GP 22 Flashcards
A to E approach
General Approach
How do they look?
“How do you feel?”
Look at obs eg overall trends, request ECG?
Airway
Speaking = patent
cyanosed/ accessory breathing muscles, see-saw breathing
check mouth : forceps to remove, not fingers
high flow oxygen and maintain airway;
headtilt/chinlift or jawthrust: consider adjuvent if breathing only clear in this position
Gurgling/Burbling?: turn head to side (gurgling/burbling) and suction
airway adjunct if compromised (try guardal first to see how unconscious, then nasopharyngeal, lubricate, 6 for female and 7 for male)
Give high flow 15l non -rebreath. If bag mask then hold right behind jaw, not under. 12/min or 1/5-6s)
anaphylaxis?
Breathing
Look/listen/feel for resp distress (sweat, accessory muscles, cyanosis)
RR (>25 may deteriate suddenly)- Count for 1m
assess depth and pattern, ueven expansion?
chest deformity? abdominal distension? raised jvp?
record sats and o2 levels (does not detect hypercapnea)
breath sounds (rattle (secretions not clearing), wheeze, stridor)
percussion
Auscultate (bronchiol breathing indicates consolidation)
position of trachea
chest wall crepitas
all critically ill get a non rebreath mask 15L/min
Can step down to Venturi 28% mask (4 L min-1) or a 24% Venturi mask (4 L min-1) initially in COPD and reassess
if depth of breathing inadequate use bag mask and call for specialist help
nebs can give 6 litres max but add 5l via nasal canula
Circulation
Temp
HR - count for 1 min (weak central= poor cardiac output, bounding = sepsis
BP
are they septic?
Quick cardio exam: temp, CRT, Pulse, heart sounds, oedema
Oliguria = sign of poor cardiac output
external/internal bleeding?
cannulate
IX; All get FBC, U&E, LFTs
Major harmorhage protocol = call blood bank or 2222 . . will need trained runner
then specific:
Sepsis: CRP, lactate, blood cultures
Haemorrhage or surgical emergency: Coagulation and cross-match
Acute coronary syndrome (ACS): Cardiac enzymes
Arrhythmia: Calcium, magnesium, phosphate, TFTs, coagulation
PE: D-dimer (depending on Well’s score)
Overdose: Toxicology screen
Electrolyte imbalance: Calcium, magnesium, phosphate
Ruptured ectopic: Coagulation, cross-match, ß-HCG levels
Anaphylaxis: Consider serial mast cell tryptase levels
ECG, Cathetarisation, bladder scan, pregnancy test, swabs/cultures?
3 lead ECG = red/right, lemon/left and green/spleen
Hyovolemic? - MC . . . IVF to all cool peripheries and tachicardic
Lay patient supine and raise legs if appropriate
Give 500ml bolus Hartmann’s solution/0.9% sodium chloride (warmed if available) over 15 mins
In heart failure: Give 250ml fluid as above; check the chest for crackles after each bolus as there is a risk of fluid overload and pulmonary oedema
Repeat up to 4 times (2000ml/1000ml), monitoring response
assess BP q5mins aiming for thir normal or >100
Stop and seek help if the patient has a negative response (e.g. increased chest crackles).
Seek senior help if the patient isn’t responding adequately to repeated boluses.
ACS : ECG,po aspirin 300mg, subliguial glyceryle trinitate spray/tablet, oxygen, morphine + antimimetic,
Disability
Consciousness;
repeart AVPU (alert, responds to voice, responds to pain, uresponsive)
assess pupils (pinpoint opioids, dilated = intracranial pathology of TCA overdose)
PEARL = pupils equal and reactive to light
Check for head injury while you are here
calculate GCS (<= 8 = anaethetist or crash team)
Movement: ‘squeeze my fingers
check drug chart (opioids, sedatives, anxiolytics and antihypertensives)
Causes of decreased consciousness:
Hypovolaemia
Hypoxia
Hypercapnia
Metabolic disturbance (hypoglycaemia)
Seizure
Raised intracranial pressure/other neurological insults
Drug overdose
Iatrogenic causes (e.g. administration of opiates for pain relief)
DIABETES Blood glucose (4.0-11.0 mmols/L)
check ketones if >15
<4 give 50ml 10% dextrose - give every minute till 250ml if no response
urine dipstic?
imaging?
Exposure
Any pain?
Bleeding? - rate/ amount .. . . ax for shock
rashes? coagulopathy/infection
calves - red swollen dvt?
Lines - any concerning?
Cathetar- puss or blood?
surgical wound?
drains- pus? blood? high/low output?
Reasses . . . who can help?
Full hx from pt or collateral
r/v notes - esp vital signs and meds
lap results?
What care? HDU? ICU?
Notes and SBAR handover
keep realtivesinformed
Antibiotic Ladder
Rules
- If sick go broad
- Escalate Rapidly
- Descalate slowly
- Target Cultures and Sensitivies
- Empiric treatment - use the lowest possible
Amnionpenicillins = g-ves etc but with b lactimase inhibitors has some +ve coverage
Cephalosporins
1st - cephalexin, cefadroxil, cephradine (strep and MSSA)
2nd-
3rd - Ceftriaxone (Strep and g +ves)
4th - cefeprime (pseudomonas coverage)
amoxicillin clavulanic acid = co-amoxicillin
Pip-Taz = Piperacillin/tazobactam aka tazocin
Tic-sulb = ticarcillin sulbactam
Aztreonam - would only jump to if severe beta lactam allergy
Daptomycin used in blood stream
Linozolid for lung infection
Fluroquinolones - need to go through each base? - used to be good for UTIs but now for pseudomonas coverage
levofloxacin ver specific infections
moxifloxacin - respiratory fluroquinolone but do not use.
IV gentamicin, amoxicillin & metronidazole: Also known as ‘triple therapy’, these antibiotics are often used together in severe intra-abdominal infections.
TMP/SMX = co-trimoxazol
Animal Bite = co amoxiclav
Pneumonia
Fever and cough = CXR and Sats for everyone
ABG if low sats
FBC - neutrophilia in bacterial
U&Es for dehydration and curb 65
CRP - raised in response to infection (<20 no abx, >100 abx, 20-100 consider delay)
Blood culture should do but only returns 10% of time and does not really alter tx
Sputum culture is low yield and we tx empiracally anyway
Nothing? - bronchitis aka atypical pneumonia (CAP lite)
-PO abx
Cavity lesion?
- usually malodorous sputum
differentiate with CT chest
Tx 3rd gen + G+ve and anaerobic coverage (clindomycin)
Consolidation?
Pneumonia
Differentiate with Time relation to hospital building
Empiric tx depending on category
Low severity community = amoxicillin (macrolide/tetracyclin if pen allergy)
more severe = Amoxacilin + macrolide (7-10d)
- consider co amoxiclav/ ceftriaxone / piperacillin with tazobactam and a macrolide
Admit?
-CURB 65 score
Confusion (AMT <=8)
Urea >7 mmol/L
RR>30/min
BP <90/60
>65yo
0 mx in community
1 - SATS and community CXR
2- MX in hospital
4 = 30% mortality by 30days
CRB65 in community - 2 = go to hospital
PCP
HIV+ve (immunosuppressed)
not solid consolidation but patchy diffue infiltrates
longer subacute presentation
ix silver sputum stain (not culture)
Tx with co trimoxazole
Give steroids if hypoxaemic
FLU
Myalgia giveaway
confirm with swab
prevent with vaccine
presdisposes to S.Aureus pneumonia
AND
Klebsiella ax with aspiration (MC righ lower lobe)
H.flu = COPD or smokers
3RD gen cephalosporin = ceftriaxone
Imaging
- Pneumonia
- PCP
- Abscess
Mycoplasma Pneumonia
Associated erythema multiforme
tx: doxycycline or a macrolide
Allergic Bronchopulmonary Aspergillosis
IX: po glucocorticoids + itraconazole
Legionella Pneumophilia
flu-like symptoms including fever (present in > 95% of patients)
dry cough
relative bradycardia
confusion
lymphopaenia
hyponatraemia
deranged liver function tests
pleural effusion: seen in around 30% of patients
Dx: Urinary Antigen
MX: erythromycin/clarithromycin
AKI full
Pre
PUMP = mi and chf
Leaky - also a bit CHF but think OSI
Hole : diuresis, dehydration, diarhoea and haemorhage
FMD (fibromuscular dysplasia) = young woman with secondary htn and renal failure
RAS (renal artery stenosis) = old man with atherosclerosis
Renal
RBC casts = glomerulonephritis - BUT r/o nephrotic syndrome (triad)
AIN - itis . .. look for infections. Look for WBC casts or eosiophils
but also some drugs (TMX-SMP, penicillins, cephalosporins)
ATN - muddy brown casts (not sensitive or specific)
Things in tubules coming into contact and damaging them
two main types (ischamia and toxins) prevent with IVF
Three main phases
Post
hydroureter/hydronephrosis
depends on level of obstruction (both kidneys = urethra. . only one dialted = ureter)
more causes the lower down you go
neurogenic = nerve damage or medications
foley kink
Approach
PRE
first rule this out
U:Cr >100 / Urins sodium <10 = pre-renal
give IVF if hypovolaemic
give diuresis if hypervolaemic
Post
Then rule out this
US or CT scan (CT better for stones)
then relieve obstruction
intra
hx/physical/UA usually enoght
eg DM with glucose and protein = diabetic nephropathy
Might need bx occosionally to prove dx
AEIOU = indications for dialysis
Staging
AKI is staged according to the serum creatinine changes, and/or the production of urine.
1 = Increase 1.5-1.9x baseline or < 0.5ml/kg/h for >6 consecutive hours
2 = Increase 2.0-2.9x baselinem or < 0.5ml/kg/h for >12 consecutive hours
3 = Increase > 3x baseline or >354 µmol/L or < 0.3ml/kg/h for > 24h or anuric for 12h
Extra
Stop NSAIDs in AKI as can worsen
Renal replacement therapy indications: (i) fluid overload that is refractory to diuresis, (ii) hyperkalaemia refractory to medical therapy, (iii) metabolic acidosis (pH <7.1) and (iv) complications arising from uraemia (e.g. encephalopathy, pericarditis).
Brain Inflammation
Fever + HA raise suspician (in real life maybe general innfection) - Photo/phono further raises this
Meningitis MC general bacterial unless specific clues
AMS for encephalitis (encephalitis leads to encephalopathy)
Encephalitis = 1000s and all just need supportive tx
- except HSV which is common and can be tx
FAILS - do not do if any one of these (brain will herniate through foramen magnum and die)
Immunosuppressed = elderly neonate who is on monoclonal antibody chemotherapy for their HIV
Unsafe you give Abx THEN CT scan (better a bad diagnosis and alive pt than dead pt and good diagnosis)
1000s of WBCs and mostly polys = bacterial . .. if not then consider something else (can still be bacterial)
No corticosteroids in suspecting bacterial meningitis if <3 months
Mass
cannot LP
HIV/AIDS - Tx for toxoplasmosis
Lymphocytes
temporal lobe/ haemoragic tap = HSV on test but means nothing in life
Cryptosporogenes Tx with Amphotericin
Lymes = Tx with ceftriaxone
TB tx with RIPE
Contact prophylaxis
Meningococcal Meningitis ciprofloxacin or rifampicin
Neisseria meningitides MC children (5% develop neurolgical sequlae and 10% mortality)
Men B 60% of meningococcal disease
Men C for 40%
the rest from travel/ uni
Neontes: Gp B Strep, E Coli, Listeria, Pneumococcus, Staph aureus.
In babies over one month and children, causes include: Meningococcus, Pneumococcus and Haemophilus influenzae B
UTI
General
Typically ascending infectino from urethra to kidneys (higher = worse)
MC young woman with contraception (having sex) and men who penetrate the anus
Uncomlicated must be a non pregnant female
Comlicated = the Ps
E.coli 85% of the time
klebsiella and proteus = other enteric GNR
Cloudy offensive urine
U/A and urine culture = the go to tsts
(>10 WBC/ high powered field)
CT/ US to ix more serious
(>10 to the 5 colonies)
Urethritis
Not really UTI but STD
gonorrhea = chlamydia (ie if you find one then you tx the other)
test urine sample now (first void urine sample NAAT test)
Gonnorhoea = IM ceftriaxone (ciprofloxacin if its known to be sesnitive)
Chlamydia = 7d Doxycycline (azithromycin if not tolerated)
HIV screen
Asx Bacteriuria
should only really be for regant or prepp for urologic procedure ( no-one else should be tx)
Tx with nitrofurentoin (amoxacillin/cefalexin 2nd line) - 7days
repeat to see if tx (only one that you repeat test)
nitrofurentoin can cause neonatal haemolysis near to term so use amoxacillin instead
Cystitis
MC young women
U/F/D (urgency, frequency and dysuria) w/o systemic symptoms (in life you can of course get sepsis from this)
Can choose the abx (TMP-SMX if CKD) but decide how long for
complicated - 7day in uk
Men get abx straight away, woman have back up prescription if not improved in 48hrs
Pyelonephritis
U/F/D but with systemic sx
CVA = costrovertebral angle
WBC casts = give away
urine culture here as long course of abx
Can give PO ciprofloxacin if ambulatory (young and still getting around but still all the sx)
want to admit them to see if perinephritic abscess
Perinephric abscess
(walled off or in parenchyma itself)
suspect if don’t improve after 72hrs confirm with US/CT
Children
Maybe more generalised sx
<3months refer to paediatrician and admit if upper UTI
>3month then usual 3 day
Plasma cell dyscrasias
Monoclonal exansion of plasma cells in BM
Multiple Myeloma = Most important
- -Raised ESR and osteoporosis represents multiple myeloma until proven otherwise*
- -raised calcium and bone pain = myeloma until proven otherwise*
Incomplete IgG
BM becomes crowded and good plasma cells not made so prone to infections
Protein gap on LFTs
Spep = serum protein electrophoresis (M spike)
IgA, IgG
Immunoglobulins: The most common type of heavy chain produced in myeloma is IgG, followed by IgA and then IgD. IgM myelomas are rare, but when IgM is elevated in the blood, the patient more likely has a related disorder, known as Waldenstrom’s Macroglobulinemia.
As MM progresses you get more light chains than heavy (more light chains = more aggressive)
A Bence Jones protein is a monoclonal globulin protein - deposits in kidneys so use Upep (M spike)
Osteoclast stimulating factor leads to Lytic lesions and subsequent pathological fractures
-detect with seletal survey (not bone scan) . . . do with MRI body (CT if not possible)
CRABBI
Calcium
- Hypercalcaemia occurs as a result of increased osteoclast activity within the bones*
- This leads to constipation, nausea, anorexia and confusion*
Renal
- Monoclonal production of immunoglobulins results in light chain deposition within the renal tubules*
- This causes renal damage which presents as dehydration and increasing thirst*
- Other causes of renal impairment in myeloma include amyloidosis, nephrocalcinosis, nephrolithiasis*
Anaemia
- Bone marrow crowding suppresses erythropoiesis leading to anaemia*
- This causes fatigue and pallor*
Bleeding
bone marrow crowding also results in thrombocytopenia which puts patients at increased risk of bleeding and bruising
Bones (middle/lower back, ribs and hips)
- Bone marrow infiltration by plasma cells and cytokine-mediated osteoclast overactivity creates lytic bone lesions*
- This may present as pain (especially in the back) and increases the risk of fragility fractures*
Infection
a reduction in the production of normal immunoglobulins results in increased susceptibility to infection
Chemotherapy often with melphalan and steroid (dexomethasone) and EITHER thalidomide (if no autologous stem cell transplant) or bortezomid (if being induced for autologous stem cell translant)
<70 possible stem cell transplant
also zolondric acid for fractures, VTE prophylaxis, vaccinations, ig replacement
Monoclonal Gammopathy of uncertain significance
monitor for conversion (2% a year)
usually die before this
key is <10%
Waldenstrom’s Macroglobulinaemia
IgM so can form petamers which lead to hyperviscosity
Key is >10% LYMPHOMA ie lymphoplasmosidic lymphoma
Constitutional sx = night sweats, fevers ,weight loss
tx rituximab based chemo
tx the hyperviscosity with plasmaphoresis
Approach To Anaemia
Symptoms represent severity not type of anaemia
Men: 135-180 g/l Women: 115-160 g/l
More 100 usually asymptomatic
HOHF = high output heart failure
<80 pallor of skin and anterior rim
Delivery of O2 = Cardiact output * Hb * SATS - depending on your reserve you exerience sx differently
It also depends on how quick the loss in hb happens
Micro and Macro = mostly production anaemias (low reticulocyte count)
Normocytic mostly destruction anaemias (increased retiulocyte count)
Megaloblastic (Impaired DNA synthesis) looking for hypersegmented neutrophils (5+ lobes)
If B12/Folate levels not clear can request methylmelonic acid to differentiate.
