Ward Prep Flashcards
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.
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
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
stable or unstable (haemodynamically) (DC cardioversion if unstable)
rate control off if 48h and give if >48hr
(sotalol, amiodarone, flecainide)
- 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.
Pain relief
po Morphine breakthrough dose, do 1/6 of total daily dose
conversion of weak opiods to morphine you divide by 10
never increase background by more than 50%
po morphine to po oxycodone = divide by 2
po morphine to sc morphine = divide by 2
po oxycodone to sc oxycodone = divide by 1.5
Patches if they don’t want to be hooked up (buprenorphine or fentanyl - convert using NICE chart)
NSAID - any stage
Neuropathic: Amytriptyline 10mg nightly or pregabalin 75mg 12 hrly
Diabetic Neuropathy: Duloxetine 60mg PO daily
An NSAID (e.g, ibuprofen 400 mg 8-hourly may be introduced at any stage regularly or ‘as required’ if not contraindicated (as discussed earlier under Contraindications). With neuropathic pain (t.e. pain arising from nerve damage or disease and usually described as ‘shooting’, stabbing’ or ‘burning) the first line of treatment is amitriptyline (10mg oral nightly) or pregabalin (75 mg oral 12-hourly): duloxetine (60 mg oral daily) is indicated in painful diabetic neuropathy
Systems R/V
Fits/Faints/Funny turns
Coughs/colds
SOB
N/V
Change in bowel habit
change in water works
Any pain anywhere
Have you lost any weight
hows your appetite been
ISBAR
Introduce
This is Luke an FY1 calling from ED. Who am I talking to?
Situation (reason)
Current problem
I am calling about Mr Brown who was admitted with severe pneumonia, he has sats of 90% despite high flow oxygen and I am very worried about him.
“The problem appears to be cardiac/respiratory/neurological/sepsis”
“I’m not sure what the problem is but the patient is deteriorating”
“The patient is unstable, getting worse and I need help”
Background (Story)
reason for admission and past medical hx
“He is 55 and previously fit and well. He has a 2 day hx of cough and fever and arrived an hour ago by ambulance”
Assessment (vital signs)
go through ABCDE approach
He looks very unwell and is tiring. Airway: . . . .. . Breathing . . . .. .
Recommendation (Plan)
State explicitally what you want to caller to do - WHAT AND WHEN
I have given him IV abx that you presecribed and he has had 1 litre of IV saline. I am worried he is getting worse. I need help, please can you come and see him right away?
“I am going to start the following tx, is there anything else that you suggest?”
“I am going to do the following ix, is there anything else you can suggest?”
“If they do not improve when would you like to be called?”
“I don’t think I can do any more: I would like you to see the patient urgently”
Blood Pressure
Home BP S1 = 135/85 mmHg
Home BP S2 = >= 150/95 mmHg
Clinic BP severe = >180/110
Abnormal lab result general questions
- *How far out of range is it?**
- what is normal in your setting?
- whats the biggest and smallest result you have seen in your setting?
- Is it always slightly out of range?
- is it within a range or group that could contain false positives?
- *Does the result make sense?**
- has the patientsjust had an operation?
- has the patinet started a new medication?
- do they have sx?
- in short, do the results match the person in front of you?
What do the family groups tell us and do they agree?
- *Is this an important blood result?**
- which are the go to blood tests in your setting, the ones people get worried about?
- Some tests are more important that others. what would be the consequences of filing vs taking action?
Labs: what are we measuring
- Cell leakage (car oil)
ALT, AST, CK, Troponin and CK
depends on healthy tissues (less troponin in HF and less liver enzymes in chronic liver disease)
K+ also in damage but this could be from blood cells, muscles, damage in tube etc
2. Clearance
Kidneys: urea, creatine, uric acid
Creatine takes longer to change as smaller amounts (increase over 5-7 days indicating AKI).
Liver: bilirubin conjugated in liver
biliary tree has lots of ALP so if increased bili and increased ALP we think post hepatic jaundice (conjugated)
3. Production
Red blood cell production (look at diagram . . . problems could arise in any of the organs)
White blood cell production: CRP makes BM make neutrophils . .. . explains lag
if WBC increased but not CRP then something happening in last 4 weeks (lifespan of WBC)
Inflamattion but no CRP or WBC? could be false -ve or could have problem with BM or Liver or just localised inflamation (poor vasc flow?)
