Ward Prep Flashcards

1
Q

CXR approach

A

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.

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2
Q

ECG take 2

A

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:

  1. rhythm
  2. conduction intervals
  3. cardiac axis
  4. description of QRS complexes
  5. description of ST segments and T waves

eg:

  1. Simus rhythm, rate 50bpm
  2. normal PR interval (100ms)
  3. Normal QRS complex duration (120ms)
  4. Normal Cardiac Axis
  5. Normal QRS complexes
  6. 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

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3
Q

Arhythmias

A

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.

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4
Q

Pain relief

A

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

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5
Q

Systems R/V

A

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

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6
Q

ISBAR

A

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”

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7
Q

Blood Pressure

A

Home BP S1 = 135/85 mmHg

Home BP S2 = >= 150/95 mmHg

Clinic BP severe = >180/110

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8
Q

Abnormal lab result general questions

A
  • *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?
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9
Q

Labs: what are we measuring

A
  1. 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)

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10
Q

Labs: Family Groups

A

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

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11
Q

Diabetes Emergencies

A

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.

  1. 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

  1. Hypovolaemia
  2. Marked Hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis
  3. 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

  1. Normalise the osmolality (gradually) . . .
  2. Replace fluid and electrolyte losses
  3. 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

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12
Q

Diabetes

A

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

  1. Lifestyle: target = 48 mmol/mol
  2. Add metformin: target = 48mmol/mol
  3. If >58 add another drug: target = 53 mmol/mol
  4. 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

  1. Lifestyle: target = 48 mmol/mol
  2. Add another drug: target = 48mmol/mol
  3. If >58 add another drug: target = 53 mmol/mol
  4. 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

  1. 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%

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13
Q

Insulin Mx

A

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.

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