Normocytic
Haemolytic or haemorhage
Haemorhage = increase LDH, decreased haptoglobin, increased bili
Haemorhage you should see evidence so find and plug
MDS = myelodysplasic syndrome
Sodium
Moderate symptoms: nausea, confusion, headache
Severe symptoms: vomiting, cardiorespiratory distress, severe somnolence, seizures, coma (GCS = 8)
Acute (<48hrs)
Severe = <125 with severe symptoms = consultant management only in with close observation ICU, HDU, Resus or maybe AMU
Moderate = <129 with mooderate symptoms
aim is to stop further decrease (stop diuretics, acei and hypotonic fluids if possible)
if strong suspician of new onset symptoms consider IC hypertonic saline (consult a consultant) aim to increase by 5 every 24hrs but no more than 10 in 1st 24hrs or 8 thereafter, receck at 1, 6 and 12 hrs
non-symptomatic = <135 without severe or moderate sx (stop further decrease as above) further mx is dx specific as there is time.
Chronic (>48hrs)
USE HANDBOOK for dx
ix: if possible, stop diuretics/angiotensin-II antagonists/ACE-inhibitors for 48 hours and then measure serum and urine osmolality, and urinary sodium. Assess clinically for volume status.
Hypovolemic tx = stop relevent drugs, IV nacl, 100mg IV hydrocortison if clincial suspician of adrenal insufficiency
euvolemic tx= stop relevent drugs, water restric 1 L/day, oral sodium chloride (slow sodium) +/- low dose furesemide, consider demeclocycline
hypervolemic tx = tx underlying cause, sodium restrict, fluid restrict 1l/day
Monitoring: CNS observations and reassess every 6 hrs till stablised?
HYPERNATRAEMIA
causes: diarrhoea, vomitting, burns, nephrogenic/central diabetes insipidus, glucosuria eg dM, excessive iV sluids, lithium, phenytoin, demeclocycline and corticosteroids
Mild = <155 (drinking may be enough)
severe/hypovolemic = > 155 with salt and water loss
tx: initially hartmann’s until haemodynamics stabalised then correct with 0.45%
Severe hypernatraemia/dehydration (water loss >155mmol/l)
tx: slow infusion of sodium chloride 0.45% or glucose 5%
AKI Guidelines
Prevention
At risk = elderly, diabetic, hypotensive and septic pt
Keep well hydrated
Recognition
Cr = 1.5x baseline
1 = Increase 1.5-1.9x baseline or < 0.5ml/kg/h for >6 consecutive hours
2 = Increase 2.0-2.9x baselinem or < 0.5ml/kg/h for >12 consecutive hours
3 = Increase > 3x baseline or >354 µmol/L or < 0.3ml/kg/h for > 24h or anuric for 12h
clarify what type and reasoning
presence or absence of immune sx (rashe, new arthritis, nasal crusting/bleeding, haemoptysis, bew deafness, mouth ulcers, alopecia, iritis/episcleritis, mononeuritis or neuropathy)
Obstructive sx? FUD, poor stream, hesitancy,, nocturia, PV bleeding, stones
Examination and Observations
Fluid status exam (inc autoimmune)
Urine Dipstick (all AKI, non dialysis CKD, DVT &PE , oedematous pt and suspected UTI)
fluid input/output (cathetarise if this is hard)
send MSU if urinalysis abnormal
send urine protein creatinine ration if protein >2+
Investigations
daily U&Es, bone profile and bicarbonate until fxn improving
autoimmune screen if glommerulonephritis/vasculitis suspected
urine sodium if oliguric (<20 implies pre-renal)
Renal US:
- urgent if >3x or > 400 or obstructions suspected
- non-urgent if 1.5-3x or suspected GN
- may not reed if recovering function or US in last 6 months
Management
Stop nephrotoxic drugs (NSAIDs, ACEi, ARB, pottassium sparing diuretics)
Diuretics should only be suspended if hypovolemic
Stop metformin if eGFR <30
optimise fluids
treat infection promptly
suspected vasculitis/ renal syndromes are a renal emergency (call nephrologist)
30% increase in Cr acceptable on starting RAAS inhibitor (ARBs/ACEi)
Calcium Aetiology and Mx
PT glands behind thyroid
PTH released by dishinibition of Ca receptors
PTH acts on gut indirectly via Vit D- 1,25 which tells gut to reabsorb Calciuma and phosphate (1 alpha hydroxylase)
kidney resabsorbs calcium and extrets phosphate
Clasts breakdown bony matrix releasing calcium and phosphate
Albumin
only 1% free (as ionised calcium)
every one change in albumin = a change in the opposite diection of calcium (from normal)
Hypocalcaemia Management
Check if symptoms
Trousseau = capal pedal spasm on cuff inflation
Chvostek = Tapping (no dulling of reflex)
Prolinged QT interval on ECG
Hypercalcaemia Mx
‘bones, stones, groans and psychic moans’
corneal calcification
shortened QT interval on ECG
hypertension
Increased risk of pseudogout
Moans = AMS
Groans = abdo pain
Sx then tx straight away with IVF (solution to polution is dilution) and Bisphosphonates
Calcitonin (calcium turn down) if severe
Can add loop directics (block calcium reabsorption) when volume resiscitated (or it could make it worse)
Hypercalcaemia Diagnosis
Hyperthyroidism MC
Primary - One hyperfunctioning
Tertiary = all Hyperfunctioning
Secondary = Appropriate response to relative hypocalcaemia in early kidney disese GIVE CINACELCET (calcium mimicker) to prevent tertiary
IX
Differentiate with Sestamibi Scan (technetium-MIBI subtraction scan)
Xray may show pepperpot skull
High calcium and as kidney is functioning it wins
brown tumours = unique to parathyroidism (not really malignancy by eat away at bone)
Tx with resection but watch out fo hypocalcaemia as remainiong PT glands atrophied as suppressed
calcimimmet compounds if unsuitable for surgery
Hypercalcaemia of cancer
Ca inhibits PT release therefore kidneys do not win
PT related protein acts on kidney so Kidney wins
differentiate with phosphate
Hypervitaminosis D
Can see with ingesting in practice
Granulomatous disease increase completed 1,25 vit D produciton so kidneys absorb more calcium an phosphate so
TB and Sarcoid presentation
Hypercalcaemia of immobility = rare, ASx ,old person, trauma, immobility with hypercalcaemia
Familial Hypecalcaemic hypocalcinuria = benign
First ones = big derangements and last = small derangements
Thiazide diuretics can cause hypercalcaemia
Bone Mets Cause
MC source: Prostate>breast>lung
MC site: Spine>Pelvis>Ribs>Skull>Long bones
Hypcalcaemai diagnosis
MC Thyroidectomy (oopsy) or appropriate repsonse to parathyroid resection
AI = very rare
tetany/perioral tingaling = post op day 1
phosphate irrelevent as no pth so no reabsorption or secretion
parathyroid should switch back on with time (or supplement with PTH in future)
Pseudoparathyroidism
end organ resistance to PT so as if its low
HIGH PHOSPHATE not low
Vit D deficiency
poor dairy intake or not going outside
Diagnose with 25 -vit D
Bisphosphonates if significantly osteopenic
Acute hypocalcaemia in pancreatitis is due to sequestration and is an ominous sign
CKD
early = impaired vitamine D formation
Cinacalcet to prevent tertiary
Late = Hyperphosphataemia
EXTRA
Prolonged QT interval on ECG
HF approach
Left HF - backs up to lungs
Right HF- backs up to body
often mixed
SX - RHF - peripheral oedema, hepatosplenomegally, raised JVP . . . dyspnoeea etc from hypoperfusion
- liver = firm, smooth, tender and pulsatile liver edge
LHF - Dyspnea, orthopnea, paroxysmal nocturnal dyspnoea, crackles, S3
IX - BNP>TTECHO>Left heart cath (ischaemic or not)
1st line N-terminal pro-B-type natriuretic peptide (NT‑proBNP)
High = > 2000 pg/ml (236 pmol/litre) = TTE <2w and specialist assessment
Raised = 400-2000 pg/ml (47-236 pmol/litre) = TTE <6w and specialist assessment
Normal = < 400 pg/ml (47 pmol/litre)
BNP levels different (H= >400, R = 100=400 and N<100)
TX
Annual influenza vaccination
One off pneumococcal vaccine
check U and Es 2 weeks after ACEi or Spironolactomne started
1st line ACEi and Beta blockers (bisoprolol, carvedilol, and nebivolol)
If still symptomatic and LVEF <35%:
second line ARBs and aldosterone antagonist (spironolactone/eplerenone) - cause hyperkalaemia along with ACEi
If still symptomatic and LVEF <35%:
Third line ;
ivabradine, sacubitril-valsartan, hydralazine in combination with nitrate, digoxin and cardiac resynchronisation therapy
Diuretics for managing fluid overload but no change in mortality
Aspirin and statin if know ischaemic cause
Pacemaker if <35% but not stage class IV
Class IV- bridge to transplant
Acute bloods for anaemia, infection, electrolyte imbalance . . . . BNP >1mg/L supports diagnosis
NYHA classification
Stage I - No limitation on ordinary physical activity (incorrect)
Stage II - Normal at rest. Ordinary physical activity causes breathlessness (correct)
Stage III - Normal at rest. Less-than-ordinary activity causes breathlessness (incorrect)
Stage IV - Symptoms at rest. (incorrect)
Extra
Measure digoxin levels 6hrs post dose
XRAY:
A - alveolar oedema (bat wing opacities)
B - Kerley B lines.
C - cardiomegaly.
D - dilated upper lobe vessels.
E - pleural effusion.
CKD
Diagnose if eGFR is <60 on 2 consecutive prsentations. Do yearly U+Es and ACR
remember ACEi can decrease by 25%+. nsaids can affect too
consider referal 3b and down or if complications start
- Stage it (when to dialysis)
- Prevent Progression
- Mx Complications
US: bilateral enlarged in diabetic nephropathy, shrunken in other types
Staging
Assume stable Cr so eGFR not reliable in AKI
ESRD = essential anuric
stage 1 - evidence of CKD but normal eGFR
Stage II usually asx
stage III you see start of complication mx here
stage IV means ESRD inevitable so prepare with a AV fistual (matures over months . . . at least 8 weeks)
HD = 4 hours three times a week
PD = every night via peritoneal cathetar
Renal transplant final option
eGFR innacurate in extremes of muscle mass
Prevention
Prevent progression at every stage
Htn
want tighter targets with ACE-I
ACE-i reduce filtration pressure therefor decrease of eGFR by 25% or increase in Cr of 30% acceptable
Can also use furesomide
DM
same goals as everyone else
do not use metformin as causes lactic acidosis
target <48 mmol/mol (6.5%)
Proteinuria
covered by ACEi/ARB + low protein diet
measure via albumin:creatine ratio via a 1st pass urine spot sample
if > 3 significant and > 70 mg/mmol should be on ACEi regardless of htn
Hyperlipidaemia
atorvastatin 20mg offered to all CKD - increase dose if 40% reduction not achieved
- <30ml/min should be mx by renal specialist
Complications
anaemia of CKD
due to EPO
dx by R/O other causes of normocytic anaemia and malnutrition (iron/folate/b12)
Tx with Fe (PO or IV)
EPO - ESAs (erythropoiesis-stimulating agents) such as erythropoietin and darbepoetin
may need transfusions
secondary hyperparathyroidism and mineral bone disease
phosphate stimulates PTH release in attempt to eliminate via kidney but kidneys unable to
Ca low as kidney cannot stimulat 1, 25 vitamine D so not absorbed
Phoshate binders =sevelamer
calcimimetics (cinecalcet) . . . act as calcium and reduce PTH
also replace Ca and vitamine D (alfacalcidol, calcitriol)
want to prevent osteopenia and pathological fractures
Volume overload
prevent with Loops (can add in thiazide later on)
not uncommon to see stage IV on furosemide and metalozone ot get the last out of kidneys
Metabolic acidosis. . . bicarb usually settles around 10-20 . . .. give po sodium bicarbonate to stop metabolic acidosis
Drugs to avoid in renal failure
antibiotics: tetracycline, nitrofurantoin
NSAIDs
lithium
metformin
Pottassium Disturbance
Hypokalaemia
symptoms = CAWP cramps, arrhythmias, muscle Weakness, Polyuria
Mild = 2.5-3.5, no symptoms tx: oral K+
Severe = <2.5 or symptomatic Tx: ECG, IV 40mmol 4-6 hrs
causes: thiazides, corticosteroids, salbutamol, theophyline, rTA, IVF, laxitive abuse, GI loss, alkalosios
Hyperkalaemia
symptoms: PHEW BPP palpitatios, hypotension, ecg changes, muscle Weakness, bradycardia, parasthesia, flacid paralysis
Mild/Moderate = 5.4 -6.4 no symptoms tx = calcium resonium 15d po t/qds
severe = >6.5 or ECG changes or severe symptoms
tx
- ecg
- 10mls 10%d calcium glucanate IV bolus over 3 minutes every 15 mins up to 50ml until ECG improves
- 10 units of actrapid with 25g glucose (250ml of 10% or 50ml of 50%) IV
- nebulised salbutamol 10mg
- if persists then renal/ critical care team
causes: acei, arbs, nsaids, heparin, digoxin, pattassium sparing diuretics, renal failure, addisons, burns, metabolic acidosis
COPD MEDED
If they have Asthma too it should have already been diagnosed
Bronchitis - low o2 leads to hypertension and RHF
Emphysema - damaged aveoli and co2 retension - cachexic and prolonged forced expiration
Diagnose - Spirometry. .. . . the other stuff is for acute
Asthma: raised eosinophil count +/- diurnal variation +/- peak flow varition over time (at least 400ml)
FEV1/FVC = <0.7
FEV1 of predicted for severity
->80% =mild stage 1
50-79 = moderate stage 2
30-49 = stage 3 severe
<30% = stage 4 very severe
Simplified drugs
beclometasone, formoterol and glycopyrronium (Trimbow) - triple therapy in one for better compliance
Non asthmatic = SAMA + LABA + LAMA
Asthmatic = LABA + ICS (can add in LAMA if refractory
Mucolytics for productive cough
SABA = Albuterol (can also use SAMA first line in uk but need to switch to SABA for second line)
LAMA = ibatropium (2ND line ICS+LABA instead if asthmatic features)
LABA- ending in -alol
COPDER - long term management
O2 and smoking cessation = only things that prelong life (and colume reduction surgery in some patients
O2 - 88-92%
- -long term - IX if FEV1 <30%/cyanosis/raised JVP*
- 2 ABG 3w apart offer if <7.3 kPa or 7.2-8 and peripheral/pulmonart oedema or polycythamia*
Exacerbation
ECG, ABC, CXR important to see if anything else causing
Add ABX if sputum looks infected. Cycle between doxycycline (ruin teeth) and azithromycin (QT prolongation so check ECG first)
- azithromycin used for prophylaxis in UK
- amoxicillin, doxycycline or clarithromycin for acute in UK
Causative organisms
Haemophilus influenzae (most common cause)
Streptococcus pneumoniae
Moraxella catarrhalis
IX
The following investigations are recommended in patients with suspected COPD:
post-bronchodilator spirometry to demonstrate airflow obstruction: FEV1/FVC ratio less than 70%
chest x-ray: hyperinflation, bullae, flat hemidiaphragm. Also important to exclude lung cancer
full blood count: exclude secondary polycythaemia
body mass index (BMI) calculation
Ventilation
Non invasive ventilation benefits pts with pH 7.25-7.35
also indicated if respiratory acidosis persists despite maximal standard medical therapy for 1 hour or more
Invasive ventilation if pH <7.25
PE
Common, high mortality, extensive topic
Continuous with DVT
Need Vircow’s Triad to get DVT
1-
2- eg central lines or smoking
3- COCP, coagulopathy, malignacy
CALF SIGNS = NO DIAGNOSTIC VALUE
- unilateral odema >2cm
Retinal haemorrhages and intra-arterial fat globules on fundoscopy can be assoicated with fat embolsim
2 Level DVT wells score
=>2 = DVT likely
<=1 do D-dimer to rule out
Post Thrombotic Syndrome
Complication following DVT
painful, heavy calves, pruritus, swelling, varicose veins, venous ulceration
tx with compression stockings
Wedge Infarct
can see on CXR
Ischaemia - pleuritic chest pain
- Pulmonary hypertension from pushing against clot
Hypoxaemia from decreased perfusion
S1Q3T3 - indicates rs heart strain (also new RBBB associated with PE)
Haemodynamically unstable + Right Heart straign indicates massive PE (thrombolyse them)
Body’s response (why PE size not important)
- platelet mediators spread over lungs leading to vasodilation and fluid to leak out
- O2 diffusion limited so hypoxaemia develops
- hypoxaemia leads to tachyC/P
- co2 perfussion limited so decreases with rachypnoea
-hypocapnaeia/alkalaemia develop
therefore Blood gas = hypoxaemia with respiratory alkalosis
IX (NICE)
ABG, ECG, CXR
Blood: fbc, u+es, clotting screen and G+S
Use well’s criteria to
>4 CTPA (ie >=5)
-V/Q scan if renaly impared and CXR clear (needs to be able to visualose ventilation)
=<4 = D-dimer to rule out (>50yo you need to age adjust)
tPA - massive PE eg drop in BP (can give IVF also). if haemodynamically unstahble after fluid challenge can consider POC echocardiogram ix right ventricular strain or to visualise thrombus. tPA (eg alteplase) also considered for haemodynamically stable patients with severe right ventricular dysfunction, extensive clot burden and cardiopulmonary arrest due to PE
if cont. haemodynamically unstable after tPA can consider cathetar directed or surgical embelectomy.
