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Year 3 > Medicine > Flashcards

Medicine Flashcards

1
Q

What scoring system is used for risk of rebleeding and mortality in upper GI bleed patients? (also state factors included)

A

Rockall Score
Mortality for upper GI bleed after endoscopy
Includes age, haemodynamic instability (tachycardia and hypotensive), comorbidities, diagnosis from endoscopy, endoscopic stigmata.

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2
Q

What scoring system is used for risk of stroke to guide decision to anticoagulate? Tell me about it

A 
CHA2DS2VASC score. Used to predict risk of stroke for decisions to anticoagulate.
CHF
HTN
Age 65-74
DM
Stroke/TIA
Vasc disease (MI, PAD)
Age >75
Sc sex category (F)
offer anticoagulation to all patients with a score >2
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3
Q

What scoring system for pneumonia?

A 
CURB-65
Confusion
BUN >7
RR >30
BP <90/<60
>65

Mild- 1 (amoxicillin 5 days). Home
Mod- 2 (amox and doxy). Hospital
Severe- 3 (Co-amox IV and doxy PO). Consider ICU

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4
Q

What scoring system is used for DVT?

A

Two-level Wells score
The risk of DVT is likely if the score is two points or more, and unlikely if the score is one point or less.
If likely, arrange proximal leg vein USS. If unlikely, do D-dimer, if positive arrange USS.
Active Ca
Swollen calf >3cm compared with asymptomatic leg
Entire leg swollen
Tender calf
Immobilised leg
Recently bedridden for 3+ days or major surgery needing GA in last 12 weeks
Pitting oedema (greater than asymptomatic leg)
Collateral superficial veins (non-varicose)
Previously documented DVT
Subtract 2 points if alternative explanation more likely

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5
Q

UC severity

A

Truelove and Witts

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6
Q

To help guide admission in upper GI bleed patients

A 
Blatchford
Early discharge considered for score of 0 
BUN 
Low BP/Hb
Abnormal poop (malaena)
Tachycardia >100
CF 
Hepatic Failure
Fall- syncope
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7
Q

To diagnose true constipation

A

Rome criteria- need 2 or more of…
25% bowel motions involve straining
Need to manually evacuate
Hard/lumpy stools

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8
Q

Severity of liver cirrhosis

A 
Child-Pugh
Bilirubin (µmol/l)	<34	34-50	>50
Albumin (g/l)	>35	28-35	<28
Prothrombin time,
prolonged by (s)	<4	4-6	>6
Encephalopathy	none	mild	marked
Ascites
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9
Q

Criteria for pleural fluid contents

A

Light’s criteria. Use if pleural fluid protein is between 25-35 so you’re not sure if it’s transudate or exudate.
Exudate if one or more of the following:
Pleural fluid LDH: serum LDH >0.6
Pleural fluid protein:serum protein >0.5
Pleural fluid LDH >2/3 of upper limit of normal

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10
Q

What is the formula to calculate acid base?

Interpret the results

A

Na - (Cl + Bicarb)
8-12 is normal
>12 means that the acidosis is due to excess acid (e.g. lactic acidosis, ketoacidosis, renal failure)
<8 means that the acidosis is due to decreased alkali (e.g. GI losses of HCO3 with diarrhoea, renal losses of HCO3 with renal tubular acidosis, Addison’s)

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11
Q

What questionnaire could be used to assess alcohol misuse?

A

CAGE

  1. Have you ever felt you should CUT down
  2. Have people ever ANNOYED you by asking about your drinking?
  3. Have you ever felt GUILTY about your drinking?
  4. Have you ever had a drink first thing in the morning to steady nerves/get rid of hangover? (EYE-OPENER)

Or the more comprehensive AUDIT questionnaire (alcohol use disorders identification test)

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12
Q

MRC dyspnoea scale

A

1- only troubled on exertion
2- breathless up hill/hurrying
3- walks slower than most people/stops after a mile
4- stop after 100m
5- too breathless to leave house/dressing breathless

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13
Q

Scoring system for severity/prognosis of acute pancreatitis

A 
Glasgow criteria- remember with PANCREAS
PaO2 <8
Age >55 
Neutrophils >15
Calcium <2 
Renal function urea >16
Enzymes LDH >600, AST >200
Albumin <32
Sugar blood glucose >10

Severe pancreatitis if >3 in first 48hrs of admission

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14
Q

Scoring system for open fractures

A 
Gustilo Anderson 
I - wound <1cm
II - wound 1-10cm 
IIIa - wound >10cm, high energy, extensive soft tissue damage, contaminated 
IIIb- Needs flap coverage
IIIc- Needs vascular repair
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15
Q

Scoring system for necessity of amputation after lower extremity trauma

A

MESS- Mangled Extremity Score

Variables: skeletal and soft tissue injury, limb ischaemia, shock and age

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16
Q

Disease progression for OA

A

WOMAC score

score range of 0-20 for Pain, 0-8 for Stiffness, and 0-68 for Physical Function

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17
Q

Scoring systems for delirium

A

CAM (confusion assessment method)
4AT
Assesses acute/fluctuating onset, inattention, disorganised thinking, altered level of consciousness

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18
Q

Describe the 3 measurements of distal radial fractures to determine whether they are displaced

A

Radial height: 11mm
Radial inclination: 22 degrees
Volat tilt (on lateral): 11 degrees

Acceptable criteria is less than 5mm/5 degrees change and can be non-operatively managed with closed reduction and cast immobolisation

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19
Q

Classification for ankle fractures

A

Weber
A - below level of syndesmosis, likely stable, can manage with reduction and cast
B- transyndesmosis, ?stable
C- suprasyndesmosis, unstable, rupture of deltoid ligament, needs ORIG

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20
Q

Scoring system for PE likelihood

A

Two-level Wells score.
PE likely if >4 (as opposed to DVT which is 2+)
Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins)
An alternative diagnosis is less likely than PE (e.g. resp, ACS, MSK pain, GORD)
Heart rate > 100 beats per minute
Immobilisation for more than 3 days or surgery in the previous 4 weeks
Previous DVT/PE
Haemoptysis
Malignancy (on treatment, treated in the last 6 months, or palliative)

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21
Q

What is D-dimer?

A

Cross-linked fibrin broken down by plasmin

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22
Q

Scoring system for PE likelihood

A

Two-level Wells score.

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23
Q

What is PE treatment:

A

Start 24hr empirical LMWH (can be outpatient) while CTPA is arranged. Then once PE is confirmed start anticoagulation:
If unprovoked PE need 6mo LMWH (potentiates ATIII)
If provoked PE 3mo LMWH
If unprovoked consider investigating undiagnosed cancer and anti-phospholipid testing (cardiolipin)
Can also use apixaban as anticoagulant (direct factor Xa inhibitor)

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24
Q

What can cause a positive D-dimer test?

A

Specificity of D-dimers decreases with aging and with co-morbid illnesses such as cancer, infection, inflammation, vasculitis, pregnancy, trauma, haemorrhage and post-surgical states.

