medicine Flashcards
batteries on a pacemaker usually last around
five years
pacemakers may be CI for
TENS machines and diathermy and MRI
indications for a pacemaker
Symptomatic bradycardias
Mobitz Type 2 AV block
Third degree heart block
Severe heart failure (biventricular pacemakers)
Hypertrophic obstructive cardiomyopathy (ICDs)
Single chamber pacemaker ECG sign is
A line before either the P or QRS but not the other indicates a single-chamber pacemaker
one an ECG A sharp vertical line before the P and QRS indicates
dual-chamber pacemaker
the two shockable cardiac arrest rhythm are
Ventricular tachycardia
Ventricular fibrillation
the two non-shockable cardiac arrest rhythms are
Pulseless electrical activity
Asystole
Tachycardia unstable patient consider
Consider up to 3 synchronised shocks
Consider an amiodarone infusion
narrow complex tachycardias are
atrial fibrillation, atrial flutter and supraventricular tachycardias
in a stable patient with atrial fibrillation consider Tx
rate control with a beta blocker or diltiazem (calcium channel blocker)
in a stable patient with atrial flutter Tx
control rate with a beta blocker
supraventricular tachycardia in a stable patient Tx
treat with vagal manoeuvres and adenosine
broad complex tachycardias
ventricular tachycardia or SVT with bundle branch block
Ventricular tachycardia broad complex Tx in stable patient
amiodarone infusion
atrial flutter pathology
“re-entrant rhythm” in either atrium. This is where the electrical signal re-circulates in a self-perpetuating loop due to an extra electrical pathway.
atrial flutter ECG appearance
“sawtooth appearance”
treatment options for atrial flutter
Radiofrequency ablation of the re-entrant rhythm
Anticoagulation based on CHA2DS2VASc score
treat underlying cause
rate/rhythm control with beta blockers or cardioversion
what conditions are associated with atrial flutter
Hypertension
Ischaemic heart disease
Cardiomyopathy
Thyrotoxicosis
Supraventricular tachycardia (SVT) pathology
electrical signal re-entering the atria from the ventricles.
what are the three types of SVT
“Atrioventricular nodal re-entrant tachycardia” - AV node
“Atrioventricular re-entrant tachycardia” (wolff-parkinson (accesory pathway))
“Atrial tachycardia” is where the electrical signal originates in the atria somewhere other than the sinoatrial node.
SVT management options
valsalva, carotid sinus massage, adenosine or direct current cardioversion.
adenosine mechanism
slowing cardiac conduction primarily though the AV node.
adenosine bolus is associated with
brief period of asystole or bradycardia
adenosine CI
Avoid if patient has asthma / COPD / heart failure / heart block / severe hypotension
adenosine dosing
6mg, then 12mg and further 12mg if no improvement between doses
long term management of SVT may include
Medication (beta blockers, calcium channel blockers or amiodarone)
Radiofrequency ablation
Wolff-Parkinson White Syndrome is often called the
Bundle of Kent.
definitive treatment of wolf parkinson syndrome is
radiofrequency ablation of the accessory pathway.
ECG changes for wolf parkinson white syndrome.
Short PR interval (< 0.12 seconds)
Wide QRS complex (> 0.12 seconds)
“Delta wave” which is a slurred upstroke on the QRS complex
AF and WPW may cause
polymorphic wide complex tachycardia
polymorphic wide complex tachycardia may be triggered by
Most antiarrhythmic medications (beta blockers, calcium channel blockers, adenosine etc) increase the risk of this by reducing conduction through the AV node and therefore promoting conduction through the accessory pathway
what medications are CI in WPW
Most antiarrhythmic medications
radiofrequency ablation is curative for what arrhythmias
Atrial Fibrillation
Atrial Flutter
Supraventricular Tachycardias
Wolff-Parkinson-White Syndrome
a prolonged QT interval represents a prolonged
repolarisation
depolarisation of the myocardium is what leads to
contraction
prolonged QT’s may result in
spontaneous depolarisation as they away repolarisation.
recurrent contractions without normal repolarisation of the mycocardium is called
torsades de pointes
torsades de pointes is a type of
polymorphic (multiple shape) ventricular tachycardia. It translates from French as “twisting of the tips”,
causes of a prolonged GT includes
Long QT Syndrome (inherited)
Medications (antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide antibiotics)
Electrolyte Disturbance (hypokalaemia, hypomagnesaemia, hypocalcaemia)
acute management of torsades de pointe is
Correct the cause (electrolyte disturbances or medications)
Magnesium infusion (even if they have a normal serum magnesium)
Defibrillation if VT occurs
long term management of torsades de pointes is
Avoid medications that prolong the QT interval Correct electrolyte disturbances Beta blockers (not sotalol) Pacemaker or implantable defibrillator
management of ectopic beats include
Check bloods for anaemia, electrolyte disturbance and thyroid abnormalities
Reassurance and no treatment in otherwise healthy people
Seek expert advice in patients with background heart conditions
types of AV node blocks
First degree heart block Second Degree Heart Block (Mobitz Type 1) Mobitz Type 2 2:1 block third degree heart block
First degree heart block pathology
there is delayed atrioventricular conduction through the AV node.
first degree heart block ECG appearance
On an ECG this presents as a PR interval greater than 0.20 seconds (5 small or 1 big square).
second degree heart block pathology
Second degree heart block is where some of the atrial impulses do not make it through the AV node to the ventricles.
second degree heart block appearance
This means that there are instances where p waves do not lead to QRS complexes.
(Mobitz Type 1) ECG appearance
increasing PR interval until the P wave no longer conducts to ventricles. This culminates in absent QRS complex after a P wave. The PR interval then returns to normal but progressively becomes longer again until another QRS complex is missed. This cycle repeats itself.
mobitz type 2 ECG appearance
This is where there is intermitted failure or interruption of AV conduction. This results in missing QRS complexes. There is usually a set ratio of P waves to QRS complexes, for example 3 P waves to each QRS complex would be referred to as a 3:1 block. The PR interval remains normal.
what complication may arise from mobitz type 2
asystole
2:1 block ECG appearance
2 P waves for each QRS complex
third degree heart block ECG appearance
This is referred to as complete heart block. This is no observable relationship between P waves and QRS complexes.
risk of what with third degree heart block
significant risk of asystole
unstable bradycardia/AV node block (risk of asystole) first line treatment
Atropine 500mcg IV
second line unstable bradycardia/AV node block (risk of asystole)
Atropine 500mcg IV repeated (up to 6 doses for a total to 3mg) Other inotropes (such as noradrenalin) Transcutaneous cardiac pacing (using a defibrillator)
high risk asystole patients consider
Temporary transvenous cardiac pacing or permanent implantable pacemaker
atropine mechanism
antimuscarinic medication and works by inhibiting the parasympathetic nervous system.
atropine SE
pupil dilatation, urinary retention, dry eyes and constipation.
