehydrogenase

A

anaemia, kidney disease, liver disease, muscle injury, heart attack, pancreatitis, infections [meningitis, encephalitis, mono], some types of cancer [lymphoma, leukaemia]

275
Q

Causes of abnormal SMA [smooth muscle antibody]

A

high- type 1 autoimmune hepatitis
low- type 2 autoimmune hepatitis
none- symptoms aren’t caused by autoimmune hepatitis

276
Q

Alcoholic Liver Disease - mx

A

*manage alcohol withdrawal [benzodiazepines, alcohol team input]
*alcohol cessation
*hydration [cautious fluid resus, use of albumin to reduce risk of ascites, hyponatraemia, precipitating GI bleed]
*nutrition [dietitian input, low threshold for NG feed and vit. supplementation]
*aggressive treatment of infections [++risk of life-threatening infections due to immune dysfunction]
*pharmacological therapy [corticosteroids can be used in severe alcoholic hepatitis]
*transplantation [6/12 abstinent from alcohol prior to transplantation]

277
Q

Non-Alcoholic Fatty Liver Disease - mx

A

Treatment centres on dietary advice, exercise and managing co-morbidities [e.g .diabetes]
*weight loss
*control htn, diabetes, high cholesterol
*liver transplantation [only curative treatment for end-stage liver disease]

278
Q

Viral Hepatitis - mx

A

A- usually resolves without treatment, supportive tx may help [analgesia]
B- antiviral medications, screen for other diseases, liver transplantation, contact tracing and informing at-risk contacts
C- antiviral treatment with direct-acting antivirals for 8-12/52
D- pegylated interferon alpha over at least 48/52
E- usually cleared within a month, no treatment aside from supportive treatment necessary

279
Q

Haemochromatosis - mx

A

*venesection [weekly blood removal to decrease total iron]
*monitoring serum ferritin
*avoid alcohol
*genetic counselling
*monitoring and treatment of complications

280
Q

Autoimmune Hepatitis - mx

A

high-dose steroids [prednisolone]
immunosuppressants [azathioprine] - useful for inducing remission
liver transplantation may be required in end-stage liver disease; autoimmune hepatitis can reoccur in the new liver

281
Q

Complications of Chronic Liver Disease

A

Hepatic encephalopathy
Ascites
Hyponatraemia
GI bleeding
Infections - SBP
AKI
Hepatocellular carcinoma
Hepatorenal syndrome
Hepatopulmonary syndrome
Acute-on-chronic liver failure

282
Q

Hepatic Encephalopathy - s/s

A

confusion, forgetfulness, personality/mood changes, stale/sweet odour on breath, poor judgement, poor concentration, change in sleep patterns, worsening of handwriting or small hand movement
asterixis, extreme anxiety, seizures, severe confusion, fatigue, severe personality changes, jumbled/slurred speech, slow movement

283
Q

Hepatic Encephalopathy - mx

A

Lactulose - changes acidity of stools to help prevent growth of bacteria that produce ammonia in the bowel
Rifaximin - abx used to stop growth of bacteria in the intestines; taken alongside lactulose
nutritional support

284
Q

Ascites - s/s

A

fluid accumulation within peritoneal cavity
swelling/distention
fluid thrill and shifting dullness

285
Q

Ascites - mx

A

low sodium diet
aldosterone antagonists [spironolactone]
paracentesis [ascetic tap or ascetic drain]
prophylactic antibiotics [ciprofloxacin]
transjugular intrahepatic portosystemic shunt [TIPS] considered in refractory ascites
liver transplantation in refractory ascites

286
Q

Oesophageal Varices [GI bleeding] - s/s

A

typically asymptomatic until they start bleeding
bleeding from varices can cause patients to bleed out due to high blood flow

287
Q

Oesophageal Varices [GI bleeding] - mx

A

immediate senior help
consider blood transfusion [activate major haemorrhage protocol]
treat any coagulopathy
vasopressin analogues [terlipressin]
prophylactic broad-spectrum antibiotics
urgent endoscopy with variceal band ligation
consider intubation and intensive care

Sengstaken-Blakemore tube to tamponade bleeding
Transjugular intrahepatic portosystemic shunt [TIPS]

288
Q

Infection [SBP] - s/s

A

can be asymptomatic
presenting features include: fever, abdominal pain, deranged bloods, ileus, hypotension

organisms: Escherichia coli, Klebsiella pneumoniae

289
Q

Infection [SBP] - mx

A

sample of ascitic fluid for culture before abx
IV broad-spec abx according to local guidelines
human albumin solution to help prevent aki and hepatorenal syndrome
long-term prophylactic antibiotics

290
Q

Infection [SBP] - mx

A

sample of ascitic fluid for culture before abx
IV broad-spec abx according to local guidelines
human albumin solution to help prevent aki and hepatorenal syndrome
long-term prophylactic antibiotics

291
Q

Portal Hypertension - s/s

A

increased resistance to blood flow to the liver due to liver cirrhosis; back pressure on the portal system
splenomegaly
oesophageal varices, caput medusae

292
Q

Portal Hypertension - mx

A

Non-selective b-blockers [propranolol]
Watchful waiting - hope varices don’t bleed