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25
Q

What is PE treatment:

A

Start 24hr empirical LMWH (can be outpatient) while CTPA is arranged. Then once PE is confirmed start anticoagulation:
If unprovoked PE need 6mo LMWH
If provoked PE 3mo LMWH
If unprovoked consider investigating undiagnosed cancer and anti-phoshoplipid testing (cardiolipin)
Can also use apixaban as anticoagulant (direct factor Xa inhibitor)

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26
Q

What is the test for ruptured Achilles’ tendon?

A

Simmonds’ Test

With knee on chair and foot hanging off, squeeze the calf. The foot should plantarflex

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27
Q

What scoring system is used for antibiotic prescription in URTI?

A 
Centor.
Tonsillar exudate
Fever 
No cough 
Tender anterior cervical lymphadenopathy?

Scoring 3 or 4 of these signs suggests they may have Group A beta-haemolytic streptococcus e.g. Streptococcus pyogenes (40-60% chance) and may benefit from Abx.

Treat with penicillin V 500mg QDS for 7 days (2nd line erythromycin)

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28
Q

How would you score for malnutrition? Man with 4k weight loss over 4 months, BMI 19, current chest infection.

A

BMI Score: >20 is 0, 18.5-20 is 1, <18.5 is 2
Weight loss over 3-6mo: <5 is 0, 5-10 is 1, >10 is 2
Has been acutely ill OR likely to be no intake for >5days then add 2

He scores 3.
2 or more is at high risk so treat: refer to dietician, set goals, monitor and review care plan

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29
Q

What is refeeding syndrome and who’s at risk?

A

Potentially fatal shift of fluids and electrolytes in malnourished patients on refeeding.

At risk: BMI <16, unintentional weight loss >15% in 3-6mo, little/no intake last >10 days, low levels of K, phosphate, Mg prior to feeding, Hx alcohol abuse, drugs

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30
Q

How should you manage someone at risk of refeeding syndrome:

A 
max 10kcal/kg/day
Restore volume and fluid balance 
Oral thiamine 200-300mg daily 
Vitamin B 
Balanced multivitamins, K, Mg
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31
Q

Patient presents with headache, neck stiffness, non-blanching rash. How will you manage?

A

2 large bore cannulas, check obs for shock
LP (CSF protein and leukocytes high, glucose low, gram stain and culture). No LP if at risk of coning
Start IV ceftriaxone (or benzypenicillin IM if GP)
Dexamethasone within 4hrs of Abx improves outcomes

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32
Q

What long term complications of meningitis might result?

A

Hearing loss- test before discharge/within 4 weeks
Epilepsy
Amputations
Cognitive, behavioural problems/memory problems, learning difficulties

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33
Q

Name most common causes of meningitis at different ages and their class of bacteria

A

Newborns- Escherichia coli (gram neg rod), listeria monocytogenes (gram pos rod)
Infants- Haemophilus influenzae (gram neg rod) (this is why babies are given Hib vaccine)
Adults- neisseria meningitidis (gram neg diplococci)
Elderly- Streptococcus pneumoniae (gram pos cocci, strings)

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34
Q

What is a notifiable disease, and which are they?

A

Registered medical practitioners have statutory duty to notify local health protection team of suspected cases (routine <3days, urgent <24hrs)

Urgent notification: poliomyelitis, Hep ABC, anthrax, botulism, cholera, diphtheria, typhoid, HUS, infectious bloody diarrhoea, invasive group A strep, legionnaire’’s, measles, meningococcal septicaemia, plague, rabies, SARS, smallpox, viral haemorrhage fever, bacterial acute meningitis, food poisoning if part of cluster, whooping cough

Routine notification: acute encephalitis, brucellosis, scarlet fever, leprosy, malaria, mumps, rubella, tetanus, TB, typhus, yellow fever

Note: HIV is NOT notifiable!!!

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35
Q

What are the different types of meningitis?

A

Pneumococcal- streptococcus pneumoniae
Meningococcal- neisseria meningitidis
Hib meningitis- Haemophilus influenza
Are the bacterial types

Viral: more common and less severe e.g. HSV, VZV, influenza

Fungal e.g. cryptococcus

Parasitic

Amebic

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36
Q

Traveller returns with pyrexia of unknown origin. What are your differentials and investigations?

A

DDx: Hep ABC, HIV, TB, dengue fever, viral haemorrhagic fever, yellow fever, malaria, East African sleeping sickness, Giardiasis, Lassa fever, Japanese encephalitis, EBV, CMV

Ix: FBC, CRP, LFTs, U&Es, urine dip, blood culture, stool sample C&S, O&P, giardia stool Agm faecal leukocytes, malaria blood films,

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37
Q

What are you at risk of being colonised with if treated in hospital abroad?

A

CRO. Screen them with rectal swab, wound swab, cannula/drain swab
Once safe can be moved out of side room

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38
Q

What do the different tests for TB tell you?

A

AFB smear and culture- tells you if active TB and what it’s sensitive to
NAAT- nucleic acid amplification test. Tells you rapidly if active TB
Quantiferon Gold- tells you if any active or latent TB

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39
Q

What is the stain for mycobacterium?

A

Ziehl-Neelson

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40
Q

What are the 4 drugs for TB, their side effects?

A

Rifampicin- orange wee, flu-like, hepatotoxicity
Isoniazid- hepatotoxicity, peripheral neuropathy, itchy
Pyrazinamide- hepatotoxicity
Ethambutol- optic neuritis

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41
Q

What is the treatment for active TB?

A

All 4 drugs for 4 months

Rifampicin and isoniazid for additional 2 months

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42
Q

What is the treatment for latent TB?

A

Either 6mo of isoniazid

Or 3mo of rifampicin and isoniazid

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43
Q

What is the treatment for meningeal TB?

A

Rifampicin and isoniazid for 12mo

Then pyrazinamide and ethambutol for 2 months

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44
Q

Causes of constipation

A

Opiates, hypercalcemia, hypothyroidism, lack of food/water/movement/fibre, lack of privacy, pain/immobility

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45
Q

What medications might cause constipation

A

Opiates, NSAIDs, amantadine, beta blockers, TCAs, calcium channel blockers e.g. verapamil

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46
Q

Name causes of urinary retention

A 
Faecal impaction
BPH 
ACEi
TCAs
NSAIDs
CCBs
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47
Q

A woman presents with urinary incontinence. How will you proceed?

A

Categorise as stress or urgency/overactive bladder.

If SI- pelvic floor muscle training >3mo, can offer duloxetine (5-HT and NA reuptake inhibitor)
Surgery- mid-urethral mesh sling

If nocturia can try desmopressin

OAB- reduce caffeine, bladder training for >6wks, start anticholinergics e.g. oxybutynin, if fails can consider augmentation cystoplasty

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48
Q

Name 4 reversible causes of cognitive decline

A

Delirium
Depression
Sensory impairment e.g. no glasses, hearing aid
Medication

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49
Q

How can dementia be diagnosed?