Submassive PE = RHS (ix with trop, bnp and echo) but haremodynamically stable
Massive = RHS + Haemodynamically unstable
-sit up, give 15L o2
IVC filter (eg DVT likely to kill and GI bleed)
The warfarin bridge is 5d/ when INR 2-3 (whichever longest)
NICE - GIVE DOAC straight off if PE likely its not contraindicated as can just cont. after - apixaban, rivaroxaban
ROH Process
Gestalt assessment = unlikely then rule out with PERC assessment
if not then Wells score (d-dimer to rule out if negative (adjust if >50))
CTPA unless <35 or pregnant/breast feeding
if can do within 4 hours then wait for treatment, if not then tx straight away
provoked? main =surgery, major trauma, pregnant or puperium, Hormone treatment (pill or HRT), immobility (bedbound, unable to walk or proprtionate part of day in bed/chair)
all unprovoked should be offered cancer screening
DOAC for most unprovoked
LMWH in Ca, pregnancy, breast feeding, eGFR <15
Lifelong = warfarin
egfr <5 = unfractionated
GI bleed Approach
Can’t rely on sx as some variation
- even upper can present as haematocetzia
Call GI when stabalised
- minimal : FBC, U&Es, LFTs, clotting, obs, crossmatch
Give Terlippressin before OGD in varicies
OGD all suspected upper GI within 24hrs of admission (first gastrographin/ barium in borhaeves)
NICE says you don’t need to do IV PPI but conflicting evidence so many still do
Mallory weiss = weekend warrier. does not usually vommit
Boorhaeves = professional vomitter
Lower GI you want to find source of bleed. . .. based on rate of bleed (hypotension?). rapidly decreasing HB?
Mesenteric Ishcaemia = ‘gut attack’ POOP (pain out of proportion to examination) - pain after meals is like angina to the heart. colonoscopy looking for ischarmic tissue.
Colonic ischaemia = watershed areas in hypotensive patient. This would be a painful bleed after someone becomes hypotensive for another reason. colonoscopy
Haemorhoids - Internal = painless + blood (not mixed in)
external = painful - blood
glasgow-blatchford bleeding score
assess upper GI bleed severity
1-6 each graded on points
>8 ICU admission
Score is “0”only if all the following are present :
- Hemoglobin level > 12.9 g/dL (men) or > 11.9 g/dL (women)
- Systolic blood pressure > 109 mm Hg 3. Pulse < 100/minute
- Blood urea nitrogen level < 39 mg/dL
- No melena or syncope
- No past or present liver disease or heart failure.
ROH Approach
A to and oxygen
2 large bore cannulas : FBC, U+Es, LFRs, Clotting, VBG, crossmatch 6 units
arrange blood transfusion/ give crystalloid vs major haemorhage protocol
correct coagulopathy (plts \> 50, vit/ffp, reverse anti-coags) Varicell bleed + 2mg IV terlipressin, 4.5g pip-tazo, metoclopromide 10mg
escalate to med reg or GI consultant
discontinue NSAIDs, aspirin and antiplatelets
Microcytic Anaemia
Go to iron studies
Silo metaphor
- tap/ output release to blood
- ferritin = iron stores
TIBC = room in the silo
Iron in from diet (mainenance is 1g . . . can take in max 3-4g)
Menometrorrhagia = prolonged or excessive uterine bleeding occurs irregularly and more frequently than normal.
IDA (iron deficiency anaemia)
1st line ix all IDA should be screened for coelic disease
slow bleed think:
- old man colon cancer
- young woman menometrorrhagia
BM biospy definitive but don’t do
silo slowly runs out
stool softeners to prevent constipation
If before surgery can give transfusion or IV iron (ferric carboxymaltose) 1g
ACID = anaemia of chronic inflammatory disease
our cells can survive longer w/o iron than bacteria therefore defence mechanism
silo tap turned off but continues to fill
Look for chronic inflammation eg RA/ Lupus
often no tx needed if asx - EPO if needed
Thalassaemias
Iron studies and silo normal
Do electrophoresis - As with something else = Beta thalasaemia
Normal = Alpha thalassaemia (beta does not bind with other)
4 copies of each gene - just one = won’t notice and all 4 = dead so have mild (don’t treat) and severe (transfusion)
tx the iron overload w deferoxamine (undo iron from me)
Beta Thalasaemia trait: disproportionatly low MCV and HbA2 raised (> 3.5%)
Sideroblastic
Increased Fe with everthing else normal l l loften show photo of BM biopsy showing ring sidoblasts (iron stuck in mitochondria)
Divide into reversible and non reversible
B6 - cannot tx with B6
MDS - Myelodysplasic syndrome
Arhythmias
Palpitations? - exclude arrhythmias with Holter Monitering (24hr potable 3 lead ecg)
fast = tachycadia?
Narrow = <3 boxes (0.12s) - wide is >
Adenosine = 6mg then 12 then 12 (IV adenosine needs to be infused via a large-calibre vein or central route)
Ventricular Fibrillation
MC cause of death following an MI
SVT
no p waves, HR>150, regular
if haemodynamically stable do vagal manouvres
if this fails give IV adenosine 6mg>12mg>12mg (veramapril if asthmatic)
AF
no p, irregularly irregular, <150
- chaotic background and flutter sawtooth
Torsades de points = turning of points around heart therefore changing amplitude
V-tach - monomorphic, wide complex, fast rhythm
Diltiazem (CCB) can be used instead of beta blocker in asthmatics
AF MX
echo: to assess left ventricular function, atrial size and valve function
Paroxysmal AF: consider antithrombotic
infrequent and/or asymptomatic antiarrhythmics may not be required. Symptomatic start bisoprolol 2.5mg OD and titrate to 10mg if needed (second line or beta blocker contraindicated = flecainide or solatol) . CAD?: amiodarone or dronedarone. poor LVF? amiodarone or non pharma
Persistent AF (longer than 7 days or terminated by cardioversion)
Rate controlled: >65, CAD, w/o CHF, contraindications for antiarrhythmics, unsuitable for cardioversion
rhythm controlled: symptomatic, younger, first time lone af, af secondary to corrected precipitant, CHF
Cardioversion: part of rhythm control . . . should be anticoagulated 4 weeks prior with warfarin . pharmacological with flecainide 2mg/kg iv over 10-30mins with monitoring
Acutre onset and haemodynamically unstable
(chest pain, SOB, hypotension/underperfusion, pulmonary oedema, myocardial ischarmia)
DC cardioverioversion stat
- if CHF then use digoxin in acute setting if already on beta blocker . . rate limiting CCB contraindicated in excerbation HF
stable and decide to cardiovert? (beneficial in young, non CAD, low risk)
<48hr - heparinise and give DC cardioversion (anticoag not needed after unless CHADVAS score) or amiodarone
>48hrs either anticoag 3 weeks before and 4 weeks after DC conversion or TOE to exclude left atrial appendage (LAA) thrombus then can heparanise and DC cardiovert immediatelly
if previous cadioversion failure should have 4w amiodarone before DC cardioversion
CHA2DV2ASC - determine anticoag strategy:
0- non aspirin no longer recommended
1- consider for males
2 - offer anticoag (NOAC or Warfarin)
HASBLED score if starting warfarin - high risk =>3
Slow
Narrow and wide not as important here
PACE if too slow or unstable
Atropine helps for the first two - maybe 3rd
Idioventricular rhythm has no p waves as only ventricles contracting
stability - American Heart Association, includes systolic blood pressure < 90 mm Hg, altered mental status, cardiac ischemia, or severely decompensated heart failure due to the underlying rhythm.
Thyroid
T4 = spark plug of the body
mentaion = brain moving
Hyperthyroidism
Hyperthyroid = thyrotoxicosis = too much T4
weight loss form diarhoea and metabolism
Oligomenorhoea leading to Amenorrhoea
Screen with TSH and confirm with free T4
Exception to decrease TSH is central where TSH drives the T4
Thyroid Storm
Hypertension
IV propanalol
antithyroid drugs ; methimazole or propylthiouracil
dexamethasone -stops T4 conversion to T3
RAIU scan = radioactive iodine uptake = nuclear scintigraphy
. . . goes wherever T4 being MADE
MNG = multinodular goitre
Graves
smoking is a risk factor
TSH receptor antibodies (also anti-TPO antibodies)
RAIU lights up
specific findings = bugg eyes and muddy shins, acropachy (clubbing)
surgery as radioactive iodine will make exo and PM worse
Anti-thyroid drug titration (40mg carbimazole then gradual reduce when euthyroid) 12-18 months
block and replace (40mg carbimazole then add thyroxine when euthyroid) 6-9 months
carbimazole can cause agranulocytosis
Thyroiditis
T4 leaks out there transient hyperthyroid state . . .will heal or die after
painfull = de querveins and painless = hashimotos
RAIU = cold
Riedel’s thyroiditis = rare, dense fibrosis, painless, usually mroe common in women
De qierveoms (subacute) -
reduced iodine uptake in scintography - usually self limiting - NSAIDs for pain
2-6w painful hyperthyroidism >1-3w euthyroid > weeks/months hypothyroidism > structure/fxn back to normal
MNG and toxic adenoma
RAIU will show nodes
factitious and stroma present stroma ovaria = both exogenous . . .. factitious = trying to lose weight
TX
can use same medications for ther conditions but go for surgery/ Radioactive iodine ablation as don’t want lifelong medication
Hypothyroidism
Menorrhagia but can lead to Amenorrhoea
Doesn’t matter how you get it, tx with levothyrxin
TSH up unless its a central problem (rare)
Iatrogenic = Graces Tx
non iatrogenic = MC hashimotos ( TPO abs to confirm)
Myxedemic coma = sever of hypo (give iv corticosteroids to tackle co-existing adrenal insufficiency)
so cold intolerant that becomes hypothermic which leads to hypotension
Tx with warm IVF and warm blankets
give IV T4 and more potent T3 if that does not work.
MX
Levothyroixine = 50-100mcg od (severe/cardiac disease/ elderly start 25mcg and titrate up)
target TSH value 0.5-2.5 mU/l
measure every 8-12 weeks
pregnancy icnrease by 50% as early as 4-6 weeks of pregnancy
REMEMBER in the vast majority of cases:
Low TSH = high T4 = hyperthroidism
High TSH = Low T4 = Hypothyroidism
EXTRA
Infective Endocarditis
Dukes Criteria technically not clinical criteria
Definite if:
Two Major (culture and echo)
one major + 3 minor
5 minor
Murmur
The most common valvular abnormality in infective endocarditis is tricuspid regurgitation. Combined with the fact that this man is showing sings of right sided heart failure (peripheral oedema)
Holosystolic Murmur louder on inspiration
RFs
h/o endocarditis (scares perfect place to set up shop)
vascular
Acute limb ischaemia
Splinter haemorages
janeways lesions (painless)
Rhematologic Sx
Roth spots (eyes)
Osler nodes (painful lesion on finger pulp)
Glomerulonephritis
Two main presentations in Practice
Acute
CHF presentation or Bacteraemia presentation
empiric tx and blood culture until nothing
not enough time for Rheum sx to present
Subacute
more insidious
keep doing cultures till you detect something (harder to grow)
no abx at first or won’t culture
TEE for IE (In practice you would probs do TTE first)
Empiric Tx
Depends on pt (what valve and how long), not organism
Vanc & Gent backbone
NICE TX
Native : amoxacillin
Prosphetic : Vanc + low dose gent + rifampicin
Pen al/MRSA/ SEVERE : vanc + low dose gentamicin (acts on biofilms well)
strep - benzylpenicillin
staph- flucloxacillin
Surgery
if risk of embolism or something the abx won’t tx
Prophylaxis (NICE actually recommonds against PPX)
If Bad Valve + mouth/Throat procedure
BV = h/o endo, prosthetic, congenital heart disease
MT - dental procedues/ biopsy of airway + GI tract + gynae obs procedures
AND
if you can’t us vanc then use dapto
If you culture S.Bovis do a colonoscopy (they have colon cancer)
Organisms
S.aureus MC
S.epididimus MC postoperative eg indwelling lines
Strep viridans (pseudotoxic term . . . MC ones are S.mitis and S. Sanguinis) (poor dental hyegine)
Strep bovis - colon cancer
Culture negative;
HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
or used abx
Post Op Fever
Fever = inflamation, not neccessarily infection
Wound healing causes fever (closer to surgery the more likely wound healing)
temp >39 is what’s alarming (or sx)
>38 after 48hrs do the fever workup
5 Ws
used to be what infections (not true) now use for prevention framwork
so fever with some sx
atechelitis does not case fever but can lead to collapsed alveoli and pneumonia
incetative spirometry not enough evidence (big breaths should open up alveoli but waliking will open more naturally)
Get cathetar out early to prevent infection
Malignant hyperthermia
AD= autosomal dominant
(ca channels stay open leading to massive sustained contraction using lots of energy and generating lots of heat)
Wound is rest of slide
predicting infxn
different types of wound
clean = does not go near any mucosa
clean contaminated = mucosa but it was deliberate without spillage
contaminated (oopsy or ruptured prior to surgery)
Dirty = dirty source eg fecal contamination, foreign object wound
wash out as things can be hinding in crevices
Nec Fac
any organism but those are most associated.
black = evidence of necrotic tissue under skin
Grey dishwater as serum with lots of dead stuff in it
Bacteraemia
no skin changes to differentiate from Nec Fac
Superficial Skin Infection
usually infection of subcutaneous fat (cellulitis)
usually don’t see alone but with wound dishenence.
Deep Peritoneal Infection
2 kinds.
free fluid is normal after surgery but if not absorbed can develop to abscess
abscess is inflamed by definition as immune system has made it
If leak then spillage is ongoing . .. will be sicker
abscess = focussed peritonitis as its walled off
Always look for these if unresolving ileus.
Ortho Trauma
Comminuted = broken in several places
Angular/oblique = curved or at angle
AD - dislocates forward . . . maybe deltoid parastheisis (axilliary neve damage)
Montegia and Galleazzi
Humerus # AX w radial nerve damage (wrist drop)
Colles- fall on outstretched wrist - damage to median nerve leads to loss of thumb abduction
Scaphoid - all proximal scaphoid fractures req surgical fixation
Knee - not swollen? probs hip
Hip- Garden classification for neck of femur fractures
iliofascial nerve block is effective pain relief
MCL/CCL - VuLgar Stress = Lateral stress = MCL injury
- vargus is the other
Tib/Fib - if tib breaks then probs fi also
Ankle - surgery as casting ankle weird and they don’t usually break well.