293
Q

Hepatorenal Syndrome - s/s

A

impaired kidney function
reduced blood pressure

294
Q

Hepatorenal Syndrome - mx

A

liver transplant - best option for pt

295
Q

Hepatocellular Carcinoma - s/s

A

jaundice, weight loss, deranged LFTs, abdominal pain, anorexia, n/v, pruritus

296
Q

Hepatocellular Carcinoma - mx

A

resection of early disease can be curative
liver transplant when isolated to liver can be curative
kinase inhibitors to inhibit proliferation of cancer cells [sorafenib]
chemo/radiotherapy don’t tend to work; but can be used as palliative treatment or clinical trials

297
Q

Sepsis - defintion

A

Body launches a large immune response to an infection that causes systemic inflammation and organ dysfunction

298
Q

Sepsis - septic shock

A

Arterial BP drops and results in organ hypo-perfusion, leading to increased anaerobic respiration
*systolic bp <90 despite fluid resuscitation
*hyperlactaemia [lactate >4mmol/L]
aggressively treated with IV fluids, inotropes [noradrenaline], as well as sepsis treatment

299
Q

Examples of organ dysfunction [signs of severe sepsis]

A

resp- –Pa02, –FiO2, need for ventilation, tachypnoea
cardio- –bp, need for inotropes
renal- oliguria, anuria, AKI
haematological- platelet count, coagulation
liver- coagulation, bilirubin
neurological- –GCS

300
Q

Sepsis - risk factors

A

very young/very old [<1 or >75]
chronic conditions [COPD, diabetes]
chemotherapy, immunosuppression, steroids
surgery or recent trauma or burns
pregnancy or peripartum
indwelling medical devices [catheters, central lines]

301
Q

Sepsis - s/s

A

features of specific infection
warm, flushed skin [vasodilation due to inflammatory mediators] or cool, mottled skin [suggests shock]
prolonged CRT
febrile [>38C] hypothermic [<36C]
tachycardic
tachypnoea
hypotension

jaundice, ileus, bleeding, bruising, altered mental status, reduced consciousness, low urine output, anuric

302
Q

Sepsis - ix

A

SEPSIS 6
should be initiated within an hour of recognition of the signs
+oxygen; +antibiotics; +IV fluids; -blood cultures; -urine output; -lactate

FBC, U&Es, CRP, clotting screen, LFTs, ongoing obs
CXR, urine MC&S, CT abdo/pelvis, lumbar puncture, blood film, joint aspiration - find source of infection

303
Q

Sepsis - mx

A

SEPSIS 6
should be initiated within an hour of recognition of the signs
+oxygen; +antibiotics; +IV fluids; -blood cultures; -urine output; -lactate

senior review - all pts with sepsis should be reviewed by a senior clinician and have ongoing monitoring
any deterioration and should be reviewed by intensive care team

304
Q

LRTI/Pneumonia - s/s

A

Symptoms- fever, malaise, cough [with purulent sputum], dyspnoea, pleuritic pain
Signs- dull percussion, reduced breath sounds, bronchial breathing, coarse crepitations, increased vocal transmission, tachycardia, hypotension, confusion, cyanosis

305
Q

LRTI/Pneumonia - ix

A

bed: sputum culture, obs
blood: FBC, U&Es, CRP, cultures
imaging: CXR

306
Q

LRTI/Pneumonia - mx

A

CURB-65 helps to guide treatment
0-1: outpatient treatment
2: consider inpatient
3+: inpatient treatment

antibiotics - amoxicillin 500mg TDS [PO] for 5/7 or co-amoxiclav 1.2g TDS [IV] and Clarithromycin 500mg BD [PO] for 5/7

307
Q

Infective Endocarditis - s/s

A

Symptoms- fever, malaise, lethargy, anorexia, weight loss, abdominal pain, haematuria, cardiac symptoms [sob, chest pain, palpitations]
Signs- cardiac murmur, features of heart failure, splinter haemorrhages, petechiae, Janeway lesions, Osler nodes, Roth spots, splenomegaly

308
Q

Infective Endocarditis - risk factors

A

IV drug use
Chronic kidney disease
Immunocompromised
Hx of infective endocarditis
Structural heart pathology:
*valvular heart disease
*congenital heart disease
*hypertrophic cardiomyopathy
*prosthetic heart valves
*implantable cardiac devices

309
Q

Infective Endocarditis - causative organisms

A

Staphylococcus aureus - IVDU
Coagulase negative staphylococcus - prosthetic devices
Viridans streptococci - poor dentition
Candida albicans, Aspergillus - poor prognosis

310
Q

Infective Endocarditis - patho

A

bacteria enters bloodstream and deposit onto the endocardial surface of the heart
once deposited, the organisms adhere and eventually lead to invasion and destruction of the valve leaflets
key pathological process is formation of infected vegetations

311
Q

Infective Endocarditis - ix

A

Microbiology- at least 3x blood cultures 30m apart before systemic antibiotics
Echocardiography- trans thoracic or oesophageal echo are imaging modalities of choice. Findings suggestive include: vegetation, abscess formation, pseudoaneurysm, valve perforation, new dehiscence of a prosthetic valve

bed: urine dip, ECG
blood: FBC, U&E, CRP/ESR, LFT, VBG
imaging: echo, CXR

312
Q

Infective Endocarditis - mx

A

Streptococci- benzylpenicillin plus low grade gentamicin
Enterococci- amoxicillin plus low grade gentamicin
Staphlococci- flucloxacillin plus gentamicin

