Renal:

Treatment of hyperkalaemia:
Calcium gluconate if evidence of ECG changes (and most people would give if severe hyperkalaemia
with K >6.5 regardless of ECG findings
Insulin and dextrose (10 units actrapid in 100ml of 20% or 200ml of 10%) for K >6.0
Salbutamol 10mg can be used as an adjunct but short lived
Calcium resonium has slow onset >24hrs and can cause gut necrosis so use with care
If hyperkalaemia is refractory to treatment (x2 medical mx) then consider haemodialysis/filtration

Of course if a patient on RRT has hyperkalaemia then you need to treat medically but they are going
to require renal replacement as the definitive treatment but medical therapy will buy you some time
to arrange this.

Renal transplant dysfunction;

Increased serum creatinine that is not explained by dehydration, urinary obstruction, high
calcineurin inhibitor (CNI) levels or other apparent causes is most likely due to an intragraft
parenchymal process, such as acute rejection, chronic allograft injury (CAI), drug toxicity, recurrent
or de novo kidney disease, obstruction or BKV nephropathy.

In acute graft dysfunction patients will need a renal ultrasound (with dopplers of transplant artery),
CNI level (tacrolimus is most common in the UK), urine protein creatinine ratio, viral testing and
donor specific antibodies. They will then often require a renal transplant biopsy as this can influence
management (although if donor specific antibodies are very high a diagnosis of antibody mediated
acute rejection may be made without biopsy).

Membranous glomerulonephritis:
Most commonly it is a primary disorder however it can be secondary to drugs, malignancy or
hepatitis B. It is more common in Caucasians males >40 years old. Anti-PLA2R antibody testing is a
relatively new test - these antibodies are found in a high proportion of patients with primary
membranous nephropathy and can be used in diagnosis and monitoring disease activity. 

Management of ATN: supportive, hold nephrotoxics. This issues with ATN is it is often caused by a
pre-renal insult e.g. hypotension secondary to bleeding. However the ongoing pathology is not pre-
renal, it is intra-renal (in the tubule) and so further IV fluids once the patient is euvolaemic and no
longer hypotensive only push the patient into fluid overload as the cannot manage the fluid burden.
Treat the underlying cause (hypotension, nephrotoxics) but excessive IV fluids will not improve their
outcomes and may force them into having dialysis.

Interstitial nephritis – renal dysfunction secondary to renal injury charactersiced by inflammation

and oedema of the renal interstitium. Generally drug induced, infection related or secondary to an
immune process.

Drug induced;

 Antibiotics – cephalosporins, ciprofloxacin, isoniazid, ethambutol, macrolides, penicillins,

rifampicin, sulphonamides
 NSAIDs
 Diuretics – furosemide, thiazide
 Other – acyclovir, allopurinol, amlodipine, azathioprine, carbamazepine, cocaine, diltiazem,
omeprazole, phenytoin, quinine, ranitidine

Infections;
  Primary renal infection – bacterial pyelonephritis, renal TB, fungal nephritis
 Viral - Cytomegalovirus, Epstein-Barr virus, hantaviruses, hepatitis C, herpes simplex virus,
human immunodeficiency virus
 Systemic - legionella, staphylococci, streptococci, Leptospira, mycobacterium, mycoplasma,
rickettsia, syphilis, toxoplasmosis

Immune; glomerulonephritis, SLE, acute transplant rejection

Chronic pyelonephritis:

Commonly secondary to chronic vesicouretral reflux. Diagnosis is clinical with imaging, histology is
rarely required. Patients will have a history of recurrent UTIs/pyelonephritis. Damage is irreversible
and patients may develop end-stage renal failure. CT/MRI will show shrunken kidney’s with scarred
renal parenchyma. Creatinine will be abnormal and patients may have tubular damage resulting in
electrolyte derangements (hyponatraemia, hyperkalaemia, acidosis).

Renal bone disease :

Chronic kidney disease mineral bone disease can be diagnosed in any patient with;

1. Abnormalities of calcium, phosphate, PTH or vitamin D metabolism

2. Vascular or soft tissue calcification
3. Abnormal bone turnover, metabolism, volume, linear growth or strength

As CKD develops there is a development of hypocalcaemia and hyperphosphataemia. This results in

secondary hyperparathyroidism. Initially this compensatrory hyperparathyroidism maintains serum
phosphate through increasing excretion however this results in worsening hypocalcaemia so
promoting PTH secretion and an ongoing cycle. This also reduces calcitriol which reduces calcium
reabsorption from the gut so worsening this issue. Hyperphosphataemia is associated with
resistance to the actions of calcitriol on the parathyroid glands, which also leads to increased PTH
secretion - and causes resistance to the action of PTH on bone.

