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fourth year > medicine > Flashcards

medicine Flashcards

1
Q

batteries on a pacemaker usually last around

A

five years

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2
Q

pacemakers may be CI for

A

TENS machines and diathermy and MRI

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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)

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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

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5
Q

one an ECG A sharp vertical line before the P and QRS indicates

A

dual-chamber pacemaker

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6
Q

the two shockable cardiac arrest rhythm are

A

Ventricular tachycardia

Ventricular fibrillation

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7
Q

the two non-shockable cardiac arrest rhythms are

A

Pulseless electrical activity

Asystole

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8
Q

Tachycardia unstable patient consider

A

Consider up to 3 synchronised shocks

Consider an amiodarone infusion

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9
Q

narrow complex tachycardias are

A

atrial fibrillation, atrial flutter and supraventricular tachycardias

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10
Q

in a stable patient with atrial fibrillation consider Tx

A

rate control with a beta blocker or diltiazem (calcium channel blocker)

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11
Q

in a stable patient with atrial flutter Tx

A

control rate with a beta blocker

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12
Q

supraventricular tachycardia in a stable patient Tx

A

treat with vagal manoeuvres and adenosine

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13
Q

broad complex tachycardias

A

ventricular tachycardia or SVT with bundle branch block

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14
Q

Ventricular tachycardia broad complex Tx in stable patient

A

amiodarone infusion

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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.

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16
Q

atrial flutter ECG appearance

A

“sawtooth appearance”

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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

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18
Q

what conditions are associated with atrial flutter

A

Hypertension
Ischaemic heart disease
Cardiomyopathy
Thyrotoxicosis

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19
Q

Supraventricular tachycardia (SVT) pathology

A

electrical signal re-entering the atria from the ventricles.

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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.

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21
Q

SVT management options

A

valsalva, carotid sinus massage, adenosine or direct current cardioversion.

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22
Q

adenosine mechanism

A

slowing cardiac conduction primarily though the AV node.

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23
Q

adenosine bolus is associated with

A

brief period of asystole or bradycardia

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24
Q

adenosine CI

A

Avoid if patient has asthma / COPD / heart failure / heart block / severe hypotension

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25
Q

adenosine dosing

A

6mg, then 12mg and further 12mg if no improvement between doses

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26
Q

long term management of SVT may include

A

Medication (beta blockers, calcium channel blockers or amiodarone)
Radiofrequency ablation

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27
Q

Wolff-Parkinson White Syndrome is often called the

A

Bundle of Kent.

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28
Q

definitive treatment of wolf parkinson syndrome is

A

radiofrequency ablation of the accessory pathway.

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29
Q

ECG changes for wolf parkinson white syndrome.

A

Short PR interval (< 0.12 seconds)
Wide QRS complex (> 0.12 seconds)
“Delta wave” which is a slurred upstroke on the QRS complex

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30
Q

AF and WPW may cause

A

polymorphic wide complex tachycardia

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31
Q

polymorphic wide complex tachycardia may be triggered by

A

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

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32
Q

what medications are CI in WPW

A

Most antiarrhythmic medications

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33
Q

radiofrequency ablation is curative for what arrhythmias

A

Atrial Fibrillation
Atrial Flutter
Supraventricular Tachycardias
Wolff-Parkinson-White Syndrome

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34
Q

a prolonged QT interval represents a prolonged

A

repolarisation

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35
Q

depolarisation of the myocardium is what leads to

A

contraction

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36
Q

prolonged QT’s may result in

A

spontaneous depolarisation as they away repolarisation.

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37
Q

recurrent contractions without normal repolarisation of the mycocardium is called

A

torsades de pointes

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38
Q

torsades de pointes is a type of

A

polymorphic (multiple shape) ventricular tachycardia. It translates from French as “twisting of the tips”,

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39
Q

causes of a prolonged GT includes

A

Long QT Syndrome (inherited)
Medications (antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide antibiotics)
Electrolyte Disturbance (hypokalaemia, hypomagnesaemia, hypocalcaemia)

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40
Q

acute management of torsades de pointe is

A

Correct the cause (electrolyte disturbances or medications)
Magnesium infusion (even if they have a normal serum magnesium)
Defibrillation if VT occurs

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41
Q

long term management of torsades de pointes is

A 
Avoid medications that prolong the QT interval
Correct electrolyte disturbances
Beta blockers (not sotalol)
Pacemaker or implantable defibrillator
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42
Q

management of ectopic beats include

A

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

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43
Q

types of AV node blocks

A 
First degree heart block
Second Degree Heart Block
(Mobitz Type 1)
Mobitz Type 2
2:1 block
third degree heart block
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44
Q

First degree heart block pathology

A

there is delayed atrioventricular conduction through the AV node.