313
Q

Infective Endocarditis - follow-up

A

Echo [1x weekly] to assess vegetation size
ECG [twice weekly] to detect conduction disturbances
Bloods [twice weekly] ESR, CRP, FBC, U&Es
Duration of abx will depend on clinical response; may require 6+wks of abx

314
Q

Infective Endocarditis - referral for surgery

A

valve dehiscence
uncontrolled infection
relapse after therapy
threatened or systemic embolism
fungal infections
valve obstruction
aortic root abscess
mod-severe cardiac failure due to valve compromise

315
Q

Meningitis - causative organisms

A

Bacterial meningitis is most commonly caused by Neisseria meningitidis and Streptococcus pneumoniae
Neonates- group B strep is most common

Can also be viral [HIV, VZV, enteroviruses, HSV] or fungal [Cryptococcus neoformans, candida]

316
Q

Neisseria meningitidis

A

Gram negative diplococci
commensal organism in 5-11% of population
Vaccinated against as part of the UK vaccination programme

317
Q

Streptococcus pneumoniae

A

Gram positive diplococci
5-10% asymptomatic carriers in adults; higher in children
Offer vaccinations to children as part of the UK vaccination programme, also offered to patients with significant co-morbidities [diabetes] and adults >65

318
Q

Meningitis - patho

A

Typically acquired through droplets or secretions from the upper respiratory tract
Causes meningeal inflammation via: a) invasion of bloodstream OR b) direct contiguous spread [as a result of ENT infections or trauma]

Mild- infection confined to subarachnoid space
Severe- brain parenchyma underneath pia mater can be affected

319
Q

Meningitis - s/s

A

Symptoms- neck stiffness, photophobia, headache, fever, n/v, fatigue, confusion, irritable or unsettled behaviours, altered mental status
Signs- tachycardia, hypotension, marked neck stiffness, photophobia, non-blanching rash, seizures, focal neurological deficits, reduced consciousness, coma

Two classic signs-
Kernig’s sign: unable to extend knee when hip is flex to 90`
Brudzinski’s sign: spontaneous flexion of knees and hips on flexion of the neck due to pain

320
Q

Meningitis - diagnosing

A

Diagnosis is typically made on clinical suspicion and treatment starts while further investigations are carried out
Definitive diagnosis- isolation of a pathogen from CSF following a lumber puncture
also can be diagnosed using blood cultures too

321
Q

Meningitis - ix

A

ABCDE approach if critically unwell
bed: throat swab, nasopharyngeal swab for viral screen
blood: FBC, U&Es, LFTs, bone profile, coagulation, CRP, blood cultures, VBG, meningococcal PCR
imaging: CT head to look for any contraindications to lumber puncture

322
Q

Meningitis - mx

A

Bacterial - first line is ceftriaxone 2g BD; caution with pen.allergic
dexamethasone can be given as an adjunct

Viral - supportive treatment w/ rest, hydration, analgesia, antipyretic

Meningitis is a notifiable disease - contact tracing, chemoprophylaxis

323
Q

Encephalitis - patho

A

Inflammation of the brain parenchyma
can be secondary to infection or secondary to other causes [cancer, autoimmunity]

324
Q

Encephalitis - s/s

A

Possible features- fever, headache, seizures, altered mental status, behavioural changes, brainstem dysfunction, memory problems, focal neurological deficits

325
Q

Encephalitis - ix

A

bed: obs, urinalysis, ECG, sputum cultures
blood: FBC, U&Es, bone profile, LFTs, CRP, blood cultures, coagulation
imaging: CXR, CT head
special: EEG to record electrical activity in the brain
CSF analysis to potentially identify a cause
Serological testing can be used to check for antibodies associated with paraneoplastic or autoimmune encephalitis

326
Q

Encephalitis - mx

A

Aim to treat the underlying cause
?infection - antibiotics or antivirals
?paraneoplastic/autoimmune/post-infective - immunosuppression [i.e. steroids]

327
Q

Gastroenteritis - define

A

Acute transient diarrhoeal illness +/- vomiting due to an enteric infection
Transmitted by a number of routes [faecal-oral; foodborne; airborne; environmental]

328
Q

Gastroenteritis - causative organisms

A

Viral - rotavirus; norovirus; adenovirus
Bacteria causing watery diarrhoea - Clostridioides difficile; Clostridium perfringens; Entertoxigenic Escherichia coli
Bacteria causing bloody diarrhoea - Non-typhoidal salmonellosis; Campylobacter spp.; Shigella spp.; Yersinia enterocolitica; Enterhaemorrhagic Escherichia coli
Parasites - Cryptosporidium parvum; Entamoeba histolytica; Giardia spp.

329
Q

Gastroenteritis - rotavirus

A

Rare in adults due to long-lasting immunity
Commonly causes watery diarrhoea with vomiting
vomiting settles in 1-3d
diarrhoea settles in 7d
Oral vaccine against virus is now part of the childhood immunisation programme

330
Q

Gastroenteritis - norovirus

A

Most common cause of gastroenteritis in UK; common in winter months
Full recovery within 2 days typically

331
Q

Gastroenteritis - campylobacter

A

Most common bacterial cause [C. jejuni]
Gram negative bacillus
Acquired through ingesting undercooked poultry
Watery or bloody diarrhoea 2-5 days after exposure
Majority of cases are self-limiting within 1wk

332
Q

Gastroenteritis - bacillus cereus

A

commonly causes vomiting illness after reheating starchy food
heat stable emetic toxin causes vomiting; heat labile diarrhoeal toxin causes diarrhoea