A

With the 6-CIT score (cognitive impairment test). Note doesn’t rule out dementia if normal score.

What year is it, what month, remember this address, months of the year in reverse, recall the address

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50
Q

What specialist tests are available for sub-types of dementia?

A

AD- FDG-PET, CSF for total tau

Frontotemporal dementia- FDG-PET

Vascular dementia- MRI

Lewy bodies- I-FP-CIT SPECT

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51
Q

How can you tell the difference between delirium and dementia?

A 
Use the CAM test as a delirium screening tool.
Features of delirium: 
1. fluctuating and acute onset
2. inattention
3. disorganised thinking 
4. altered level of consciousness

If 1+2 plus 3 OR 4 are present, this suggests delirium

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52
Q

Should enteral feeding be used in patients with dementia?

A

Normally, not in severe dementia no. Should only be used if it is a treatable cause expected to resolve afterwards.

Has no benefit to mortality, no benefit to weight/nourishment, more likely to get aspiration pneumonia.

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53
Q

What feeding safely principles should be used in dementia?

A

Conscious, reduce distractions, upright, give time, oral hygiene, glasses and hearing aids

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54
Q

How can you determine mental capacity?

A 
Assume capacity. 
Understand info 
Weigh up info 
Retain info 
Communicate decision
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55
Q

What is involved in an advance care plan?

A

Discussion with patient and carers, and family if they wish. Involves advance statement about wishes, preferences, beliefs and values, advance decisions to refuse treatment, place of care and death. Chances to review and change

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56
Q

Categorise causes of a fall

A 
Mechanical- trip
Cardiac- arrhythmias, MI 
Vascular- stroke, TIA, vasovagal, postural hypotension
Metabolic- hypoglycemia, hypovolemia
MSK- weakness, movement difficulties 
Sensory- vision, balance
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57
Q

Name some MDT strategies to help before discharging patient with fall

A 
Home assessment/OT 
Physio- strength and balance training 
Vision assessment and referral 
Med review 
Education on prevention, how to cope if they fall (avoiding long lie)
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58
Q

What commonly prescribed drugs increase the risk of falls in older people?

A

Sedatives - benzodiazepines, amitriptyline

ACEi (accumulate in renal failure/dehydration)
Thiazides (hypokalaemia and hyponatremia)
Beta blockers (hypotension, bradycardia)

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59
Q

Summarise tests for acute confusion, delirium and dementia?

A

Confusion - MMSE ??
Delirium- CAM (confusion assessment method), 4-AT
Dementia- 6CIT (cognitive impairment test) Is best, maybe AMT (abbreviated mental test)

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60
Q

Common causes of AKI

A

Pre-renal- dehydration/hypovolemia, NSAIDs, HF

Intrinsic

Post-renal

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61
Q

Common causes of AKI

A

Pre-renal- dehydration/hypovolemia, NSAIDs, HF

Intrinsic- gentamicin, post-streptococcal GN, rhabdomylosis, ATN

Post-renal- ACEi, BPH, bladder Ca, nephrolithiasis, urinary retention

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62
Q

Causes of nephrotic and nephritic syndrome

A 
Nephrotic is losing protein <3.5g. (MADFucker throwing steaks around) 
Minimal change disease
Membranous nephropathy 
Amyloidosis 
Diabetic nephropathy 
FSGS
Nephritic is blood. PIGPEAL. 
Post-streptococcal GN 
IgA nephropathy 
Goodpasture's 
Polyangitis with granulomatosis (ELK) (actually gran comes first) 
Eosinophilic polyangitis with granulomatosis (Churg-Strauss)
Alport syndrome 
Lupus nephritis
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63
Q

What hormones (and how) regulate fluid balance in the body?

A

Renin, released from juxtaglomerular cells in the kidney, converts angiotensinogen (from liver) to angiotensin I. This is converted by ACE from the lungs to angiotensin II. This acts to vasoconstrict, increase ADH (from post pit), and increase aldosterone (from zona glomerulosa of adrenal glands).

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64
Q

What are the three categories of fluid a patient might need?

A

Resus- if haemodynamically unstable
Replacement- once stable but unable to meet fluid/electrolyte needs orally/enterally. Existing deficits or excesses, ongoing losses, abnormal distribution or other complex issues.
Routine- if none of the above issues but still can’t meet needs

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65
Q

What is the grading for AKI stage 1,2,3?

A

stage 1 - UO <0.5ml/kg/hr >6hrs
stage 2 - UO <0.5ml/kg/hr >12hrs
stage 3 - UO <0.3ml/kg/hr 24hrs or anuric 12hrs

Or by creatinine rise from baseline:
50-99%
100-199%
>200%

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66
Q

Define stages for CKD

A

Abnormalities of kidney structure/function for at least 3 months
Note CKD is now measured with GFR categories + ACR categories (albumin:creatinine ratio)

1 - >90 
2- 60-89
3-  30-59
4- 15-29
5- <15

A1- <3
A2- 3-30
A3- >30
Albumin should be kept inside, creatinine outside

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67
Q

How can CKD be related to HTN?

A

HTN –> damages kidney –> CKD
Renal artery stenosis –> CKD
CKD –> impaired sodium excretion –> fluid overload –> HTN
Activated RAAS?

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68
Q

5 common causes of CKD

A 
DM 40%
HTN 33%
Polycystic Kidney Disease (most common form is ADPKD, gene PKD1. Also have hepatic cysts, LVH, intracranial aneurysm, haemorrhage stroke) 
FSGS 
Lupus nephritis 
Amyloidosis 
Sickle cell 
Granulomatosis with polyangitis (c-ANCA, anti-PR3) 
Alport's 
IgA nephropathy

(remember nephrotic MADF Membranous GN, MCD, Amyloidosis, Diabetes, FSGS)
(Nephritic PIGPEAL Post-strep, IgA, Goodpasture’s, Polyang, Eosinophilic, Alport’s, Lupus)

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69
Q

Signs of CKD

A 
Fluid overload (peripheral, pulmonary oedema) 
Excoriations (uremia) 
Signs of anaemia (pale conjunctiva) 
HTN 
Peripheral neuropathy
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70
Q

What investigations would you do to find cause of CKD?

A 
HbA1c (number 1 cause) 
BP (number 2 cause) 
Urinalysis (casts suggest GN, WCCs infection)
USS for renal cysts, obstructive cause 
Antibodies- 
anti-GBM for Goodpasture's 
anti-ANA for SLE 
anti-c-ANCA/PR3 for granulomatosis with polyangitis 
anti-p-ANCA/MPO for eosinophilic
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71
Q

Patient has been told they have CKD. How will you change meds?

A 
Stop NSAIDs 
Control HTN: ACEi 
Consider B12 and folate supplementation 
Offer statins 
Offer aspirin 
Offer dietary advice about potassium, phosphate, calorie and salt intake appropriate to the severity of CKD.
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72
Q

Name some extra renal complications of CKD

A

Anemia
Hyperkalemia
MBD (increased phosphate and PTH, decreased Ca and calcitriol)
Metabolic acidosis (from decreased acid secretion)
Sodium retention/fluid overload

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73
Q

How does CKD cause renal osteodystrophy?