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45
Q

first degree heart block ECG appearance

A

On an ECG this presents as a PR interval greater than 0.20 seconds (5 small or 1 big square).

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46
Q

second degree heart block pathology

A

Second degree heart block is where some of the atrial impulses do not make it through the AV node to the ventricles.

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47
Q

second degree heart block appearance

A

This means that there are instances where p waves do not lead to QRS complexes.

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48
Q

(Mobitz Type 1) ECG appearance

A

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.

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49
Q

mobitz type 2 ECG appearance

A

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.

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50
Q

what complication may arise from mobitz type 2

A

asystole

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51
Q

2:1 block ECG appearance

A

2 P waves for each QRS complex

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52
Q

third degree heart block ECG appearance

A

This is referred to as complete heart block. This is no observable relationship between P waves and QRS complexes.

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53
Q

risk of what with third degree heart block

A

significant risk of asystole

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54
Q

unstable bradycardia/AV node block (risk of asystole) first line treatment

A

Atropine 500mcg IV

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55
Q

second line unstable bradycardia/AV node block (risk of asystole)

A 
Atropine 500mcg IV repeated (up to 6 doses for a total to 3mg)
Other inotropes (such as noradrenalin)
Transcutaneous cardiac pacing (using a defibrillator)
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56
Q

high risk asystole patients consider

A

Temporary transvenous cardiac pacing or permanent implantable pacemaker

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57
Q

atropine mechanism

A

antimuscarinic medication and works by inhibiting the parasympathetic nervous system.

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58
Q

atropine SE

A

pupil dilatation, urinary retention, dry eyes and constipation.

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59
Q

Atrial fibrillation may result in

A

Irregularly irregular ventricular contractions
Tachycardia
Heart failure due to poor filling of the ventricles during diastole
Risk of stroke(emboli)

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60
Q

presenting symptoms of Atrial fibrillation are

A

Palpitations
Shortness of breath
Syncope (dizziness or fainting)
Symptoms of associated conditions (e.g. stroke, sepsis or thyrotoxicosis)

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61
Q

two differentials for irregularly irregular pulse are

A

Atrial fibrillation

Ventricular ectopics

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62
Q

ventricular ectopic disappear often

A

when HR gets over a certain threshold,

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63
Q

atrial fibrillation signs

A

Absent P waves
Narrow QRS Complex Tachycardia
Irregularly irregular ventricular rhythm

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64
Q

valvular atrial fibrillation may be caused by

A

severe mitral stenosis or a mechanical heart valve

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65
Q

common causes of atrial fibrillation includes

A 
Sepsis
Mitral Valve Pathology (stenosis or regurgitation)
Ischemic Heart Disease
Thyrotoxicosis
Hypertension
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66
Q

goal of rate control with atrial fibrillation

A

The aim is to get the heart rate below 100 to extend the time during diastole when the ventricles can fill with blood.

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67
Q

first line option for rate control in atrial fibrillation

A

Beta blocker is first line (e.g. atenolol 50-100mg once daily)

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68
Q

other options for rate control in atrial fibrillation

A

Calcium-channel blocker (e.g. diltiazem) (not preferable in heart failure)
Digoxin (only in sedentary people, needs monitoring and risk of toxicity)

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69
Q

rhythm control for atrial fibrillation is offered for patients where

A

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

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70
Q

immediate cardioversion for atrial fibrillation if

A

the AF has been present for less than 48 hours or they are severely haemodynamically unstable.

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71
Q

delayed cardioversion for atrial fibrillation if

A

AF has been present for more than 48 hours and they are stable.

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72
Q

delayed cardioversion requires

A

anticoagulation.

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73
Q

pharmacological cardioversion first line is

A

Flecanide

Amiodarone

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74
Q

long term medical rhythm control options are

A

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

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75
Q

Paroxysmal atrial fibrillation Tx

A

Pill in pocket approach -> flecanide.