‘Bone involvement in CKD-MBD can be divided into high turnover states and low turnover states.
High turnover states (osteitis fibrosa) are a consequence of hyperparathyroidism which increases
bone turnover and bone resorption. This then contributes to bone pain and fractures at skeletal sites
and systemic vascular injury including vascular calcification that is associated with an increased
cardiovascular mortality.

Low turnover states are a consequence of PTH oversuppression and also vitamin D deficiency and
(uncommonly) aluminium deposition in bone. Low turnover states are also associated with bone
pain and an increased fracture rate and cardiovascular disease progression.
High turnover and low turnover changes can co-exist. Whilst the pathogenic pathways associated
with this are different, ultimately they have the same clinical consequences for the patient.’
‘http://www.renalmed.co.uk/database/chronic-kidney-disease---mineral-bone-disorder-ckd-mbd#’
Resp:
Blood gas analysis:

1. Are they hypoxic? If yes = respiratory failure, type 1 has hypoxia only (with low or normal
PCO2), type 2 has low pO2 and high pCO2 (2 issues)
2. pH – are they acidotic or alkalotic?
3. What is the pCO2? How does this relate to the pH – if pCO2 raised and acidosis then
respiratory acidosis, if low pCO2 and acidosis then metabolic acidosis (with attempt to
compensate)
4. What is the bicarbonate? Renal compensation is slow so acute pathology will not change the
bicarbonate. If bicarbonate is low and acidosis then metabolic acidosis. If bicarbonate is high
then this patient likely has respiratory acidosis with compensation (they have a chronic
underlying resp pathology or their issue has been ongoing for many hours/days)
5. Base excess – if negative (<-2) then metabolic is primary issue. If positive (>2) then
respiratory likely primary issue

Compensation – compensation is aiming to return the pH to the normal range. There are two ways
for the body to compensate – respiratory compensation can be attempted quickly while bicarbonate
buffering takes time and so occurs more slowly. In the case of acidosis the body should be trying to
clear pCO2 by raising respiratory rate. In the case of alkalosis the body would only reduce respiratory
rate in very extreme cases. Bicarbonate should rise in acidosis and fall in response to alkalosis (but
again rarely is alkalosis so prolonged unless drug related). If the pH is not normal then compensation
is not complete (partial compensation). This is common in acute events or decompensation of a
chronic condition. If the pCO2 is raised but bicarbonate is also raised and so pH is normal then this is
fully compensated. IT IS ONLY RESPIRATORY FAILURE IF THEY ARE HYPOXIC

Asthma:
Most recent guidelines are the BTS guidelines from 2019.

Acute asthma management is easy –

 Salbutamol nebuliser 5mg

 Steroids
 If this fails add in ipratropium nebulisation 500mcg (or 0.5mg) and continue with salbutamol
nebulisers (every 15 minutes)
 If this fails add in IV magnesium

IV salbutamol is not the correct answer in PLAB – this is an intervention which can only be done on
ITU, you are doing patients initial management. IV aminophylline is also not in the algorithm – it is a
senior decision to use and so should not be the correct answer (as you won’t be at that point in
management in the question).

NIV in asthma – this is beyond the scope of PLAB. This should only be done in an ITU environment
and is an ITU decision vs whether the mechanically ventilate. There is some evidence of good results
but this should only ever be done in a level 3 environment to allow rapid intubation and is never the
correct answer in plab (or to be done by your general medic).

Chronic asthma diagnosis and management is more difficult;

Diagnosis – BTS recommend trial of treatment if highly likely and if intermediate use spirometry.
NICE recommends using spirometry for everyone. So if in doubt select spirometry for diagnosis.
Management (cheat sheet) – BTS recommends SABA then ICS then LABA then LTRA or increasing ICS
dose then increasing ICS dose or LTRA (whichever one you didn’t do). NICE recommends SABA and
ICS then LTRA then LABA then MART (ICS and fast acting SABA) then increasing ICS dose. So the main
difference is the timing of introducing the LTRA (e.g. monteleukast).