333
Q

Gastroenteritis - salmonella

A

acquired through ingestion of contaminated food [i.e undercooked poultry]
typically causes water diarrhoea but can be bloody, associated with abdo pain/fever/vomiting
illness starts within 3d of exposure and resolves within a week
caused by S. enteritidis and S. typhimurium

334
Q

Gastroenteritis - shigella

A

cause of bloody/mucoid diarrhoea associated with fever/abdo pain in young childrne [<5y]
common in late summer
spreads via direct human-to-human contact
illness begins within 1-3d of exposure and resolves within a week

335
Q

Gastroenteritis - escherichia coli

A

there are different types of E.coli:
*enterohaemorrhagic E.coli [EHEC]
*enterotixigenic E.coli [ETEC]
*enteropathogenic E.coli [EPEC]

336
Q

Gastroenteritis - EHEC

A

cause a bloody diarrhoeal illness/may also be asymptomatic
E.coli 0157 is most common in children <5
begins within 3-4d of exposure and resolves within 10d
transmitted through contaminated food; also seen from direct human-to-human contact and contact with infected animals
can cause haemolytic uraemic syndrome in children

337
Q

Gastroenteritis - ETEC

A

commonly associated with water diarrhoeal illness in travellers or resource limited countries

338
Q

Gastroenteritis - entamoeba

A

entamoeba histolytica - anaeorbic parasite
majority of cases are asymptomatic
if symptoms, usually subacute onset over weeks
s/s range from mild diarrhoeal illness to severe dysentery

339
Q

Gastroenteritis - giardia

A

Giardi lambila is commonly implicated in Travellers’ diarrhoea
classically watery diarrhoea alongside abdo pain/anorexia/flatulence/bloating
if left untreated may lead to malabsorption and weight loss

340
Q

Gastroenteritis - s/s

A

Characterised by acute onset of diarrhoea +/- vomiting
Hx- food+drink, foreign travel, contacts, occupation, co-morbidities
Symptoms- diarrhoea, n/v, fever, abdo pain, general malaise, bloating/cramping, weight loss
Signs- features of dehydration, features of shock, abdominal tenderness

341
Q

Gastroenteritis - ix

A

stool- MC&S, virology, C.diff toxin, OCP
blood- FBC, U&Es, bone profile, CRP, VBG, blood cultures
imaging- not routinely recommended in pts with gastroenteritis

342
Q

Gastroenteritis - mx

A

mainly supportive treatment - good oral intake, rest, good basic hygiene
consider hospital admission if: systemically unwell, persistent vomiting or high output diarrhoea, suspected sepsis, failure to respond to supportive treatment, major co-morbidities

343
Q

Gastroenteritis - notifiable diseases

A

cholera
food poisoning
infectious bloody diarrhoea
HUS
enteric fever [typhoid or paratyphoid]

344
Q

Gastroenteritis - notifiable microorganisms

A

bacillus cereus
campylobacter spp.
clostridium perfringens
cryptosporidium spp.
entamoeba histolytica
giardia lambila
salmonella spp.
shigella spp.

345
Q

Acute Cholecystitis - patho

A

inflammation of the gallbladder most commonly due to impacted gallstones

346
Q

Acute Cholecystitis - s/s

A

Symptoms- RUQ pain, epigastric pain, n/v, fever
Signs- RUQ/epigastric tenderness +/- guarding, pyrexia, tachycardia, hypotension

Murphy’s sign- as pt breathes out, place hand below the right costal margin. as pt breathes, inflamed gallbladder moves inferiorly and hits the hand, causing patient to catch their breath.

347
Q

Acute Cholecystitis - ix

A

bed: obs, urine dip, pregnancy test
blood: FBC, U&Es, CRP, LFTs, amylase
imaging: ultrasound, CT abdo w/contrast, MRCP
special: ERCP

348
Q

Acute Cholecystitis - mx

A

Medical: A-E if critically unwell; abx [augmentin +stat dose of gentamicin]; IV fluids; analgesia
Percutaneous cholecystostomy - drain inside the gallbladder placed by IR
Cholecystectomy - definitive management in simple cholecystitis

349
Q

Acute Cholangitis - patho

A

Infection of the biliary tree caused by bacterial infection secondary to biliary obstruction
obstruction can be due to gallstones or biliary strictures [benign and malignant]

350
Q

Acute Cholangitis - s/s

A

Charcot’s triad - fever, jaundice, RUQ pain

Symptoms- RUQ/epigastric pain; fever; malaise; n/v
Signs- RUQ/epigastric tenderness; pyrexia; jaundice; hypotension; confusion

351
Q

Acute Cholangitis - ix

A

bed: obs, urine dip, pregnancy test
blood: FBC, U&Es, CRP, LFTs, amylase
imaging: ultrasound, CT abdo w/contrast, MRCP
special: ERCP

352
Q

Acute Cholangitis - mx

A

Medical- A-E if unwell, IV abx [augmentin + stat dose of gentamicin]; IV fluids; analgesia
Biliary drainage: ERCP or PTC [percutaneous transhepatic cholangiography]

353
Q

Acute Pancreatitis - causes ‘I GET SMASHED’

A

Idiopathic

Gallstones
Ethanol
Trauma

Steroids
Mumps
Autoimmune
Scorpion sting
Hyperlipidaemia/Hypercalcaemia
ERCP
Drugs

