medicine Flashcards
(432 cards)
1
Q
batteries on a pacemaker usually last around
A
five years
2
Q
pacemakers may be CI for
A
TENS machines and diathermy and MRI
3
Q
indications for a pacemaker
A
Symptomatic bradycardias
Mobitz Type 2 AV block
Third degree heart block
Severe heart failure (biventricular pacemakers)
Hypertrophic obstructive cardiomyopathy (ICDs)
4
Q
Single chamber pacemaker ECG sign is
A
A line before either the P or QRS but not the other indicates a single-chamber pacemaker
5
Q
one an ECG A sharp vertical line before the P and QRS indicates
A
dual-chamber pacemaker
6
Q
the two shockable cardiac arrest rhythm are
A
Ventricular tachycardia
Ventricular fibrillation
7
Q
the two non-shockable cardiac arrest rhythms are
A
Pulseless electrical activity
Asystole
8
Q
Tachycardia unstable patient consider
A
Consider up to 3 synchronised shocks
Consider an amiodarone infusion
9
Q
narrow complex tachycardias are
A
atrial fibrillation, atrial flutter and supraventricular tachycardias
10
Q
in a stable patient with atrial fibrillation consider Tx
A
rate control with a beta blocker or diltiazem (calcium channel blocker)
11
Q
in a stable patient with atrial flutter Tx
A
control rate with a beta blocker
12
Q
supraventricular tachycardia in a stable patient Tx
A
treat with vagal manoeuvres and adenosine
13
Q
broad complex tachycardias
A
ventricular tachycardia or SVT with bundle branch block
14
Q
Ventricular tachycardia broad complex Tx in stable patient
A
amiodarone infusion
15
Q
atrial flutter pathology
A
“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.
16
Q
atrial flutter ECG appearance
A
“sawtooth appearance”
17
Q
treatment options for atrial flutter
A
Radiofrequency ablation of the re-entrant rhythm
Anticoagulation based on CHA2DS2VASc score
treat underlying cause
rate/rhythm control with beta blockers or cardioversion
18
Q
what conditions are associated with atrial flutter
A
Hypertension
Ischaemic heart disease
Cardiomyopathy
Thyrotoxicosis
19
Q
Supraventricular tachycardia (SVT) pathology
A
electrical signal re-entering the atria from the ventricles.
20
Q
what are the three types of SVT
A
“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.
21
Q
SVT management options
A
valsalva, carotid sinus massage, adenosine or direct current cardioversion.
22
Q
adenosine mechanism
A
slowing cardiac conduction primarily though the AV node.
23
Q
adenosine bolus is associated with
A
brief period of asystole or bradycardia
24
Q
adenosine CI
A
Avoid if patient has asthma / COPD / heart failure / heart block / severe hypotension
25
adenosine dosing
6mg, then 12mg and further 12mg if no improvement between doses
26
long term management of SVT may include
Medication (beta blockers, calcium channel blockers or amiodarone)
Radiofrequency ablation
27
Wolff-Parkinson White Syndrome is often called the
Bundle of Kent.
28
definitive treatment of wolf parkinson syndrome is
radiofrequency ablation of the accessory pathway.
29
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
30
AF and WPW may cause
polymorphic wide complex tachycardia
31
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
32
what medications are CI in WPW
Most antiarrhythmic medications
33
radiofrequency ablation is curative for what arrhythmias
Atrial Fibrillation
Atrial Flutter
Supraventricular Tachycardias
Wolff-Parkinson-White Syndrome
34
a prolonged QT interval represents a prolonged
repolarisation
35
depolarisation of the myocardium is what leads to
contraction
36
prolonged QT's may result in
spontaneous depolarisation as they away repolarisation.
37
recurrent contractions without normal repolarisation of the mycocardium is called
torsades de pointes
38
torsades de pointes is a type of
polymorphic (multiple shape) ventricular tachycardia. It translates from French as “twisting of the tips”,
39
causes of a prolonged GT includes
Long QT Syndrome (inherited)
Medications (antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide antibiotics)
Electrolyte Disturbance (hypokalaemia, hypomagnesaemia, hypocalcaemia)
40
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
41
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
```
42
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
43
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
```
44
First degree heart block pathology
there is delayed atrioventricular conduction through the AV node.
45
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).
46
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.
47
second degree heart block appearance
This means that there are instances where p waves do not lead to QRS complexes.
48
(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.
49
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.
50
what complication may arise from mobitz type 2
asystole
51
2:1 block ECG appearance
2 P waves for each QRS complex
52
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.