Atrial fibrillation may result in
Irregularly irregular ventricular contractions
Tachycardia
Heart failure due to poor filling of the ventricles during diastole
Risk of stroke(emboli)
presenting symptoms of Atrial fibrillation are
Palpitations
Shortness of breath
Syncope (dizziness or fainting)
Symptoms of associated conditions (e.g. stroke, sepsis or thyrotoxicosis)
two differentials for irregularly irregular pulse are
Atrial fibrillation
Ventricular ectopics
ventricular ectopic disappear often
when HR gets over a certain threshold,
atrial fibrillation signs
Absent P waves
Narrow QRS Complex Tachycardia
Irregularly irregular ventricular rhythm
valvular atrial fibrillation may be caused by
severe mitral stenosis or a mechanical heart valve
common causes of atrial fibrillation includes
Sepsis Mitral Valve Pathology (stenosis or regurgitation) Ischemic Heart Disease Thyrotoxicosis Hypertension
goal of rate control with atrial fibrillation
The aim is to get the heart rate below 100 to extend the time during diastole when the ventricles can fill with blood.
first line option for rate control in atrial fibrillation
Beta blocker is first line (e.g. atenolol 50-100mg once daily)
other options for rate control in atrial fibrillation
Calcium-channel blocker (e.g. diltiazem) (not preferable in heart failure)
Digoxin (only in sedentary people, needs monitoring and risk of toxicity)
rhythm control for atrial fibrillation is offered for patients where
There is a reversible cause for their AF
Their AF is of new onset (<48 hours)
Their AF is causing heart failure
They remain symptomatic despite being effectively rate controlled
immediate cardioversion for atrial fibrillation if
the AF has been present for less than 48 hours or they are severely haemodynamically unstable.
delayed cardioversion for atrial fibrillation if
AF has been present for more than 48 hours and they are stable.
delayed cardioversion requires
anticoagulation.
pharmacological cardioversion first line is
Flecanide
Amiodarone
long term medical rhythm control options are
Beta blockers are first line for rhythm control
Dronedarone is second line for maintaining normal rhythm where patients have had successful cardioversion
Amiodarone is useful in patients with heart failure or left ventricular dysfunction
Paroxysmal atrial fibrillation Tx
Pill in pocket approach -> flecanide.
warfarin prolongs
prothrombin time
with anticoagulation atrial fibrillation risk of ischaemic stroke is reduced by
two thirds
warfarin is effected by what liver enzyme
cytochrome P450
target INR for atrial fibrillation is
2-3
what CHA2DS2-VASc score would be indicative for anticoagulation
> 1
CHA2DS2-VASc mnemonic
C – Congestive heart failure H – Hypertension A2 – Age >75 (Scores 2) D – Diabetes S2 – Stroke or TIA previously (Scores 2) V – Vascular disease A – Age 65-74 S – Sex (female)
HAS-BLED mnemonic for risk of haemorrhage on anticoagulation
H – Hypertension A – Abnormal renal and liver function S – Stroke B – Bleeding L – Labile INRs (whilst on warfarin) E – Elderly D – Drugs or alcohol
common mechanical valve used is the
St Jude valve.
bioprosthetic valve lifespan is
1o years
mechanical valve lifespan
over twenty years but requires lifelong anticoagulation with warfarin
INR range for mechanical valve is
2.5-3.5
complications of a mechanical heart valve are
thrombus, infective endocarditis, and haemolysis
gram positive cocci responsible for infective endocarditis with heart valves
Staphylococcus
Streptococcus
Enterococcus
3rd heart sound is the result of
rapid ventricular filling (chordae tendineae twang)
> 40 a third heart sound may be a sign of
heart failure.
4th heart sound is caused by
an atria contracting against a non-compliant ventricle.
“Erb’s point” is
third intercostal space on the left sternal boarder and is the best area for listening to heart sounds (S1 and S2).
leaning a patient onto their left hand side helps to listen for
mitral stenosis
having a patient leaning forward and holding exhalation is for
aortic regurgitation.
mitral stenosis causes
Rheumatic Heart Disease
Infective Endocarditis
mitral stenosis murmur
mid-diastolic, low pitched “rumbling” murmur
mitral stenosis associations
malar flush, atrial fibrillation and tapping apex beat.
mitral regurgitation causes
Idiopathic weakening of the valve with age
Ischaemic heart disease
Infective Endocarditis
Rheumatic Heart Disease
Connective tissue disorders such as Ehlers Danlos syndrome or Marfan syndrome
mitral regurgitation murmur
pan-systolic, high pitched “whistling” murmur due to high velocity blood flow that radiated to left axilla
aortic stenosis causes
Idiopathic age related calcification
Rheumatic Heart Disease
aortic stenosis murmur
ejection-systolic, high pitched murmur (high velocity of systole). This has a crescendo-decrescendo character
aortic stenosis associations
carotid radiation, slow rising pulse, narrow pulse pressure, exertional syncope.
aortic regurgitation murmur
early diastolic, soft murmur.
aortic regurgitation associations
collapsing pulse, austin flint murmur
austin flint murmur is
heard at the apex and is an early diastolic “rumbling” murmur.
causes of aortic regurgitation
Idiopathic age related weakness
Connective tissue disorders such as Ehlers Danlos syndrome or Marfan syndrome
essential hypertension (idiopathic) accounts for what percentage of cases
95%
secondary causes of hypertension include
Renal disease
Obesity
Pregnancy
Endocrine (Conn’s syndrome, hyperaldosteronism)
stage 1 hypertension clinic and ambulatory
clinical: >140/90
ambulatory: >135/85
stage 2 hypertension clinic and ambulatory
clinical: >160/100
ambulatory: >150/95
stage 3 hypertension
> 180/120
new diagnosis of hypertension should receive what further Ix
Urine albumin:creatinine ratio for proteinuria and dipstick
Bloods for HbA1c, renal function and lipids
fundus examination
ECG
medications for hypertension
A – ACE inhibitor (e.g. ramipril 1.25mg up to 10mg once daily)
B – Beta blocker (e.g. bisoprolol 5mg up to 20mg once daily)
C – Calcium channel blocker (e.g. amlodipine 5mg up to 10mg once daily)
D – Thiazide-like diuretic (e.g. indapamide 2.5mg once daily)
ARB – Angiotensin II receptor blocker (e.g. candesartan 8mg to up 32mg once daily)
step 1 for hypertension management (stage 2)
Aged less than 55 and non-black use A ((e.g. ramipril 1.25mg up to 10mg once daily)). Aged over 55 or black of African or African-Caribbean descent use C. Calcium channel blocker (e.g. amlodipine 5mg up to 10mg once daily)
step 2 hypertension management
A – ACE inhibitor (e.g. ramipril 1.25mg up to 10mg once daily) + C – Calcium channel blocker (e.g. amlodipine 5mg up to 10mg once daily)
step 3 hypertension management
A – ACE inhibitor (e.g. ramipril 1.25mg up to 10mg once daily)
C – Calcium channel blocker (e.g. amlodipine 5mg up to 10mg once daily)
D – Thiazide-like diuretic (e.g. indapamide 2.5mg once daily)
Step 4 hypertension Mx additional options if potassium less or equal to 4.5mmol/l
potassium sparing diuretic such as spironolactone.