There is no such thing as exercise induced asthma – only poorly controlled asthma. If you are asked
do not pick sodium cromoglicate! They can use SABA before exercise but if they are regularly
symptomatic you should increase their management as above.

MART – maintanence and reliever therapy (ICS + short acting LABA) in the same inhaler. E.g. fostair,
Symbicort and duoresp. For example if using Symbicort MART take 2 puffs BD and if symptomatic
can take up to 8 puffs during the day as well (max 6 at a time).

Spacers should be cleaned once a month with soapy water and left to dry.

Management in children under 5 –

Step 1: SABA
Step 2: 8 week trial of moderate paediatric dose of ICS
Step 3: stop ICS – if symptoms recur within 4 weeks then restart low dose ICS (test of treatment
confirmed asthma)
Step 4: LTRA
Step 5: refer to specialist

Controlled oxygen in COPD:

A minority of COPD patients are oxygen sensitive. This is identified by a chronically raised
bicarbonate and pCO2 (can be normal when hyperventilating). In these cases the target sats of these
patient should be 88-92% and target pO2 of 8. However these patients can still receive home oxygen
with monitoring of response. This is outside the scope of PLAB. They should have the same
assessment for home oxygen as any other patient. Home oxygen is typically low flow via nasal specs
– usually starts at 1L but can be very small amounts in oxygen sensitive patients. It is patient specific
and this is why you will not be asked about it. You just need to know when to refer someone for
assessment, the pO2 cut offs (on the slide) and that assessment is made when well with 2 ABGs >3
weeks apart.

Setting up nocturnal NIV is well beyond the scope of PLAB. However if they have a chronically raised
PCO2 when well then they may be suitable for referral for assessment at a specialist centre
(assuming this is something they want). NICE guidelines ‘Refer people who are adequately treated
but have chronic hypercapnic respiratory failure and have needed assisted ventilation (whether
invasive or non-invasive) during an exacerbation, or who are hypercapnic or acidotic on long-term
oxygen therapy, to a specialist centre for consideration of long-term non-invasive ventilation.’

PE:
In most patients CTPA is the appropriate diagnostic tool for PE. There are some special cases – young
women with no underlying lung disease may select V/Q to reduce radiation dose. However
remember VQ cannot be used in people with underlying lung disease or CXR changes. ALL PATIENTS
WITH ? PE MUST HAVE A CXR BEFORE FURTHER IMAGING. D-dimer is a rule out test for patients
unlikely to have a PE.

The most significant time VQ is used is in pregnancy. Based on RCOG guidelines. In pregnancy D-
dimer has no value. If the patient has evidence of a DVT then Doppler is the first line investigation as
if it confirms clot then there is not need for VQ or CTPA. If there is no evidence of DVT then patient
needs imaging. It is patient choice regarding scan (assuming no CXR changes – all patients must have
a CXR first). ‘Women with suspected PE should be advised that, compared with CTPA, V/Q scanning
may carry a slightly increased risk of childhood cancer but is associated with a lower risk of maternal
breast cancer; in both situations, the absolute risk is very small.’ Therefore if asked to choose
PLABable recommends selecting VQ scan as the woman is your patient (not the fetus). If the patient
expresses a strong preference for CTPA (usually due to the concern re:childhood cancer) then this
should be done at her request. Treatment in pregnancy is with LMWH (cannot use other agents).

Pneumothorax:

Types of pleural procedure;

- Needle decompression – you place a cannula into

the chest. This is done in an emergency (tension
pneumothorax only) to buy you time to put in a
chest drain (as they may arrest before you finish a
drain otherwise). For spontaneous pneumothorax
guidelines remain for needle decompression in 2nd
intercostal space mid-clavicular line. ATLS 10 th
edition recommends 4th or 5th intercostal space
mid-axillary line in tension pneumothorax in the context of trauma. Ultimately this
recommendation is only based on cadaver studies so most important is to detect a tension
(remember this is an obstructive form of shock so patients are compromised) and treat with
decompression.
- Pleural aspiration - a small (6F) thoracocentesis catheter– (picture on the right) is inserted
into the chest and used to aspirate up to 1.5L (maximum) of air or fluid. The catheter is then
removed. The procedure takes about 30 minutes in total and nothing remains in the patient.
- Medical chest drain – a medical chest drain (picture
on the left) (typically 12-18F) is inserted using
seldinger technique into the pleural space which
continuously drains air/fluid (you would clamp after
draining first 1.5L of fluid and wait 4 hours before
re-opening but MUST NEVER clamp a chest drain for
pneumothorax). A chest drain remains in situ usually
for hours to days (until resolution)
- Surgical chest drain – less commonly used, bigger in
size (up to 40F!), used in ATLS for haemopneumothorax/haemothorax or post-operatively.
Inserted via an incision and
blunt dissection down to the
pleura.