A

Impaired Ca absorption and phosphate excretion
Get hyperparathyroidism
stimulates bones to release calcium, resulting in ongoing bone resorption, remodeling, and redistribution
PTH also stimulates the proximal tubules in the kidneys to produce calcitriol, but it can’t due to decreasing nephrons so PTH becomes ineffective

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74
Q

What can be done for patients with CKD-MBD?

A

Hyperphosphataemia: Give information about controlling intake of phosphate-rich food, offer calcium acetate as phosphate binder

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75
Q

What are the two types of peritoneal dialysis?

A

CAPD- change solution x4 day, keep new solution for 4-6hrs. Have total control. But restricts you in the day.

APD- machine exchanges 3-5 times in night, fresh solution in am. All taken care of for you.

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76
Q

When should someone with CKD be referred to specialists?

A

GFR <30
Decrease in GFR <25% in 1yr
ACR >70
HTN w 4 HTN drugs

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77
Q

What monitoring should you do for patients with ESRD?

A

If eGFR <30 then measure Ca, PTH, phosphate and vit D

Every 3 months measure % of hypo chromic RBCs OR reticulocyte Hb content (NOT EPO or ferritin)

78
Q

How can you manage ESRD patients with anaemia?

A
  1. Consider ESA therapy (EPO stimulating agent)
  2. Patient education (support, diet, exercise)
  3. Iron therapy
79
Q

Name agents that can be used for immunosuppression post renal transplant, and what monitoring is needed?

A

Induction- Basiliximab
Maintenance-
Tacrolimus (calcineurin inhibitor, decreases IL-2)
Mycophenolate mofetil

Monitor tacrolimus and ciclosporin trough levels

80
Q

Name some complications of renal transplantation?

A

Surgical: infection, bleed, thrombosis, hernia
NODAT- new onset diabetes after transplant
40% have delayed graft function (ATN due to Uischaemia-reperfusion injury)
Acute or chronic rejection (will need more immunosuppression)
x5 risk of cancer with immunosuppression
Increased BP in 50% and CVS is leading cause of death in transplant patients

81
Q

Classify the forms of asthma

A

Mod- PEF 50-75%
Severe- 33-50%, RR>25, HR >110, can’t complete sentences
Life threatening- <33%, normal CO2, cyanosis, altered consciousness, silent chest, O2 <92%
Near fatal- high CO2

82
Q

Acute asthma management

A 
Oxygen 15L non-rebreathe high flow 
Salbutamol 5mg NEB
Hydrocortisone IV 100mg or pred 40mg PO 
Ipratropium bromide 500micrograms IV 
Call ICU, aminophylline, theophylline, magnesium
83
Q

When can you prescribe a SABA alone for asthma?

A

If infrequent, short-lived wheeze and normal lung function, consider treatment with SABA reliever therapy alone.

84
Q

When should you prescribe SABA + ICS for asthma?

A

symptoms at presentation that clearly indicate the need for maintenance therapy (for example, asthma-related symptoms 3 times a week or more, or causing waking at night) or

asthma that is uncontrolled with a SABA alone.

85
Q

Patient presents with uncontrolled asthma on SABA + ICS, what are your next steps?

A

Add a LABA (formoterol)

Then add LAMA (tiotropium), LTRA (montelukast), theophylline (phosphodiesterase inhibitor)

86
Q

What is included in an asthma safe discharge bundle?

A
  1. Inhaler technique
  2. Asthma action plan
  3. Med review
  4. Consider triggers
  5. Community follow up in 2 days and specialist follow up in 2 weeks
87
Q

Signs of COPD?

A

Clubbing, peripheral cyanosis, hypertrophy of accessory muscles (scalene, traps, SCM), chest crackles, tachypnoea, decreased cricosternal distance (<3cm), hyper resonant percussion, wheeze

88
Q

What are the muscles of respiration?

A

Inspiration- diaphragm contracts, external intercostals
Accessory of inspiration- SCM, scalenus anterior, medius and posterior, serratus anterior and latissimus dorsi,

Expiration- relaxes
Forceful expiration- abdominal (rectus abdominus, external oblique, internal oblique), internal intercostals

89
Q

How do you define emphysema and chronic bronchitis?

A

Chronic bronchitis is defined clinically as sputum production on most days for 3 months of 2 successive years

Emphysema is defined histologically as enlarged air spaces distal to terminal bronchioles with destruction of alveolar walls

90
Q

What signs may be seen on CXR of COPD?

A

Flattened hemidiaphragms
Hyperinflation (>8 posterior ribs or >6 anterior ribs)
Upper lobe diversion
Cardiomegaly (from cor pulmonale following RV strain)

91
Q

Why do patients with COPD get ankle oedema?

A
  1. Ventilation:perfusion matching, constriction of pulmonary vessels, increased after load to R ventricle, increased hydrostatic pressure back flow to ankle
  2. Hypoxia so increased RAAS
  3. Hypoxia also damages pulmonary vessels, leading to remodelling, become less compliant and more resistant
92
Q

Definition of cor pulmonale

A

right ventricular enlargement secondary to a lung disorder that causes pulmonary artery hypertension

93
Q

What is in a COPD discharge care bundle?

A
  1. Med review/check inhaler technique
  2. Self management plan and emergency drug pack
  3. Smoking cessation
  4. Pulmonary rehab
  5. Arrange follow up call within 72hrs of discharge
94
Q

What 5 things should happen when a COPD patient is admitted?

A
  1. CXR and ECG
  2. If ?resp acidosis ABG
  3. O2 and target range
  4. Salbutamol and nebs within 4hrs of admission
  5. Resp team review in 24hrs
95
Q

What interventions in COPD alter mortality?

A

Smoking cessation
Oxygen
Rest is symptom control

96
Q

What’s involved in pulmonary rehab for COPD? (and when should it be offered?)

A

When MRC dyspnoea score 3+

Exercise (e.g breathing techniques for exercise)
Education
Diet
Psych

97
Q

What are meds for COPD?

A

Start with SAMA or SABA
Then if not asthamtic/steroid responsive try LAMA + LABA
If asthmatic features/seems steroid responsive try LABA + ICS
Then try LABA + LAMA

98
Q

Tell me about sarcoidosis

A

Multisystem granulomatosis disorder of unknown cause
Females, 20-40yo
20-40% incidental CXR
Presents: erythema nodosum +/- polyarthralgia, dry cough, progressive dyspnoea, reduced exercise tolerance, chest pain , hepatosplenomegaly, lymphadenopathy, hypercalcemia
Most recover spontaneously! Bed rest and NSAIDs
60% resolve in 2years, 20% respond to steroids

99
Q

Name 4 diseases involving granulomas

A 
Sarcoidosis 
TB (non-caseating) 
Crohn's disease 
Granulomatosis with polyangitis (c-ANCA, PR3) 
Churg-Strauss
Syphilis 
Cat-scratch disease
100
Q

4 drugs that cause fibrosis

A

Methotrexate
Nitrofurantoin
Amiodarone
Cyclophosphamide

101
Q

What are the different types of staph and strep?