Compartment Syndrome - on repurfusion, after crush injury, very tense, check compartment pressure, tx - fasciotomy
Ottawa Rules
Xray if: pain in malleolar zone and one of
bony tenderness at the lateral malleolar zone (from the tip of the lateral malleolus to include the lower 6 cm of posterior border of the fibular)
bony tenderness at the medial malleolar zone (from the tip of the medial malleolus to the lower 6 cm of the posterior border of the tibia)
inability to walk four weight bearing steps immediately after the injury and in the emergency department
Subluxation of the radial head
Pulled Elbow
MC upper limb injury in >6
elbow pain with limited supination and extension of the elbow
MX: analgesia and passively supination of the elbow joint whilst the elbow is flexed to 90 degrees
Iliotibial band syndrome (not trauma)
a common cause of lateral knee pain in runners. Athletes commonly present with a sharp or burning pain around the lateral knee joint line.
Plantar Fasciitis (not trauma)
Plantar fasciitis is the most common cause of heel pain seen in adults. The pain is usually worse around the medial calcaneal tuberosity.
Management
rest the feet where possible
wear shoes with good arch support and cushioned heels
insoles and heel pads may be helpful
trochanteric bursitis (non trauma)
aka Greater trochanteric pain syndrom
MC women 50-70
from repeated movement of the fibroelastic iliotibial band
pain over the lateral side of hip/thigh
tenderness on palpation of the greater trochanter
ECG Rhythm
Key Approach
Relationship of p waves to QRS
Width of QRS
Sinus Arrhythmia
changes in rate associated with respiration normally seen in young
sUpraventricular rhytms have narrow QRSs and ventricular are wide (except supraventricular with bbb or WPW syndrome)
Escape Rhythms
normal sinus then SAN fails to discharge. you then get:
atrial escape (abnormal p wave followed by qrs then back to normal)
junctional escape (no p waves and normal qrs
ventricular escape (larger delay then abnormal qrs . . . t wave often inverted)
Extrasystoles
This is the same as escape rhythms but occur early rather than late)
again have atrial, junctional and ventricular.
extrasystoles rarely require mx
Supraventricular Tachicardias
Atrial Tachicardia (subtype)
atria depolorise faster than 150bpm
if >200 then av block occurs preventing higher rates in ventricles
Atrial Flutter (subtype)
atrial rate >250 (no flat baseline between p waves)
often associated with 2:1 block
a narrow complex tachicardia with a ventricular rate of 125-150 should always alert you to possibility of atrial flutter with 2:1 block
Junctional Tachicardia (subtype)
P waves v close or not seen at all with normal QRSs
Carotid Sinus Massage
Do in SVT to tx but also make nature of arrythmia more obvious
rub along one carotid artery at the point of maximal pulsation for 5-10s
do not attempt in pts with known carotid artery stenosis or in those with recent TIAs or strokes because of risk of dislodging emboli
Diagnostic use:
sinus tachicardia = temporary slowing of HR
atria or junctional tachicardia = may terminate or have no effect
atrial flutter = usually causes temporary increase in block
atrial fibrillation or ventricular tachicardia = no effect
Ventricular Tachicardia
= very tidy
wide abnormal QRSs
Atrial Fibrillation
No p waves, irregular baseline, irregular QRS, Normal QRS morphology
Ventricular Fibrillation
= very fuzzy (ecg totally disorganised)
pt will quickly lose conciousness
Bundle branch block complications
compare to sinus rhythm
if qrs> 4 squares its probs ventricular origin
in context of MI invariably ventricular tachicardia
LAD indicates ventricular origin
very irregular may have AF on top
Wolff-parkinson-white syndrome
short PR interval with slurred upstroke on QRS complex
What to do:
- For fast or slow sinus rhytm treat the underlying cause, not the rhythm itself
- extrasystoles rarely need treatment
- in patients with acute HF or low BP due to rachycardia, DC cardioversion should be considered early on
- Patients with any bradycardia that is affecting the circulation can be treated with atropin, but if this is innefective they will need temporaty or permanent pacing
- Consider Vagal manouvres such as CSM, valsalva or eyeball compression in abnormal narrow wave tachycardia
ECG Rhythm
Key Approach
Relationship of p waves to QRS
Width of QRS
Sinus Arrhythmia
changes in rate associated with respiration normally seen in young
sUpraventricular rhytms have narrow QRSs and ventricular are wide (except supraventricular with bbb or WPW syndrome)
Escape Rhythms
normal sinus then SAN fails to discharge. you then get:
atrial escape (abnormal p wave followed by qrs then back to normal)
junctional escape (no p waves and normal qrs
ventricular escape (larger delay then abnormal qrs . . . t wave often inverted)
Extrasystoles
This is the same as escape rhythms but occur early rather than late)
again have atrial, junctional and ventricular.
extrasystoles rarely require mx
Supraventricular Tachicardias
Atrial Tachicardia (subtype)
atria depolorise faster than 150bpm
if >200 then av block occurs preventing higher rates in ventricles
Atrial Flutter (subtype)
atrial rate >250 (no flat baseline between p waves)
often associated with 2:1 block
a narrow complex tachicardia with a ventricular rate of 125-150 should always alert you to possibility of atrial flutter with 2:1 block
Junctional Tachicardia (subtype)
P waves v close or not seen at all with normal QRSs
Carotid Sinus Massage
Do in SVT to tx but also make nature of arrythmia more obvious
rub along one carotid artery at the point of maximal pulsation for 5-10s
do not attempt in pts with known carotid artery stenosis or in those with recent TIAs or strokes because of risk of dislodging emboli
Diagnostic use:
sinus tachicardia = temporary slowing of HR
atria or junctional tachicardia = may terminate or have no effect
atrial flutter = usually causes temporary increase in block
atrial fibrillation or ventricular tachicardia = no effect
Ventricular Tachicardia
= very tidy
wide abnormal QRSs
Atrial Fibrillation
No p waves, irregular baseline, irregular QRS, Normal QRS morphology
Ventricular Fibrillation
= very fuzzy (ecg totally disorganised)
pt will quickly lose conciousness
Bundle branch block complications
compare to sinus rhythm
if qrs> 4 squares its probs ventricular origin
in context of MI invariably ventricular tachicardia
LAD indicates ventricular origin
very irregular may have AF on top
Wolff-parkinson-white syndrome
short PR interval with slurred upstroke on QRS complex
What to do:
- For fast or slow sinus rhytm treat the underlying cause, not the rhythm itself
- extrasystoles rarely need treatment
- in patients with acute HF or low BP due to rachycardia, DC cardioversion should be considered early on
- Patients with any bradycardia that is affecting the circulation can be treated with atropin, but if this is innefective they will need temporaty or permanent pacing
- Consider Vagal manouvres such as CSM, valsalva or eyeball compression in abnormal narrow wave tachycardia
Hip Fractures
CF: shortened, externally rotated flexed leg
IX: AP pelvis and lateral xray
MX :
Pre-operatively
Analgesia including a fascia iliaca block, stop anticoagulants/anti-platelets & early surgery.
Post operatively
Thromboprophylaxis, early mobilisation Beware of delirium!
Garden Classification ( for intracapsular fractures)
Principoles of fracture Mx
Resuscitate > Reduce > Hold > Rehabilitate
Reduce
Reduction in the taction of soft tissues (to reduce swelling) of transversing nerves ( to reduce neuropraxia) and reduction of pressures on blood vessels (restoring blood supply).
Some use an initial exaggeration of fraction to uncouple distal and proximal fragments
can be done open or closed
Requires analgesia e.g. local/regional blockade or conscious sedation
requires at least two people (one apply reduction force and another counter reduction . . . . often 3rd for casting)
Hold
immonilising fracture
consider need of traction where strong muscles pull across facture sites eg femur fractures
most commonly simple splints or casts
casts non circumferential in first 2 weeks due to risk of compartment syndrome
axial instability: casts need to cross both the joint above and below if # able to rotate along axis eg combined tibia/fibula metaphyseal # or radius/ula metaphyseal #
weight bear? always let pt know if they can
Thromboprophylaxis: common if immobilised and non-weight bearing
safety net pt on sx of compartment syndrome.
Rehabilitate
Intensive period of physiotherapy as pts stiff after immobilisation
encourage movement of non-immobilised unaffected joints from outset
Frailty a significant risk factor so therapists essential to making sure suitable adaptions implemented for their recovery
Orthopedic Radiology
Projection
- -2 views generally AP and lateral
- -if shaft of long bone image joint above and below
- -Comment on skeletal maturity (fused epiphyses/growth plates)
Patient Details
-name, DOB, date taken
Technical Adequacy
- -Penetrance? – make out bones and soft tissue
- -rotation/?
- Obvious Abnormalities?
- -fractures, subluxations/dislocations
Systemic r/v of the xray
- -look at disruption of smooth continuous cortex (fractures)
- -then medulla for fracturs (trabecular disruption and sclerotic/lucent lines)
- -soft tissue swelling and join effusion
- -joint surfaces for subluxation or dislocation
- assess joints for degenerative changes (loss of joint space, subchondral sclerosis, subchondral cysts and osteophytes)
- -assess joints for inflammatory changes (periarticular osteoporosis, soft tissue swelling and bony erosions)
- -r/v bone densitiy for lucent and sclerotic areas.
Summary
- -State key findings (description or findings)
- -differential diagnosis
- further relevant imaging
- appropriate initial mx
Fracture Description
- What bone involved
- What part of bone (proximal/middle/distal third, intraarticular)
- Fracture pattern (simple/open, comminuted (>2 fragments), impacted (fragments driven into eacchother))
- Type of fracture (Transverse(perpendicular), oblique(<90degrees), vertical (parallel), spiral, greenstick (break in once cortex but not other)
- Subluxation (some contact between articular surfaces) vs dislocation (no contact)
- Translational Displacement (relation of distal to proximal fragment . . . . anterior/posterior/medial/lateral displacement) . . . AP view displacement = medial/lateral and lateral view displament = anterior/posterior
- Angulation (movement of distal fragment relative to proximal in degrees
- Rotation (internal or external, measured along long axis – might be easier on examination)
- Shortening
- Joint space (smaller/larger, asymmetrical, fragments/foreign bodies)
- Joint cartilage (symmetrical outline of cartilage?)
- Bone texture
- Mostly radiolucent with thin cortices = osteopenia
- Radiolucent around joint = inflammation/infected joint
- Focal lucent areas indicate lesion (tumour/infection)
- Sclerotic lesions (rarer – paget’s, osteochondritis, sclerotic bone mets)
General Surgical Approach
End of bed o gram
look at patient
look at obs
speak to nurse
then . . . .
Lower Limb Fracture
Ottowa rules
General mx
Closed reduction with propafol (try in A&E)
RICE = Rest, Ice, Compression, Elevation
Webber Classification
lateral malleolus classification
based on level of fracture of fubual compared to syndesmosis
Extra
Trimalleolar includes posterior malleolus
Lauge-Hansen classification used in orthopaedics. . . . depends on position at time of fracture
immobilised with below knee backslab
Any signs of NV compromise requires immediate surgical review (check pulses)
lightbulb sign on xray is aposterior shluder dislocation
Back Pain
- Cord Compression?
- Non-specific = MSK
- can jump to others if you do not think msk (XRAY/MRI)
- If not MSK then tx is surgery based on sx and lifestyle
Thoracic back pain is a red flag symptom
acute = <6w, subacute = 6-12 and chronic >12
MSK
lower backpain first line NSAID (ibuprofen/naproxen)
+ ppi if >45
encourage exercise ( print excercise sheet) but physiotherapy only if sx no resolving or likely to become disabled.
after 2-4 weeks encourage graded return to work even if pain . . .. won’t make worse
Spinal cord compression - seems the same as cauda equina syndrome (this can be caused by massive disk herniation) - surgical emergency
- sensory loss, lowe limb weaknes
- urinary incontinence/retention
- reduced sensationin perianal area
- reduced anal tone
MRI spine WHOLE spine in 24hr
urgent oncology referal
high dose dex
Cauda Equina vs cord compression
Cauda equina = flaccid paralysis + loss of reflexes
Cord compression = spastic paralysis + brisk reflexes.
Both = sensory + power loss.
Sciatica = shooting pain from bottom down back of legs to toes
Do not offer X-ray in UK - MRI only if you suspec someting sinister - red flag symptoms
pseudoclaudication (spinal stenosins - only upper thigh and buttocks - don’t get climbing stairs or bent over on bike
- resolves on sitting down
Herniation- AKA prolapsed disk
Leg pain usually worse than back
pain worse on sitting
pain ins dermantological according to which level affected
NSAIDs/exercise/physiotherapy . . MRI if no imporovement after 4-6 weeks
nerve route compression unlikely if SLR not limited or pain does not extend below knee on slr
look for L5/S1 compression (loss of sensatino of lateral border of lower leg and foot, weakness of dorsiflexion and plantarflexion of foot or impaired ankle reflex)
Compression fracture - dont forget f/u dexa scanand osteoporosis tx
Ankylosing Spondylitis should be here:
Typically a young man who presents with lower back pain and stiffness
Stiffness is usually worse in morning and improves with activity
Peripheral arthritis (25%, more common if female)
NSAIDS - remember PPI if over 45
psoas abscess
Back/flank pain worse which is worse when the hip is flexed, with associated fever and raised inflammatory markers in an IVDU. ix CT Abdo
TX = IV abx and percutaneous drainage
EXTRAS
Previous hx of Ca? - always orthopaedic referal
Discitis
CF
backpain, fever, sepsis, lower limb neurological sx
RF: IVDU MC Staph Aureus . . . may present with endocarditis
Dx: MRI
Tx: 6-8w abx
Hyperlipedaemia
QRISK2 score calculated for >40y and <84y to assess CVD risk
More specific guidlines or DM, CKD and Familial hyperlipidaemia
Safetynet for muscle pain and weakness .. .. check cK if the complain of it. >10 times upper limit stop immediatelly (rhabdo). <5 times rarely significant.
Might underestimate for HIV,
NICE suggest QRISK2 may underestimate CVD risk in the following population groups:
people treated for HIV, SLE, antipsychotics, steroids and immunosuppresent drugs
Measuring lipid levels
A full lipid profile should also be checked (i.e. including triglycerides) before starting a statin. The samples does not need to be fasting.
Can feed lipid measurements into QRISK score. Consider familial hyperlipidaemia if very high
If >10% statin indicated (offer period of lifestyle modification first)
also offer statin for DM as above and CKD
Other tests
TFTs - can be caused by hypothyroidsim
Bloood Glucose: DM can cause
Anorexia nervosa can also cause
Secondary prevention
All patients with CVD should be taking a statin in the absence of any contraindication.
Atorvastatin 80mg should be offered first-line.
Follow-up of people started on statins (asthenia (physical weakness), flatulance, headaches)
NICE recommend we follow-up patients at 3 months
repeat a full lipid profile
if the non-HDL cholesterol has not fallen by at least 40% concordance and lifestyle changes should be discussed with the patient
NICE recommend we consider increasing the dose of atorvastatin up to 80mg
Familial Hyperlipidaemia
Ezetimibe inhibits the absorption of cholesterol
Bezafibrate reduce serum triglycerides.
Lifestyle modifications
These are in many ways predictable but NICE make a number of specific points:
Cardioprotective diet
total fat intake should be <= 30% of total energy intake
saturated fats should be <= 7% of total energy intake
intake of dietary cholesterol should be < 300 mg/day
saturated fats should be replaced by monounsaturated and polyunsaturated fats where possible
replace saturated and monounsaturated fat intake with olive oil, rapeseed oil or spreads based on these oils
choose wholegrain varieties of starchy food
reduce their intake of sugar and food products containing refined sugars including fructose
eat at least 5 portions of fruit and vegetables per day
eat at least 2 portions of fish per week, including a portion of oily fish
eat at least 4 to 5 portions of unsalted nuts, seeds and legumes per week
Physical activity
each week aim for at least 150 minutes of moderate intensity aerobic activity or 75 minutes of vigorous intensity aerobic activity or a mix of moderate and vigorous aerobic activity
do musclestrengthening activities on 2 or more days a week that work all major muscle groups (legs, hips, back, abdomen, chest, shoulders and arms) in line with national guidance for the general population
Weight management
no specific advice is given, overweight patients should be managed in keeping with relevant NICE guidance
Alcohol intake
again no specific advice, other than the general recommendation that males drink no more than 3-4 units/day and females no more than 2-3 units/day
Smoking cessation
smokers should be encouraged to quit
Hypertension Dx
can ix primarty hyperaldosteronism after two drugs if suspected (aldo:renin ratio)
Stage 1 hypertension
- Clinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg*
- lifestyle changes + consider antihypertensives*
- *Stage 2 hypertension**
- Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg*
Antihypertensives regardless
Severe hypertension
- Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 110 mmHg*
- immediate tx*
admit if worryig signs (pappilodema, retnal haemorhages, confusion)
if no worry signs do urgent ECG, urine tests and bloods lookinf for end-organ damage
Clinic BP
Take readings in both arms (if >20 dif recheck then go with highest if persistent)
Take two readings in consultation and use lowest
Ambulatory blood pressure monitoring (ABPM)
at least 2 measurements per hour during the person’s usual waking hours (for example, between 08:00 and 22:00)
use the average value of at least 14 measurements
If ABPM is not tolerated or declined HBPM should be offered.