53
risk of what with third degree heart block
significant risk of asystole
54
unstable bradycardia/AV node block (risk of asystole) first line treatment
Atropine 500mcg IV
55
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)
```
56
high risk asystole patients consider
Temporary transvenous cardiac pacing or permanent implantable pacemaker
57
atropine mechanism
antimuscarinic medication and works by inhibiting the parasympathetic nervous system.
58
atropine SE
pupil dilatation, urinary retention, dry eyes and constipation.
59
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)
60
presenting symptoms of Atrial fibrillation are
Palpitations
Shortness of breath
Syncope (dizziness or fainting)
Symptoms of associated conditions (e.g. stroke, sepsis or thyrotoxicosis)
61
two differentials for irregularly irregular pulse are
Atrial fibrillation
| Ventricular ectopics
62
ventricular ectopic disappear often
when HR gets over a certain threshold,
63
atrial fibrillation signs
Absent P waves
Narrow QRS Complex Tachycardia
Irregularly irregular ventricular rhythm
64
valvular atrial fibrillation may be caused by
severe mitral stenosis or a mechanical heart valve
65
common causes of atrial fibrillation includes
```
Sepsis
Mitral Valve Pathology (stenosis or regurgitation)
Ischemic Heart Disease
Thyrotoxicosis
Hypertension
```
66
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.
67
first line option for rate control in atrial fibrillation
Beta blocker is first line (e.g. atenolol 50-100mg once daily)
68
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)
69
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
70
immediate cardioversion for atrial fibrillation if
the AF has been present for less than 48 hours or they are severely haemodynamically unstable.
71
delayed cardioversion for atrial fibrillation if
AF has been present for more than 48 hours and they are stable.
72
delayed cardioversion requires
anticoagulation.
73
pharmacological cardioversion first line is
Flecanide
| Amiodarone
74
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
75
Paroxysmal atrial fibrillation Tx
Pill in pocket approach -> flecanide.
76
warfarin prolongs
prothrombin time
77
with anticoagulation atrial fibrillation risk of ischaemic stroke is reduced by
two thirds
78
warfarin is effected by what liver enzyme
cytochrome P450
79
target INR for atrial fibrillation is
2-3
80
what CHA2DS2-VASc score would be indicative for anticoagulation
>1
81
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)
```
82
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
```
83
common mechanical valve used is the
St Jude valve.
84
bioprosthetic valve lifespan is
1o years
85
mechanical valve lifespan
over twenty years but requires lifelong anticoagulation with warfarin
86
INR range for mechanical valve is
2.5-3.5
87
complications of a mechanical heart valve are
thrombus, infective endocarditis, and haemolysis
88
gram positive cocci responsible for infective endocarditis with heart valves
Staphylococcus
Streptococcus
Enterococcus
89
3rd heart sound is the result of
rapid ventricular filling (chordae tendineae twang)
90
>40 a third heart sound may be a sign of
heart failure.
91
4th heart sound is caused by
an atria contracting against a non-compliant ventricle.
92
“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).
93
leaning a patient onto their left hand side helps to listen for
mitral stenosis
94
having a patient leaning forward and holding exhalation is for
aortic regurgitation.
95
mitral stenosis causes
Rheumatic Heart Disease
| Infective Endocarditis
96
mitral stenosis murmur
mid-diastolic, low pitched “rumbling” murmur
97
mitral stenosis associations
malar flush, atrial fibrillation and tapping apex beat.
98
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
99
mitral regurgitation murmur
pan-systolic, high pitched “whistling” murmur due to high velocity blood flow that radiated to left axilla
100
aortic stenosis causes
Idiopathic age related calcification
| Rheumatic Heart Disease
101
aortic stenosis murmur
ejection-systolic, high pitched murmur (high velocity of systole). This has a crescendo-decrescendo character
102
aortic stenosis associations
carotid radiation, slow rising pulse, narrow pulse pressure, exertional syncope.
103
aortic regurgitation murmur
early diastolic, soft murmur.
104
aortic regurgitation associations
collapsing pulse, austin flint murmur
105
austin flint murmur is
heard at the apex and is an early diastolic “rumbling” murmur.
106
causes of aortic regurgitation
Idiopathic age related weakness
| Connective tissue disorders such as Ehlers Danlos syndrome or Marfan syndrome
107
essential hypertension (idiopathic) accounts for what percentage of cases
95%
108
secondary causes of hypertension include
Renal disease
Obesity
Pregnancy
Endocrine (Conn's syndrome, hyperaldosteronism)
109
stage 1 hypertension clinic and ambulatory
clinical: >140/90
ambulatory: >135/85
110
stage 2 hypertension clinic and ambulatory
clinical: >160/100
ambulatory: >150/95
111
stage 3 hypertension
>180/120
112
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
113
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)
114
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)
115
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)
116
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)
117
Step 4 hypertension Mx additional options if potassium less or equal to 4.5mmol/l
potassium sparing diuretic such as spironolactone.