4. Interaction
multiple systems involved
Albumin produced by liver and kept in blood by kidney .. . . a decrease could be because of either
HBA1C: glucose stuck o haemoglobin. glucose sticks to everything so indicates it will also be stuck to nerves or eyes (3 month lifespan)
Labs: Family Groups
Full Blood Count
Hb, WBC and Plt
leukemia = increased WBC and reduced Hb and Plt
but this could also be explained by infection (wbc), infxn and medicaiotn (plts) and anaemia (hb) . . . . all in context of pt presentation
RBCs
Hb + Hct (RBC % of whole blood) and RBC (absolute amount
all low indicates anaemia and pushedot look at MCV. this guides further tests of ferritin b12 and folate
WBCs
MC neutrophils (75%) - responds to CRP
lymphocytes = 25-30%
monocytes, eosinophils and basophils = 5-10%
LFTs
ALT = actual liver cell content (leaks when damaged)
ALB = liver production
Bilirubin = liver waste removal
ALP = biliary tree (post hepatic obstructive jaundice
AST = Liver but also found in heart (beware if isolated)
GGT (bile duct cells)
if ALT, ALB and Bili normal but ALP raised its probably another source:
kidney look at urea and creatine
bone look at bone profile and Calcium
placenta - no test
Diabetes Emergencies
Iatrogenic eg Insulin or other diabetic medications
Hypoglycaemic = <4 mmol/l
Once corrected to tx cause
sx - also hungry, tired, tingling lips
Non diabetic
Factitious and insulinoma
(also liver disease, addison’s, alcohol)
endogenoius insulin would have C-peptide breakdown
Also do a secretogog screen as drugs such as Sulphonylureas induces endogenous insulin (insulinoma also has raised proinsulin:insulin ratio)
Suspected insulinoma bring into hospital and fast till hypoglycaemic . . .. then further CT/MRI (pancreas) to diagnose
diazoxide and somatostatin if not suitable for surgery
Insulinoma CF
Whipple’s Triad:
1) hypoglycaemia with fasting or exercise
2) reversal of symptoms with glucose
3) recorded low BMs at the time of symptoms
DKA
symtoms:
abdominal pain
polyuria, polydipsia, dehydration
Kussmaul respiration (deep hyperventilation)
Acetone-smelling breath (‘pear drops’ smell)
Think T1 but can be T2
Glucose in blood and not cells > cells think starving so induce lipolysis so ketones > sugar gets out kidneys causis osmotic diareusis > BMs not as high as ketones make sick
U&Es will show hypokalaemia and increased protein GAP
Joint British Diabetes Society Criteria:
glucose > 11 mmol/l or known diabetes mellitus
pH < 7.3
bicarbonate < 15 mmol/l
ketones > 3 mmol/l or urine ketones ++ on dipstick
Mx - local DKA protocol!
Insulin to correct Glucose
but correct K first as Insulin will make hypokalaemia worse
GAP fixed by Insulin overall but fluids (isotonic) needed in meantime
introduce glucose when GAP closing and glucose falling
finally when GAP closed take off drip and trial food
TX THE CAUSE
Passmed mx
fluid replacement: most patients with DKA are deplete around 5-8 litres. Isotonic saline is used initially. Please see an example fluid regime below.
- 9% sodium chloride 1L over first hour PRIORITY OVER INSULIN
insulin: an intravenous infusion should be started at 0.1 unit/kg/hour. Once blood glucose is < 15 mmol/l an infusion of 5% dextrose should be started
correction of hypokalaemia
long-acting insulin should be continued, short-acting insulin should be stopped
DKA resolution is defined as:
pH >7.3 and
blood ketones < 0.6 mmol/L and
bicarbonate > 15.0mmol/L
Hyperosmolar Hyperglycaemic State
Small amount of glucose into cells therefore BMs can climb a lot higher
CFs
General: fatigue, lethargy, nausea and vomiting
Neurological: altered level of consciousness, headaches, papilloedema, weakness
Haematological: hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)
Cardiovascular: dehydration, hypotension, tachycardia
Diagnosis
- Hypovolaemia
- Marked Hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis
- Significantly raised serum osmolarity (> 320 mosmol/kg)
Note: A precise definition of HHS does not exist, however the above 3 criteria are helpful in distinguishing between HHS and DKA. It is also important to remember that a mixed HHS / DKA picture can occur.
Mx Goals
- Normalise the osmolality (gradually) . . .
- Replace fluid and electrolyte losses
- Normalise blood glucose (gradually)
Start by giving IV normla saline and LMWH (due to hyperviscousity) not insulin! - manage in high dependency unit
Alcoholic Ketoacidosis
Ketoacidosis with nromal or low BG
Tx with Iv thiamine and 09% saline
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%
Insulin Mx
Normal
Your body dose basal bolus
basal = always a baseline there
body releases insulin in respons to BG
qHs = before bedtime
qAc = before meals
Types
Best to do basal bolus with the first two
can kind of replicate with the last two but not as good
mixed is easier but not as effective
NPH equivalent to long active
Regular = normal insulin = rapid
Basal Bolus
start long acting insulin and titrate up based on morning BG (until normal level)
Measure BM before each meal. . .if long not enough on its own add a rapid insulin before a meal (etc etc until all meals)
remember each BG measurement is because of the PREVIOUS meal/insulin dose if you need to adjust
No meal = no insulin and vice versa
Mixed
if all the measurements and injections are too much then use this
still bm before injections to titrate
Sliding Scale Insulin
is wrong
give insulin based on BG but BG based on previous insulin
Hospital
do basal bolus with SSI on top
TDI = total daily insulin . . . can estimate usuing 0.5U/kg (0.3 if >65, >creatinin or glucose <10mmol/l
Split 50/50 for basal bolus and 2/3 - 1/3 for mixed
add in the SSI requirment to their TDI at end of the day until BG under control.