Step 4 hypertension Mx additional options if potassium more than 4.5mmol/l
alpha blocker (e.g. doxazosin) or a beta blocker (e.g. atenolol).
spironolactone mechanism
blocking the action of aldosterone in the kidneys, resulting in sodium excretion and potassium reabsorption.
thiazide effect on potassium
reduced
ACEI effect on potassium
hyperkalaemia
presentation of cor pulmonale
asymptomatic, SOB, Hypoxia
Cyanosis
Raised JVP (due to a back-log of blood in the jugular veins)
Peripheral oedema
Third heart sound
Murmurs (e.g. pan-systolic in tricuspid regurgitation)
Hepatomegaly
presentation of chronic heart failure
Breathlessness worsened by exertion
Cough. They may produce frothy white/pink sputum.
Orthopnoea (the sensation of shortness of breathing when lying flat, relieves by sitting or standing). Ask them how many pillows they use at night.
Paroxysmal Nocturnal Dyspnoea
Peripheral oedema (swollen ankles)
diagnosis of chronic heart failure is with
Clinical presentation
BNP blood test (specifically “N-terminal pro-B-type natriuretic peptide” – NT‑proBNP)
Echocardiogram
ECG
causes of chronic heart failure include
Ischaemic Heart Disease
Valvular Heart Disease (commonly aortic stenosis)
Hypertension
Arrhythmias (commonly atrial fibrillation)
management for chronic heart failure
Yearly flu and pneumococcal vaccine
Stop smoking
Optimise treatment of co-morbidities
Exercise at tolerated
first line treatment for chronic heart failure
ACE inhibitor (e.g. ramipril titrated as tolerated up to 10mg once daily) Beta Blocker (e.g. bisoprolol titrated as tolerated up to 10mg once daily) Aldosterone antagonist when symptoms not controlled with A and B (spironolactone or eplerenone) Loop diuretics improves symptoms (e.g. furosemide 40mg once daily)
(ABAL)
acute Left ventricular failure can cause
type 1 respiratory failure (low o2 normal CO2)
symptoms of LVF
Shortness of breath
Looking and feeling unwell
Cough (frothy white/pink sputum)
signs of LVF
Increase respiratory rate
Reduced oxygen saturations
Tachycardia
3rd Heart Sound
Bilateral basal crackles (sounding “wet”) on auscultation
Hypotension in severe cases (cardiogenic shock)
85 year old lady with chronic kidney disease and aortic stenosis is prescribed 2 litres of fluid over 4 hours and then starts to drop her oxygen saturations. what treatment would help with the deteriorating sats?
IV furosemide
other causes aside from Chronic heart failure and LVF of a raised BNP include
Tachycardia Sepsis Pulmonary embolism Renal impairment COPD
and ejection fraction above what percentage is considered normal?
50%
CXR findings of LVF
cardiomegaly, upper lobe venous diversion, bilateral pleural effusion, fluid in interlobar fissures and fluid in septal lines (Kerley lines)
management of LVF
POUR SOD
pour away fluid (STOP fluids)
Sit up
O2
Diuretics (IV furosemide 40mg stat)
right coronary artery supplies the
Right atrium
Right ventricle
Inferior aspect of left ventricle
Posterior septal area
circumflex artery supplies
Left atrium
Posterior aspect of left ventricle
left anterior descending artery supplies
Anterior aspect of left ventricle
Anterior aspect of septum
diagnosis of acute coronary syndrome
ST elevation or new left bundle branch block -> STEMI
raised troponin and ECG (ST depression or T wave inversion or Q waves) -> NSTEMI
troponin normal and no ECG changes -> unstable angina
Left coronary artery ECG lead
I, aVL, V3-6
LAD ECG lead
V1-4
Circumflex ECG lead
I, aVL, V5-6
right coronary artery ECG lead
II, III, aVF
other than normal angina investigations for acute coronary syndrome you would also consider
CXR, ECHO, CT coronary angiogram
Acute STEMI presenting within 12 hours, within 2 hours you would
Primary PCI
Acute STEMI presenting within 12 hours but after 2 hours you would
thrombolysis
acute NSTEMI treatment
B – Beta blockers unless contraindicated
A – Aspirin 300mg stat dose
T – Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative)
M – Morphine titrated to control pain
A – Anticoagulant: Low Molecular Weight Heparin (LMWH) at treatment dose (e.g. enoxaparin 1mg/kg twice daily for 2-8 days)
N – Nitrates (e.g. GTN) to relieve coronary artery spasm
complications of MI
D – Death
R – Rupture of the heart septum or papillary muscles
E – “Edema” (Heart Failure)
A – Arrhythmia and Aneurysm
D – Dressler’s Syndrome
dressler’s syndrome usually occurs how long after an MI?
2-3 weeks
patholgoy of dressler’s syndrome
localised immune response causing pericarditis
presentation of dressler’s syndrome
pleuritis chest pain, pericardial rub, ericardial effusion
ECG changes with dressler’s is
ECG (global ST elevation and T wave inversion),
Dressler’s Dx
ECG, echocardiogram (pericardial effusion) and raised inflammatory markers (CRP and ESR).