118
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).
119
spironolactone mechanism
blocking the action of aldosterone in the kidneys, resulting in sodium excretion and potassium reabsorption.
120
thiazide effect on potassium
reduced
121
ACEI effect on potassium
hyperkalaemia
122
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
123
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)
124
diagnosis of chronic heart failure is with
Clinical presentation
BNP blood test (specifically “N-terminal pro-B-type natriuretic peptide” – NT‑proBNP)
Echocardiogram
ECG
125
causes of chronic heart failure include
Ischaemic Heart Disease
Valvular Heart Disease (commonly aortic stenosis)
Hypertension
Arrhythmias (commonly atrial fibrillation)
126
management for chronic heart failure
Yearly flu and pneumococcal vaccine
Stop smoking
Optimise treatment of co-morbidities
Exercise at tolerated
127
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)
128
acute Left ventricular failure can cause
type 1 respiratory failure (low o2 normal CO2)
129
symptoms of LVF
Shortness of breath
Looking and feeling unwell
Cough (frothy white/pink sputum)
130
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)
131
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
132
other causes aside from Chronic heart failure and LVF of a raised BNP include
```
Tachycardia
Sepsis
Pulmonary embolism
Renal impairment
COPD
```
133
and ejection fraction above what percentage is considered normal?
50%
134
CXR findings of LVF
cardiomegaly, upper lobe venous diversion, bilateral pleural effusion, fluid in interlobar fissures and fluid in septal lines (Kerley lines)
135
management of LVF
POUR SOD
pour away fluid (STOP fluids)
Sit up
O2
Diuretics (IV furosemide 40mg stat)
136
right coronary artery supplies the
Right atrium
Right ventricle
Inferior aspect of left ventricle
Posterior septal area
137
circumflex artery supplies
Left atrium
| Posterior aspect of left ventricle
138
left anterior descending artery supplies
Anterior aspect of left ventricle
| Anterior aspect of septum
139
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
140
Left coronary artery ECG lead
I, aVL, V3-6
141
LAD ECG lead
V1-4
142
Circumflex ECG lead
I, aVL, V5-6
143
right coronary artery ECG lead
II, III, aVF
144
other than normal angina investigations for acute coronary syndrome you would also consider
CXR, ECHO, CT coronary angiogram
145
Acute STEMI presenting within 12 hours, within 2 hours you would
Primary PCI
146
Acute STEMI presenting within 12 hours but after 2 hours you would
thrombolysis
147
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
148
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
149
dressler's syndrome usually occurs how long after an MI?
2-3 weeks
150
patholgoy of dressler's syndrome
localised immune response causing pericarditis
151
presentation of dressler's syndrome
pleuritis chest pain, pericardial rub, ericardial effusion
152
ECG changes with dressler's is
ECG (global ST elevation and T wave inversion),
153
Dressler's Dx
ECG, echocardiogram (pericardial effusion) and raised inflammatory markers (CRP and ESR).
154
Mx of dressler's is with
NSAIDs (aspirin / ibuprofen) and in more severe cases steroids (prednisolone). They may need pericardiocentesis
155
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)
156
gold standard Ix for angina is
CT angiography
157
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)
```
158
immediate relief for angina is
GTN spray
159
long term symptom relief
```
Beta blocker (e.g. bisoprolol 5mg once daily) or;
Calcium channel blocker (e.g. amlodipine 5mg once daily)
```
160
surgical intervention of angina includes
percutaneous coronary intervention or coronary artery bypass graft.
161
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
```
162
non-modifiable risk factors for atherosclerosis
Older age
Family history
Male
163
score system for atherosclerosis for primary prevention
Qrisk3 score
164
Qrisk 3 score is
the percentage risk that a patient will have a stroke or myocardial infarction in the next 10 years.
165
Qrisk 3 score >10% then
atorvastatin 20mg at night).
166
all patients with CKD or type 1 diabetes for more than 10 years should receive
atorvastatin 20mg.
167
SE of statins
Myopathy (check creatine kinase in patients with muscle pain or weakness)
Type 2 Diabetes
Haemorrhagic Strokes (very rarely)
168
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
169
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
```
170
three broad causes of an AKI
pre renal, intrinsic or post renal
171
pre-renal causes of an AKI
Dehydration
Hypotension (shock)
Heart failure
172
renal causes of an AKI
Glomerulonephritis
Interstitial nephritis
Acute tubular necrosis
173
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
174
Ix for AKI
urinanalysis, US
175
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
176
Mx of an AKI
fluids, stop nephrotoxic meds and relieve obstruction.