You need to know the different

management of primary and secondary
pneumothorax. You measure a
pneumothorax at the level of the
hilum. This excellent BTS flow chart
may help you (BTS guidelines on
pneumothorax). Tracheal deviation has
a poor sensitivity for tension pneumothorax ~60% - look for the important signs of compromise as
this is a clinical diagnosis!

How to differentiate just plain pneumothorax from hemopneumothorax especially if there's an RTA,
decreased Blood pressure. – this is challenging. Clinically a hemopneumothorax they will say there is
deviation of the trachea but that there is areas dull to percussion or that the is increased vocal
fremitus (which is reduced in pneumothorax). I think in the context of trauma hemopneumothorax
has to be high on your differential. In the UK this patient would get a trauma series which would
identify it. The change in management is that these patients require a surgical chest drain.

Simple spirometry:

Obstructive = FEV1 low, FVC low (but less reduced than FEV1), FEV1:FVC ratio low <0.7 = COPD,
poorly controlled asthma, bronchiectasis

Restrictive = FEV1 low, FVC low, FEV1:FVC ratio normal >0.7 = interstitial lung disease/fibrosis,
lobectomy/pneumonectomy

Chest radiograph stages of sarcoidosis;

1. Bihilar lymphadenopathy
2. Bihilar lymphadenopathy and pulmonary infiltrates
3. Pulmonary infiltrates with no lymphadenopathy
4. Fibrosis

Pneumonia:
Hospitalisation in pneumonia is at clinical discretion however CURB65 >2 has a significant mortality
risk and likely too unwell to go home (considering that they will likely either be confused,
hypotensive or tachypnoeic to score 3). However remember this is a scoring system for mortality
and is largely validated in older people – it depends why they are scoring, scoring 1 for age 66 is very
different than scoring 1 for hypotension or tachypnoea.
ID:

Latent TB:
Offer Mantoux testing to diagnose latent TB to close contacts of those with pulmonary or laryngeal
TB, new NHS employees and new entrants from high risk countries who have not had the BCG
vaccine.
If Mantoux positive assess for active TB and if no signs of active treat as latent TB.
If immunocompromised off interferon-gamma release assay and Mantoux.

For people <65, including those with HIV with latent TB offer;
3 months of isoniazid (with pyridoxine) and rifampicin or
6 months of isoniazid (with pyridoxine).

Isolation for TB;

If suspected TB then put in side room, if suspected MDRTB put in negative pressure room. Unless
clear need (e.g. homelessness) patients should not be admitted to hospital for diagnostics. Do not
admit anyone with TB to a ward with immunocompromised patients unless they can be in negative
pressure room. With pulmonary TB remain in side room until completed 2 weeks tx, then can
consider de-escalation if negative/low risk of MDRTB. If MDRTB need care in negative pressure room
until x 3 smear negative at weekly intervals, ideally with a negative culture.

BCG (in UK);