Mx of dressler’s is with
NSAIDs (aspirin / ibuprofen) and in more severe cases steroids (prednisolone). They may need pericardiocentesis
secondary prevention following from acute coronary syndrome
Aspirin 75mg once daily
Another antiplatelet: e.g. clopidogrel or ticagrelor for up to 12 months
Atorvastatin 80mg once daily
ACE inhibitors (e.g. ramipril titrated as tolerated to 10mg once daily)
Atenolol (or other beta blocker titrated as high as tolerated)
Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)
gold standard Ix for angina is
CT angiography
Ix for angina are
Physical Examination (heart sounds, signs of heart failure, BMI) ECG FBC (check for anaemia) U&Es (prior to ACEi and other meds) LFTs (prior to statins) Lipid profile Thyroid function tests (check for hypo / hyper thyroid) HbA1C and fasting glucose (for diabetes)
immediate relief for angina is
GTN spray
long term symptom relief
Beta blocker (e.g. bisoprolol 5mg once daily) or; Calcium channel blocker (e.g. amlodipine 5mg once daily)
surgical intervention of angina includes
percutaneous coronary intervention or coronary artery bypass graft.
risk factors modifiable for atherosclerosis
Smoking Alcohol consumption Poor diet (high sugar and trans-fat and reduced fruit and vegetables and omega 3 consumption) Low exercise Obesity Poor sleep Stres
non-modifiable risk factors for atherosclerosis
Older age
Family history
Male
score system for atherosclerosis for primary prevention
Qrisk3 score
Qrisk 3 score is
the percentage risk that a patient will have a stroke or myocardial infarction in the next 10 years.
Qrisk 3 score >10% then
atorvastatin 20mg at night).
all patients with CKD or type 1 diabetes for more than 10 years should receive
atorvastatin 20mg.
SE of statins
Myopathy (check creatine kinase in patients with muscle pain or weakness)
Type 2 Diabetes
Haemorrhagic Strokes (very rarely)
NICE criteria for an AKI
Rise in creatinine of ≥ 25 micromol/L in 48 hours
Rise in creatinine of ≥ 50% in 7 days
Urine output of < 0.5ml/kg/hour for > 6 hours
risk factors for a AKI
Chronic kidney disease Heart failure Diabetes Liver disease Older age (above 65 years) Cognitive impairment Nephrotoxic medications such as NSAIDS and ACE inhibitors Use of a contrast medium such as during CT scans
three broad causes of an AKI
pre renal, intrinsic or post renal
pre-renal causes of an AKI
Dehydration
Hypotension (shock)
Heart failure
renal causes of an AKI
Glomerulonephritis
Interstitial nephritis
Acute tubular necrosis
post renal causes of an AKI
Kidney stones
Masses such as cancer in the abdomen or pelvis
Ureter or uretral strictures
Enlarged prostate or prostate cancer
Ix for AKI
urinanalysis, US
urinalysis details for an AKI cause
Urinalysis for protein, blood, leucocytes, nitrites and glucose.
Leucocytes and nitrites suggest infection
Protein and blood suggest acute nephritis (but can be positive in infection)
Glucose suggests diabetes
Mx of an AKI
fluids, stop nephrotoxic meds and relieve obstruction.
complications of an AKI
Hyperkalaemia
Fluid overload, heart failure and pulmonary oedema
Metabolic acidosis
Uraemia (high urea) can lead to encephalopathy or pericarditis
presentation of CKD
asymptomatic Pruritus (itching) Loss of appetite Nausea Oedema Muscle cramps Peripheral neuropathy Pallor Hypertension
Ix for CKD
eGFR
urine albumin:creatinine ratio
haematuria (Dipstick)
renal US
significant urine albumin:creatinine ratio result is
> 3mg/mmol
CKD diagnosis requires at least
eGFR of < 60 or proteinuria
complications of CKD
Anaemia Renal bone disease Cardiovascular disease Peripheral neuropathy Dialysis related problems
Tx of complications involve
Oral sodium bicarbonate to treat metabolic acidosis
Iron supplementation and erythropoietin to treat anaemia
Vitamin D to treat renal bone disease
Dialysis in end stage renal failure
Renal transplant in end stage renal failure
first line for CKD hypertension is
ACEI
features of CKD bone disease are
Osteomalacia (softening of bones)
Osteoporosis (brittle bones)
Osteosclerosis (hardening of bones)
X-ray changes of CKD bone disease are
sclerosis of the ends of the vertebrae, osteomalacia in the centre of the vertebrae known as “rugger jersey sign”
pathophysiology of CKD bone disease
high serum phosphate from reduced excretion and reduced vitamin D reduces calcium absorption and regulation of bone turnover
what thyroid complication arises in CKD
secondary hyperparathyroidism
CKD and secondary hyperparathyroidism pathology
glands react to low calcium and excrete more PTH resulting in increased osteoclast activity.
osteomalacia in CKD is because of
increased bone turnover
osteosclerosis in CKD arises from
osteoblasts trying to match osteoclasts but lack calcium so new bone is nor properly mineralised
management of CKD bone disease is with
Active forms of vitamin D (alfacalcidol and calcitriol)
Low phosphate diet
Bisphosphonates can be used to treat osteoporosis
indications for acute dialysis
A – Acidosis (severe and not responding to treatment)
E – Electrolyte abnormalities (severe and unresponsive hyperkalaemia)
I – Intoxication (overdose of certain medications)
O – Oedema (severe and unresponsive pulmonary oedema)
U – Uraemia symptoms such as seizures or reduced consciousness
options for dialysis include
Continuous Ambulatory Peritoneal Dialysis
Automated Peritoneal Dialysis
Haemodialysis
complications of peritoneal dialysis include
peritonitis, sclerosis, ultrafiltration failure, weight gain and pyschosocial.
a tunnelled cuffed catheter for haemodialysis may be inserted into
subclavian or jugular vein
A-V fistula complications are
Aneurysm Infection Thrombosis Stenosis STEAL syndrome High output heart failure
STEAL syndrome refers too
inadequate blood flow to the limb distal to the AV fistula. The AV fistula “steals” blood from the distal limb. This causes distal ischaemia
high output heart failure in AV fistula refers too
blood is flowing very quickly from the arterial to the venous system through the fistula. This means there is rapid return of blood to the heart. This increases the pre-load in the heart (how full the heart is before it pumps). This leads to hypertrophy of the heart muscle and heart failure.
kidney transplant donor matching requires
HLA matches
what is the incision used to a kidney transplant?
hockey stick incision
what immunosupressants are used in a post renal transplant
Tacrolimus
Mycophenolate
Prednisolone
nephritic syndrome refers too
Haematuria means blood in the urine. This can be microscopic (not visible) or macroscopic (visible).
Oliguria means there is a significantly reduced urine output.
Proteinuria is protein in the urine. In nephritic syndrome there is less than 3g / 24 hours. Any more and it starts being classified as nephrotic syndrome.