177
complications of an AKI
Hyperkalaemia
Fluid overload, heart failure and pulmonary oedema
Metabolic acidosis
Uraemia (high urea) can lead to encephalopathy or pericarditis
178
presentation of CKD
```
asymptomatic
Pruritus (itching)
Loss of appetite
Nausea
Oedema
Muscle cramps
Peripheral neuropathy
Pallor
Hypertension
```
179
Ix for CKD
eGFR
urine albumin:creatinine ratio
haematuria (Dipstick)
renal US
180
significant urine albumin:creatinine ratio result is
>3mg/mmol
181
CKD diagnosis requires at least
eGFR of < 60 or proteinuria
182
complications of CKD
```
Anaemia
Renal bone disease
Cardiovascular disease
Peripheral neuropathy
Dialysis related problems
```
183
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
184
first line for CKD hypertension is
ACEI
185
features of CKD bone disease are
Osteomalacia (softening of bones)
Osteoporosis (brittle bones)
Osteosclerosis (hardening of bones)
186
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"
187
pathophysiology of CKD bone disease
high serum phosphate from reduced excretion and reduced vitamin D reduces calcium absorption and regulation of bone turnover
188
what thyroid complication arises in CKD
secondary hyperparathyroidism
189
CKD and secondary hyperparathyroidism pathology
glands react to low calcium and excrete more PTH resulting in increased osteoclast activity.
190
osteomalacia in CKD is because of
increased bone turnover
191
osteosclerosis in CKD arises from
osteoblasts trying to match osteoclasts but lack calcium so new bone is nor properly mineralised
192
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
193
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
194
options for dialysis include
Continuous Ambulatory Peritoneal Dialysis
Automated Peritoneal Dialysis
Haemodialysis
195
complications of peritoneal dialysis include
peritonitis, sclerosis, ultrafiltration failure, weight gain and pyschosocial.
196
a tunnelled cuffed catheter for haemodialysis may be inserted into
subclavian or jugular vein
197
A-V fistula complications are
```
Aneurysm
Infection
Thrombosis
Stenosis
STEAL syndrome
High output heart failure
```
198
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
199
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.
200
kidney transplant donor matching requires
HLA matches
201
what is the incision used to a kidney transplant?
hockey stick incision
202
what immunosupressants are used in a post renal transplant
Tacrolimus
Mycophenolate
Prednisolone
203
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
204
nephrotic syndrome refers too
Peripheral oedema
Proteinuria more than 3g / 24 hours
Serum albumin less than 25g / L
Hypercholesterolaemia
205
glomerulonephritis refers too
an umbrella term applied to conditions that cause inflammation of or around the glomerulus
206
interstitial nephritis refers too
nflammation of the space between cells and tubules (the interstitium) within the kidney
207
glomerulosclerosis is referred to as
pathological process of scarring of the tissue in the glomerulus.
208
glomerulosclerosis can be caused by
glomerulonephritis or obstructive uropathy (blockage of urine outflow), and by a disease called focal segmental glomerulosclerosis.
209
glomerulonephritis Tx is
Immunosuppression (e.g. steroids)
| Blood pressure control by blocking renin-angiotensin system (i.e. ACEi or ARBs)
210
nephrotic syndrome common cause in kids is
minimal change disease
211
nephrotic syndrome common cause in adults is
focal segmental glomerulosclerosis
212
common cause of primary glomerulonephritis is
IgA nephropathy
213
IgA nephropathy histology
gA deposits and glomerular mesangial proliferation”
214
commonest overall glomerulonephritis is
membranous glomerulonephritis
215
histology of membranous glomerulonephritis is
IgG and complement deposits on the basement membrane
216
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
217
good pasture syndrome pathology
Anti-GBM (glomerular basement membrane) antibodies attack glomerulus and pulmonary basement membranes.
218
good pasture syndrome causes
This causes glomerulonephritis and pulmonary haemorrhage
219
rapidly progressive glomerulonephritis histology shows
crescentic glomerulonephritis
220
what is the commonest cause of glomerular pathology and CKD in the UK?
diabetic nephropathy
221
key feature of diabetic nephropathy is
proteinuria
222
what are the two types of interstitial nephritis?
acute interstitial nephritis and chronic tubulointerstitial nephritis.
223
Acute interstitial nephritis presents with
acute kidney injury and hypertension. As well as rash, fever and eosinophilia.