354
Q

Acute Pancreatitis - s/s

A

Symptoms- abdo pain; n/v; anorexia; diarrhoea
Signs- abdo tenderness; abdo distention; tachycardia; tachypnoea; pyrexia

Cullen’s sign- peri-umbilical bruising
Grey-Turner’s sign- flank bruising

355
Q

Acute Pancreatitis - ix

A

bed: obs, ECG
blood: FBC, U&Es, LFTs, CRP, amylase, lipase, glucose, lipids, bone profile, ABG
imaging: ultrasound; CT; MRCP

356
Q

Acute Pancreatitis - Glasgow score

A

Completed within first 48hrs, hleps to assess severity of acute pancreatitis
P- PaO2 <8kPa
A- Age >55
N- Neutrophils, WCC >15x10[9]0/L
C- Calcium <2mmol/L
R- Renal, urea >16mmol/L
E- Enzymes, AST >200iu/L or LDH >600iu/L
A- Albumin <32g/L
S- sugar, glucose >10mmol/L

> =3 is a sign of severe disease [should have HDU/ITU input]

357
Q

Acute Pancreatitis - mx

A

General management consists of analgesia, appropriate fluids and nutritional support
antibiotics not routinely indicated in acute pancreatitis

358
Q

Acute Pancreatitis - complications

A

Pancreatic necrosis
Pancreatic pseudocyst
Pseudoaneurysm
Venous thrombosis

systemic:
Acute respiratory distress syndrome
Renal failure
Shock

359
Q

Cystitis - patho

A

cystitis results from colonisation and ascending spread of microorganisms from the urethra to the bladder
typically Escherichia coli
uncommon in men

360
Q

Cystitis - risk factors

A

recent sexual intercourse
diabetes
history of UTIs
spermicide use
catheters

361
Q

Cystitis - s/s

A

Symptoms- dysuria; frequency; urgency; incontinence; suprapubic pain; haematuria; n/v
Signs- fever; rigors; flank pain; confusion; costovertebral angle tenderness

362
Q

Cystitis - ix

A

Definitive diagnosis of UTI is based on typical clinical features and positive lab evidence of pyuria +/- bacteriuria

bed: urine dip, urine MC&S, obs, pregnancy test, STI screen
blood: FBC, U&Es, CRP
imaging: not routinely used but can use ultrasonography and CT

363
Q

Cystitis - mx

A

Appropriate antibiotic therapy according to local guidelines

consider delaying if not unwell
unwell/men/pregnant/diabetes/others - immediate treatment

Nitrofurantoin 100mg BD for 3/7; 7/7 if pregnant/men/complications

364
Q

Pyelonephritis - patho

A

pyelonephritis results from colonisation and ascending spread of microorganisms from the urethra to the bladder
typically Escherichia coli
uncommon in men

365
Q

Pyelonephritis - s/s

A

Symptoms- dysuria; frequency; urgency; incontinence; suprapubic pain; haematuria; n/v
Signs- fever; rigors; flank pain; confusion; costovertebral angle tenderness

366
Q

Pyelonephritis - ix

A

Definitive diagnosis of UTI is based on typical clinical features and positive lab evidence of pyuria +/- bacteriuria

bed: urine dip, urine MC&S, obs, pregnancy test, STI screen
blood: FBC, U&Es, CRP
imaging: not routinely used but can use ultrasonography and CT

367
Q

Pyelonephritis - mx

A

Abx according to local guidelines

Co-amoxiclav 625mg TDS for 10/7
pregnant- cefalexin 500mg BD for 10/7

368
Q

Cellulitis - patho

A

Acute bacterial infection of the skin
Affects both dermis and subcutaneous tissue
Occurs anywhere on the body; ranges from self-limiting to necrotising infection

369
Q

Cellulitis - causative organisms

A

Beta-haemolytic streptococcus
Staphylococcus aureus
^^ commonly

370
Q

Cellulitis - s/s

A

Symptoms- pain, redness, swelling, malaise, fever
Signs- tenderness on palpation, erythema, skin warmth, superficial bullae/blisters, abscess, lymphadenopathy

371
Q

Cellulitis - ix

A

Diagnosis usually made clinically based on the classic appearance
Lab investigations are often unnecessary

bed: skin swabs, blood glucose
blood: FBC, U&Es, LFTs, CRP, blood cultures, HbA1c
imaging: ultrasound, X-ray

372
Q

Cellulitis - mx

A

Mild cellulitis can be treated in community with oral antibiotics - penicillin or flucloxacillin or erythromycin
Severe cellulitis/unwell pt/lymphoedema/complications may warrant hospital admission; IV abx [flucloxacillin, clindamycin, vancomycin]

373
Q

Necrotising Fasciitis - patho

A

rapidly progressive infection resulting in extensive tissue destruction

374
Q

Necrotising Fasciitis - s/s

A

Can be confused with cellulitis
Disproportionate pain compared with physical findings

Skin changes:
Stage I- erythema, tenderness, swelling, warmth
Stage II- bullae formation, blistering, fluctuation of the ksin
Stage III- haemorrhagic bullae, crepitus, tissue necrosis

375
Q

Necrotising Fasciitis - ix

A

Diagnosis is essentially clinical
Gold standard is surgical exploration and tissue biopsy
Fascial necrosis with loss of natural tissue planes is diagnositc
If suspected, do not delay surgical exploration and debridement