A

Staph can be coagulase positive (aureus) or negative (saprophyticus, epidermidis)
Strep can be alpha which is green (viridans, pnemoniae)
Beta which is clear (pyogenes)
or gamma haemolytic (enterococci, faecalis)

102
Q

Patient with HAP- when should you follow up?

A

Within 6 weeks outpatient appointment/GP

CXR 6 weeks post discharge in high risk patients for malignancy (e.g. smoker, >50yo)

103
Q

Patient with HAP- when should you follow up?

A

Within 6 weeks outpatient appointment/GP

CXR 6 weeks post discharge in high risk patients for malignancy (e.g. smoker, >50yo)

104
Q

What are the types of lung cancer and tell me about them

A

Small cell (less common)

Non-small cell:
Squamous cell (40% of NSC)
Adenocarcinoma 35% (commonest in non-smokers)
Large cell 5%

Rare: carcinoid

105
Q

Name paraneoplastic syndromes of lung cancer and which are more common in which types

A

Squamous cell :
PTHrP (hypercalcemia, thirst, constipation)
Clubbing
Ectopic TSH –> hyperthyroidism

Adenocarcinoma –> gynaecomastia

Small cell:
SIADH –> hyponatremia
Ectopic ACTH secretion –> atypical Cushing’s, hypertension, hyperglycaemia
Lambert-Eaton Myasthenic Syndrome –> autoimmune at NMJ pre-synaptic Ca channels causing proximal limb weakness legs >arms, dry mouth

106
Q

Define paraneoplastic syndrome

A

Effects of a cancer that are not caused by invasion of the tumour or its mets

107
Q

Where do lung mets go?

A

Liver, brain, spine, pericardium

108
Q

What do the different stages of lung cancer mean for treatment options?

A

TNM combines to make a stage I-IV score

Stage I and II radical treatment
Stage III non-operable
Stage IV- palliative (any M1)

109
Q

Why is the prognosis for lung cancer generally so poor?

A

2/3rds mets at presentation

110
Q

What is ILD?

A

Umbrella term for conditions leading to pulmonary fibrosis/affecting lung parenchyma
15% usual interstitial pneumonia, which is normally idiopathic
8% sarcoidosis
Asbestosis
Pneumoconiosis
Extrinsic allergic alveolitis
Drug-induced (methotrexate, amiodarone, nitrofurantoin, cyclophosphamide)
Post-infectious
Autoimmune (SLE and RA)

111
Q

What signs might a patient with ILD present with?

A

Dyspnoea, dry cough

Abnormal CXR/CT
Honeycombing
Restrictive spirometry

If extrinsic allergic alveolitis, 4-6hrs post exposure fever, riggers, dry cough, dyspnoea crackles (no wheeze). If continue to be exposed, with lose weight, cor pulmonale, worsening dyspnoea

112
Q

What scoring system is used for obstructive sleep apnoea?

A

Epworth Sleepiness Scale
>9
Points for chance of sleeping during activities e.g. sitting and talking

113
Q

What antibody tests might you want to do in patient with ?ILD and why

A

Anti-ANA for SLE
Rheumatoid factor/CCP for RA
Anti-GBM for Goodpasture’s (pulmonary haemorrhage)
c-ANCA for GwP (ELK)
ACE (sarcoidosis) from MO in granulomas (Ca increased from calcitriol from MO in granulomas too)

114
Q

Management for obstructive sleep apnoea?

A

Advice: don’t drink alcohol in evening, weight loss, sleep decubitus
Mandibular advancement devices
Nasal CPAP

115
Q

Name small, medium and large vessel vasculitis types?

A

Small- GwP, Churg-Strauss
Medium- Kawasaki, polyarteritis nodosa
Large- Takayasu, GCA, Polymyalgia rheumatica

116
Q

What criteria can you use to differentiate transudate and exudate?

A

Exudate is >35g/L protein
Transudate is <25
If between 25-35 then use Light’s criteria

If LDH > 0.6 it’s exudate
If pleural fluid/serum protein >0.5 then exudate

117
Q

What are the common causes of bronchiectasis?

A

Most common is post-infective e.g. TB, H.influenzae, s. aureus
CF
Hypoglammaglobulinaemia, CGD
Obstruction (eg. from tumour, foreign body)
Gastric aspiration, inhalation of toxic gases
RA
HIV

118
Q

What is bronchiectasis and how would you diagnose?

A

Chronic dilatation of 1+ bronchi

High resolution CT (signet ring, tram track sign- thickened bronchial walls with no tapering)

119
Q

Common pathogens seen in bronchiectasis

A

Pseudomonas aeruginosa
Haemophilus influenzae
Moraxella catarrhalis
Aspergillus

120
Q

How would you manage bronchiectasis?

A 
Manage infective exacerbations 
Exercises for airway clearance 
If breathless refer to pulmonary rehab 
If severe ++ can consider lung transplant 
Flu and strep pneumoniae vaccination
Smoking cessation
121
Q

How common is CF and it’s carrier gene?

A

1/25 carriers

1/3000 CF

122
Q

Name some effects of CF

A

Commonest genetic cause of bronchiectasis
Meconium ileus
DIOS - distal intestinal obstruction syndrome
Osteoporosis (malnutrition)
Pancreatitis
T2DM
Low body weight (no enzymes)
Gallstones
Inflam hepatic response from delayed bile passage causing cirrhosis, portal HTN
Infertility (absence of vas deferens)
Recurrent chest infections

123
Q

How do you make a CF diagnosis?

A

Characteristic features/sibling/newborn positive result
PLUS

Sweat test chloride >60mmol/L
Or identification of 2 CF mutations with genotyping

124
Q

What lifestyle advice should you offer CF patients?

A 
No smoking 
Avoid other CF patients 
Avoid jacuzzis (pseudomonas) 
Avoid people with chest infections 
Clean and dry nebulisers 
Avoid stables, rotting vegetation, compost (risk of aspergillus fumigatus inhalation) 
Annual influenza jab 
Sodium chloride tablets in hot weather/exercise

Staph aureus chest Ifx should make you think of CF too

125
Q

Which joints are affected in RA?

A

MCP and PIP of hands, feet
Wrists (ulnar styloid)
Cervical spine (50%)

126
Q

What signs are there with RA?

A

Rheumatoid nodules over extensor surfaces
Swan neck deformity
Ulnar deviation
Boutonierre deformity

127
Q

What signs are there with OA?

A

Heberden’s nodes

Bouchard’s nodes

128
Q

What are some systemic complications of RA?