224
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
225
acute tubular necrosis refers too
death of the epithelial cells in the renal tubals
226
commonest cause of an AKI is
acute tubal necrosis
227
urinalysis of acute tubular necrosis will show
Muddy brown casts
228
Mx of acute tubular necrosis
Supportive management
IV fluids
Stop nephrotoxic medications
Treat complications
229
type 1 renal tubular acidosis pathology
pathology in the distal tubule as it is unable to excrete hydrogen ions
230
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
```
231
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)
232
results of type 1 renal tubular acidosis
Hypokalaemia
Metabolic acidosis
High urinary pH (above 6)
233
Tx of type 1 renal tubular acidosis
bicarbonate
234
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
235
commonest cause of renal tubular acidosis?
type 4 - > reduced aldosterone
236
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.
237
results of type 4 renal tubular acidosis
Hyperkalaemia
High chloride
Metabolic acidosis
Low urinary pH
238
management of type 4 renal tubular acidosis
Management is with fludrocortisone. Sodium bicarbonate and treatment of the hyperkalaemia may also be required.
239
HUS classic triad
Haemolytic anaemia
Acute kidney injury
Low platelet count (thrombocytopenia)
240
presentation of HUS
```
Reduced urine output
Haematuria or dark brown urine
Abdominal pain
Lethargy and irritability
Confusion
Hypertension
Bruising
```
241
Tx of HUS
Antihypertensives
Blood transfusions
Dialysis
242
cell death in rhabdomyolysis releases
Myoglobin (causing myoglobinurea)
Potassium
Phosphate
Creatine Kinase
243
what cell content is particularly harmful to the kidney during rhabdomyolysis
myoglobin
244
causes of rhabdomyolysis
prolonged immobility, extremely rigorous exercise, crush injuries and seizures
245
symptoms of rhabdomyolysis
```
Muscle aches and pain
Oedema
Fatigue
Confusion (particularly in elderly frail patients)
Red-brown urine
```
246
Ix for rhabdomyolysis
creatine kinase, urine dipstick (blood positive due to myoglobin), U+E's and ECG
247
Tx for rhabdomyolysis
IV fluids, IV sodium carbonate, IV mannitol and hyperkalaemia Tx
248
conditions that can cause a raised potassium level
```
Acute kidney injury
Chronic kidney disease
Rhabdomyolysis
Adrenal insufficiency
Tumour lysis syndrome
```
249
medications that can cause a raised potassium level
```
Aldosterone antagonists (spironolactone and eplerenone)
ACE inhibitors
Angiotensin II receptor blockers
NSAIDS
Potassium supplements
```
250
ECG changes with hyperkalaemia
Tall peaked T waves
Flattening or absence of P waves
Broad QRS complexes
251
treatment for lowering potassium is
insulin and dextrose infusion and IV calcium gluconate:
252
alternative treatments for lowering potassium are
nebulised salbutamol, IV fluids, oral calcium resonium and sodium bicarbonate and dialysis
253
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
254
what drug can slow the development of cysts in autosomal dominant polycystic kidney disease
Tolvaptan (a vasopressin receptor antagonist)
255
anterior pituitary releases
```
Thyroid Stimulating Hormone (TSH)
Adrenocorticotropic Hormone (ACTH)
Follicle Stimulating Hormone (FSH) and Luteinising Hormone (LH)
Growth Hormone (GH)
Prolactin
```
256
posterior pituitary releases
```
Oxytocin
Antidiuretic Hormone (ADH)
```
257
cortisol release pattern.
diurnal variation
258
cortisol function
```
Inhibits the immune system
Inhibits bone formation
Raises blood glucose
Increases metabolism
Increases alertness
```
259
growth hormone function
Stimulates muscle growth
Increases bone density and strength
Stimulates cell regeneration and reproduction
Stimulates growth of internal organs
260
GH stimulates the release of
insulin like growth factor 1 from the liver
261
PTH is released in response to
low serum calcium, low magnesium and high serum phosphate
262
PTH role
stimulates activity and number of osteoclasts, calcium reabsorption in the kidney and conversation of D3-> calcitriol
263
Renin is secreted by the
juxtaglomerular cells
264
juxtaglomerular cells secrete renin in response too
low blood pressure
265
renin's role
converts angiotensin into angiotensin 1
266
angiotensin 1 becomes
angiotensin 2 in the lungs via angiotensin converting enzyme ACE
267
angiotensin 2 role
vasoconstriction and the secretion of aldosterone
268
aldosterone is what type of hormone?