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76
Q

warfarin prolongs

A

prothrombin time

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77
Q

with anticoagulation atrial fibrillation risk of ischaemic stroke is reduced by

A

two thirds

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78
Q

warfarin is effected by what liver enzyme

A

cytochrome P450

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79
Q

target INR for atrial fibrillation is

A

2-3

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80
Q

what CHA2DS2-VASc score would be indicative for anticoagulation

A

> 1

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81
Q

CHA2DS2-VASc mnemonic

A 
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)
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82
Q

HAS-BLED mnemonic for risk of haemorrhage on anticoagulation

A 
H – Hypertension
A – Abnormal renal and liver function
S – Stroke
B – Bleeding
L – Labile INRs (whilst on warfarin)
E – Elderly
D – Drugs or alcohol
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83
Q

common mechanical valve used is the

A

St Jude valve.

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84
Q

bioprosthetic valve lifespan is

A

1o years

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85
Q

mechanical valve lifespan

A

over twenty years but requires lifelong anticoagulation with warfarin

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86
Q

INR range for mechanical valve is

A

2.5-3.5

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87
Q

complications of a mechanical heart valve are

A

thrombus, infective endocarditis, and haemolysis

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88
Q

gram positive cocci responsible for infective endocarditis with heart valves

A

Staphylococcus
Streptococcus
Enterococcus

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89
Q

3rd heart sound is the result of

A

rapid ventricular filling (chordae tendineae twang)

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90
Q

> 40 a third heart sound may be a sign of

A

heart failure.

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91
Q

4th heart sound is caused by

A

an atria contracting against a non-compliant ventricle.

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92
Q

“Erb’s point” is

A

third intercostal space on the left sternal boarder and is the best area for listening to heart sounds (S1 and S2).

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93
Q

leaning a patient onto their left hand side helps to listen for

A

mitral stenosis

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94
Q

having a patient leaning forward and holding exhalation is for

A

aortic regurgitation.

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95
Q

mitral stenosis causes

A

Rheumatic Heart Disease

Infective Endocarditis

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96
Q

mitral stenosis murmur

A

mid-diastolic, low pitched “rumbling” murmur

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97
Q

mitral stenosis associations

A

malar flush, atrial fibrillation and tapping apex beat.

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98
Q

mitral regurgitation causes

A

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

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99
Q

mitral regurgitation murmur

A

pan-systolic, high pitched “whistling” murmur due to high velocity blood flow that radiated to left axilla

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100
Q

aortic stenosis causes

A

Idiopathic age related calcification

Rheumatic Heart Disease

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101
Q

aortic stenosis murmur

A

ejection-systolic, high pitched murmur (high velocity of systole). This has a crescendo-decrescendo character

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102
Q

aortic stenosis associations

A

carotid radiation, slow rising pulse, narrow pulse pressure, exertional syncope.

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103
Q

aortic regurgitation murmur

A

early diastolic, soft murmur.

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104
Q

aortic regurgitation associations

A

collapsing pulse, austin flint murmur

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105
Q

austin flint murmur is

A

heard at the apex and is an early diastolic “rumbling” murmur.

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106
Q

causes of aortic regurgitation

A

Idiopathic age related weakness

Connective tissue disorders such as Ehlers Danlos syndrome or Marfan syndrome

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107
Q

essential hypertension (idiopathic) accounts for what percentage of cases

A

95%

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108
Q

secondary causes of hypertension include

A

Renal disease
Obesity
Pregnancy
Endocrine (Conn’s syndrome, hyperaldosteronism)

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109
Q

stage 1 hypertension clinic and ambulatory

A

clinical: >140/90
ambulatory: >135/85

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110
Q

stage 2 hypertension clinic and ambulatory

A

clinical: >160/100
ambulatory: >150/95

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111
Q

stage 3 hypertension

A

> 180/120

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112
Q

new diagnosis of hypertension should receive what further Ix

A

Urine albumin:creatinine ratio for proteinuria and dipstick
Bloods for HbA1c, renal function and lipids
fundus examination
ECG

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113
Q

medications for hypertension

A

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)

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114
Q

step 1 for hypertension management (stage 2)

A

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)

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115
Q

step 2 hypertension management

A

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)

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116
Q

step 3 hypertension management

A

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)

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117
Q

Step 4 hypertension Mx additional options if potassium less or equal to 4.5mmol/l

A

potassium sparing diuretic such as spironolactone.

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118
Q

Step 4 hypertension Mx additional options if potassium more than 4.5mmol/l

A

alpha blocker (e.g. doxazosin) or a beta blocker (e.g. atenolol).