376
Q

Necrotising Fasciitis - mx

A

Prompt resuscitation
Antibiotics- Tazocin, meropenem, clindamycin
Surgical debridement- early and aggressive surgical debridement is priority
Supportive care
Reconstruction- should only be considered when the infection is completely eradicated; can include skin grating, local/regional flaps/free tissue transfer

377
Q

Diabetic Foot Infection - patho

A

Defined as any type of skin, soft tissue or bone infection below the ankle in patients with diabetes

378
Q

Diabetic Foot Infection - s/s

A

ulcer, pain, loss of protective sensation
malaise, anorexia, foot erythema, oedema of foot/ankle/calf, absent pedal pulses, fluctuance

379
Q

Diabetic Foot Infection - ix

A

bed: swabs for culture, glucose
blood: FBC, U&Es, CRP, HbA1c
imaging: X-ray; MRI or CT
special: ABPI; duplex ultrasound

380
Q

Diabetic Foot Infection - mx

A

Debridement
Supportive treatment
Antibiotics
Diabetic review - better control to stop further progression
Negative pressure wound therapy
Skin grafts
Surgery

381
Q

Septic Arthritis - patho

A

Commonly a bacterial infection of one or more joints; typically Staphylococcus aureus
Haematogenous spread is most common mechanism of infection; direct inoculation can occur through an animal bite, surgery, wounds or joint injection

382
Q

Septic Arthritis - risk factors

A

Diabetes
Advancing age
Prosthesis
Immunodeficiency/immunosuppression
IV drug use

383
Q

Septic Arthritis - s/s

A

High index of suspicion for any patient presenting with acute atraumatic joint pain
Symptoms- pain, swelling, fevers, inability to weight bear
Signs- pain on active and passive movement, reduced ROM, erythema, warmth, joint effusion

384
Q

Septic Arthritis - ix

A

bed: obs, glucose, urine dip, consider sexual health screen
blood: FBCV, U&Es, CRP, LFTs, ESR, urate, blood cultures
imaging: plain X-ray; ultrasound; CT/MRI
special: joint aspiration [gold standard for diagnosing; should be send for WBC, gram stain, culture and crystal microscopy]; synovial tissue culture

385
Q

Septic Arthritis - mx

A

Should be referred to and managed by orthopaedics
Antibiotics- typically a long course of antibiotics 6wks with 2 weeks of IV therapy; refer to local guidelines [flucloxacillin 2g QDS]
Joint drainage- joint should be aspirated to dryness; arthroscopic drainage and washout considered

386
Q

Osteomyelitis - patho/causative organism

A

Infection of the bone
Most common cause- Staphylococcus aureus [Gram positive cocci]
Haematogenous spread [rf: indwelling intravascular catheter, haemodialysis, endocarditis, IVDU]
Non-haematogenous spread occurs due to skin ulcers, trauma, surgery, animal/insect bites

387
Q

Osteomyelitis - s/s

A

Symptoms- fever, pain, overlying redness, swelling, malaise
Signs- erythema, swelling, evidence of previous surgery or trauma, tenderness, discharging sinus, ulcers/skin breaks

388
Q

Osteomyelitis - ix

A

bed: obs, glucose, urine dip
blood: FBC, U&Es, CRP, LFTs, ESR, HbA1c
microbiology: urine MSU, blood cultures, wound swab, bone culture
imaging: diagnosed on MRI usually; X-ray; CT

389
Q

Osteomyelitis - mx

A

Antibiotics +/- surgical debridement is main focus of treatment

390
Q

Spondylodiscitis - patho

A

involves infection of the vertebra and infection of the vertebral disc
Similar to osteomyelitis but also affects the disc
Staphylococcus aureus

391
Q

Spondylodiscitis - s/s

A

Symptoms- fever, pain, overlying redness, swelling, malaise
Signs- erythema, swelling, evidence of previous surgery or trauma, tenderness, discharging sinus, ulcers/skin breaks

392
Q

Spondylodiscitis - ix

A

bed: obs, glucose, urine dip
blood: FBC, U&Es, CRP, LFTs, ESR, HbA1c
microbiology: urine MSU, blood cultures, wound swab, bone culture
imaging: diagnosed on MRI usually; X-ray; CT

393
Q

Spondylodiscitis - mx

A

Referral to infectious disease specialist and a spinal surgeon
Antibiotics
Monitoring for neurological changes, sepsis, spinal instability, intraspinal empyema
^ indications for surgical treatment

394
Q

Returning Traveller with Fever - s/s

A

febrile illness, diarrhoea +/- vomiting, jaundice, lymphadenopathy, hepatosplenomegaly, cough, sob, rash
^ any combination of symptoms

395
Q

Returning Traveller with Fever - history and examination

A

*geographic region of travel within last 12m
*dates of travel and duration of stay
*careful documentation of time of onset and nature of various symptoms/signs
*type of accommodation [hotels vs more rural backpacker areas have different levels of exposure to certain things]
*recreational activities and exposures [insects, animals, lakes and streams, canal water]
*type of food/drink consumed
*sexual history [condom use, sex with commercial sex worker, MSM]
*past medical history and predisposition to infection

396
Q

Returning Traveller with Fever - typical time frame

A

0-10d: dengue fever, rickettsia, viral [inc. mono], GI [bacterial/amoeba]
10-21d: malaria, typhoid, primary HIV
>21d: malaria, chronic bacterial infection, TB, parasitic infections