BCG immunisation should be offered to:
● all infants (aged 0 to 12 months) with a parent or grandparent who was born in a country where
the annual incidence of TB is 40/100,000 or greater
● all infants (aged 0 to 12 months) living in areas of the UK where the annual incidence of TB is
40/100,000 or greater
● previously unvaccinated children aged one to five years with a parent or grandparent who was
born in a country where the annual incidence of TB is 40/100,000 or greater. Can normally be
vaccinated without tuberculin testing
● previously unvaccinated, tuberculin-negative children aged from six to under 16 years of age with
a parent or grandparent who was born in a country where the annual incidence of TB is 40/100,000
or greater. Tuberculin tested and vaccinated if negative
● previously unvaccinated tuberculin-negative individuals under 16 years of age household or
equivalent close contacts of cases of sputum smear-positive pulmonary or laryngeal TB following
contact management
● previously unvaccinated, tuberculin-negative individuals under 16 years of age who were born in
or who have lived for a prolonged period (at least three months) in a country with an annual TB
incidence of 40/100,000 or greater (new entrants)
● Healthcare worker (HCW) or laboratory worker, who has either direct contact with TB patients or
with potentially infectious clinical materials or derived isolates. Should be done for new employees
● Veterinary and staff such as abattoir workers who handle animals or animal materials, which could
be infected with TB
The vaccine should not be given to:
● those who have already had a BCG vaccination
● those with a past history of TB
● those with an induration of 5mm or more following Mantoux (AJV) tuberculin skin testing
● those who have had a confirmed anaphylactic reaction to a component of the vaccine
● children less than two years of age in a household where an active TB case is suspected or
confirmed
● infants born to a mother who received immunosuppressive biological therapy during pregnancy
● Those who are receiving, or have received in the past 6 months, - immunosuppressive
chemotherapy or radiotherapy for malignant disease or nonmalignant disorders -
immunosuppressive therapy for a solid organ transplant (with exceptions, depending upon the type
of transplant and the immune status of the patient)
● Those who are receiving or have received in the past 12 months - immunosuppressive biological
therapy (e.g. anti-TNF therapy such as alemtuzumab, ofatumumab and rituximab) unless otherwise
directed by a specialist.
● Those who are receiving or have received in the past 3 months immunosuppressive therapy
including: high dose corticosteroids for >1 week, low dose corticosteroids for >2 weeks, DMARDs
●BCG vaccine is absolutely contraindicated in all HIV-positive persons regardless of CD4 cell count,
ART use, viral load, and clinical status
HIV and vaccinations;
Great table from https://www.bhiva.org/file/NriBJHDVKGwzZ/2015-Vaccination-Guidelines.pdf

WHO guidelines of management of Malaria -

https://apps.who.int/iris/bitstream/handle/10665/162441/9789241549127_eng.pdf;jsessionid=F60
0DEDF2F7692DB911CF5AA5912219B?sequence=1

But in summary;
Uncomplicated falciparum malaria (except in 1 st trimester of pregnancy) – artemether+lumefantrine
Uncomplicated falciparum malaria in 1 st trimester – quinine + clindamycin
Uncomplicated non-falciparum malaria (except in 1 st trimester) in chlorquinine sensitive areas – treat
with artemether+lumefantrine or chloroquine. If chloroquinine resistance use
artemether+lumefantrine
To prevent relapse then a 14 day course of primaquine unless pregnant, breastfeeding or <6months
If pregnant or breast feeding weekly chloroquine as chemoprophylaxis.
Severe malaria – IV artesunate
Cut offs for various opportunistic infections;
Any CD4; increased risk of TB and Kaposi’s sarcoma (but worse if CD4 <500)
CD4 <300; diarrhoea secondary to microsporidia and cryptosporidia, candida
CD4 <200; PCP, toxoplasmosis
CD4 <100; mycobacterium avium complex, cryptococcus
CD4<50; CMV retinitis
Features of PCP on CXR – fine reticular interstitial changes in a perihilar distribution.

Herpes in pregnancy before 3rd trimester – oral acyclovir (well tolerated in pregnancy). If delivery not
in the next 6 weeks can deliver vaginally.

What is a test of cure? A post-treatment test to ensure resolution

CNS listeria infection can be treated with ampicillin or amoxicillin

I cannot find an more updated guideline for tetanus – if you send this guideline on the group I will
happily review it but I have tried to search for it and cannot find a more up to date guideline than
those included in the slides. Sorry!

VZV exposure immunosuppressed: oral acyclovir PEP 800mg QDS from day 7 post-exposure to day
14. It is delayed (given day 7 post-exposure based on clinical trial data – if you’re interested its on
page 10 https://assets.publishing.service.gov.uk/government/uploads/system/uploads/
attachment_data/file/812526/PHE_PEP_VZIG_guidance_for_health_professionals.pdf).
VZV exposure in pregnant patients: All pregnant women who are exposed to chickenpox or shingles
should be assessed for susceptibility. If previous history of chickenpox in the pregnant woman, she
can be re-assured and no PEP is required. If there is no/unknown previous history of chickenpox in
the pregnant woman, test for the presence of varicella antibodies in line with national guidelines.
• for susceptible women (quantitative assay < 100mIU/ml) exposed in the first 20 weeks of
pregnancy, VZIG is recommended
• for susceptible women (quantitative assay < 100mIU/ml) exposed from 20 weeks of pregnancy,
either VZIG or aciclovir (800mg 4 times a day from days 7 to 14 after exposure) is recommended for
susceptible contacts. Oral valaciclovir 1000mg 3 times a day can be used as a suitable alternative

If the woman presents later than day 7 after exposure, a 7- day course of antivirals can be started up
to day 14 after exposure, if necessary.
Other stuff I’ve been asked previously/miscellaneous

Endo:
Acromegaly vs marfans:
Marfans is a genetic connective tissue disorder therefore often clinically obvious in
childhood/adolescence.. It causes overgrowth of long bones (tall stature), scoliosis, pectus
excavatum/carinatum, joint hyper-mobility, high-arched palate, regurgitant valve disease, aortic
aneurysm/dissection and spontaneous pneumothorax.