A 
ILD 
Vasculitis 
Pericarditis 
Pleuritis 
Scleritis/uveitis 
Carpal tunnel 
Anemia 
Amyloidosis 
Sjogren's (xerophthalmia and xerostomia), affects exocrine glands, initially salivary, then vaginal dryness, arthralgias and myalgias; peripheral neuropathies; pulmonary, thyroid, and renal disorders; and lymphoma. Often occurs with another autoimmune disease e.g. RA, SLE, systemic sclerosis). 
Splenomegaly
129
Q

How would you manage RA?

A 
DMARDs: 
Methotrexate 
Also sulfasalazine, hydroxychloroquine 
Symptoms with NSAIDs 
Biologics e.g. etanercept (anti-TNF), rituximab (B cell), infliximab (anti-TNFa)

Can offer short term bridging treatment with corticosteroids e.g. pred

130
Q

Tell me about Sjogren’s

A

More common with another autoimmune problem (e.g. RA, systemic sclerosis, SLE)
(xerophthalmia and xerostomia), affects exocrine glands, initially salivary, then vaginal dryness, arthralgias and myalgias; peripheral neuropathies; pulmonary, thyroid, and renal disorders; and lymphoma. Often occurs with another autoimmune disease e.g. RA, SLE, systemic
May get Raynaud’s, enlarged parotids
Pregnant mothers with SS are at risk of fetal loss
5-10% lifetime risk of B cell lymphoma

Biopsy will show lymphocytic infiltrate of exocrine glands

90% have positie anti Ro and anti La

131
Q

What monitoring should take place with DMARDs?

A

FBC - bone marrow suppression
LFTs- liver cirrhosis
U&E/eGFR makes toxicity more likely

Methotrexate also causes GI toxicity (stomatitis first sign)

132
Q

Tell me clinical manifestations of SLE

A

Skin - malar rash, photosensitive, oral ulcers, alopecia
Heart - pericarditis, myocarditis, endocarditis, premature atherosclerotic CAD
Lungs - pleuritis, pleural effusions, ILD
GI- oral ulcers, abdo pain, D&V, pancreatitis, hepatitis
Joints- arthralgia
Kidneys- lupus nephritis –> HTN
Vascular- Raynaud’s, vasculitis, haemolytic anaemia
Neuro- seizures, psychosis

133
Q

What immunological criteria are there for SLE?

A 
ANA positive 
dsDNA 
SM
thrombocytopenia 
Leukpenia 
Low complement 
Antiphospholipid Abs 
Direct Coombs test
134
Q

What clinical criteria are there for SLE?

A 
Acute cutaneous lupus 
Chronic cutaneous lupus 
Oral ulcers 
Nonscarring alopecia 
Synovitis >2 joints with >30mins am stiffness 
Serositis 
REnal 
Neurologic 
Haemolytic anemia 
Leukopenia 
Thrombocytopenia
135
Q

What features might suggest an SLE flare up?

A

Thrombocytopenia
Low complement
Red cell casts in urine microscopy

136
Q

How can you manage SLE?

A

Hydroxychloroquine (DMARD)
Naproxen (NOT ibuprofen, has risk of aseptic meningitis)
Add on methotrexate if above inadequate
Plus for lupus nephritis: ciclosporin, tacrolimus, cyclophosphamide

Lifestyle: stop smoking, SPF 50, exercise, diet (avoid trans fats as already have CAD risk)

137
Q

Tell me about drug monitoring in SLE

A

Hydroxychloroquine - retinopathy so need annual eye assessment (fundus photograph, OCT scan)

Prednisolone- DEXA

Remember, don’t give ibuprofen in SLE (risk of aseptic meningitis)

138
Q

How can you diagnose ankylosing spondylitis?

A

HLA-B27 90%
FH x16
Normally <45yo, back pain >3mo, back pain better with movement and worse with rest, back pain wakes in night, improves with NSAIDs within 48hrs, buttock pain

Sacroiliac XR
If negative do MRI

139
Q

What might someone with ank spond present with other than back pain?

A 
Enthesitis (heel pain) 
Costochondritis 
Uveitis 
Psoriasis 
IBD 
Recent infective diarrhoea/STI 
Dactylitis 
Limitation of lumbar spine in sagittal and frontal planes
140
Q

What are long term complications of ank spond?

A

Bamboo spine (fusion of
Spine fracture
Increase risk of CVS mortality
Anterior uveitis can lead to vision loss

141
Q

What special test is there for ank spond?

A

Schober’s test. Mark skin 10cm above and 5cm below PSIS
Measure this and check it is 15cm
Ask patient to bend forward with straight legs
Measure again
Distance increase to >20cm is normal (i.e. +5cm gained in flexion)

142
Q

When should you do a joint aspiration?

A

If ?septic arthritis or the diagnosis of gout is uncertain

If certain of gout, don’t need to aspirate normally

143
Q

When can you prescribe prophylaxis for gout?

A

Allopurinol for 2-3 attacks a year

144
Q

What can gout cause?

A

Acute and chronic arthritis
Urate nephropathy
Uric acid neprolithiasis
Top

145
Q

What are modifiable risk factors for gout

A 
Beer 
Seafood and meat (purine intake) 
High fructose intake 
Obesity 
HTN 
Smoking 
DM 
Urate-elevating drugs e.g. diuretics (loop/thiazide)
Renal disease 
CHF 
Dyslipidaemia
146
Q

Compare gout and pseudo gout crystals

A

Gout- negatively birefringent needle shaped monosodium urate crystals
Pseudogout- rhomboid shaped positively birefringent calcium pyrophosphate crystals

147
Q

What is the treatment for DVT?

A

Therapeutic dalteparin for at least 5days
Can consider catheter directed thrombolytic therapy

THEN: rivaroxiban or warfarin for at least 3 months!!

148
Q

Causes of provoked PE

A

COCP/HRT, pregnancy, cancer, surgery, immobility

149
Q

What is a massive PE?

A

PE with sustained hypotension (systolic BP <90 for >15mins)

150
Q

How do you treat massive PE?

A

Thrombolysis (as opposed to LMWH which just ensures new clots don’t form)
Give alteplase 10mg IV over 1 min

CT will show R sided heart strain

OR catheter-directed lysis

OR surgical embolectomy

If absolute contraindication to thrombosis can insert IVC filter (e.g. if recent stroke, recent trauma/surgery, recent GI bleed, bleeding disorder, aortic dissection)

Admit to ICU- 85% die within 6h of symptom onset

151
Q

How would you manage anaphylaxis?

A 
500micrograms adrenaline IM every 5mins 
Fluids 0.9% NaCl resus 500ml
High flow oxygen 15L non-rebreathe 
Once haemodynamically stable: 
Hydrocortisone 200mg slow IV/IM
Chlorphenamine 10mg slow IV/IM

Early prophylactic airway management

152
Q

Explain the pathophysiology of anaphylaxis

A

Exposure to pre-sensitised antigen
Type 1 hypersensitivity reaction
Re-exposure stimulates IgE mediated degranulation of mast cells (PGs, leukotrienes, histamine, PAF) and basophils via high affinity Fc R
Cytokine release, increased permeability of vessels
Systemic vasodilation resulting in hypotension
Bronchoconstriction induced by histamine

153
Q

After initial management, what should you do for anaphylaxis?