Fluid retention
nephrotic syndrome refers too
Peripheral oedema
Proteinuria more than 3g / 24 hours
Serum albumin less than 25g / L
Hypercholesterolaemia
glomerulonephritis refers too
an umbrella term applied to conditions that cause inflammation of or around the glomerulus
interstitial nephritis refers too
nflammation of the space between cells and tubules (the interstitium) within the kidney
glomerulosclerosis is referred to as
pathological process of scarring of the tissue in the glomerulus.
glomerulosclerosis can be caused by
glomerulonephritis or obstructive uropathy (blockage of urine outflow), and by a disease called focal segmental glomerulosclerosis.
glomerulonephritis Tx is
Immunosuppression (e.g. steroids)
Blood pressure control by blocking renin-angiotensin system (i.e. ACEi or ARBs)
nephrotic syndrome common cause in kids is
minimal change disease
nephrotic syndrome common cause in adults is
focal segmental glomerulosclerosis
common cause of primary glomerulonephritis is
IgA nephropathy
IgA nephropathy histology
gA deposits and glomerular mesangial proliferation”
commonest overall glomerulonephritis is
membranous glomerulonephritis
histology of membranous glomerulonephritis is
IgG and complement deposits on the basement membrane
post streptococcal glomerulonephritis presentation
Patients are typically under 30 years. It presents as:
1-3 weeks after a streptococcal infection (e.g. tonsillitis or impetigo)
They develop a nephritic syndrome
good pasture syndrome pathology
Anti-GBM (glomerular basement membrane) antibodies attack glomerulus and pulmonary basement membranes.
good pasture syndrome causes
This causes glomerulonephritis and pulmonary haemorrhage
rapidly progressive glomerulonephritis histology shows
crescentic glomerulonephritis
what is the commonest cause of glomerular pathology and CKD in the UK?
diabetic nephropathy
key feature of diabetic nephropathy is
proteinuria
what are the two types of interstitial nephritis?
acute interstitial nephritis and chronic tubulointerstitial nephritis.
Acute interstitial nephritis presents with
acute kidney injury and hypertension. As well as rash, fever and eosinophilia.
pathology of acute interstitial nephritis is
inflammation of the tubules and interstitium. This is usually caused by a hypersensitivity reaction to:
Drugs (e.g. NSAIDS or antibiotics)
Infection
acute tubular necrosis refers too
death of the epithelial cells in the renal tubals
commonest cause of an AKI is
acute tubal necrosis
urinalysis of acute tubular necrosis will show
Muddy brown casts
Mx of acute tubular necrosis
Supportive management
IV fluids
Stop nephrotoxic medications
Treat complications
type 1 renal tubular acidosis pathology
pathology in the distal tubule as it is unable to excrete hydrogen ions
causes of type 1 renal tubular acidosis
Genetic. There are both autosomal dominant and recessive forms. Systemic lupus erythematosus Sjogrens syndrome Primary biliary cirrhosis Hyperthyroidism Sickle cell anaemia Marfan’s syndrome
presentation of type 1 renal tubular acidosis
Failure to thrive in children
Hyperventilation to compensate for the metabolic acidosis
Chronic kidney disease
Bone disease (osteomalacia)
results of type 1 renal tubular acidosis
Hypokalaemia
Metabolic acidosis
High urinary pH (above 6)
Tx of type 1 renal tubular acidosis
bicarbonate
type 2 renal tubular acidosis pathology
Type 2 renal tubular acidosis is due to pathology in the proximal tubule. The proximal tubule is unable to reabsorb bicarbonate
commonest cause of renal tubular acidosis?
type 4 - > reduced aldosterone
type 4 tubular acidosis aetiology
can be due to adrenal insufficiency, medications such as ACE inhibitors and spironolactone or systemic conditions that affect the kidneys such as systemic lupus erythematosus, diabetes or HIV.
results of type 4 renal tubular acidosis
Hyperkalaemia
High chloride
Metabolic acidosis
Low urinary pH
management of type 4 renal tubular acidosis
Management is with fludrocortisone. Sodium bicarbonate and treatment of the hyperkalaemia may also be required.
HUS classic triad
Haemolytic anaemia
Acute kidney injury
Low platelet count (thrombocytopenia)
presentation of HUS
Reduced urine output Haematuria or dark brown urine Abdominal pain Lethargy and irritability Confusion Hypertension Bruising
Tx of HUS
Antihypertensives
Blood transfusions
Dialysis
cell death in rhabdomyolysis releases
Myoglobin (causing myoglobinurea)
Potassium
Phosphate
Creatine Kinase
what cell content is particularly harmful to the kidney during rhabdomyolysis
myoglobin
causes of rhabdomyolysis
prolonged immobility, extremely rigorous exercise, crush injuries and seizures
symptoms of rhabdomyolysis
Muscle aches and pain Oedema Fatigue Confusion (particularly in elderly frail patients) Red-brown urine
Ix for rhabdomyolysis
creatine kinase, urine dipstick (blood positive due to myoglobin), U+E’s and ECG
Tx for rhabdomyolysis
IV fluids, IV sodium carbonate, IV mannitol and hyperkalaemia Tx
conditions that can cause a raised potassium level
Acute kidney injury Chronic kidney disease Rhabdomyolysis Adrenal insufficiency Tumour lysis syndrome
medications that can cause a raised potassium level
Aldosterone antagonists (spironolactone and eplerenone) ACE inhibitors Angiotensin II receptor blockers NSAIDS Potassium supplements
ECG changes with hyperkalaemia
Tall peaked T waves
Flattening or absence of P waves
Broad QRS complexes
treatment for lowering potassium is
insulin and dextrose infusion and IV calcium gluconate:
alternative treatments for lowering potassium are
nebulised salbutamol, IV fluids, oral calcium resonium and sodium bicarbonate and dialysis
complications of the autosomal dominant type polycystic kidney disease
Chronic loin pain
Hypertension
Cardiovascular disease
Gross haematuria can occur with cyst rupture. This usually resolves within a few days.
Renal stones are more common in patients with PKD
End stage renal failure
what drug can slow the development of cysts in autosomal dominant polycystic kidney disease
Tolvaptan (a vasopressin receptor antagonist)
anterior pituitary releases
Thyroid Stimulating Hormone (TSH) Adrenocorticotropic Hormone (ACTH) Follicle Stimulating Hormone (FSH) and Luteinising Hormone (LH) Growth Hormone (GH) Prolactin
posterior pituitary releases
Oxytocin Antidiuretic Hormone (ADH)
cortisol release pattern.
diurnal variation
cortisol function
Inhibits the immune system Inhibits bone formation Raises blood glucose Increases metabolism Increases alertness
growth hormone function
Stimulates muscle growth
Increases bone density and strength
Stimulates cell regeneration and reproduction
Stimulates growth of internal organs
GH stimulates the release of
insulin like growth factor 1 from the liver
PTH is released in response to
low serum calcium, low magnesium and high serum phosphate
PTH role
stimulates activity and number of osteoclasts, calcium reabsorption in the kidney and conversation of D3-> calcitriol
Renin is secreted by the
juxtaglomerular cells
juxtaglomerular cells secrete renin in response too
low blood pressure
renin’s role
converts angiotensin into angiotensin 1
angiotensin 1 becomes
angiotensin 2 in the lungs via angiotensin converting enzyme ACE
angiotensin 2 role
vasoconstriction and the secretion of aldosterone
aldosterone is what type of hormone?