Home blood pressure monitoring (HBPM)
for each BP recording, two consecutive measurements need to be taken, at least 1 minute apart and with the person seated
BP should be recorded twice daily, ideally in the morning and evening
BP should be recorded for at least 4 days, ideally for 7 days
discard the measurements taken on the first day and use the average value of all the remaining measurements
If however the blood pressure is >= 180/110 mmHg:
immediate treatment should be considered
if there are signs of papilloedema or retinal haemorrhages NICE recommend same day assessment by a specialist
NICE also recommend referral if a phaeochromocytoma is suspected (labile or postural hypotension, headache, palpitations, pallor and diaphoresis)
Hypertension Mx
ACEi - enalapril, lisinopril, perindopril and ramipril.
ARBs - candesartan, irbesartan, losartan, valsatan
CCBs - amlodipine, felodipine and nifedipine.
Diuretics - indapamide and bendroflumethiazide.
Bendroflumethiazide
first, check for:
- confirm elevated clinic BP with ABPM or HBPM*
- assess for postural hypotension.*
- discuss adherence*
Step 1 treatment
patients < 55-years-old or a background of type 2 diabetes mellitus: ACE inhibitor or a Angiotension receptor blocker (ACE-i or ARB): (A)
angiotensin receptor blockers should be used where ACE inhibitors are not tolerated (e.g. due to a cough)
patients >= 55-years-old or of Afro-Caribbean origin: Calcium channel blocker (C)
ACE inhibitors have reduced efficacy in patients of Afro-Caribbean origin are therefore not used first-line
If CCB give peripheral oedema it can be switched for 2nd line indapamide to relieve symptoms
Step 2 treatment
if already taking an ACE-i or ARB add a Calcium channel blocker or a thiazide-like Diuretic
if already taking a Calcium channel blocker add an ACE-i or ARB
for patients of Afro-Caribbean origin taking a calcium channel blocker for hypertension, if they require a second agent consider an ARB in preference to an ACE inhibitor
(A + C) or (A + D)
Step 3 treatment
add a third drug to make, i.e.:
if already taking an (A + C) then add a D
if already (A + D) then add a C
(A + C + D)
Step 4 treatment
NICE define step 4 as resistant hypertension and suggest either adding a 4th drug (as below) or seeking specialist advice
if potassium < 4.5 mmol/l add low-dose spironolactone
if potassium > 4.5 mmol/l add an alpha- or beta-blocker
Approach To Dyspnoea
Acid base balance not a Dx but a catch all
Bad blood = carboxyhaemoglobin/ Methemoglobinemia
Anaemia - don’t worry about the type at first. Just Dx
- SOB, fatigue, tiredness, pale skin, dizziness
Same w CHF - exacerbation the same whichever type
-SOB, Orthopnoea, PND, Crackles, chest pain
Pleuritic Pain + SOB narrows it
- pneumothorx, pneumonia, PE, pulmonary effusion, CA
- Obstructive and restrictive
- DAH = diffuse alveolar Haemorhage
IX
Always these (BNP debatable)
ABG - covers top two
CXR - covers bottoms two
ECG - arythmia/MI
BNP- CHF
SATS - also do these. generally want >92%
order all before you get there and cancel if you don’t need
Pneumothroax
<2cm rim and not SOB discharge
if <2cm SOB then aspiration
if >2cm and >50 or SOB after aspiration then instert chest drain
Approach To Abdo Pain
Type + Location = Shortlist
Somatic Pain = pinpoint pain (correct target)
Neuropathic pain (tingling/burning) - not frome target
Visceral organs = no innvervation . . hijack somatic overlay from EMBRYOLOGICAL origin
Feel obstruction/stretch/inflammation (not stabbing/buring)
Obstructive
Hollow organs
-increase pain as peristalsis approachs obstruction
Restless trying to find position of comfort
Inflammatory
Constant and restlesss with inflammatory markers
Perforation
Peritoneal does have innvervations and very sensitve so SAS , very paifull, motionless
peritoneal pain will illicit rebound tenderness (percuss non tende area and tender area will hurt) hollow viscous to perf - PUD/ Diverticulitis
Ischaemic
POOP - ie very painful but not at all tender to touch . . . . lactate gives it away
Some sort of vascular history (AF/CAD/PVD) or ischaemic colits?
Functional
Reffered pain - can have pain from bad constipation or bloating from periods
ANGRY ROBOT
PM BAD BRUNG = randos . . .NOT periumbilical
Epigastric Chest and Epigastric Abdo (remember Qs for both)
RUQ = US
Everwhere else use CT
O/E
not very useful except
peritoneal pain/ absent bowel sounds
Rovsing’s Sign = pain in LIF when palpation of RIF
boas’ sign = hyperaesthesia below right scapula in Cholecystitis
PM BAD LUNCH:
- *Porphyria**
- *Mediterranean** Fever (Familial Mediterranean Fever): Armenian heritage; FHx of FMF. History paroxsymal fever/abdominal pain x 72 hrs.
- *Black Widow** Spider bite
- *Addison’s:** Associated hypotension; history of steroid use, auto-immune disease, or tuberculosis (the most common causes of Addison’s disease)
- *Diabetic Ketoacidosis**
- *Lead** poisoning
- *Uremia**
- *Narrow angle glaucoma**: Red, painful eye.
- *Calcium:** Hypercalcemia causes chronic constipation due to chronic bowel contraction.
- *Herpes Zoste**r: Dermatomal pain may precede vesicular rash by 1-2 days.
Cough Approach
Acute = always infection
subacute = alwasys post infection
dex/benz = sx releief
don’t worry in practice if <8weeks
ACEi/Cigs = stop
-smoking cessation initial worsening for 8 weeks
CXR to see if primary pathology (resp referal if +ve)
- empirit tx if not (8 weeks each)
Further ix if not
primary pathology missed by CXR
if still nothing then idiopathic and tx symptoms
ENT infections +
OM
URTIs - S. pneumoniae, H. influenzae, M. catarrhalis
erythromycin or clarithromycin if pen allergy
Antibiotics should be prescribed immediately if:
- Symptoms lasting more than 4 days or not improving*
- Systemically unwell but not requiring admission*
- Immunocompromise or high risk of complications secondary to significant heart, lung, kidney, liver, or neuromuscular disease*
- Younger than 2 years with bilateral otitis media*
- Otitis media with perforation and/or discharge in the canal*
If an antibiotic is given, a 5-day course of amoxicillin is first-line. In patients with penicillin allergy, erythromycin or clarithromycin should be given.
OE
swimmers ear from not drying after - pseudomonas
digital - cotton buds
Tx - usully resolves spontaneously
1st line - topical abx or topical abx/steroid combo
cipro topical if bad
Flucloxacillin if sreading
Ref to ENT if toical abx not working
Consider malignant OE in diabetes and immunocompromised -CT and emergerncy ent ref + IV antiseudomonal
Mastoiditis
hx of OE/OM
CT often not needed
Sinusitis
vral v bacterial
purulent thick bilateral discage
don’t really need imaging
TX - analgesia + nasal decongestants
maybe steroids if >10 days
phenoxymethylpenicillin first-line, co-amoxiclav if very unwell
Consider causes of poor drainage (predisposes) eg polyps
Double sickening indicates bacterial sinusitis (initial recovery before worsening
Nasal virla - coryzal
bilateral copius and clear
supportive
Pharyngitis
viral vs strep A
tx strep A to avoid rhematic fever
EBV? - do the monospot
centor criteria (3 or 4 = more likely to benefit from antibiotics);
- presence of tonsillar exudate*
- tender anterior cervical lymphadenopathy or lymphadenitis*
- history of fever*
absence of cough
Tx: Penicillin V (erythromycin/clarithromycin in pennicilln allergy)
epistaxis
normal = unilateral for <30mins
if posterior bleed then pack + prophylactic Abx for toxic shock
anterior = 1st silver nitrite cautery and 2nd line rapid rhino for 24hrs (tampon thigng . . . . different ones for anterior and posterior bleed
Choanal atresia
= blockage from nose to throat
blue on feeding
dx - fail to cathetarise
tx surgery
foreign body
remove it and tx infection with abx
homeless may be insect – do not use light - lidocaine to parylise first.
Perforated Tympanic membrane
ENT referal if does not heal in 6-8 weeks
abx if caused by acute OM
Infectious Mononucleosis
EBV aka HVV-4
Classic triad = sore throat, pyrexia, lymphadenopathy
Also: palatial petechiae, splenomegaly, hepatitis, lymphocytosis, haemolytic anaemia, maculopapular rash with amoxicilin/ampicillin
Ix: Monospot tests and FBC in second week of illness (NICE)
Tx: rest/fluids/avoid alcohol, simple analgesia for aches and pains, avoid contact sports for 8 weeks
Approach to dysphagia
Diffulculty swallowing (not pain)
often desribed as getting stuck - ask where they feel its getting stuck (above or below clavicle
Oropharyngeal
- ENT laryngoscope
- usually a neuro problem
- problem with initiating (cough/choke/gag)
Vagus nerve
MS - multiple sclerosis
TM = transverse myolitis
Stroke is most common
SALT referal (automatic if stroke)
Pharyngogram = radiolabel different cosistencies
If NBM then NG tube
PEG you would still need to get gastro involved
OESOPHAGEAL
GI referall and endoscope
Motility
funcitional (muscle fine)
liquid and food problems from get go
Mechanicl
obstructive worsening and progessive
food then liquid
BOTH - barium swallow and OGD
monometry - maybe in the community but wont as OGD in hospital if admitted
IX UK
All OGD, FBC
maybe barium
ambulatory oesophageal ph and monometry for GORD and achalesia
causes
oesophageal cancer
oesophagitis
oesophageal candidasis
achalasia
pharyngeal pouch
systemic sclerosis
myasthesia gravis
globus hystericus
Rashes
EI
Slapped cheek syndrome is giveaway . . .but can be on arms and legs
Aplastic crisis if Sicle Cell disease
Keep away from pregnacy
M
the 4 Cs giveaway
remember subacute sclerosing Panencephalitis later in life ( brain problems)
Maccular
otitis media = MC complication
Rubella
Genralised Tender Lymphadenopathy is the giveway.
Maccular
Roseola
High spiking fever THEN rash
paracetamol for high temperature
febrile seizures more likely as higher temperature v quickly
Varicella
Rash w/o fever?
Adults - never croses midline
can be painfull before and after (gabapentin/ pregabalin)
Can give varicella vaccine in old too
acyclavir to reduce length in elderly
exclude from school until all lesions dry and crusted over
Mumps pretty obvious
Hand foot and mouth disease
Like Varicella but on the hands, feet and face
no need to stay away from school if feels well
Joint Pain Approach
REMEMBER THESE ARE GENERAL RULES
First differentiate by numbers then acuity/ toxicity
High acuity/toxicity you admit - low one harder to spot
Ser -ve = PAIR
Poly = VIRUSSSSS
SLEs like big joints. RA likes small joints
AP = lower back OA = weight bearing joints (shoulder/hip) or joints with previous trauma/surgery Acute = red hot swollen tender and immobile
Reactive = ive got gonorhoea and my joint hurts.
Infective = I have gonourhea in my joint
The (A)s are for acute toxicity
Abs most important to learn from top to bottom
Asthma
Not all wheezing asthma but should always consider
Ominous = lots of air trapping and not much room for air movement
PFTS = spirometry
ach agonist = Methacholine
Negavite Spirometry does not exclude asthma: ix further with fractional exhaled nitric oxide (FeNO) testing
Tx
Bronchoconstricion with bronchodilators
Inflammation with anti-inflammatories
Stabalisers can be used for athletic asthma as you can take pre-emptivly (cromolyn/ nedocromil)
short course of prednisolone for acute episodes (eg 5day hx of wheeze and cough and already on medicaiton)
Adult Tx
2- jump in here if Newly-diagnosed asthma with symptoms >= 3 / week or night-time waking
Salmeterol = LABA aka a ‘controller’
Child 5-16 tx
The same as adult but stop LRTA at 4
Jump to 2 if Newly-diagnosed asthma with symptoms >= 3 / week or night-time waking
8 week trial:
After 8-weeks stop the ICS and monitor the child’s symptoms:
if symptoms did not resolve during the trial period, review whether an alternative diagnosis is likely
if symptoms resolved then reoccurred within 4 weeks of stopping ICS treatment, restart the ICS at a paediatric low dose as first-line maintenance therapy
if symptoms resolved but reoccurred beyond 4 weeks after stopping ICS treatment, repeat the 8‑week trial of a paediatric moderate dose of ICS
Exacerbation
Life threatening:
SpO2 <92%
PEF <33% best or predicted
Silent chest
Poor respiratory effort
Agitation
Altered consciousness
Cyanosis
Nebs = Ipratropium (muscarinic antagonist)/ salbutamol
PEFR = peak espiratory flow rate ( they should know their best)
All patients to receive PO prednisolone
Oxygen through non rebreath
MDI = metered dose inhalors
Rescue medication :
Racemic adrenaline neb, subq adrenaline, IV magnesium all used to try and prevent intubation
Grades
1 - intermitent
2/3/4 = intermittent
- mild
- moderate
- severe
Refractory = tx not working
Adult Corticosteroid Doses
<= 400 micrograms budesonide or equivalent = low dose
400 micrograms - 800 micrograms budesonide or equivalent = moderate dose
> 800 micrograms budesonide or equivalent= high dose.
Paeds Corticosteroid Doses
<= 200 micrograms budesonide or equivalent = paediatric low dose
200 micrograms - 400 micrograms budesonide or equivalent = paediatric moderate dose
> 400 micrograms budesonide or equivalent= paediatric high dose.