mineralocorticoid
269
aldosterone role for sodium
Increase sodium reabsorption from the distal tubule
270
aldosterone role for potassium
Increase potassium secretion from the distal tubule
271
aldosterone role for hydrogen
Increase hydrogen secretion from the collecting ducts
272
aldosterone effect on intravascular volume
increase via sodium
273
cushing syndrome refers too
abnormal elevation of cortisol
274
cushing disease refers too
pituitary adenoma secreting excessive ACTH
275
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
```
276
presentation of cushing's due to high level or stress hormone
```
Hypertension
Cardiac hypertrophy
Hyperglycaemia (Type 2 Diabetes)
Depression
Insomnia
```
277
extra effects of cushing's syndrome
Osteoporosis
| Easy bruising and poor skin healing
278
causes of cushing's syndrome
adrenal ademona, cushing's disease, exogenous, paraneoplastic
279
common cause of paraneoplastic cushing's syndrome
“ectopic ACTH”. Small Cell Lung Cancer
280
diagnostic test of choice for cushing's is
dexamethasone suppression test
281
how to perform a dex suppression test?
dose of dex. at night then cortisol and ACTH measured in the morning
282
low dose dexamethasone suppression test
1mg normal response is to be reduced cortisol and ACTH abnormal means cushing's syndrome
283
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.
284
low dose dex test normal/high cortisol then
cushing's syndrome
285
high dose dex test low cortisol then
cushing's disease
286
high dose dex test low ACTH high/normal cortisol then
adrenal cushings
287
high dose dex test high cortisol high ACTH
ectopic ACTH
288
other Ix for cushings are
24 hour urinary free cortisol, FBC, U+E's, MRI brain, chest CT, abdo CT
289
TX for cushings
trans sphenoidal surgery, surgical removal.
290
primary adrenal insufficiency (Addison's disease) refers too
adrenal glands have been damaged, usually autoimmune. reduced cortisol and aldosterone.
291
secondary adrenal insufficiency refers too
inadequate ACTH to stimulate adrenal glands.
292
tertiary adrenal insufficiency refers too
inadequate CRH from the hypothalamus
293
causes of tertiary adrenal insufficiency
long term oral steroids (>3 weeks)
294
symptoms of adrenal insufficiency
```
Fatigue
Nausea
Cramps
Abdominal pain
Reduced libido
```
295
signs of adrenal insufficiency
Bronze hyperpigmentation to skin (ACTH stimulates melanocytes to produce melanin)
Hypotension (particularly postural hypotension)
296
Ix for adrenal insufficiency
sodium lo, high potassium, early morning cortisol, short synacthen test, adrenal autoantibodies, CT/MRI or MRI pituitary
297
test of choice for adrenal insufficiency is
short synacthen test
298
adrenal autoantibodies are
adrenal cortex antibodies and 21-hydroxylase antibodies
299
short synacthen test method
cortisol measured at baseline, 30 and then 60 minutes after. should normally double baseline.
300
Tx of adrenal insufficiency
hydrocortisone (glucocorticoid) and fludrocortisone (mineralcorticoid)
301
patients with adrenal insufficiency are also given
steroid card and emergency ID
302
adrenal crisis presentation
Reduced consciousness
Hypotension
Hypoglycaemia, hyponatraemia, hyperkaemia
Patients can be very unwell
303
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
304
secondary hypothyroidism levels
low TSH low T3 and T4
305
antibodies against the thyroid gland itself are
Antithyroid Peroxidase (anti-TPO) Antibodies
306
Antithyroid Peroxidase (anti-TPO) Antibodies are usually present in
Grave’s Disease and Hashimoto’s Thyroiditis
307
antithyroglobulin antibodies are usually present in
Grave’s Disease, Hashimoto’s Thyroiditis and thyroid cancer.
308
TSH Receptor Antibodies are usually cause
Grave’s Disease
309
radioisotope scan with iodine in Grave's disease will show
Diffuse high uptake
310
radioisotope scan with iodine in toxic multinodular goitre and adenomas will show
focal high uptake
311
radioisotope scan with iodine will show cold areas
thyroid cancer
312
commonest cause of hyperthyroidism is
Grave's disease
313
toxic multinodular goitre causes
hyperthyroidism
314
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.
315
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.
316
features of hyperthyroidism
```
Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss
Fatigue
Frequent loose stools
Sexual dysfunction
```
317
features specific to grave's disease
Diffuse Goitre (without nodules)
Graves Eye Disease
Bilateral Exopthalmos
Pretibial Myxoedema
318
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)
319
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
320
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.
321
thyroid storm presentation
severe presentation of hyperthyroidism with pyrexia, tachycardia and delirium
322
first line for hyperthyroidism
carbimazole
323
two therapies for carbimazole treatment of hyperthyroidism
titration-block or block and replace
324
second line drug for hyperthyroidism
Propylthiouracil
325
other treatments for hyperthyroidism include
radioactive iodine, beta blockers, and surgery.