397
Q

Returning Traveller with Fever - o/e

A

pulse: brady can indicate typhoid
skin: maculopapular rash can be indicative of dengue fever, mono, rubella, parvovirus B19, primary HIV
skin: rose spots, pink macules 2-3mm in diameter on chest/abdomen indicates typhoid
skin: black necrotic ulcer with erythematous margins - rickettsia [tick exposure]
skin: petechiae, ecchymoses, or haemorrhagic lesions - dengue fever, meningococcaemia, viral haemorrhagic fever
eye: conjunctival suffusion - leptospirosis
spleen: splenomegaly - mono, malaria, typhoid fever
neurological system: fever+altered mental status may represent meningo-encephalitis

398
Q

Returning Traveller with Fever - ix

A

bed: obs, urinalysis+/-culture
blood: FBC, U&Es, LFTs, blood film, blood cultures [x2 with biohazard labels], serology for hep b/c/hiv/syphilis
stool: culture +/- stool for ova, cysts and parasites [OCP]

399
Q

Malaria - patho

A

Caused by parasite - plasmodium falciparum [can be f. vivax and p. ovale too]

400
Q

Malaria - s/s

A

Symptoms- fever +/- rigours and sweating, fatigue, malaise, headache, anorexia, n/v/d, myalgia, arthralgia, confusion, sore throat, cough
Signs- pallor, splenomegaly, jaundice

Signs of severe malaria:
*cerebral malaria [seizures/low GCS]
*AKI [oliguria/anuria]
*metabolic acidosis
*hypoglycaemia
*respiratory distress [sob/hypoxia due to ARDS]
*severe anaemia [<70g/L] [breathlessness, chest pain, dizziness, syncope, severe pallor]
*spontaneous bruising or bleeding [suggestive of DIC]
*thrombocytopenia
*hypovolaemia and shock

401
Q

Malaria - ix

A

Diagnosis is based on thick and thin slides [gold standard diagnostic tool for malaria] 3x in 36hrs
rapid diagnostic test [detection of malarial antigens]; can be completed in 15-20m

blood: FBC, U&Es, LFTs, bone profile, CRP, VBG, blood glucose
imaging: CXR, CT head [if low GCS]
cultures: septic screen

402
Q

Malaria - mx

A

Riamet - 4 tablets
OR Malarone - 4 tablets daily for 3d

403
Q

Typhoid Fever - patho

A

caused by salmonella typhi
faecal-oral route of transmission

404
Q

Typhoid Fever - s/s

A

Persistent fever
Dull frontal headache
Anorexia
Apathetic-lethargic state
Constipation
Cough
Diarrhoea
Malaise
Nausea
Prostration- extreme physical weakness
Chills; hepatomegaly; pneumonia; relative bradycardia; rigors; rose spots; splenomegaly

405
Q

Typhoid Fever - o/e

A

Pulse-temperature dissociation [high fever, low pulse]
Hepatosplenomegaly
Rose spots, but may disappear before presentation

406
Q

Typhoid Fever - ix

A

bed: obs, stool MS&U+culture, urine culture
blood: FBC, U&Es, LFTs, TFTs, CRP, blood cultures
imaging: ?CT head for headache/altered mental status
special: bone marrow culture, rose spot culture

407
Q

Typhoid Fever - mx

A

Antibiotic therapy and supportive care
IV ceftriaxone 2g OD, the nonce sensitivities known switch to an appropriate abx

408
Q

Pyrexia of Unknown Origin - patho

A

Classical definition:
Temperature >38` on multiple occasions
Illness of >3wks duration
No diagnosis despite >1wk inpatient investigation

409
Q

Pyrexia of Unknown Origin - ix

A

hx- chronology of events/symptoms; pets/animal exposure; travel; occupation; medications; family history; vaccination history; sexual history
o/e- lymph nodes; stigmata of endocarditis; evidence of weight loss; joint abnormalities; abdominal exam
blood: FBC, U&Es, LFTs, bone profile, CRP, clotting, TFTs, multiple blood cultures, LDH, ferritin, B12, folate, ?immunoglobulins, ?autoimmune screen
micro: HIV, hepB/C, syphilis, MSU, sputum cultures, ?malria films, ?atypical pneumonia screen, viral swabs, CMV/EBV serology
imaging: CXR, CTthorax/abdo/pelvis, transthoracic echo, ?MRI, ?PET

410
Q

Pyrexia of Unknown Origin - mx

A

Aim to find a diagnosis to treat instead of going in blind
Don’t use abx, steroids, antifungals without speaking to a senior
Rheumatology, haematology are asked to see patients
Stable patients can be managed as outpatients
Prognosis does tend to be good, even without a diagnosis

411
Q

Pyrexia of Unknown Origin - causes

A

infection: TB, abscess, infective endocarditis, brucellosis
autoimmune/connective tissue: adult onset Still’s disease, temporal arteritis, Wegner’s granulomatosis
Neoplastic: leukaemias, lymphomas, renal cell carcinoma
Other: drugs, thromboembolism, hyperthyroidism, adrenal insufficiency

412
Q

Causes for immunosuppression

A

*age
*chronic disease
*malnutrition
*immunosuppression drugs - for crohn’s or rheumatoid arthritis - azathioprine/methotrexate/monoclonal antibodies/anti-tnf drugs
*oral steroids
*anti-rejection drugs for after a transplant
*chemotherapy or radiotherapy for cancer
*some types of cancer - particularly lymphomas, leukaemias, myelomas
*splenectomy patients
*HIV/AIDS
*genetic conditions - SCID, DiGeorge’s syndrome

413
Q

Immunosuppression - mx regarding infection

A

*avoid eating food that would put you at risk of food poisoning
*handle raw meat safely
*good hygiene
*avoid close contact with people with infections
*ensure all routine vaccinations are up to date
*extra vaccinations - i.e. annual flu-jab; COVID-19 vaccination; shingles vaccine
*don’t take live vaccines - ask your doctor if this is suitable for you
*post-splenectomy patients tend to take prophylactic antibiotics

414
Q

What is a CGA?