Maintenance and reliever therapy (MART)
a form of combined ICS and LABA treatment in which a single inhaler, containing both ICS and a fast-acting LABA, is used for both daily maintenance therapy and the relief of symptoms as required
MART is only available for ICS and LABA combinations in which the LABA has a fast-acting component (for example, formoterol)
Criteria for discharge
been stable on their discharge medication (i.e. no nebulisers or oxygen) for 12–24 hours
inhaler technique checked and recorded
PEF >75% of best or predicted
Oesophagitis
Oesophagitis in general
As you often have to do a biopsy and take a PIECE
E for GORD and everything else
MC presents with odynophagia but sometimes just dysphagia
Give some sort of antacid for all as if its not the cause it can make it worse
Pill induced
Gets stuck and inflames surface
Non-entric coated NSAIDs notorious for it
Pill often not still there but remove if it is
Should recover with PPI
PPX but taking pills with a whole glass of water adn not when lying down
Infectious
Pretty much anything can cause but remember these four
Candida - oral candidasis with oesophagitis symptoms (tx with fluconazol
HSV = herpes = painful prodrome, vesicles on erythematous base and ulcers at multiple stages of healing cal or acyclavir
CMV - wont see anything
HIV - opportunitstic infections and to remind you infectious oesophagitis often in immunosuppressed
Eosinophilic
allergic reaction in oesophagus
EGD with >15eos per high powered field then you trial PPI as GORD often causes . . .. if they were origionally tx for GORD before biopsy then they now get oral aerosolised steroids
Caustic
Kid eg drinking drain cleaner
Aduld = suicide attempt
Touches all on way down inc larynx
OGD to determine severity
Low = trial liquid diet and monitor
High severity = strictures with necrotic black looking oesophagus
Never neutralise pH as it can cause a exothermic reaction and burn again . .. .. or expose again on induced emesis
NGT and flush and suck multiple tiems
Incontinence
Initial IX in general
bladder diaries should be completed for a minimum of 3 days
vaginal examination to exclude pelvic organ prolapse and ability to initiate voluntary contraction of pelvic floor muscles (‘Kegel’ exercises)
urine dipstick and culture
urodynamic studies
Stress
have to have given birth
cardinal ligament hlds uterus/bladder/vagina in place
Leads to cystocel and IAP thne only increases bladder pressure and not sphincter
anything that IAP (coughing, laughing, running)
no nocturnal as no IAP
Q-tip test = apply q tip to urethra and IAP .. . . if it rotates >30 degress then you have urethral mobility
Strengthen pelvic floor with kegal exerises then use pessaries if fails
surgery MC calposuspension (NICE = retropubic mid-urethral tape procedures)
Duloxetine 2nd life if decline surgical procedures
ALL the following applicable to men and women
Hyertonic
random spasms of detrussor (not predictable)
nocturnal (as random)
U/A to ro infection
Cystometry = empty and then allow to fill . . . random detrusor activity throughout
Too much antispasmotics can lead to hypotonic
Bladder training by graduall increasing intervals
oxybutynin (avoid in old frail women), tolterodine or darifenacin
mirabegron (a beta-3 agonist) if concern anticholinergic burden
Hypotonic (neurogenic bladder)]
leak before you explode (bladder pressure intermittently exceeds sphincter pressure)
nocturnal (if bladder full)
Physical might also find underlying FND (eg multiple in MS)
Bethanacol induces spasms but in chronic irreversibele conditions consider intermittent/indwelling catheters
Cystometry shows no activity
Irritated
FUD = frequency/urgency/dysuria
not neccessarily incontinence
might wake up with bladder symptoms but not incontinence
U/A gives the answer (use in other to r/o)
WBC = infection and RBC = stones, Ca
UTI abx (amoxicillin, nitrofurentoin, trimethrorim sulphate)
Fistula
Epithelial line tract between bladder and anything
from inflammation/radiation (so look for hx of Surgery, Ca, IBD-crohns)
Physical . ..look for fistula
Tampton test = put tampon where you think it is and inject dye up urethra
Vagina = vaginal leak
skin = they might have ad to catch it
rectum = air/stool in urin (or urin in rectum)
tx with fistulotomy
Vaginal Bleeding Overview
Differentiate by age
Most common causes
foreign body mc inserted by herself
vaginal atrophy esp after sex
What you most worry about
sexual abuse if trauma or STI
Pregnancy = PAD
DUB (dysfunctional uterine bleeding) = AUB (abdnormal uterine bleeding)
also be aware of
= precocious puberty/HRT
what to do
speculum can be traumatising in young so under GA
UPT = urinary pregnancy test
post menopausal = Ca until proved otherwise
Bleeding a lot
ABC including two peripheral cannulae, 14 gauge
IV syntocinon (oxytocin) 10 units or IV ergometrine 500 micrograms
IM carboprost
- for access
- support BP until blood
- crossmatch and transfuse as needed
- IV oestrogen to stop bleeding
- if above fail some sort of surgical intervention
Assess
Hb key but assess after IVF as before normal
<7 = absolute transfusion indicaiton
orthostatics to assess haemodynamic stablity
surgical intervention
Intracavitary Tamponade = absolute tamponade
Dilattion and cuterage = get at source to stop bleeding and preserve fertility
Uteine arter embolisation reserved for AVM and fibroids (by intervential radiology)
TAH = definitive tx for unrelenting haemorhage ( does not preserve fertility)
Headache
Secondary
want to first consider secondary and ask RED FLAGS
SAH = worst HA
Tumour = FND with progressive N/V
Abscess = fever/HA/FND
Meningitis = Fever and HA
will proabbly follow up with one or more of those IX
Primary HA
Tension
Common one that people usualy tx themselves
Bilateral vice like pain that starts in the front and radiates backt to the neck
might be exacerbated by loud noise and exercise but no photo/phonophobia
If they have > 2 days a week consider prophylaxis (10 sessions of accupuncture or amitriptyline 25mg-150mg ON). trail of prphylaxis after 4-6 months.
Analgesic Rebound or medication overuse
most at risk are those using triptans barbituates and opiates >10/month to tx HA
can also be caused by withdrawl from NSAIDS/Paracetamol and even caffeine
tx = push through withdrawl
consider if HA 15 days a month for three months
advised to stop abruptly, not gradually and push through at least a month (but can also do naproxen 250mg TDS for 4 weeks first?!)- give antiemetics
Cluster HA
Asx for months and then a cluster of HAs
increased duration means decreased frequence and vice versa
same each time
unilateral eye pain associated with horner’s syndrome:
rhinorhea, lacrimation, conjunctival injection and lid sags
2nd line triptans
MRI to r/o 2are HA
give parenteral triptan (IN zomitriptam 5-10mg or SC sumatriptan 6mg to terminate or 100% oxygen no rebreath 12l/min for 10-20 mins to terminate in ED) no paracetamol, nsaids, opioids, ergots or oral triptans
Migraine
do dual treatment of NSAID and triptan straight away
nsal triptan in 12-17yo
give antiemetic if naeusea eg prcholorperazine3-6mg bucacal tablets or domperidone 10mg po
prophylaxs with topiramate or propanaol
vascular . . .generally vasodilation
Aura can be any FND
Trigger : eg MSG, menstrule cycle, chocolate, caffeine
Sleep usually aborts but ‘hangover’ following day
NSAIDs best if you get in early
Triptans (can cause vasospasm in CAD)
Idiopathic Intracranial Hten
increased ICP w/o cause
ICP sx esp papiilloedema
associated OCPs
CT scan will be -ve
LP has high opening pressure and releives sx
tx = acetazolamide
refractory tx = serial LPs
last resort = VP shunt
Migraine triggers include the mnemonic CHOCOLATE: chocolate, hangovers, orgasms, cheese/caffeine, oral contraceptives, lie-ins, alcohol, travel, exercise
Menstrual Migraine
ID relationhip with period for at least two cycles. give triptans or nsaids a couple of days before and after expected HA
Trigeminal Neuralgia
ear to chin shooting pain on eating or cold liquids
tx with carbamazapine
Temporal arteritis
Typically patient > 60 years old
Usually rapid onset (e.g. < 1 month) of unilateral headache
Jaw claudication (65%)
Tender, palpable temporal artery
Raised ESR
Asoociated with polymyalgia
Low Pressure Headache
post lumbar puncture
worse on standing up
tx with caffeine and fluids
Vertigo
r/o syncope and disequilibrium (syncope can pose immediate risk)
Vestibular system begins in semi circular canal of ears and connected to brainstem by CN8
Central
NS = neighbourhoods sx, esp FND
FND usually cerebellar
MC MS, CVA and tumour
IX: MRI head looking at posterior Fossa
Peripheral
Benign paroxysmal positional vertigo
lasts <1min, eg every time i lie on my left side
Dx: Hallpike manouvre looking for rotary nystagmas
Tx: Epley Manouvre
Labrynthitis and vestibular neuritis
the same but labrynthitis has hearing loss
vertigo lasts 1-10 mins
horizontal nystagmus
can confuse for central but will be negative scan
can tx with steroids if get straght awau but mosly wait it out with antivertigo meds
URI = URTI
tx: prochlorperazine for sx mx but only for 3 days (vertigo and nausea sx)
Vestibular neuronitis urgernt referal to balance specialist for rehabilitation in the first week
Menier’s
Triad of . . .
last for life so prescribe anti vertigo meds
Stop driving until sx under control
sx tx with prochlorperazine
ppx with betahistine
Anxiety Disorders
Anxiety
Feeling + Physical
Individual experience
Bad experience so risk of mood disorders and to self medicate
Generalised Anxiery Disorder
At least 6 months
somatic sx ie impairs normal fxn
chronic problem so psychotherapy best
Panic Disorder
Presents like physical problem so r/o others
Benzos to abort attack
SSRIs can be used to decrease frequency
CBT can be used to get out of panic attack
agoraphobia = fear of leaving home alone
Phobias
Irrational or/and irrational fear
Flooding = medicate then rapid exposure to stimulus
Desensitisation = gradual exposure (floor by floor analagy
Social Phobia
non selective BB eg propanalol
ABG interpretation
Normal Ranges
pH: 7.35 – 7.45
PaCO2: 4.7 – 6.0 kPa || 35.2 – 45 mmHg
PaO2: 11 – 13 kPa || 82.5 – 97.5 mmHg
HCO3–: 22 – 26 mEq/L
Base excess (BE): -2 to +2 mmol/L
Hypoxic?
<10 kPa on air = hypoxaemic
<8 kPa on air = severely hypoxaemic
Type 1 or 2?
Type 1 respiratory failure involves hypoxaemia (PaO2 <8 kPa) with normocapnia (PaCO2 <6.0 kPa).
V/Q (ventilation/perfusion) mismatch>hypoxia + hypercapnaei > increased RR then blows off CO2
causes: alveolar hypoventilation (pneumonia, ARDS, pulmonary oedema), distribution/diffusion) (pulmonary fibrosis), perfusion (pulmonary embolism)
Type 2 respiratory failure involves hypoxaemia (PaO2 <8 kPa) with hypercapnia (PaCO2 >6.0 kPa).
Alveolar hypoventilation:
Central (coma, intracerebral haemorhage), Neuromuscular (muscular dystrophy), obstruction (COPD/ Asthma), restriction (pulmonary fibroisis, pneumothorax)
-airway obstruction (COPD) -reduced compliance (pneumonia/rib fracturs/ obesity - reduced respiratory muscle strength (Guilian-barre/MND) -Drugs reducing resp rate (opiates)
pH?
Acidotic: pH <7.35
Normal: pH 7.35 – 7.45
Alkalotic: pH >7.45
imbalance in the CO2 (respiratory) or HCO3– (metabolic).
PaCO2?
Does it correlate or not>
Bicarbonate?
Does this correlate?
(Base Excess)
High base excess = > +2mmol/L = high HCO3- = primary metabolic alkalosis or compensated respiratory alkalosis
Low base excess = < -2mmol/L = low HCO3- =
primary metabolic acidosis or compensated respiratory alkalosis
respiratory compensation is quicker than metabolic (days)
Compensation?
Assess compared to primary disturbance
Anion Gap?
Normal = 4-12 mmol/L
Anion gap formula: Anion gap = Na+ – (Cl- + HCO3-)
An increased anion gap indicates increased acid production or ingestion:
Diabetic ketoacidosis (↑ production)
Lactic acidosis (↑ production)
Aspirin overdose (ingestion of acid)
A decreased anion gap indicates decreased acid excretion or loss of HCO3–:
Gastrointestinal loss of HCO3– (e.g. diarrhoea, ileostomy, proximal colostomy)
Renal tubular acidosis (retaining H+)
Addison’s disease (retaining H+)
Mixed acidosis/alkalsosis
CO2 and HCO3- will be moving in oppositie directions
tx each primary acid/base disturbance
Context
A ‘normal’ PaO2 in a patient on high flow oxygen: this is abnormal as you would expect the patient to have a PaO2 well above the normal range with this level of oxygen therapy.
A ‘normal’ PaCO2 in a hypoxic asthmatic patient: a sign they are tiring and need ITU intervention.
A ‘very low’ PaO2 in a patient who looks completely well, is not short of breath and has normal O2 saturations: this is likely a venous sample.
Examination of Eyes And Vision
WIPE
Visual Acuity
6metres from snellen chart
one eye to the lowest possible line
improvement through pin-hole indicates refractive component
6 (distance read)/ 6(lowest line read) -2 (two letters wrong)
if more than two letters wrong go to previous line
U/A = unnaided, PH = pinhole
3metres >1 metres > fingers holding up
Can assess near vision with fine print reading
Decreased accuity differentials
Refractive errors
Amblyopia
Ocular media opacities such as cataract or corneal scarring
Retinal diseases such as age-related macular degeneration
Optic nerve (CN II) pathology such as optic neuritis
Lesions higher in the visual pathways
Colour Vision
Ischihara plates
wear reading glasses if they have
number of plates corrctly idied = x/13
Visual fields
Bitemporal Hemianopia (optic chiasm pressure)
Homonymous Field defects = same side of visual field in each eye
Scotoma = area of reduced vision surrounded by normal
Monocular vision loss = total loss of one eye . . . secondary to optic nerve pathology (vascular neuropathy) or occular diseae (retinal detachment or retinal artery/vein problems)
External Eye Inspection
Eyelids (lumps/oumps/ ectropions)
Eyelashes
diffuse conjunctival injection (whole conjunctive: viral, bacterial , allergic)
Cicumcilliary injection (circular around cornea suggesting intraocular inflammation
Discharge: watery (corneal abraisn/foreign body/ viral/allergic) or purulent (bacterial)
Hyphema = blood in anterior chamber eg trauma
Hypopyon (pus in anterior chamber)
Periorbital erythema and swelling (preseptal cellulitis or orbital cellulitis
foreign bodies
corneal abrasion
corneal ulcer
Inspect pupil (size, shape, symmetry)
Pupil reflexes
Direct
Consensual
accommodation
swinging light test (relative afferent pupillary defect)
- normally both constrict same amount on shining light in either eye*
- if efferent damage then when light shone in affect eye both constrict a reduced amount*
- shining light in swinging eye test gives the effect of relative dilation*
- either significant retinal damage (retinal vein/artery occlusion or large retinal detachment) or optic neuropathy (optic neuritis, unilaterlal advanced glaucoma, compression of secondary tumour or abscess and ischaemic optic neuropathy)*
Strabismus
- Light reflex test/ corneal reflex test/ hirschbeg test:*
- focus on half a metre away and shine light in both eyes . .. should reflect equally*
Cover test
If contralateral eye does not move then orthotropic (normal alignment) if it does then heterotropia . .. see diagram for specifics
Eye movments
H pattern
restricted movement or nystagmus?
Fundoscopy
darkened room, ideal with short acting mydriatic eye drops (tropicamide 1%)
ask to look straight ahead for duration of test
Red light reflex
about arms length
absent in adults :cataracts vitreous haemorrhage and retinal detachment
absent in children = congenital cataracts, retinla detachment, vitreous haemorrhage and retinoblastoma
white reflex (lekocoria) in any age can be above pathologies
Anterior segment
use green 10 or 15
hand on forehead to prevent colision
idealy with dye . .. white opacities can be coreanl ulcer
Fundus
Optic disk
45 degree angle slighlt temportal
follow vessels to optiv disc
comment on 3 Cs:
Contour (clear and well defined . . .blurrred = papilloedema secondary to raised ICP)
Colour: disc should be orange pink doughnut with pale centre . .. pale disc = aptiv atrophy (optic neuritis, advanced glaucoma and ischamic vascular events)
Cup: cup to disc ratio should be around 3 Iie cup occupies 3rd of disc) . .. . if increaseed ratio reduced neural teinal tissue (glaucoma)
Retina
clockwise/anticlockwise: superior temportal, superior nalsa, inferior nasal, inferior temportal
Look for arteriolar narrowing, arteriovenous nipping.bicking, dot and blot haemorhages, flame haemorrhages, cotton wool spots, hard exudates, neovascularisation, pan retinal photocoagulation, branch retinal vein occlusion
assess macula
fovea should be same size as optiv disk
look for haed exudates, drusen, cheery red spot
Complete
thank patient
remind can’t drive if had mdriatic drops for 3-4 hours till wear off
for completeness : slit lamp exam, cranial nerve examination, blod pressure, capilliary blood glucose, retinal photography
Obstructive Jaundice (Painless)
Prehepatic
Haematoma (reabsorption of it)
Conjugation = bilirubin rate limiting step (2,3 UDP gluconyltransferase)
Intrahepatic
Liver three main steps (entry, conjugation, excretion (genetic rotors, duben johnson etc)
Post hepatic = obstruction
Gallstones
choledocholithiasis = stone from GB stuck in biliary tree
sudden so only mild dilation of tree but inflammation of biliary tree and gallbladder (cholecystitis)
Inflammation = mild fever, leukocytosis, pain and maybe murphy’s sign
US first, MRCP best (ERCP w/o ro complication)
ERCP usually opted for as faster than cholecystectomy with retrogrrade cholangiopancreatography
Stricture/cancer
Slowly obstruction so system has time to adapt
massivly dilated and thin walled distended gallbladder
courvoisier sign = painless jaundice and enlarged gallbladder
Flow
all three things point ot obstructive jaundice
Bili levels higher (20-26 as opposed to single digits of gallstones)
Workup = CT first in test if not sure?