A

Advice on avoiding triggers
Always carry epipen x2
Advice on early symptoms
Test mast cell tryptase 1-2hrs later

154
Q

What is red flag sepsis

A 
Need one of: 
Systolic BP <90
Tachycardia >130 
Tachypnoea >25
New need to keep Sats <92% 
Altered consciousness 
Only responds to pain/unresponsive 
Non-blanching rash/cyanotic/mottled 
18hr anuric or <0.5ml/kg
Lactate >2mmol
Recent chemo
155
Q

What are the common causes of sepsis?

A 
90% bacteria (staph aureus, strep, E.coli) 
60% resp source 
26% abdominal source
20% blood source 
14% skin
12% urinary
156
Q

What criteria should be met before discharging a paracetamol OD patient?

A 
Paracetamol level below treatment line
Normal INR (liver function)
Normal ALT (liver hurt)
Normal creatinine (kidneys)
157
Q

What is the time limit for treating paracetamol OD with acetylcysteine and activated charcoal?

A

Acetylcysteine- most effective <8hrs but up to 24hrs

Activated charcoal up to 2hrs

158
Q

Patient presents (feeling fine) 6hrs post paracetamol ingestion. What will you do?

A

Most have no symptoms in first 24hrs and then 2-3days later ALT, AST and PT rise, encephalopathy/coma, hepatorenal syndrome. May have N&V, headache, change in conscious level, anorexia, abdominal pain.

Ix: LFTs, serum paracetamol, electrolytes, U&Es, PT & INR, ABG

Mx: Consult TOXBASE. Use Rumack-Matthew nomogram-check paracetamol level 4hrs post ingestion and plot. If it falls on or above line, treat with acetylcysteine.

150 mg/kg over 1 hour, dose to be administered in 200 mL Glucose Intravenous Infusion 5%

159
Q

Why is alcohol protective with paracetamol OD?

A

Changes cytochrome enzymes so less NAPQI is oxidised

160
Q

Name two types of NAFLD

A

NASH- steatohepatitis. Involves inflam of the liver which can cause fibrosis, can lead to cirrhosis or liver cancer

Simple fatty liver (also called NAFL). No inflammation, normally no complications.

161
Q

What monitoring should liver cirrhosis patients undergo?

A

Every 6mo USS +/- serum AFP for hepatocellular carcinoma

At diagnosis offer OGD for oesophageal varies then again every 3 years

162
Q

Difference between delirium tremens and WE?

A

Delirium tremens has no neurological signs (only symptoms).

WE has neurological signs (ophthalmoplegia, confusion, ataxia).

163
Q

Manage Wernicke’s encephalopathy (and describe presentation)

A

Classic triad of acute confusion, ataxia and ophthalmoplegia. However only occurs in 10% of patients. Treat if no more likely explanation with any one+ of confusion, ataxia, opthalmoplegia, memory disturbance, unexplained hypotension with hypothermia, nystagmus.

Give pabrinex IV

After can give thiamine 100mg TDS and vitamin B OD, continue for 2-6wks

164
Q

Manage alcohol withdrawal

A

Chlordiazepoxide (anxiolytic, anticonvulsant) 25-50mg. This is better than diazepam because has less potential for abuse. May need dose reduction in liver failure. Reduced does by 20% per day.
Pabrinex (to avoid Wernicke’s encephalopathy)

Obs every 2 hours:

  • use alcohol withdrawal scale CIWA-Ar
  • BP, PR, RR
165
Q

Patient presents polyuric, thirsty, nauseous, constipated, confused, with muscle weakness. What will you do?

A

Indicates hypercalcemia.
?spine mets
Skeletal survey/CXR/CT abdominal/PTH (should be normal/low)
Do an ECG (shortened QT)

High calcium and high PTH = primary or tertiary hyperparathyroidism
High calcium and low PTH = malignancy or other rarer causes

Treat with IV 0.9% NaCl 4-6L in 24hrs
When rehydrated give IV bisphosphanates (zoledronic acid) which blocks osteoclastic bone resorption, takes 2-4days.
Can give IV calcitonin if no response

80% hyper cal from tumour secretion of PTHrP (most common lung, multiple myeloma, RCC, breast, colorectal)
20% is local osteolytic hypercalcemia caused by bony mets

166
Q

Patient following recent thyroidectomy presents with numbness/tingling around mouth and in hands, wrists are is spasm, and difficulty breathing with laryngeal spasm. What will you do?

A

So parathyroid glands have been damaged in thyroidectomy, meaning they do not release PTH to increase Ca absorption/levels. She is hypocalcemic.

Do ECG (cardiac hyperexcitability)
Check Mg (can't fix Ca if Mg low) 
Give IV calcium gluconate 10ml slow IV 10% in 50ml 5% glucose

PT glands often recover in 6-8wks. If not, can give levothyroxine, Ca +/- vit D for life

Other common causes of hypocalcemia: vit D deficiency, IBD, PPIs/phenytoin (also lead to vit D def), renal disease so can’t make calcitriol, hypomagnesaemia

167
Q

Name 4 complications of hypernatremia and proposed management of hypernatremia

A
  1. ECG changes- prolonged QT
  2. Muscle weakness/cramps/rhabdomyolysis –> renal failure
  3. Brain cell shrinkage –> vascular rupture/intracerebral haemorrhage
  4. Myelinolysis also possible (but more common in rapid correction of hyponatremia)

Correct with IV Hartmann’s
Risk of too rapid correction is cerebral oedema (the opposite to hypo)

168
Q

Manage acute hyponatremia (has just run a triathlon)

A

IV 3% NaCl (if less than 48hrs onset) 2-4ml/kg

(beware central pontine myelinolysis if corrected too quickly. Sudden water moving out of cells destroys myelin)

If has developed <48hrs has risk of cerebral oedema

169
Q

Manage a patient who has suddenly stopped long term prednisolone for RA

A

IV fluids 0.9% NaCl 1L rapidly

IV hydrocortisone

170
Q

Which diabetes meds should be used with caution for CKD 3-5?