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119
Q

spironolactone mechanism

A

blocking the action of aldosterone in the kidneys, resulting in sodium excretion and potassium reabsorption.

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120
Q

thiazide effect on potassium

A

reduced

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121
Q

ACEI effect on potassium

A

hyperkalaemia

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122
Q

presentation of cor pulmonale

A

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

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123
Q

presentation of chronic heart failure

A

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)

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124
Q

diagnosis of chronic heart failure is with

A

Clinical presentation
BNP blood test (specifically “N-terminal pro-B-type natriuretic peptide” – NT‑proBNP)
Echocardiogram
ECG

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125
Q

causes of chronic heart failure include

A

Ischaemic Heart Disease
Valvular Heart Disease (commonly aortic stenosis)
Hypertension
Arrhythmias (commonly atrial fibrillation)

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126
Q

management for chronic heart failure

A

Yearly flu and pneumococcal vaccine
Stop smoking
Optimise treatment of co-morbidities
Exercise at tolerated

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127
Q

first line treatment for chronic heart failure

A 
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)

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128
Q

acute Left ventricular failure can cause

A

type 1 respiratory failure (low o2 normal CO2)

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129
Q

symptoms of LVF

A

Shortness of breath
Looking and feeling unwell
Cough (frothy white/pink sputum)

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130
Q

signs of LVF

A

Increase respiratory rate
Reduced oxygen saturations
Tachycardia
3rd Heart Sound
Bilateral basal crackles (sounding “wet”) on auscultation
Hypotension in severe cases (cardiogenic shock)

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131
Q

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?

A

IV furosemide

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132
Q

other causes aside from Chronic heart failure and LVF of a raised BNP include

A 
Tachycardia
Sepsis
Pulmonary embolism
Renal impairment
COPD
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133
Q

and ejection fraction above what percentage is considered normal?

A

50%

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134
Q

CXR findings of LVF

A

cardiomegaly, upper lobe venous diversion, bilateral pleural effusion, fluid in interlobar fissures and fluid in septal lines (Kerley lines)

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135
Q

management of LVF

A

POUR SOD

pour away fluid (STOP fluids)
Sit up
O2
Diuretics (IV furosemide 40mg stat)

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136
Q

right coronary artery supplies the

A

Right atrium
Right ventricle
Inferior aspect of left ventricle
Posterior septal area

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137
Q

circumflex artery supplies

A

Left atrium

Posterior aspect of left ventricle

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138
Q

left anterior descending artery supplies

A

Anterior aspect of left ventricle

Anterior aspect of septum

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139
Q

diagnosis of acute coronary syndrome

A

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

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140
Q

Left coronary artery ECG lead

A

I, aVL, V3-6

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141
Q

LAD ECG lead

A

V1-4

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142
Q

Circumflex ECG lead

A

I, aVL, V5-6

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143
Q

right coronary artery ECG lead

A

II, III, aVF

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144
Q

other than normal angina investigations for acute coronary syndrome you would also consider

A

CXR, ECHO, CT coronary angiogram

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145
Q

Acute STEMI presenting within 12 hours, within 2 hours you would

A

Primary PCI

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146
Q

Acute STEMI presenting within 12 hours but after 2 hours you would

A

thrombolysis

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147
Q

acute NSTEMI treatment

A

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

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148
Q

complications of MI

A

D – Death

R – Rupture of the heart septum or papillary muscles

E – “Edema” (Heart Failure)

A – Arrhythmia and Aneurysm

D – Dressler’s Syndrome

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149
Q

dressler’s syndrome usually occurs how long after an MI?

A

2-3 weeks

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150
Q

patholgoy of dressler’s syndrome

A

localised immune response causing pericarditis

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151
Q

presentation of dressler’s syndrome

A

pleuritis chest pain, pericardial rub, ericardial effusion

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152
Q

ECG changes with dressler’s is

A

ECG (global ST elevation and T wave inversion),

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153
Q

Dressler’s Dx

A

ECG, echocardiogram (pericardial effusion) and raised inflammatory markers (CRP and ESR).