mineralocorticoid
aldosterone role for sodium
Increase sodium reabsorption from the distal tubule
aldosterone role for potassium
Increase potassium secretion from the distal tubule
aldosterone role for hydrogen
Increase hydrogen secretion from the collecting ducts
aldosterone effect on intravascular volume
increase via sodium
cushing syndrome refers too
abnormal elevation of cortisol
cushing disease refers too
pituitary adenoma secreting excessive ACTH
presentation of cushings: round in the middle with thin limbs
Round “moon” face Central Obesity Abdominal striae Buffalo Hump (fat pad on upper back) Proximal limb muscle wasting
presentation of cushing’s due to high level or stress hormone
Hypertension Cardiac hypertrophy Hyperglycaemia (Type 2 Diabetes) Depression Insomnia
extra effects of cushing’s syndrome
Osteoporosis
Easy bruising and poor skin healing
causes of cushing’s syndrome
adrenal ademona, cushing’s disease, exogenous, paraneoplastic
common cause of paraneoplastic cushing’s syndrome
“ectopic ACTH”. Small Cell Lung Cancer
diagnostic test of choice for cushing’s is
dexamethasone suppression test
how to perform a dex suppression test?
dose of dex. at night then cortisol and ACTH measured in the morning
low dose dexamethasone suppression test
1mg normal response is to be reduced cortisol and ACTH abnormal means cushing’s syndrome
high dexamethasone test
follows abnormal low dose. 8mg will be enough to suppress cortisol in cushing’s disease.
adrenal adenoma ACTH is suppressed but cortisol raised.
ectopic ACTH neither ACTH or cortisol will be reduced.
low dose dex test normal/high cortisol then
cushing’s syndrome
high dose dex test low cortisol then
cushing’s disease
high dose dex test low ACTH high/normal cortisol then
adrenal cushings
high dose dex test high cortisol high ACTH
ectopic ACTH
other Ix for cushings are
24 hour urinary free cortisol, FBC, U+E’s, MRI brain, chest CT, abdo CT
TX for cushings
trans sphenoidal surgery, surgical removal.
primary adrenal insufficiency (Addison’s disease) refers too
adrenal glands have been damaged, usually autoimmune. reduced cortisol and aldosterone.
secondary adrenal insufficiency refers too
inadequate ACTH to stimulate adrenal glands.
tertiary adrenal insufficiency refers too
inadequate CRH from the hypothalamus
causes of tertiary adrenal insufficiency
long term oral steroids (>3 weeks)
symptoms of adrenal insufficiency
Fatigue Nausea Cramps Abdominal pain Reduced libido
signs of adrenal insufficiency
Bronze hyperpigmentation to skin (ACTH stimulates melanocytes to produce melanin)
Hypotension (particularly postural hypotension)
Ix for adrenal insufficiency
sodium lo, high potassium, early morning cortisol, short synacthen test, adrenal autoantibodies, CT/MRI or MRI pituitary
test of choice for adrenal insufficiency is
short synacthen test
adrenal autoantibodies are
adrenal cortex antibodies and 21-hydroxylase antibodies
short synacthen test method
cortisol measured at baseline, 30 and then 60 minutes after. should normally double baseline.
Tx of adrenal insufficiency
hydrocortisone (glucocorticoid) and fludrocortisone (mineralcorticoid)
patients with adrenal insufficiency are also given
steroid card and emergency ID
adrenal crisis presentation
Reduced consciousness
Hypotension
Hypoglycaemia, hyponatraemia, hyperkaemia
Patients can be very unwell
adrenal crisis managment
Intensive monitoring if unwell
Parenteral steroids (i.e. IV hydrocortisone 100mg stat then 100mg every 6 hours)
IV fluid resuscitation
Correct hypoglycaemia
Careful monitoring of electrolytes and fluid balance
secondary hypothyroidism levels
low TSH low T3 and T4
antibodies against the thyroid gland itself are
Antithyroid Peroxidase (anti-TPO) Antibodies
Antithyroid Peroxidase (anti-TPO) Antibodies are usually present in
Grave’s Disease and Hashimoto’s Thyroiditis
antithyroglobulin antibodies are usually present in
Grave’s Disease, Hashimoto’s Thyroiditis and thyroid cancer.
TSH Receptor Antibodies are usually cause
Grave’s Disease
radioisotope scan with iodine in Grave’s disease will show
Diffuse high uptake
radioisotope scan with iodine in toxic multinodular goitre and adenomas will show
focal high uptake
radioisotope scan with iodine will show cold areas
thyroid cancer
commonest cause of hyperthyroidism is
Grave’s disease
toxic multinodular goitre causes
hyperthyroidism
Exopthalmos refers too
bulging of eyeball out of the socket caused by Graves Disease. This is due to inflammation, swelling and hypertrophy of the tissue behind the eyeball that forces the eyeball forward.
Pretibial Myxoedema refers too
deposits of mucin under the skin on the anterior aspect of the leg (the pre-tibial area). This gives a discoloured, waxy, oedematous appearance to the skin over this area. It is specific to Grave’s disease and is a reaction to the TSH receptor antibodies.
features of hyperthyroidism
Anxiety and irritability Sweating and heat intolerance Tachycardia Weight loss Fatigue Frequent loose stools Sexual dysfunction
features specific to grave’s disease
Diffuse Goitre (without nodules)
Graves Eye Disease
Bilateral Exopthalmos
Pretibial Myxoedema
features specific to toxic multinodular goitre
Goitre with firm nodules
Most patients are aged over 50
Second most common cause of thyrotoxicosis (after Grave’s)
De Quervain’s Thyroiditis describes
presentation of a viral infection with fever, neck pain and tenderness, dysphagia and features of hyperthyroidism. This progresses to hypothyroid phase
De Quervain’s thyroiditis Tx
It is a self-limiting condition and supportive treatment with NSAIDs for pain and inflammation and beta blockers for symptomatic relief of hyperthyroidism is usually all that is necessary.
thyroid storm presentation
severe presentation of hyperthyroidism with pyrexia, tachycardia and delirium
first line for hyperthyroidism
carbimazole
two therapies for carbimazole treatment of hyperthyroidism
titration-block or block and replace
second line drug for hyperthyroidism
Propylthiouracil
other treatments for hyperthyroidism include
radioactive iodine, beta blockers, and surgery.
common cause of hypothyroidism in the developed world is
hashimoto’s thyroiditis
common cause of hypothyroidism in the developing world is
iodine deficiency
secondary causes of hypothyroidism
Carbimazole Prophylthiouracil Radioactive iodine Thyroid surgery lithium and amiodarone
presentation of hypothyroidism
Weight gain Fatigue Dry skin Coarse hair and hair loss Fluid retention (oedema, pleural effusions, ascites) Heavy or irregular periods Constipation
Tx of hypothyroidism
levothyroxine which is synthetic T4 that metabolises into T3
ideal blood glucose level
between 4.4. and 6.1 mmol/l.
insulin is produced by
beta cells in the islets of langerhans in the pancreas
glucagon is produced by
alpha cells in the islets of langerhans in the pancreas
glucagon role
glycogenolysis and gluconeogenesis
glycogenolysis refers too
the liver to break down stored glycogen into glucose
gluconeogenesis refers too
liver to convert proteins and fats into glucose.
triad of DKA
dehydration, potassium imbalance, ketoacidosis
why dehydration in DKA?