326
common cause of hypothyroidism in the developed world is
hashimoto's thyroiditis
327
common cause of hypothyroidism in the developing world is
iodine deficiency
328
secondary causes of hypothyroidism
```
Carbimazole
Prophylthiouracil
Radioactive iodine
Thyroid surgery
lithium and amiodarone
```
329
presentation of hypothyroidism
```
Weight gain
Fatigue
Dry skin
Coarse hair and hair loss
Fluid retention (oedema, pleural effusions, ascites)
Heavy or irregular periods
Constipation
```
330
Tx of hypothyroidism
levothyroxine which is synthetic T4 that metabolises into T3
331
ideal blood glucose level
between 4.4. and 6.1 mmol/l.
332
insulin is produced by
beta cells in the islets of langerhans in the pancreas
333
glucagon is produced by
alpha cells in the islets of langerhans in the pancreas
334
glucagon role
glycogenolysis and gluconeogenesis
335
glycogenolysis refers too
the liver to break down stored glycogen into glucose
336
gluconeogenesis refers too
liver to convert proteins and fats into glucose.
337
triad of DKA
dehydration, potassium imbalance, ketoacidosis
338
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.
339
excessive thirst is called
polydipsia
340
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.
341
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)
```
342
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)
343
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
344
long term complications of hyperglycaemia
macrovascular, microvascular and infection
345
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
346
microvascular complications of hyperglycaemia
Peripheral neuropathy
Retinopathy
Kidney disease, particularly glomerulosclerosis
347
monitoring of glucose can be conducted via
HBA1c, capillary blood glucose, flash glucose monitoring
348
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)
```
349
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.
350
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
351
diabetes Dx
HbA1c > 48 mmol/mol
Random Glucose > 11 mmol/l
Fasting Glucose > 7 mmol/l
OGTT 2 hour result > 11 mmol/l
352
HBA1c target for new type 2 diabetics
48 mmol/mol for new type 2 diabetics
353
first line for type 2 diabetes
metformin titrated from initially 500mg once daily as tolerated.
354
second therapy for t2dm
sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor.
355
T2dm + CV consider
SGLT-2 inhibitors and GLP-1 inhibitors
356
metformin mechanism
biguanide”. It increases insulin sensitivity and decreases liver production of glucose. It is considered to be “weight neutral”
357
metformin SE
Diarrhoea and abdominal pain. This is dose dependent and reducing the dose often resolves the symptoms
Lactic acidosis
358
pioglitazone mechanism
“thiazolidinedione”. It increases insulin sensitivity and decreases liver production of glucose.
359
pioglitazone SE
```
Weight gain
Fluid retention
Anaemia
Heart failure
Extended use may increase the risk of bladder cancer
```
360
sulfonylurea mechanism
The most common sulfonyluria is “gliclazide”. Sulfonylureas stimulate insulin release from the pancreas.
361
sulfonylurea SE
Weight gain
Hypoglycaemia
Increased risk of cardiovascular disease and myocardial infarction when used as monotherapy
362
incretins are
hormones produced by the GI tract. They are secreted in response to large meals and act to reduce blood sugar.
363
incretins role
Increase insulin secretions
Inhibit glucagon production
Slow absorption by the GI tract
364
main incretin is
glucagon-like peptide-1” (GLP-1).
365
incretins are inhibited by
dipeptidyl peptidase-4” (DPP-4).
366
GLP-1 mimetic example
exenatide
367
SE of GLP-1 mimetic
GI tract upset
Weight loss
Dizziness
Low risk of hypoglycaemia
368
SGLT-2 inhibitor examples
-gliflozin”, such as empagliflozin, canagliflozin and dapagliflozin.
369
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.
370
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
371
rapid acting insulin examples
Novorapid
Humalog
Apidra
372
short acting insulin examples
Actrapid
Humulin S
Insuman Rapid
373
intermediate acting insulin examples
Insulatard
Humulin I
Insuman Basal
374
long acting insulin examples
Lantus
Levemir
Degludec (lasts over 40 hours)
375
combination insulins
```
Humalog 25 (25:75)
Humalog 50 (50:50)
Novomix 30 (30:70)
```
376
commonest cause of acromegaly is
pituitary adenoma
377
visual problem associated with acromegaly is
bitemporal hemianopia (loss of vision of outer half)
378
space occupying lesion symptoms of acromegaly
Headaches
| Visual field defect (“bitemporal hemianopia”)
379
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
380
GH organ dysfunction
Hypertrophic heart
Hypertension
Type 2 diabetes
Colorectal cancer
381
other symptoms that may suggest acromegaly
Development of new skin tags
| Profuse sweating
382
Ix for acromegaly
IGF-1 screening, OGTT, MRI, ophthalmology referral
383
surgical Tx for acromegaly
trans sphenoidal resection
384
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)
385
what cells specifically produce PTH
chief cells
386
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
387
primary hyperparathyroidism is
excess PTH from tumour leading to hypercalcaemia
388
secondary hyperparathyroidism is caused by
lack of vit D or CKD leads to low calcium. the glands react by producing PTH and undergo hyperplasia.