A

Metformin (risk of lactic acidosis) avoid if eGFR <30
DDP-4 (renally excreted) e.g. saxagliptin decrease dose if <60
SGLT-2 inhibitors e.g. dapaglifozin <60 avoid use

171
Q

Manage a diabetic foot ulcer

A

ABPI, Doppler, foot XR for osteomyelitis
Clean ulcer with saline then dry and dress (low-adherent)
High compression multi-layer bandaging but not if infected
Offloading footwear to minimise repetitive trauma

Features suggestive of osteomyelitis: depth >3mm, probe to bone test (probe ulcer with sterile blunt probe and see if reaches bone)

Neuropathic arthropathy = Charcot joint. Bone and joint changes secondary to loss of sensation from DM, syphilis, leprosy. Includes destruction of articular surfaces, opaque subchondral bones, joint debris, deformity, and dislocation

172
Q

Education programmes for T1DM and T2DM

A

DAFNE for T1

DESMOND for T2

173
Q

Meds for diabetes

A

Biguanide e.g. Metformin. Inhibits hepatic gluconeogenesis to overcome insulin resistance

DDP4 inhibitors e.g. linagliptin- inhibits DDP4, which normally inhibits incretin, which increases insulin

GLP1 analogues e.g. exenatide which increase incretins
(increasing tide)

Sulfonylureas e.g. gliclazide which squeezes all the insulin out of the pancreas
(zide, zesty, squeezing)

SGLT2 inhibitors e.g. dapagliflozin which reduces glucose absorbed in kidneys so more is excreted
(flo out)

174
Q

Meds for diabetes

A

Bigunide e.g. Metformin. Inhibits hepatic gluconeogenesis to overcome insulin resistance

DDP4 inhibitors e.g. linagliptin- destroy the hormone incretin, which increases insulin

Sulfonylureas e.g. gliclazide which squeezes all the insulin out of the pancreas

175
Q

Manage HHS

A

Hyperosmolar hyperglycaemic state.

Give IV 0.9% NaCl, 1L in first hour
Add KCl 40mmol/L if K is normal (insulin drives K into cells)
Glucose will fall with hydration, but insulin if it doesn’t (fixed rate of 0.05 unit/kg/hr)
DVT prophylaxis (stroke, MI, PE, DIC risk from hypovolemia with increased viscosity)
Stop fixed rate insulin when blood ketones <0.3 and cap glucose <15mmol/L

Then if eating and drinking return to normal SC regimen
If not, start VRIII

Do urinalysis, CRP, WCC because 30-60% of HHS is due to infection. Note also cortisol inhibits insulin.

176
Q

Manage DKA

A

Hyperglycemic, acidotic, ketotic
Average fluid deficit of 6L

IV fluids 0.9% NaCl, 1st litre over 1 hr
Include KCl with fluids unless anuric
IV insulin at fixed rate 0.1units/kg/hour at 1unit/1ml
VTE

ICU if haemodynamic instability

Once stable (ketones <0.6 and pH >7.3) can either change to normal SC insulin regimen or VRIII and dextrose-saline infusion if unable to eat

177
Q

Manage hypoglycemia

A

ABCDE approach
Insert 2 wide bore cannulas
CBG every 10 mins until >4mmol/L
ECG
Stat glucose 10g PO (orange juice/glucose gel)
If unconscious give 1mg glucagon IM once only
If not effective in 10 mins give 100ml IV glucose 20%
Follow with long acting carbohydrate 20g (e.g. two biscuits) or 40g if glucagon was given

DVLA: if >1 episode of severe hypoglycaemia in 12 months no driving
Must check BM <2hrs pre driving and every 2 hours whilst driving if insulin treated

178
Q

Anti-hypertensive drugs and their side effects

A

ACEi- dry cough
Beta blockers- bronchospasm, coldness of extremities
CCBs- vasodilation –> flushing, headache

179
Q

Manage infective endocarditis

A

Normally gentamicin + amoxicillin IV for 4-6wks if native valves
Prosthetic valves for 6wks
(often viridans streptococci, or staph aureus if IVDU)

Needs ECG, TTE (trans thoracic echocardiography)
Blood cultures x3 from 3 separate sites
If decompensated HF and severe sepsis then needs surgery

180
Q

Manage heart failure (acute and chronic)

A

Fluid restriction and IV furosemide

Longer term ACEi and beta blockers reduce mortality
Give pneumococcal and influenza vaccinations
Smoking cessation

181
Q

Manage AF (acute and chronic)

A

Acute:
1. treat underlying condition (e.g. pneumonia, sepsis, MI, hypertension, hyperthyroidism, IHD, valvular heart disease)
2. Normally rate control:
Rate control- beta blocker or CCB
If haemodynamically unstable may need DC cardioversion in ITU, or if AF >48hrs
3. Assess stroke risk (CHA2DS2VASC) and risk of bleeding with anticoagulation (HAS-BLED inc. HTN, stroke, abnormal liver/renal function, alcohol)
4. Prophylactic heparin

Chronic:
Beta blockers/CCBs PLUS warfarin/apixaban to reduce VTE risk

182
Q

Manage an acute MI and post MI

A

Slow IV morphine 5mg (PLUS 10mg slow IV metochlopramide for anti-emetic)
Oxygen if sats <94
Aspirin 300mg chewable
Clopidogrel 300mg PO
PCI if available, must be within 120mins of when thrombolyis (alteplase + LMWH) could have been given

Post-MI: 
Dual anti platelet therapy (e.g. aspirin 75mg OD + ticagrelor 90mg BD 12/12) 
Statins 
ACEi
Beta blocker 
Lifestyle- smoking cessation, exercise,
183
Q

Tell me about systemic sclerosis

A

Previously known as scleroderma
It’s two main subtypes are limited scleroderma (=CREST) and diffuse scleroderma (less common with high risk of mortality)

184
Q

What is CREST?

A

Also known as limited scleroderma. Calcinosis, Raynaud’s, Esophageal dysmotility, Sclerodactyl, Telangiectasia

185
Q

What is diffuse scleroderma?

A

Diffuse skin involvement
Early organ fibrosis: lung, cardiac, GI, renal
Do annual BP and spirometry

186
Q

What antibodies are involved in systemic sclerosis?

A

ANA in 90% of patients

Anti-centromere in limited scleroderma/CREST

187
Q

What treatment is there for systemic sclerosis?

A 
Calcium antagonist for Raynaud's 
Methotrexate to reduce skin thickening 
Prednisolone for flares 
PPIs for GI symptoms 
ACEi reduce mortality from renal complications
188
Q

What is Raynaud’s?

A

Painful vasospasm of the digits with colour change sequence in response to cold:
White (inadequate blood flow)
Blue (venous stasis)
Red (re-warming hyperaemia)

Common in young women, may improve with age
FH
Keep warm, stop smoking, start CCBs

If Raynaud’s develops >30yo may be underlying disease (systemic sclerosis, SLE, Sjogren’s)

189
Q

What are some causes of Raynaud’s

A

SLE, systemic sclerosis, Sjogren’s
Use of heavy vibrating tools
Beta blocker induced

190
Q

What imaging tool is useful for diagnosing Raynaud’s?

A

Nail-fold capillaroscopy

191
Q

What is the diagnostic criteria for infective endocarditis?

A

Dukes.

Major criteria: typical organism in 2 separate blood cultures/ or persistently positive blood cultures 
Endocardium involved (positive echo e.g. vegetation, abscess, dehiscence of prosthetic valve) or new valvular regurgitation

Minor criteria: predisposition (IVDU, cardiac lesion), fever >38, vascular/immunological signs, positive blood culture, positive echo

Need 2 major, 1 major and 3 minor, or all 5 minors

Year 3 (7 decks)

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