Hyperglycaemia overwhelms the kidneys and glucose starts being filtered into the urine. The glucose in the urine draws water out with it in a process called osmotic diuresis. This causes the patient to urinate a lot (polyuria). This results in severe dehydration.
excessive thirst is called
polydipsia
why potassium imbalance in DKA
Insulin normally drives potassium into cells. Without insulin potassium is not added to and stored in cells. Serum potassium can be high or normal but total body potassium is low.
presentation of DKA
Polyuria Polydipsia Nausea and vomiting Acetone smell to their breath Dehydration and subsequent hypotension Altered Consciousness They may have symptoms of an underlying trigger (i.e. sepsis)
diagnosing DKA is through
Hyperglycaemia (i.e. blood glucose > 11 mmol/l)
Ketosis (i.e. blood ketones > 3 mmol/l)
Acidosis (i.e. pH < 7.3)
DKA TX
FIGPICK
F – Fluids – IV fluid resuscitation with normal saline (e.g. 1 litre stat, then 4 litres with added potassium over the next 12 hours)
I – Insulin – Add an insulin infusion (e.g. Actrapid at 0.1 Unit/kg/hour)
G – Glucose – Closely monitor blood glucose and add a dextrose infusion if below a certain level (e.g. 14 mmol/l)
P – Potassium – Closely monitor serum potassium (e.g. 4 hourly) and correct as required
I – Infection – Treat underlying triggers such as infection
C – Chart fluid balance
K – Ketones – Monitor blood ketones
long term complications of hyperglycaemia
macrovascular, microvascular and infection
macrovascular complications of hyperglycaemia
Coronary artery disease is a major cause of death in diabetics
Peripheral ischaemia causes poor healing, ulcers and “diabetic foot”
Stroke
Hypertension
microvascular complications of hyperglycaemia
Peripheral neuropathy
Retinopathy
Kidney disease, particularly glomerulosclerosis
monitoring of glucose can be conducted via
HBA1c, capillary blood glucose, flash glucose monitoring
presentation of type 2 diabetes
Fatigue Polydipsia and polyuria (thirsty and urinating a lot) Unintentional weight loss Opportunistic infections Slow healing Glucose in urine (on dipstick)
oral glucose tolerance test method
involves taking a baseline fasting plasma glucose result, giving a 75g glucose drink and then measuring plasma glucose 2 hours later.
pre diabetes Dx
HbA1c – 42-47 mmol/mol
Impaired fasting glucose – fasting glucose 6.1 – 6.9 mmol/l
Impaired glucose tolerance – plasma glucose at 2 hours 7.8 – 11.1 mmol/l on an OGTT
diabetes Dx
HbA1c > 48 mmol/mol
Random Glucose > 11 mmol/l
Fasting Glucose > 7 mmol/l
OGTT 2 hour result > 11 mmol/l
HBA1c target for new type 2 diabetics
48 mmol/mol for new type 2 diabetics
first line for type 2 diabetes
metformin titrated from initially 500mg once daily as tolerated.
second therapy for t2dm
sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor.
T2dm + CV consider
SGLT-2 inhibitors and GLP-1 inhibitors
metformin mechanism
biguanide”. It increases insulin sensitivity and decreases liver production of glucose. It is considered to be “weight neutral”
metformin SE
Diarrhoea and abdominal pain. This is dose dependent and reducing the dose often resolves the symptoms
Lactic acidosis
pioglitazone mechanism
“thiazolidinedione”. It increases insulin sensitivity and decreases liver production of glucose.
pioglitazone SE
Weight gain Fluid retention Anaemia Heart failure Extended use may increase the risk of bladder cancer
sulfonylurea mechanism
The most common sulfonyluria is “gliclazide”. Sulfonylureas stimulate insulin release from the pancreas.
sulfonylurea SE
Weight gain
Hypoglycaemia
Increased risk of cardiovascular disease and myocardial infarction when used as monotherapy
incretins are
hormones produced by the GI tract. They are secreted in response to large meals and act to reduce blood sugar.
incretins role
Increase insulin secretions
Inhibit glucagon production
Slow absorption by the GI tract
main incretin is
glucagon-like peptide-1” (GLP-1).
incretins are inhibited by
dipeptidyl peptidase-4” (DPP-4).
GLP-1 mimetic example
exenatide
SE of GLP-1 mimetic
GI tract upset
Weight loss
Dizziness
Low risk of hypoglycaemia
SGLT-2 inhibitor examples
-gliflozin”, such as empagliflozin, canagliflozin and dapagliflozin.
SGLT-2 inhibitor mechanism
The SGLT-2 protein is responsible for reabsorbing glucose from the urine in to the blood in the proximal tubules of the kidneys. SGLT-2 inhibitors block the action of this protein and cause glucose to be excreted in the urine.