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154
Q

Mx of dressler’s is with

A

NSAIDs (aspirin / ibuprofen) and in more severe cases steroids (prednisolone). They may need pericardiocentesis

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155
Q

secondary prevention following from acute coronary syndrome

A

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)

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156
Q

gold standard Ix for angina is

A

CT angiography

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157
Q

Ix for angina are

A 
Physical Examination (heart sounds, signs of heart failure, BMI)
ECG
FBC (check for anaemia)
U&amp;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)
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158
Q

immediate relief for angina is

A

GTN spray

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159
Q

long term symptom relief

A 
Beta blocker (e.g. bisoprolol 5mg once daily) or;
Calcium channel blocker (e.g. amlodipine 5mg once daily)
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160
Q

surgical intervention of angina includes

A

percutaneous coronary intervention or coronary artery bypass graft.

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161
Q

risk factors modifiable for atherosclerosis

A 
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
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162
Q

non-modifiable risk factors for atherosclerosis

A

Older age
Family history
Male

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163
Q

score system for atherosclerosis for primary prevention

A

Qrisk3 score

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164
Q

Qrisk 3 score is

A

the percentage risk that a patient will have a stroke or myocardial infarction in the next 10 years.

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165
Q

Qrisk 3 score >10% then

A

atorvastatin 20mg at night).

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166
Q

all patients with CKD or type 1 diabetes for more than 10 years should receive

A

atorvastatin 20mg.

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167
Q

SE of statins

A

Myopathy (check creatine kinase in patients with muscle pain or weakness)
Type 2 Diabetes
Haemorrhagic Strokes (very rarely)

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168
Q

NICE criteria for an AKI

A

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

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169
Q

risk factors for a AKI

A 
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
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170
Q

three broad causes of an AKI

A

pre renal, intrinsic or post renal

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171
Q

pre-renal causes of an AKI

A

Dehydration
Hypotension (shock)
Heart failure

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172
Q

renal causes of an AKI

A

Glomerulonephritis
Interstitial nephritis
Acute tubular necrosis

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173
Q

post renal causes of an AKI

A

Kidney stones
Masses such as cancer in the abdomen or pelvis
Ureter or uretral strictures
Enlarged prostate or prostate cancer

174
Q

Ix for AKI

A

urinanalysis, US

175
Q

urinalysis details for an AKI cause

A

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
Q

Mx of an AKI

A

fluids, stop nephrotoxic meds and relieve obstruction.

177
Q

complications of an AKI

A

Hyperkalaemia
Fluid overload, heart failure and pulmonary oedema
Metabolic acidosis
Uraemia (high urea) can lead to encephalopathy or pericarditis

178
Q

presentation of CKD

A 
asymptomatic 
Pruritus (itching)
Loss of appetite
Nausea
Oedema
Muscle cramps
Peripheral neuropathy
Pallor
Hypertension
179
Q

Ix for CKD

A

eGFR
urine albumin:creatinine ratio
haematuria (Dipstick)
renal US

180
Q

significant urine albumin:creatinine ratio result is

A

> 3mg/mmol

181
Q

CKD diagnosis requires at least

A

eGFR of < 60 or proteinuria

182
Q

complications of CKD

A 
Anaemia
Renal bone disease
Cardiovascular disease
Peripheral neuropathy
Dialysis related problems
183
Q

Tx of complications involve

A

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
Q

first line for CKD hypertension is

A

ACEI

185
Q

features of CKD bone disease are

A

Osteomalacia (softening of bones)
Osteoporosis (brittle bones)
Osteosclerosis (hardening of bones)

186
Q

X-ray changes of CKD bone disease are

A

sclerosis of the ends of the vertebrae, osteomalacia in the centre of the vertebrae known as “rugger jersey sign”

187
Q

pathophysiology of CKD bone disease

A

high serum phosphate from reduced excretion and reduced vitamin D reduces calcium absorption and regulation of bone turnover

188
Q

what thyroid complication arises in CKD

A

secondary hyperparathyroidism

189
Q

CKD and secondary hyperparathyroidism pathology

A

glands react to low calcium and excrete more PTH resulting in increased osteoclast activity.

190
Q

osteomalacia in CKD is because of

A

increased bone turnover

191
Q

osteosclerosis in CKD arises from

A

osteoblasts trying to match osteoclasts but lack calcium so new bone is nor properly mineralised

192
Q

management of CKD bone disease is with

A

Active forms of vitamin D (alfacalcidol and calcitriol)
Low phosphate diet
Bisphosphonates can be used to treat osteoporosis

193
Q

indications for acute dialysis

A

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
Q

options for dialysis include

A

Continuous Ambulatory Peritoneal Dialysis
Automated Peritoneal Dialysis
Haemodialysis

195
Q

complications of peritoneal dialysis include

A

peritonitis, sclerosis, ultrafiltration failure, weight gain and pyschosocial.