Pacnreatic
grows in peritenium so asx till large or mets (terrible prognosis)
Migratory thrombophlebitis = clot moves around body (eg leg) = pancreatic cancer (or maybe lung cancer?)
Endoscopic US with biopsy as outside the biliary tree
Double duct sign on CT (dilated common bile duct and dilated pancreatic duct)
Monitor with Ca 19-9
Cholangiocarcinoma
biliary tree mass
associated with primary sclerosing cholangitis which would have beeds on a string sign
ERCP as in biliary tree
Ampulla of Vater
as too small on CT but entrance to biliary tree so can cause significant obstruction
FOBT would be positive but nothing on colonoscopy as too far up
ERCP as in biliary tree
Gall Bladder
Cholelithiasis
means gallstones in gallbladder
stones in two forms: cholesterol = green and haemolysis = black
does’t really matter as present the same
Fat makes GB squeeze out bile but squeezes stones
US great as solid against liquid
Ursodoxycholic acid if not surgical candidate
Cholecystitis
inflammation
US to look for 1,2,3
Murphy’s sign (hand on ribs and thumb on GB . . . big breath in and out and then put thumb in. . . will stop breathing out in positive)
HIDA san if US not all 1,2,3 (gallbladder won’t fill with ijected isotope)
tx with urgent (<72hrs) cholecystectomy as could perforate
Cholecystotomy in non surgical candidate
Boas sign refers to this hyperaesthesia (increased sensitivity). It occurs because the abdominal wall innervation of this region is from the spinal roots that lie at this level. (beneath right scapula)
Choledocolithiasis
Gallstones in CBD presents with painful jaundice (consider everyting else a maybe)
might have gallstone pancreatitis or hepatitis too
US looks for dilated CBD
Want ERCP (but ok to NP,E VF, IVabx as don’t know if infective and can progress to cholangitis)
tx with urgent ERCP and can do cholecystectomy at a later date (can do straight away but ERCP quicker)
Ball-valve . . . .painful and deranged LFTs correct then come back as its acting as a valve
Cholangitis
Dilated ducts with stagnant fluid is ready for infection . . .. SAS
GNR = gram -ve rods
Don’t bother with MRCP and ERCP as this is emergency tx (ERCP diagnostic)
can give IVF, IV abx and NPO when prepping for surgery
Cholecystectiomy still urgent after
ABX p cipro (GNR) and metronidazole (anaerobe) - pip tazo wastes the +ve coverage
Extra
Pigmented Stones associated with Sickel Cell Anaemia
Diabetes
Who
CVD RFs : old fat and hypertensive
Thrush: sore itchy foreskin in men
polyuria, polydipsia, blurred vision
How
The randam blood glucose is useful for the T1DM who comes in with all the sx
The tests are better as they go down.
HbA1C measures glycosylated end products so is therefore an average over 90 days
But cannot r/o diabetes as haemaglobinopathies affect levels
IFG/IGT
Impaired fasting glucose = FPG >6.1 but <7.0 mmol/L and should be offered OGTT to r/o DM
Impaired glucose tolerace = Pre-diabetes
T1 DM
AI desruction of pancrease
old person with normal BMs last year presenting with polydisia, polyuria and very high BMs is same as young
anti-GAD (anti-glutamic acid decarboxylase) and IA-2 are antibodies (to differentiate from T2DM in older patients)
Tx with insulin
Monitor at least 4 times a day, including before each meal and before bed
Pre-Diabetes
Mx
lifestyle modification = weight loss, increase exercise, change diet
At least yearly F/U blood tests
Metformin for their FPG or HbA1c is progressing towards T2DM
T2DM
Mx
Check HbA1c q3-6 months then every 6 months when stable
- Lifestyle: target = 48 mmol/mol
- Add metformin: target = 48mmol/mol
- If >58 add another drug: target = 53 mmol/mol
- If still >58 add another or consider Insulin
Keep metformin when starting insulin and consider the others
If metformin not initially tolerated then:
First try modified release meformin
- Lifestyle: target = 48 mmol/mol
- Add another drug: target = 48mmol/mol
- If >58 add another drug: target = 53 mmol/mol
- If still >58 consider Insulin
Drugs
Metformin: the diarhoea will go away
Sulfonylureas (pick as cheap and been around ages): watch out for the hypoglycaemia esp in CKD pts- increases insulin expression
TZD = thiazolidinedione = pioglitazone : can cause CHF
GLP1 mimetic (exenatide) criteria = BMI>35 and unable to lose weight or <35 but insulin would have significant occupational implicatons . . . only continue if a 1% HbA1c reduction or weight loss of 3% in 6 months
SGLT-2i can cause DKA so avoid
Alpha Glucosidase inhibitors mean that glucose not absorbed so dirahoea and smeel flatulance
RF modification
Htn: 1st line ACEi
<80 target 140/90 clinic (135/85)
>80 target 150/90 (145/85)
Antiolatelets offered
Lipids = QRISK2 score = atorvastatin 20mg ON
Retinopathy - sudden vision loss = vitrious haemorhage
Nephropathy
All diabetic patients require annual screening for albumin:creatinine ratio (ACR) in early morning specimens
ACR > 2.5 = microalbuminuria
Mx: Start ACEi
diet restrict protein
gd control of BP, BM, Lipids
Neuropathy
1st line: amitriptyline, duloxetine, gabapentin or pregabalin
2nd- try another one of the drugs
- tramadol can be used as rescue therapy
4 - refer to pain mx clinic]
Charcot Foot
Mild pain considering of joint dysruption
swollen, red and warm
DM sick day rules
increase frequency of BG monitoring
drink at least 3 litres/24hrs
have sugary drinks if struggling to eat
keep phone on you
MODY
maturity onset diabetes of the young (MODY) - type Hepatic Nuclear Factor 1 Alpha (HNF1A). HNF1A accounts for 70% of MODY cases. Sulfonylureas (e.g. gliclazide) are the optimal treatment in HNF1A-MODY.
Small bowel bacterial overgrowth syndrome (SBBOS)
DM at ro this
excessive gut bateria
sx: chronic diarhoea, bloating, flatulance, abdo pain
dx: hyrodogen breath test
tx: rifaximin and DM control
Dietary advice
encourage high fibre, low glycaemic index sources of carbohydrates
include low-fat dairy products and oily fish
control the intake of foods containing saturated fats and trans fatty acids
limited substitution of sucrose-containing foods for other carbohydrates is allowable, but care should be taken to avoid excess energy intake
discourage use of foods marketed specifically at people with diabetes
initial target weight loss in an overweight person is 5-10%
Peptic Ulcer Disease
Gastric usully H pylori
Duodenal always H pylori
H. pylori usually single ulcer (malignancy can start like this though)
Malignancy - necrotic as outgrowing blood supply (can present with gastric outlet obstruction)
Curling irons burn and cushions are squishy
Presentation
20% asx so present with the complications:
GI bleed, perforation, G/O obstruction
Sx worsened by eating in gastric and improve with duodenal (this is unreliable in life though)
Almost always OGD
TX for everyone
stop smoking and drinking (not direct RF but inhibit healing)
PPI almost everyone
Flow
if its NSAIDs presentation don’t need to bx but probs will
(tx with high dose PPI then lower dose ppx if you restart NSAID)
if bx shows normal then PPI tx
H-pylori
often present with complications as Asx
OGD best: rapid urease, histology (expensive and time consuming), histology (best . ..actually see it)
Stool ag: check it eradicated
serology - will be positive if had once (Tx if +ve + sx + not previously dx)
Urea breath test need to be off PPI so not that much in practice (good for initial dx though)
Tripple therapy; use metro if pennicillin allergy
ZE
gastrin stimulates parietal cells to produce acid . .. acid inhibits gastrin production
Gastrinoma produces gastrin regardless
OGD will see lots . .. high dose PPI doesn’t work. . . .. repeat OGD and still loads . . . suspect gastrinoma
Gastrin in triple digits diagnostic
if in between secretin stim test will lead to increased gastrin
Locate with CT but best is somatostatin receptor scintography
resect for ulcers but also it can induce gastric carcinoma
Syncope Approach
Tx:
W- BB
O- IVF or stockings if ANS - (Volume down from th e4 Ds (dehydration, diarhoea, diuresis or haemorage) - LOOK AT MEDS)
M- Surgery
LOC?
- How long did it take them to come round?
- 2010 rule for shakes-
- the rest ask for sake of OSCE but pretty useless
WOMAN 3-2-1 PE (321 for first three sub categories)
W- acetylcholline released by cagus leads to bradycardia and vasodilation
Orhostatics - Volume down from th e4 Ds (dehydration, diarhoea, diuresis or haemorage) - LOOK AT MEDS
- sitting/standing BP 5 minutes lying down, then in 1st minute standing, then after 3 minutes standing
ANS - old, PD, DM . . . if IVF does not help its this . . . stockings
MA - admit as heart ones . . . . M usually valvular and old eg aortic stenosis (old man shovling ice) could be Hypertrophic obstruct cardiomyopathy in young.
N - very rare- . . . only consider if focal deficit
P = psych . . . faking it . . . arm drop test
E= electrolytes Na and ca for altered mental staus and K and mg for weakness
If you suspect cardiac, admit and do echo and ecg (inc 24hr)
PE - different as if they fall to the floor it won’t help them
Valvular Disease
Only work up if diastolic or systolic 3+
MS
aortic dilation thereofre af
Only one you can do ballo valvuloplasty as not calcified. Want ot avoid valve replacement until older
AI (aka aortic regurgitation)
May have chest pain as less blood coronary artery ostia
Acute and chronic both need replacement
Floppy valve leads to floppy heart
AS
atherosclerosis leads ot calcium deposition
also leads to ventricuolar dilation
Mostly old men but bicuspic valve in younger
tx as soon as symptomatic (syncope)
Nitrates contraindicated due to theoretical hypotension
narrow pulse pressure
MI
aortic dilation therefore af
holosystolic so may not hear s1 or s2
- all above improve worsen with increase venous return (squatting/leg lift increase and valsalvar decreases)*
- Following are opposite*
- Pansystolic murmur can also be caused by ventricular septal defect following an MI*
HCM
less blood and ventricle smaller so ventricle outlet closes (can kill)
you won’t see the sudden deaths
Like Aortic stenosis but more blood makes better
beta blockers increase preload
MVP (mitral valve prolapse)
Like MS but better with more blood
valve too big so ends don’t touch . . .more blood means they can
Endocarditis
The most common valvular abnormality in infective endocarditis is tricuspid regurgitation. Combined with the fact that this man is showing sings of right sided heart failure (peripheral oedema)
Holosystolic murmur louder during inspiratio
Replacement for all 1st four but can medically manage by afterload reduction and diuresis
Patterns of the 4
Left diastolic/ right systolic
up is heart apex+aortic dilation/ down is base +VD
Insufficiency = more acute/ stenotic = more insidius
Extra
Venous hum is a benign murmur heard in children and sounds like a continuous blowing noise heard below the clavicles
A pansystolic murmur is associated with mitral regurgitation.
An ejection systolic murmur is associated with aortic stenosis.
A continuous ‘machinery’ murmur is associated with a patent ductus arteriosus.
A late diastolic murmur is associated with mitral stenosis.
ECG take 2
What it represents
P wave = depolorisation of atrial muscle
PR interval = time for electricle impulse to spread from atria to ventricles (3-5 small squares)
QRS = depolorisation of the ventricles (<3 squares)
ST segment = period when ventricles are completely activated
T wave = repolorisation of ventricular muscle
U wave = repolorisation of pappilary muscles (abnormal if after flattened T wave)
Context
note BP/HR consciouness when taking ECG
RRPWQST
RATE: 300, 150, 100, 75, 60, 50 (small = 4ms and large = 200ms
RHYTHM: regular = equal distance between QRS complexes
P WAVES: P wave before every QRS = sinus (impulse from SAN to ventricles) - no P = abnormal rhythm. >1 P = heart block (abnormal coduction to the ventricles)
WIDTH: QRS >3 squares = slow ventricle conduction (abnormal conduction or eronously starting in ventricular tissue)
Q WAVE: if QRS starts with deep downward deflection could be old MI
ST segment: should be level with baseline. elevated = MI and depressed = MC Ischaemia
T wave: normally upside down in VR and V1 .. in other leads could be ischamie or ventricular hyertrohy
QT interval: varies with heart rate, prolonged with some drugs (>12 small squares)
Calibration: 1 square wide and two high . . .. . should be included on every record (25mm/s)
AXIS
serves to alert of other pathology eg PE/ conudction abnormality
Normal = +ve I and II
Left leaving = positive in I and Negative in II
Right reaching = -ve in 1 and +ve in 2
90 degrees from isoelectric lead, see if +ve at +90 or -90
RAD ax Right ventricluar hypertrophy (2ary pulmoary conditions causeing right heart strain)
LAD ax wtih conduction abnormalities
V leads
V1,V2 look at right ventricle
V3/V4 look at septum
V5/V6 look at left ventricle
V leads QRS - first septal depolorisation from left to right (intial R wave in V1/V2 but q wave in V5/V6) then ventricular depolorisation
RS trasition point represents the position of interventricular septum (normal V3/V4), right ventricle hypertrophy pushes to V4/V5/V6
Reporting ECG
Always:
- rhythm
- conduction intervals
- cardiac axis
- description of QRS complexes
- description of ST segments and T waves
eg:
- Simus rhythm, rate 50bpm
- normal PR interval (100ms)
- Normal QRS complex duration (120ms)
- Normal Cardiac Axis
- Normal QRS complexes
- Normal T waves (inverted in VR is normal)
Setup
attache electrodes to correct limbs
ensure ggod elecrical contact
check the calibrationand speed settings
make patient comfortable and relaxed
ECG red flags
Paeds Hx
Systems Review
Head – History of injury, headaches or infection?
Eyes – Visual acuity/glasses? History of injury, headaches or surgery?
Nervous system – Fits, faints, or funny turns? History of hearing concerns, seizures (febrile or afebrile), abnormal or impaired movements, tremors or change in behaviour? School performance? History of hyperactivity?
ENT – Earache, throat infections, snoring or noisy breathing (stridor)?
Chest – Cough, wheeze, breathing problems? Smokers in the family? Exposure to smoke?
Heart – Cyanosis, exercise tolerance, chest pain, fainting episodes? History of heart murmurs or rheumatic fever in the child or the family?
GIT – Vomiting, diarrhoea/constipation, abdominal pain? Rectal bleeding?
Genitourinary – Dysuria, frequency, wetting/accidents, toilet training?
Joints/Limbs – Gait, limb pain or swelling, other functional abnormalities?
Skin – General rashes? Birthmarks or unusual marks?
Pubertal development – Age of menarche?
HEEADSSS
Home and relationships
Who lives at home with you?
Do you have your own room?
Who do you get on with best and/or fight with most?
Who do you turn to when you’re feeling down?
Education and employment
Are you in school/college at the moment?
Which year are you in?
What do you like the best/least at school/college?
How are you doing at school?
What do you want to do when you finish?
Do you have friends at school?
How do you get along with others at school?
Do you work? How much?
Eating
Are you worried about your weight or body shape?
Have you noticed any change in your weight recently?
Have you been on a diet? Do you mind telling me, how?
Activities and hobbies
How do you spend your spare time?
What do you do to relax?
What kind of physical activities do you do?
Drugs, alcohol and tobacco
At this stage – reassure about confidentiality
Does anyone smoke at home?
Lots of people your age smoke. Have you been offered cigarettes? How many do you smoke each day?
Many people start drinking alcohol around your age. Have you tried or been offered alcohol? How much/how often?
Some young people use cannabis. Have you tried it? How much/how often?
What about other drugs, such as ecstasy and cocaine?
Sex and relationships
Are you seeing anyone at the moment?
Are they a boy or a girl?
Young people are often starting to develop intimate relationships? How have you handled that part of your relationship?
Have you ever had sex?
What contraception do you use?
Self-harm, depression and self-image
How is life going in general?
Are you worried about your weight?
What do you do when you feel stressed?
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Cardiovascular Examination
WIPE
Postion/Exposure
General Inspection
General Examination
Chext examination:
Inspection
Palpation
Auscultation
Special Manouvres
Additional Examination
Bedside Investigations
Proffesionalism
Presentation
Name and Age
5 things of general inspection/ exam:
warm peripheries, pulse rate was xxx, regular rhythm and normal volume, CRT <2s, non cyanotic and no appreviable JVP
On Inspection of the chest there were not notable scars
On Palpation . . . .