Acromegaly occurs in adulthood (before fusion of the growth plates excessive growth hormone
causes gigantism). It is almost always due to a pituitary adenoma (very rarely due to tumours at
other sites secreting GH or GHRH). Progressive symptoms over time, often onset is very uncertain. It
causes headaches, soft tissue swelling of the facial features (lips/nose/ears), hands and feet and
thickening of the skin, expansion of the skull causing frontal bossing, prognathism, macroglossia and
teeth spacing. Complications include cardiomyopathy, nerve compression syndromes, diabetes
mellitus, hypertension and colorectal cancer.

Diagnosis of diabetes:
One of four tests can be used:

 Fasting plasma glucose ≥7.0 mmol/L

 Random plasma glucose ≥11.1 mmol/L with diabetic symptoms 
 Blood glucose of ≥11.1 mmol/L  following a 2-hour oral glucose tolerance test   
 HbA1c ≥48 mmol/mol (6.5%)

If the patient is asymptomatic, diabetes should be confirmed with a second test, either the same or a
different modality. So if you find a random plasma glucose of >11.1 in a patient having a pre-
operative assessment they should then have another confirmatory test. However be aware in a
stress response secondary to critical illness or secondary to steroids administered for many medical
conditions patients may have an elevated plasma glucose. It would be better in these cases to check
a HbA1c or to wait until the patient has recovered and steroids stopped (if a short course) before
assessing them for underlying diabetes mellitus.

Mx htn in diabetes;
NICE HTN guidelines include specific guidelines for management of hypertension in type 2 diabetes.
1st line ACE (regardless of age)
2nd line add in CCB
3rd line thiazide

Management of type 2 diabetes;

 Lifestyle advice
o Balanced diet with high fibre, low glycemic index sources of carbohydrates,
increased physical activity, weight loss if overweight (aim initial body weight loss
target of 5-10%)
 If HbA1c is >48 mmol/mol on lifestyle advice offer standard release metformin, increasing
the dose over several weeks
 If HbA1c remains uncontrolled on maximum tolerable dose of metformin consider dual
therapy with;
o Metformin and a DPP-4 inhibitor (gliptin)
o Metformin and a sulfonylurea (gliclazide)
o Metformin and an sodium-glucose cotransporter 2 inhibitor (SGLT-2i) (gliflozin)
 o Metformin and pioglitazone*
 If HbA1c remains uncontrolled on dual therapy consider triple therapy with;
o Metformin, a DPP-4 inhibitor and a sulfonylurea
o Metformin, a sulfonylurea and an SGLT-2i
o Metformin, pioglitazone* and a sulfonylurea
o OR starting insulin based therapy
 If triple therapy is not effective consider metformin, a sulfonylurea and a glucagon-like
peptide-1 (GLP-1) mimetic if BMI ≥35kg/m² with medical problems associated with obesity
or a BMI <35kg/m² where weight loss would help obesity related comorbidities
 If symptomatic hyperglycaemia on presentation consider initiating a sulphonylurea or insulin

If metformin is contraindicated initial drug treatment can be with a DPP-4 inhibitor, pioglitazone or a
sulphonylurea. 

Metformin can promote weight loss and may reduce cardiovascular events and mortality. SGLT2i
improve glycaemic control, promote weight loss and have a diuretic effect. They have been shown to
reduce cardiovascular risk and may have renal benefit. 

*Patients should not receive pioglitazone if they have heart failure, liver impairment, a history of
bladder cancer, uninvestigated macroscopic haematuria or diabetic ketoacidosis. 

Treatment targets;
 If managed with lifestyle alone +/- a single agent not associated with hypoglycemia aim for a
HbA1c ≤48mmol/mol
 If on a drug which can cause hypoglycemia aim for a HbA1c of ≤53mmol/mol
 Consider relaxing targets in patients who are older, frail, with a reduced life expectancy
unlikely to see any benefits, those with impaired awareness of hypoglycaemia or for whom
intensive management would not be appropriate

Recheck HbA1c every 3-6 months until HbA1c stable on unchanging therapy and then 6 monthly
thereafter.