196
Q

a tunnelled cuffed catheter for haemodialysis may be inserted into

A

subclavian or jugular vein

197
Q

A-V fistula complications are

A 
Aneurysm
Infection
Thrombosis
Stenosis
STEAL syndrome
High output heart failure
198
Q

STEAL syndrome refers too

A

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
Q

high output heart failure in AV fistula refers too

A

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
Q

kidney transplant donor matching requires

A

HLA matches

201
Q

what is the incision used to a kidney transplant?

A

hockey stick incision

202
Q

what immunosupressants are used in a post renal transplant

A

Tacrolimus
Mycophenolate
Prednisolone

203
Q

nephritic syndrome refers too

A

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
Q

nephrotic syndrome refers too

A

Peripheral oedema
Proteinuria more than 3g / 24 hours
Serum albumin less than 25g / L
Hypercholesterolaemia

205
Q

glomerulonephritis refers too

A

an umbrella term applied to conditions that cause inflammation of or around the glomerulus

206
Q

interstitial nephritis refers too

A

nflammation of the space between cells and tubules (the interstitium) within the kidney

207
Q

glomerulosclerosis is referred to as

A

pathological process of scarring of the tissue in the glomerulus.

208
Q

glomerulosclerosis can be caused by

A

glomerulonephritis or obstructive uropathy (blockage of urine outflow), and by a disease called focal segmental glomerulosclerosis.

209
Q

glomerulonephritis Tx is

A

Immunosuppression (e.g. steroids)

Blood pressure control by blocking renin-angiotensin system (i.e. ACEi or ARBs)

210
Q

nephrotic syndrome common cause in kids is

A

minimal change disease

211
Q

nephrotic syndrome common cause in adults is

A

focal segmental glomerulosclerosis

212
Q

common cause of primary glomerulonephritis is

A

IgA nephropathy

213
Q

IgA nephropathy histology

A

gA deposits and glomerular mesangial proliferation”

214
Q

commonest overall glomerulonephritis is

A

membranous glomerulonephritis

215
Q

histology of membranous glomerulonephritis is

A

IgG and complement deposits on the basement membrane

216
Q

post streptococcal glomerulonephritis presentation

A

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
Q

good pasture syndrome pathology

A

Anti-GBM (glomerular basement membrane) antibodies attack glomerulus and pulmonary basement membranes.

218
Q

good pasture syndrome causes

A

This causes glomerulonephritis and pulmonary haemorrhage

219
Q

rapidly progressive glomerulonephritis histology shows

A

crescentic glomerulonephritis

220
Q

what is the commonest cause of glomerular pathology and CKD in the UK?

A

diabetic nephropathy

221
Q

key feature of diabetic nephropathy is

A

proteinuria

222
Q

what are the two types of interstitial nephritis?

A

acute interstitial nephritis and chronic tubulointerstitial nephritis.

223
Q

Acute interstitial nephritis presents with

A

acute kidney injury and hypertension. As well as rash, fever and eosinophilia.

224
Q

pathology of acute interstitial nephritis is

A

inflammation of the tubules and interstitium. This is usually caused by a hypersensitivity reaction to:

Drugs (e.g. NSAIDS or antibiotics)
Infection

225
Q

acute tubular necrosis refers too

A

death of the epithelial cells in the renal tubals

226
Q

commonest cause of an AKI is

A

acute tubal necrosis

227
Q

urinalysis of acute tubular necrosis will show

A

Muddy brown casts

228
Q

Mx of acute tubular necrosis

A

Supportive management
IV fluids
Stop nephrotoxic medications
Treat complications

229
Q

type 1 renal tubular acidosis pathology

A

pathology in the distal tubule as it is unable to excrete hydrogen ions

230
Q

causes of type 1 renal tubular acidosis

A 
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
Q

presentation of type 1 renal tubular acidosis

A

Failure to thrive in children
Hyperventilation to compensate for the metabolic acidosis
Chronic kidney disease
Bone disease (osteomalacia)

232
Q

results of type 1 renal tubular acidosis

A

Hypokalaemia
Metabolic acidosis
High urinary pH (above 6)

233
Q

Tx of type 1 renal tubular acidosis

A

bicarbonate

234
Q

type 2 renal tubular acidosis pathology

A

Type 2 renal tubular acidosis is due to pathology in the proximal tubule. The proximal tubule is unable to reabsorb bicarbonate

235
Q

commonest cause of renal tubular acidosis?