On auscultation . . ..
There was no eveidence of peripheral oedema
My THREE top differentials are:
For further Ix I would like . ..
WIPE
Correct position and adequate exposure
General Inspection
General Examination (vital signs)
Hands and anils
radial pulse
BP
Eyes
Face/mouth
Neck
Carotid pulse
Inspection
Palapation
Apex Beat
Heaves and thrills
Auscultation
Mitral
Aortic
Tricuspid
Pulmonary
Special Manouvres
Mitral stenosis
Aortic Regurgitation
Mitral regurgitation
Aortic stenosis
Additional Examination
Lung bases
periperal pulses
Peripheral odema
Abdominal Examination
Bedside Investication
Professionalism
Look, point and touch everything you exam eg scars/marks
Ankle oedema
Hold for 10s, look at face to see if painful, then check how pitted
Anaemia
Remove glasses and pulldown eyelids yourself.
get patint to look dows and check for icterus
JVP
‘No appreciatable JVP’
Extra
Collapsing pulse is a feature of aortic regurgitation, PDA, and hyperdynamic states (anaemia, thyrotoxicosis, fever, exercise/pregnancy)
A pansystolic murmur is associated with mitral regurgitation.
An ejection systolic murmur is associated with aortic stenosis.
A continuous ‘machinery’ murmur is associated with a patent ductus arteriosus.
A late diastolic murmur is associated with mitral stenosis.
CXR approach
Projection
PA = best (check scaulae are lateral
AP = crAP (for haemodynamically unstable)
Patient details
Name, gender, DOB, date of xray (check previous xrays)
technical Adequacy
Nothing imortant cut off/ RIP
Obvious Abnormalities
Where, size, texture, density
Systemic r/v of xray
Zoom out first then close up for subtle abnormalities
ABCDD
Airway
Trachea Central? check not rotation
deviates towards lobar/lung collapse
Deviates away from pleural effusion/mediastinal mass
Breathing/Borders
Apices down to costrophrenic angles comparing both sides
left hilum should never be lower than right (look for volum pulling right u or or pulling left down)
Hila should be same density with no lumbs or convex margins
look at edge of lung for pneumotharaces (if you dont look for it you wont see it
Cardiac and Mediastinum
Heart size - cardiomegally = heart >50% maximal internal thoracic diametre (on technically adequate PA . . . but if not enlarge on AP then won’t on PA)
Mediastinal borders should be clearly visible (look for lung pathology if not)
heart/mediastinum should be positioned over thoracix vertebra . . . . assess volume change in lungs if not
Mediastinal weidnicg (technical factors, masses or haemorhage)
Heart should have uniform density (consider retrocardiac pathology if not)
linear lucencies in suerior mediastinum = pneumomediastinum
Diaphragm
Both hemidiaphragms should be seen
Upwardly convex (flattened in COPD)
Righ should be slightly higher due to liver
lungs can distend beyone diaphragm so look behind
look for free air under diaphragm (stomach bubble would have thicker membrane and on the left)
costrophrenic angles should be sharp (fluid if not)
Delicates
Ax for fracturs
intercostal spaces should be equal
soft tissues - gas = surgical emphysaema
Lines
Endotracheal tube must have tip b4 carina ( if goes down a bronchi the other can collapse)
Tip of NG tube well below diaphragm
Central lines in midlower SVC
review areas
Apices, Hila, Behind the heart, Costrophrenic Angles, Under diaphragm
summary
Maind finding with differentialss
state will r/v any previous
suggest further investigations
suggest mx plan
Presenting
This is a PA chest radiograph
which has been anomynised - i would like to confirm date and patient details
No important areas have been excluded, there is no rotation, there is adequate inspiration and penetrance therefore the chest radiograph is technically adequate
What strikes me about the xray is . . . .
on review airway is central, lung fields are clear, there a clear cardiac borders w/o evidence of cardiomegally, diaphragms are bilaterally convex with no free air below, there are no discernable abnormalities of bony or soft tissue.
HEART FAILURE
A - alveolar oedema (bat wing opacities)
B - Kerley B lines.
C - cardiomegaly.
D - dilated upper lobe vessels.
E - pleural effusion.
ALS
PULSE
In practice not may options - its about team managment
Sinus bradycardia is kind of an arythmia
Stable is not emergency management
Unstable = they will die unlesss you do something
CP = chest pain
AMS = altered mental status (same time as arythmia
Shock = synchronised cardioversion (not during T wave)
F+W = likely VTAC - amiodarone
F+N = likely SVT - adenosine
Slow get atropine to prepare pace
Only pattern you need to know is Afib/flutter
-but even if you missed this you still go to BB/CCB after adenosine
NO PULSE (if in doubt always CPR)
Shockable (120-150j then same or higher in subsequent)
CPR = 30:2 (2mins)
Ventilation = supraglottic airway continuous 10/min if excessive leak then do breaths very 30 compressions
Rhythm check should be <5s (only check at appropriate time unles signs of ROSC (ie not if normal rhythm on defib)
- 1mg IV adrenaline (1mg/10mls, 1:10,000) after 3rd shock (then alternate) - flush with 20ml for 10-20s after every drug)
- 300mg amiodarone after 3rd shock (consider 150mg after 5th)
Non shockable
- adrenaline IV asap and then every 3-5m (2 CPR cycles)
ALL THIS ONLY WORKS IF YOU TREAT THE CAUSE
4 Hs and 4Ts
- Hypoxia (ensure ventilation with 100% o2, equal expansion, correct tracheal placement)*
- Hypovolaemia (most common severe haemorhagh . . obvious (trauma) or occult (GI, ruptured AAA)*
- Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders (blood tests)*
- Hypothermia/ Hyperthermia (suspec in drowning and low thermometre reading)*
- Thrombosis (coronary or pulmonary)*
- Tension pneumothorax*
- Tamponade – cardiac*
- Toxins*
Airway Managment
choking without efffective cough = 5 back blows and 5 abdominal thrusts back to back
simple airway manouvres = head tilt + chin lif or jaw thrust
guedel = from incisors to angle of mandible. too big>too small. if suspect cervical spine injury then maintain immobilisation of head and neck
oxygen: max possible ie non-rebreath
suction: caution in gag reflex. fine bor flexible suction tubes if limited mouth opening
EXTRAS
Precordal thump: if no interuption and no defib immediately available (VT/VF)
If you see person go into VT/VF in before any ALS intiiated call for help and deliver 3 shocks back to back (check for ROSC each time)
?true asystole: check for p waves . . . . if present pacing may be effective
Waveform capnography helps with: esure tarcheal tube placement, monitoring ventilation rate, monitoring quality of chest compressions, identifying ROSC and ? prognostication during CPR
Intraosseous access: requires training, prox tibial, prox humerus and distal tibia, contraindicated if trauma, infection or prosthesus at site, withdraw blood to confirm position and flush to conifrm patency.
inspiratory wheeze = laryngeal level or above
snoring = phaynx parially occluded by tongue or palate
blood oxygen (on blood gas) shoud be about 10 less that fio2
Acid- Base Interpreation
-aemia not -osi as you can have lots of osi but eventually something wins
Look at PH to see what it is
Look at CO2 to determine type
Hypoventilation
Look for air trapping disease
osa = obstructive slee anoea
muscle strenght eg intubated too long
Hyperventilation
look for high RR (could be tidal volume related though)
Metabolic Alkalosis
Do a urine chloride to determine if volume resonsive or not (Volume down means activated RAS and increased aldo which means retention of Na AND Cl- ) . . . tx with colume
Emesis especialy bad as volume down and acid lost
Not low see if hypertensive or not
hyperaldo = Conn’s or RAS/MDS
Metabolic acidosis
Calculate anion gap (Na - Cl - Bicarb)
Non Gap do a Urine anion gap (Na + k - Cl) - >20 think RTA, normal/-ve think diarhoea/vom
positive is renal tubular acidosis and -ve = diarhoea (yes volume down but loses bicarb)
MUDPILERS (rhabdomyolysis)
CAD
Angina is Demand ischaemia - reducing load will help
ANGINA
Tx: GTN spray, BB or CCB (titrate up till max tolerated) > BB + CCB
Diagnosis
Work from STEMI back
Troponins only for initial presentation as they do not go back down
Stable chest pain : Contrast-enhanced CT coronary angiogram is the first line investigation for stable chest pain of suspected coronary artery disease aetiology
Types of MI
Type 1 = acute palaque rupture (ischaemia/infarction)
Type 2 = supply and demand (whole body problem - sepsis/hypoxia)
Cath lab
>3 or big and proximal = surgery (stents for everything else)
stop metformin 24hr (contrast media decreased renal clearance and along with metformin can cause lactic acidosis)
General ACS
Aspirin 300mg
Nitrates (sublinguinal glyceryl trinitrate - avoid if hypotensive though) and morphine to relieve pain
Anti-emetic eg metoclopromide
02 if sats <94%
STEMI
above and:
P2Y12-receptor antagonist = Prasugrel>Ticagrelor>Clopidogrel
Unfractionated heparin if PIC (LMWH is an alternative)
tPA (Alteplase/Tenecteplase) if PCI <120mins of presentation not possible (perform ECG 90 mins after and if ST elevation not reduced by 50% then rescue PCI better than repeat tPA) - give antithrombin (fonadparinux) at same time and ticagrelor after
Blood glucose < 11.0 mmol/L
NSTEMI
Unstable = immediate coronary angiography
Fondaparinux (antithrombin) - if no immediate PCI planned
Estimate 6 month mortalitly (GRACE)
if low risk (<3%) then give Ticagrelor
If intermediate/high (.3%) :
PCI immediate if unstable and within 72hrs if stable
give prasugrel/ticagrelor
give unfractionated heparin
drug elucidating stents prefered.
Ticagrelor and prasugrel antiplatelets prefered to clopidogral. continue for at least 12m Prasugrel if going to have PCI (also 12m if stented.
Complications
DARTH VADER
Death
Arrythmia/Heart block
Ruptured Aneurysm
Thrombus
Heart Failure
VSD
Another MI
Dressler’s Syndrome
Embolus
Regurgitant Valve
RIGHT SIDED INFRACTS = PRELOAD DEPENDENT
RS = V1>V2
ST eleveation in V1 and depression in V2 is highly specific to RSHF
Lead III > Lead II
Give IV fluids and do not give nitrates as they cause hypotension
Extra
Diclofenac Contraindicated
deeply inverted or biphasic waves in V2-3 in a person with the previous history of angina is characteristic of Wellen’s syndrome. This is highly specific for a critical stenosis of the left anterior descending artery
CAD Tx
aspirin
a second antiplatelet if appropriate (e.g. clopidogrel)
a beta-blocker
an ACE inhibitor
a statin
Paediatrics Upper Airway
Croup
Classic Presentation
Racemic Adrenaline is the diagnositc step
Steelple sign (subglottic narrowing not sensitive or specific so don’t bother with xray)
CKS recommend giving a single dose of oral dexamethasone (0.15mg/kg) to all children regardless of severity
adrenaline/ O2 for emergency
Bacterial Tracheaitis
Almost always S.aureus following viral prodrome
presents like not improving croup (esp Racemic adrenaline)
IX- ENT scope eg laryngoscopy (purulent = abx + culuture)
Epiglotitis
quirte rare - SAS
classic presentation - check if had HIB vaccine
if not straight to ER (diagnosis will be on scoping to secure airway)
Retropharyngeal Abscess
Pretty much the same but lump on neck
CT instead of OR
PT (quinsy)
going to be older - mainly adolescents
deviated uvela = key
urgent ent referal (maybe tonsillectomy)
trismus = dificullty opening mouth
Laryngomalacia
Congenital abnormality of the larynx.
Infants typical present at 4 weeks of age with:
stridor
Noisy breathing . . . worse on eating
Paeds Lower Airway
Four seperate entities here as opposed to upper airway
Foreign body Airway obstruction
Intrathoracic location + stridor as airways narrow on exhalation
Extrathoracic = oposite true
Coin sign +ve lateral as floppy bit is at back
Depending on these clues it tells you who to contact for help
Asthma (high yield summary)
OLD = obstructive lung disease
Dx on spirometry (reversible on bronchodilator)
- if normal can induce with Methacholine
GET PARENTS TO STOP SMOKNIG
Bronchiolitis
Beta agonists don’t do anything as its not bronchoconstriction but cells sloughing off.
non of the investigations or Tx really help
even o2 and IVF is just so they are well enough to eat so they don’t FTT
BUT not a nonsense illness as can lead to acute hypoxic respiratory failure and ARDS
Immediate hospital referal
>70 breaths per min
central cyanosis
looks SAS
persistent <92% O2 saturation
Grunting
Consider hospital referal
>60 breaths per minute
dehydration
feeding <50% normal
TX
O2, consider NGT, consider suction (upper airway secretions)
CF
Triad of;
Typical pulmonary and/or gastrointestinal tract manifestations
A family history
A positive result on ‘sweat-test’ (based on Cl-ion concentration). (pilocarpine given to induce sweating. . >60 diagnostic and >30 in infant is highly suggestive
Common infections:
S.aureus
Klebsiella Pneumoniae
Pseudeomonas Aeruginosa
Burkholderia Cepacia
50-55y life expectancy
Cirhosis
VW Happens
Viral
Needs to be chronic infection
both transmitted via blood (eg transfusions)
Hep C can now be treated with Direct acting antogonists and cured (no longer year long SEs of rubavirin and interferon)
Wilson’s
sx depending where Cu deposited
also speach, behaviour and psychiatric problems
IX ceulopkasmin or urinary cu
pencillamine to bridge to transplant (which cures the disease as well as cirhosis)
Haemochromatosis
iron deposition in skin, pancreas, liver and heart
usually switch in gut to stop absorbing Fe
Ix Ferritin >1000 w/o inflammation or hepatic necrosis
transferin is a better test
tx with phlebotomy
deferoxamine is a chelator
transplant treats the cirhosis but not the disease asa its in the gut
Alpha-1 anti-trypsin deficiency
look for the young non smokers iwth COPD and Cirhosis
this enzyme opposies elastase in the lungs
it can’t get out of liver so causes cirhosis
elastase unchecked in lungs so causes COPD
transplant stops further lung damage
Primary Sclerosing Cholangitis
(S for son’s of bitches)
manly and overt so extrahepatic and dx on imaging
painless jaundice
Don’t need ERCP if beads on a string on MRCP
tx with transplant and bridge with ursodeoxycholic acid
don’t stent as althought provides relief makes transplant harder
Primary Billiary CIrhosis
B is for bitches
coy therefore intrahepatic and have to dx with imaging (AMA not always detectable)
the M rule = IgM, anti-Mitochondrial antibodies, M2 subtype ,Middle aged females
Sicca Syndrome: 70% cases : dry moyth (xerostomia)
ETOH
long alc hx
stop drinking or can’t get transplant
NASH = non alcoholic steatohepatitis
NAFLD = non alcoholic fatty liver disease
Liver Function Tests
TP = total proptein
tp - alb = protein gap
TB = total bili. d bili = direct
thinks in black form hpuse. . .stuff liver makes therefore an assessment of chronic liver disease
t - direct = unconjugated
d bili and alp green as linked and post hepatic
TAKE 2
blue are things you should order
alb made by liver but used and lost elsewhere (think ossi)
nephrosis = nephropathy
gastrosis = protein losing enteropathy or probs malnutritianb
pre albumin = tells if its just nutritional statis
u/a or u proteinm tells us if its coming from kidney
protein gap over 4 tells us something is wrong (lots of immunoglobulins eg hiv hep c , mm) but can also be sepsis
ast also made in muscle (check cpk or ck to see if from mjscle)
alt can be from bone (check ggt) but rarely need to do these extra steps as can tell from patterns/context
2:1 ratio esp if not that elevated
if get into 1000s then think of the 6 as
aflatoxin = mushrooms
bud chiari you can check with doppler
Hepatocellular = 1ary intrahepatic (large increase ast and alt). ALP/ Bili also a little as has portal triads etc
alk phos and d bili = post . . .
painful almost always gallstones (at lwat choledocolithiasis to be affecting liver) small numbers as acute
small alt/ast as back up to liver
jaundive
haemolysis needed to generate haemoglobin
pre = mostly from haemolysis
intra = 3 steps (uptake, conjucation, release) . .. mix probs intra
infiltrative (islolated alp not from bone do a liver bx). . . more for completedness