A

Comprehensive Geriatric Assessment
multidimensional, interdisciplinary diagnostic process to determine all of the capabilities of a frail older person in order to develop a coordinated and integrated plan for treatment and long-term follow-up

415
Q

What are the components of a CGA?

A

*problem list - current and past
*medication review
*nutritional status
*mental health - cognition, mood, anxiety, fears
*functional capacity - ADLs, gait/balance, activity/exercise status, instrumental ADLs [cooking, cleaning, laundry, transport]
*social circumstances - support from family/friends, social network from visitors/daytime activities, eligibility for being offered care resources
*environment - home, facilities and safety at home, transport, accessibility to local resources

416
Q

What is frailty?

A

Frailty is a distinctive health state related to the ageing process in which multiple body systems gradually lose their in-built reserves
This group of people are most at risk of adverse health outcomes

417
Q

What is the frailty score?

A

Tool to quickly and simply assess frailty
Has been validated in adults over 65y
Can help optimise quality of life outcomes for geriatric patients
Score >=5 is a marker for completing a CGA

418
Q

What is polypharmacy?

A

When 6 or more drugs are prescribed at any one time

419
Q

What is the STOPP/START tool?

A

Screening Tool of Older Persons’ Prescriptions
and
Screening Tool to Alert to Right Treatment
-criteria used as a tool for clinicians to review potentially inappropriate medications in older adults

420
Q

What is included in the STOPP/START tool?

A

Medications for clinicians to consider stopping or starting in >65 patients
Some medications may not be useful for patient anymore, some medications may provide extra benefit for patient
Lots of evidence based medicine

421
Q

Blackout/Collapse in Elderly Patient - ix

A

bed: obs [bp standing/lying], ECG, cranial nerve exam, nutritional status
blood: FBC, U&Es, CRP, CK, blood cultures
imaging: X-ray/s, CT head
other investigations may be indicated depending on patient history and other investigation findings

422
Q

Constipation - ix

A

bed: PR, medication review
blood:
imaging: AXR, CT abdo/pelvis

423
Q

Urinary Incontinence - ix

A

review of bladder and bowel diary
abdominal examination
urine dipstick and msu
PR examination
external genitalia review - particularly looking for atrophic vaginitis in females
post micturition bladder scan

424
Q

Falls - ix

A

good history - witnessed/unwitnessed? how did fall happen? dizziness/light-headedness? LOC? cardiac symptoms? weak? happened before? medication history? normal mobilisation?
o/e- CVS exam, ECG, neurological examination, MSK exam, functional assessment of mobility

suspicion of a specific cause may warrant further investigations - CT head for example

425
Q

Delirium - definition

A

Acute confused state, with sudden onset and fluctuating in course
Develops over 1-2 days and is recognised by a change in consciousness - either hyper or hypoalert and inattention

426
Q

Delirium - causes

A

*underlying medical problem
*substance intoxication
*substance withdrawal
*combination of any of ^

Good to exclude these causes:
*infection
*electrolyte imbalances
*hypoxia
*drugs - inc. opiates
*urinary retention
*constipation
*uncontrolled pain

427
Q

Dementia - definition

A

A progressive decline in cognitive functioning usually occurring over several months
Affects many areas of function including: retention of new information; managing complex tasks; language and word finding difficulty; orientation; recognition; ability to self care; reasoning

428
Q

Dementia - types

A

*Alzheimer’s disease
*Vascular dementia
*Dementia with Lewy Body
*Parkinson’s disease with dementia
*Frontotemporal dementia

429
Q

How to assess capcity

A

Always assume somebody has capacity
A person has capacity if they can do all of the following:
*understand information relevant to the decision in question
*retain that information
*use the information to make their decision
*communicate a decision

430
Q

At what point does a patient reach ‘end of life’ care?

A

Patients who are likely to die within the next 12months
Patients with advanced, progressive, incurable conditions
Generally frail with co-existing conditions that mean they are expected to die within 12m
Patients with existing conditions if they’re at risk of dying from a sudden acute crisis in their condition
Patients with life-threatening acute conditions caused by sudden catastrophic events

431
Q

What are some symptoms patients may face at the end of their life?

A

pain
n/v
dyspnoea
agitation
confusion
constipation
anorexia
terminal secretions

432
Q

What is a DNAR?

A

Form used by medical professionals to communicate that a decision has been made to not attempt CPR

433
Q

What goes into a conversation surrounding DNAR forms?

A

*patient’s diagnosis, prognosis, and current situation
*what outcomes the patient would value and fear
*what treatments might help to achieve their desired outcomes
*you must tell them if a clinical decision has been made that CPR is not appropriate and a DNAR has been added to their records
*forms can be reviewed when necessary - if patient’s wishes have changed or their health has improved/declined

Year 3 (5 decks)

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