SIADH;

Diagnostic criteria for SIADH

  Plasma osmolality < 270 mosmol/kg
  Inappropriate urinary concentration (Uosm > 100 mosmol/kg)
  Patient is clinically euvolaemic
  Elevated urinary sodium (> 40 mmol/l), with normal salt and water intake
  Exclude hypothyroidism and glucocorticoid deficiency

Management
 Treat any underlying cause
 Fluid restriction - 800-1200 ml/day

Hypercalcaemia;
Always use adjusted calcium!
Mild hypercalcaemia  2.6–3.00 mmol/L.
Moderate hypercalcaemia  3.01–3.40 mmol/L.
Severe hypercalcaemia > 3.40 mmol/L.
In cases of hypercalcaemia check a PTH. High or normal PTH with a raised calcium suggests primary
hyperparathyroidism (as PTH should be suppressed when calcium is high). If low consider
malignancy or rarer causes such as granulomatous disease.

Treatment is with IV fluids – patients should be aggressively filled (3L/day) and if required can be
given furosemide once adequately hydrated. If ongoing hypercalcaemia despite adequate IVF can
consider a IV bisphosphonate (zolendronic acid/pamidronate) however these take at least 48hrs to
have an effect so if you see an improvement before then this is likely related to the fluids.

DKA;
Best guidelines are these https://www.diabetes.org.uk/resources-s3/2017-09/Management-of-DKA-
241013.pdf. It has sections on ABG vs VBG and urinary vs blood ketones as these are recognised
areas of contention when comparing to previous guidelines. Well worth a read and not too long!

VBG is performed if there is no indication to perform an ABG (respiratory distress, hypoxia,

compromise) as it is more comfortable for the patient. You will be doing serial measurements and so
it is easier to compare like with like. The difference in pH between ABG and VBG is minimal (it will
not affect diagnosis).

Capillary blood ketones are preferred as they don’t lag and you will be doing capillary blood glucose
regularly while on fixed rate insulin but will not be passing urine as frequently so also allow closer
monitoring of whether ketone suppression is being achieved.

In DKA normal saline is used instead of Hartmann’s to allow the addition of potassium as significant
dosing of potassium (40mmol/L) is required for most patients which is more than is in Hartmann’s
(~5mmol). In the UK there is a control on what fluids potassium can be added to due to clinical
incidents and in many institutions you can now only use pre-made bags of 0.9% saline with 20 or
40mmol potassium to prevent errors in potassium chloride and do not stock potassium to be added
to fluids.

Cerebral oedema in DKA – this is more common in children and fluid administration should be more
cautious in young people than in older adults with DKA. However this must be balanced against the
risk of them being profoundly volume deplete. (see guidelines above for a more considered debate
about this).

Stopping fixed rate insulin – convert to subcutaneous regime when biochemically stable (blood
ketones less than 0.6mmol/L, pH over 7.3) and the patient is ready and able to eat.

Insulin pump with DKA – in DKA the pump has failed and the patient should receive IV fixed rate
insulin in addition to continuing their continuous infusion pump. If not in DKA but uncontrolled
hyperglycaemia you should consider insulin catheter blockage/pump failure (technical issues) and
increase the basal rate in the first instance however this should be managed by the diabetes team
(patients will often have done these basic things before presenting and continuous pumps as still not
very common in the UK so experience can be limited).

Management of hyperprolactinaemia;
Consider potential underlying causes (pregnancy, hypothyroidism, drug induced) including
medications (look for SSRIs, CCBs, ranitidine, metoclopramide). Adjust/treat if present.
First line treatment is cabergoline (more effect/less treatment resistance than bromocriptine). If
there is no response to medical therapy or in very large tumours causing visual impairments despite
medical therapy (which can reduce tumour size) then patients should have trans-sphenoidal surgery.
Patients with visual field defects require close monitoring with regards to their vision during
initiation of treatment as progression on medical therapy would be an indication for surgery. These
patients are cared for in pituitary MDTs involving endocrinology and neurosurgery as the decision
when to perform surgery can be contentious.