A

type 4 - > reduced aldosterone

236
Q

type 4 tubular acidosis aetiology

A

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
Q

results of type 4 renal tubular acidosis

A

Hyperkalaemia
High chloride
Metabolic acidosis
Low urinary pH

238
Q

management of type 4 renal tubular acidosis

A

Management is with fludrocortisone. Sodium bicarbonate and treatment of the hyperkalaemia may also be required.

239
Q

HUS classic triad

A

Haemolytic anaemia
Acute kidney injury
Low platelet count (thrombocytopenia)

240
Q

presentation of HUS

A 
Reduced urine output
Haematuria or dark brown urine
Abdominal pain
Lethargy and irritability
Confusion
Hypertension
Bruising
241
Q

Tx of HUS

A

Antihypertensives
Blood transfusions
Dialysis

242
Q

cell death in rhabdomyolysis releases

A

Myoglobin (causing myoglobinurea)
Potassium
Phosphate
Creatine Kinase

243
Q

what cell content is particularly harmful to the kidney during rhabdomyolysis

A

myoglobin

244
Q

causes of rhabdomyolysis

A

prolonged immobility, extremely rigorous exercise, crush injuries and seizures

245
Q

symptoms of rhabdomyolysis

A 
Muscle aches and pain
Oedema
Fatigue
Confusion (particularly in elderly frail patients)
Red-brown urine
246
Q

Ix for rhabdomyolysis

A

creatine kinase, urine dipstick (blood positive due to myoglobin), U+E’s and ECG

247
Q

Tx for rhabdomyolysis

A

IV fluids, IV sodium carbonate, IV mannitol and hyperkalaemia Tx

248
Q

conditions that can cause a raised potassium level

A 
Acute kidney injury
Chronic kidney disease
Rhabdomyolysis
Adrenal insufficiency
Tumour lysis syndrome
249
Q

medications that can cause a raised potassium level

A 
Aldosterone antagonists (spironolactone and eplerenone)
ACE inhibitors
Angiotensin II receptor blockers
NSAIDS
Potassium supplements
250
Q

ECG changes with hyperkalaemia

A

Tall peaked T waves
Flattening or absence of P waves
Broad QRS complexes

251
Q

treatment for lowering potassium is

A

insulin and dextrose infusion and IV calcium gluconate:

252
Q

alternative treatments for lowering potassium are

A

nebulised salbutamol, IV fluids, oral calcium resonium and sodium bicarbonate and dialysis

253
Q

complications of the autosomal dominant type polycystic kidney disease

A

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
Q

what drug can slow the development of cysts in autosomal dominant polycystic kidney disease

A

Tolvaptan (a vasopressin receptor antagonist)

255
Q

anterior pituitary releases

A 
Thyroid Stimulating Hormone (TSH)
Adrenocorticotropic Hormone (ACTH)
Follicle Stimulating Hormone (FSH) and Luteinising Hormone (LH)
Growth Hormone (GH)
Prolactin
256
Q

posterior pituitary releases

A 
Oxytocin
Antidiuretic Hormone (ADH)
257
Q

cortisol release pattern.

A

diurnal variation

258
Q

cortisol function

A 
Inhibits the immune system
Inhibits bone formation
Raises blood glucose
Increases metabolism
Increases alertness
259
Q

growth hormone function

A

Stimulates muscle growth
Increases bone density and strength
Stimulates cell regeneration and reproduction
Stimulates growth of internal organs

260
Q

GH stimulates the release of

A

insulin like growth factor 1 from the liver

261
Q

PTH is released in response to

A

low serum calcium, low magnesium and high serum phosphate

262
Q

PTH role

A

stimulates activity and number of osteoclasts, calcium reabsorption in the kidney and conversation of D3-> calcitriol

263
Q

Renin is secreted by the

A

juxtaglomerular cells

264
Q

juxtaglomerular cells secrete renin in response too

A

low blood pressure

265
Q

renin’s role

A

converts angiotensin into angiotensin 1

266
Q

angiotensin 1 becomes

A

angiotensin 2 in the lungs via angiotensin converting enzyme ACE

267
Q

angiotensin 2 role

A

vasoconstriction and the secretion of aldosterone

268
Q

aldosterone is what type of hormone?