SE of SGLT-2 inhibitors
Glucoseuria (glucose in the urine)
Increased rate of urinary tract infections
Weight loss
Diabetic ketoacidosis, notably with only moderately raised glucose. This is a rare complication
Lower limb amputation appears to be more common in patients on canagliflozin. It is not clear if this applies to other SGLT-2 inhibitors
rapid acting insulin examples
Novorapid
Humalog
Apidra
short acting insulin examples
Actrapid
Humulin S
Insuman Rapid
intermediate acting insulin examples
Insulatard
Humulin I
Insuman Basal
long acting insulin examples
Lantus
Levemir
Degludec (lasts over 40 hours)
combination insulins
Humalog 25 (25:75) Humalog 50 (50:50) Novomix 30 (30:70)
commonest cause of acromegaly is
pituitary adenoma
visual problem associated with acromegaly is
bitemporal hemianopia (loss of vision of outer half)
space occupying lesion symptoms of acromegaly
Headaches
Visual field defect (“bitemporal hemianopia”)
overgrowth of tissues symptoms in acromegaly
Prominent forehead and brow (“frontal bossing”)
Large nose
Large tongue (“macroglossia”)
Large hands and feet
Large protruding jaw (”prognathism”)
Arthritis from imbalanced growth of joints
GH organ dysfunction
Hypertrophic heart
Hypertension
Type 2 diabetes
Colorectal cancer
other symptoms that may suggest acromegaly
Development of new skin tags
Profuse sweating
Ix for acromegaly
IGF-1 screening, OGTT, MRI, ophthalmology referral
surgical Tx for acromegaly
trans sphenoidal resection
medical Tx for acromegaly
Pegvisomant (GH antagonist given subcutaneously and daily)
Somatostatin analogues to block GH release (e.g. ocreotide)
Dopamine agonists to block GH release (e.g. bromocriptine)
what cells specifically produce PTH
chief cells
PTH raises calcium by
Increasing osteoclast activity in bones (reabsorbing calcium from bones)
Increasing calcium absorption from the gut
Increasing calcium absorption from the kidneys
Increasing vitamin D activity
primary hyperparathyroidism is
excess PTH from tumour leading to hypercalcaemia
secondary hyperparathyroidism is caused by
lack of vit D or CKD leads to low calcium. the glands react by producing PTH and undergo hyperplasia.
tertiary hyperparathyroidism is caused by
chronic secondary hyperparathyroidism leading to hypercalcaemia even post treatment of underlying cause
high PTH and high calcium may be
primary or tertiary
high PTH low/normal calcium may be
secondary
Conn’s syndrome (primary hyperaldosteronism) pathology
he adrenal glands are directly responsible for producing too much aldosterone. Serum renin will be low as it is suppressed by the high blood pressure.
causes of conn’s include
An adrenal adenoma secreting aldosterone (most common) Bilateral adrenal hyperplasia Familial hyperaldosteronism type 1 and type 2 (rare) Adrenal carcinoma (rare)
secondary hyperaldosteronism is caused by
excessive renin stimulating the adrenal glands to produce more aldosterone. Serum renin will be high.
causes of secondary hyperaldosteronism include
Renal artery stenosis
Renal artery obstruction
Heart failure
Renal artery stenosis maybe confirmed by
doppler ultrasound, CT angiogram or magnetic resonance angiography (MRA).
Ix for hyperaldosteronism
renin / aldosterone ratio: Blood pressure (hypertension) Serum electrolytes (hypokalaemia) Blood gas analysis (alkalosis) CT / MRI to look for an adrenal tumour Renal doppler ultrasound, CT angiogram or MRA for renal artery stenosis or obstruction
High aldosterone and low renin indicates
primary hyperaldosteronism
High aldosterone and high renin indicates
secondary hyperaldosteronism
aldosterone antagonists include
Eplerenone
Spironolactone
renal artery stenosis TX
Percutaneous renal artery angioplasty via the femoral artery to treat in renal artery stenosis
common cause of secondary hypertension is
hyperaldosteronism (pot. low K+)
ADH is produced by
hypothalamus and secreted by the posterior pituitary gland. It is also known as “vasopressin”.
ADH role
DH stimulates water reabsorption from the collecting ducts in the kidneys.
SIADH may be caused by
posterior pituitary secreting too much ADH or the ADH may be coming from somewhere else, for example a small cell lung cancer.
SIAD commonly causes
euvolaemic hyponatraemia”.
SIADH euvolaemic hyponatreamia is demonstrated by
“high urine osmolality” and “high urine sodium”.
symptoms of SIADH
Headache Fatigue Muscle aches and cramps Confusion Severe hyponatraemia can cause seizures and reduced consciousness
rapid correction of serum sodium may cause
central pontine myelinolysis.
Mx of SIADH
Fluid restriction
Tolvaptan. “Vaptans” are ADH receptor blockers.
Demeclocycline is a tetracycline antibiotic that inhibits ADH.
first stage of central pontine myelinolysis
encephalopathic and confused. They may have a headache or nausea and vomiting.
second stage of central pontine myelinolysis
occurs few days post correction. This may present as spastic quadriparesis, pseudobulbar palsy and cognitive and behavioural changes
Diabetes insipidus is a lack of
antidiuretic hormone (ADH) or a lack of response to ADH.
Nephrogenic diabetes insipidus is when
the collecting ducts of the kidneys do not respond to ADH.
causes of nephrogenic diabetes insipidus include
Drugs, particularly lithium used in bipolar affective disorder
Mutations in the AVPR2 gene on the X chromosome that codes for the ADH receptor
Intrinsic kidney disease
Electrolyte disturbance (hypokalaemia and hypercalcaemia)
Cranial diabetes insipidus is when the
hypothalamus does not produce ADH
cranial diabetes insipidus can be caused by
Brain tumours Head injury Brain malformations Brain infections (meningitis, encephalitis and tuberculosis) Brain surgery or radiotherapy
presentation of cranial diabetes insipidus
Polyuria (excessive urine production) Polydipsia (excessive thirst) Dehydration Postural hypotension Hypernatraemia
Ix for cranial diabetes insipidus
Low urine osmolality
High serum osmolality
Water deprivation test
water deprivation test method
Initially the patient should avoid taking in any fluids for 8 hours. This is referred to as fluid deprivation. Then, urine osmolality is measured and synthetic ADH (desmopressin) is administered. 8 hours later urine osmolality is measured again.
after deprivation low urine osmolality and after ADH high points to
Cranial Diabetes Insipidus
after deprivation high urine osmolality and after ADH high points to
Primary Polydipsia
after deprivation low urine osmolality low and after ADH urine osmolality low
nephrogenic diabetes insipidus
Mx of diabetes insipidus is
Desmopressin (synthetic ADH) can be used in:
Cranial diabetes insipidus to replace ADH
Nephrogenic diabetes insipidus in higher doses under close monitoring
adrenal is produced by what cells
chromaffin cells
phaeochromocytoma is a tumour of the
chromaffin cells
adrenaline is an example of
catecholamine” hormone
what is the genetic association with phaeochromocytoma
25% are familial and associated with multiple endocrine neoplasia type 2 (MEN 2).
what is the pattern of a phaeochromocytoma
10% bilateral
10% cancerous
10% outside the adrenal gland
Dx of a phaeochromocytoma is with
24 hour urine catecholamines
Plasma free metanephrines
presentation of a phaeochromocytoma is
Anxiety Sweating Headache Hypertension Palpitations, tachycardia and paroxysmal atrial fibrillation
Mx of a phaeochromocytoma is with
Alpha blockers (i.e. phenoxybenzamine) Beta blockers once established on alpha blockers Adrenalectomy to remove tumour is the definitive management