Eye signs in graves disease;

This is complex and Wikipedia has a phenomenal list of various eponymous Grave’s eyes signs. This
is not useful for general medicine or the exam. Things to remember – Grave’s can cause a complex
ophthalmoplegia (eye signs which are not explained by a single cranial nerve defect) with
exophthalmos and lid lag. If you can identify a complex ophthalmoplegia then the list of important
causes are quite small (demyelination, cavernous sinus syndrome, neuromuscular disorder e.g.
myasthenia gravis, Grave’s, botulism) so I recommend learning the findings in simple cranial nerve
disorders then you can identify when there is more than one issue!

Cardio:

Posterior MI – horizontal ST depression in V1-3 with upright T waves and dominant R wave in V2. If
evidence of this get an ECG with lead positions V7-9 which will have STE in a posterior STEMI.

When to pick rhythm control in AF management – in young patients with acute onset AF in whom it
is likely reversible. There is no prognostic benefit to rhythm control. Otherwise consider if patients
remain symptomatic despite adequate rate control following appropriate period of anticoagulation.

Warfarin vs DOAC – warfarin is being phased out in preference for DOACs. Warfarin is still used in AF
associated with severe valvular disease (particularly mitral valve disease) and in patients with renal
failure. Otherwise only reason to choose warfarin would be for patient preference or significant
history of bleeding issues.

Torsades vs VF – torsades is secondary to QTc prolongation. It can degenerate into VF. In torsades
the amplitudes of the QRS oscillate as it twists around the isoelectric line but they change in a
predictable fashion. In VF there is variation in amplitude and rate which has no regular pattern to it.

Bradyarrhythmia acute mx - Typically to be compromised from bradycardia heart rate is <45bpm. In

these cases regardless of the underlying rhythm the most appropriate first step is to give IV atropine
500mcg and assess for a response. If there is no response the patient should be transcutaneously
paced with a view to transvenous pacing. If there is a response to atropine but this wears off then it
can be repeated every 3-5 minutes up to a maximum dose of 3mg. If transcutaneous pacing is not
available or it is appropriate to bridge the patient to transvenous pacing with second line drugs then
an isoprenaline or adrenaline infusion can be used.

LBBB - Dominant S wave in V1 (making your W) and notched R wave in V6 (making your M) with left
axis deviation and a broad QRS. T waves go in the opposite direction to the main defection (so up in
V1 and down in V6).

RBBB - Broad QRS with RSR in V1-V3 making an M (so an up deflection then down deflection then up
deflection before returning to baseline). Usually TWI in V1-V3.

Why ARB and not ACE for afrocaribbeans – this is a 2019 update in the NICE guidelines for HTN but
following the NICE guidelines references I cannot find the original source material. It is to do with the
low efficacy of ACEi in black people whoever I cannot quote you a study.

Why avoid morphine in pulmonary oedema – reduces heart rate and cardiac output and can cause
respiratory depression.
NSAIDs and CCF – recommend avoiding in CCF due to increased salt and water retention and
increased risk of cardiovascular events.

Rheumatology:

When steroids in RA – to manage symptoms in an acute flare to decrease inflammation. Patient

should be established on DMARDs and long-courses should only be considered by specialists in face
of treatment failure.

Ibuprofen and aspirin use together – aspirin and ibuprofen can be taken together however the
duration of this should be minimised and patients should have GI protection. It does increase the risk
of GI bleeding.

Bullous pemphigoid is an autoimmune bullous skin condition that primarily affects the elderly with
no gender predominance. There is typically an urticarial prodrome followed by the development of
crops of large, tense, fluid filled blisters on the trunk, proximal limbs and flexural areas. Mucosal
involvement is not typically a feature. Histologically a subepidermal blister is seen and there is an
inflammatory cell infiltrate which can form small abscesses in the superficial dermis. The epidermis is
intact. Autoantibodies, primarily IgG, are directed against the basement membrane which can be
seen on immunofluorescence.

Pemphigus Vulgaris is also an autoimmune bullous skin disease of the elderly but it commonly
involves the mucosa and the bullae are flaccid and fragile. They often deroof leaving erosions and
ulcerated areas. It is associated with the Asboe Hansen sign – direct pressure to the centre of the
lesion results in lateral extension. It is caused by IgG against intraepidermal cell adhesion molecules,
desmoglein 1 and 3 present in the desmosomes. Histologically there are numerous suprabasilar
bullae. Direct immunofluorescence shows intercellular deposition of IgG/C3 in the epidermis in a
‘fishnet like pattern’.