389
tertiary hyperparathyroidism is caused by
chronic secondary hyperparathyroidism leading to hypercalcaemia even post treatment of underlying cause
390
high PTH and high calcium may be
primary or tertiary
391
high PTH low/normal calcium may be
secondary
392
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.
393
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)
```
394
secondary hyperaldosteronism is caused by
excessive renin stimulating the adrenal glands to produce more aldosterone. Serum renin will be high.
395
causes of secondary hyperaldosteronism include
Renal artery stenosis
Renal artery obstruction
Heart failure
396
Renal artery stenosis maybe confirmed by
doppler ultrasound, CT angiogram or magnetic resonance angiography (MRA).
397
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
```
398
High aldosterone and low renin indicates
primary hyperaldosteronism
399
High aldosterone and high renin indicates
secondary hyperaldosteronism
400
aldosterone antagonists include
Eplerenone
| Spironolactone
401
renal artery stenosis TX
Percutaneous renal artery angioplasty via the femoral artery to treat in renal artery stenosis
402
common cause of secondary hypertension is
hyperaldosteronism (pot. low K+)
403
ADH is produced by
hypothalamus and secreted by the posterior pituitary gland. It is also known as “vasopressin”.
404
ADH role
DH stimulates water reabsorption from the collecting ducts in the kidneys.
405
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.
406
SIAD commonly causes
euvolaemic hyponatraemia”.
407
SIADH euvolaemic hyponatreamia is demonstrated by
“high urine osmolality” and “high urine sodium”.
408
symptoms of SIADH
```
Headache
Fatigue
Muscle aches and cramps
Confusion
Severe hyponatraemia can cause seizures and reduced consciousness
```
409
rapid correction of serum sodium may cause
central pontine myelinolysis.
410
Mx of SIADH
Fluid restriction
Tolvaptan. “Vaptans” are ADH receptor blockers.
Demeclocycline is a tetracycline antibiotic that inhibits ADH.
411
first stage of central pontine myelinolysis
encephalopathic and confused. They may have a headache or nausea and vomiting.
412
second stage of central pontine myelinolysis
occurs few days post correction. This may present as spastic quadriparesis, pseudobulbar palsy and cognitive and behavioural changes
413
Diabetes insipidus is a lack of
antidiuretic hormone (ADH) or a lack of response to ADH.
414
Nephrogenic diabetes insipidus is when
the collecting ducts of the kidneys do not respond to ADH.
415
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)
416
Cranial diabetes insipidus is when the
hypothalamus does not produce ADH
417
cranial diabetes insipidus can be caused by
```
Brain tumours
Head injury
Brain malformations
Brain infections (meningitis, encephalitis and tuberculosis)
Brain surgery or radiotherapy
```
418
presentation of cranial diabetes insipidus
```
Polyuria (excessive urine production)
Polydipsia (excessive thirst)
Dehydration
Postural hypotension
Hypernatraemia
```
419
Ix for cranial diabetes insipidus
Low urine osmolality
High serum osmolality
Water deprivation test
420
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.
421
after deprivation low urine osmolality and after ADH high points to
Cranial Diabetes Insipidus
422
after deprivation high urine osmolality and after ADH high points to
Primary Polydipsia
423
after deprivation low urine osmolality low and after ADH urine osmolality low
nephrogenic diabetes insipidus
424
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
425
adrenal is produced by what cells
chromaffin cells
426
phaeochromocytoma is a tumour of the
chromaffin cells
427
adrenaline is an example of
catecholamine” hormone
428
what is the genetic association with phaeochromocytoma
25% are familial and associated with multiple endocrine neoplasia type 2 (MEN 2).
429
what is the pattern of a phaeochromocytoma
10% bilateral
10% cancerous
10% outside the adrenal gland
430
Dx of a phaeochromocytoma is with
24 hour urine catecholamines
| Plasma free metanephrines
431
presentation of a phaeochromocytoma is
```
Anxiety
Sweating
Headache
Hypertension
Palpitations, tachycardia and paroxysmal atrial fibrillation
```
432
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
```