A

mineralocorticoid

269
Q

aldosterone role for sodium

A

Increase sodium reabsorption from the distal tubule

270
Q

aldosterone role for potassium

A

Increase potassium secretion from the distal tubule

271
Q

aldosterone role for hydrogen

A

Increase hydrogen secretion from the collecting ducts

272
Q

aldosterone effect on intravascular volume

A

increase via sodium

273
Q

cushing syndrome refers too

A

abnormal elevation of cortisol

274
Q

cushing disease refers too

A

pituitary adenoma secreting excessive ACTH

275
Q

presentation of cushings: round in the middle with thin limbs

A 
Round “moon” face
Central Obesity
Abdominal striae
Buffalo Hump (fat pad on upper back)
Proximal limb muscle wasting
276
Q

presentation of cushing’s due to high level or stress hormone

A 
Hypertension
Cardiac hypertrophy
Hyperglycaemia (Type 2 Diabetes)
Depression
Insomnia
277
Q

extra effects of cushing’s syndrome

A

Osteoporosis

Easy bruising and poor skin healing

278
Q

causes of cushing’s syndrome

A

adrenal ademona, cushing’s disease, exogenous, paraneoplastic

279
Q

common cause of paraneoplastic cushing’s syndrome

A

“ectopic ACTH”. Small Cell Lung Cancer

280
Q

diagnostic test of choice for cushing’s is

A

dexamethasone suppression test

281
Q

how to perform a dex suppression test?

A

dose of dex. at night then cortisol and ACTH measured in the morning

282
Q

low dose dexamethasone suppression test

A

1mg normal response is to be reduced cortisol and ACTH abnormal means cushing’s syndrome

283
Q

high dexamethasone test

A

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
Q

low dose dex test normal/high cortisol then

A

cushing’s syndrome

285
Q

high dose dex test low cortisol then

A

cushing’s disease

286
Q

high dose dex test low ACTH high/normal cortisol then

A

adrenal cushings

287
Q

high dose dex test high cortisol high ACTH

A

ectopic ACTH

288
Q

other Ix for cushings are

A

24 hour urinary free cortisol, FBC, U+E’s, MRI brain, chest CT, abdo CT

289
Q

TX for cushings

A

trans sphenoidal surgery, surgical removal.

290
Q

primary adrenal insufficiency (Addison’s disease) refers too

A

adrenal glands have been damaged, usually autoimmune. reduced cortisol and aldosterone.

291
Q

secondary adrenal insufficiency refers too

A

inadequate ACTH to stimulate adrenal glands.

292
Q

tertiary adrenal insufficiency refers too

A

inadequate CRH from the hypothalamus

293
Q

causes of tertiary adrenal insufficiency

A

long term oral steroids (>3 weeks)

294
Q

symptoms of adrenal insufficiency

A 
Fatigue
Nausea
Cramps
Abdominal pain
Reduced libido
295
Q

signs of adrenal insufficiency

A

Bronze hyperpigmentation to skin (ACTH stimulates melanocytes to produce melanin)
Hypotension (particularly postural hypotension)

296
Q

Ix for adrenal insufficiency

A

sodium lo, high potassium, early morning cortisol, short synacthen test, adrenal autoantibodies, CT/MRI or MRI pituitary

297
Q

test of choice for adrenal insufficiency is

A

short synacthen test

298
Q

adrenal autoantibodies are

A

adrenal cortex antibodies and 21-hydroxylase antibodies

299
Q

short synacthen test method

A

cortisol measured at baseline, 30 and then 60 minutes after. should normally double baseline.

300
Q

Tx of adrenal insufficiency

A

hydrocortisone (glucocorticoid) and fludrocortisone (mineralcorticoid)

301
Q

patients with adrenal insufficiency are also given

A

steroid card and emergency ID

302
Q

adrenal crisis presentation

A

Reduced consciousness
Hypotension
Hypoglycaemia, hyponatraemia, hyperkaemia
Patients can be very unwell

303
Q

adrenal crisis managment

A

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
Q

secondary hypothyroidism levels

A

low TSH low T3 and T4

305
Q

antibodies against the thyroid gland itself are

A

Antithyroid Peroxidase (anti-TPO) Antibodies

306
Q

Antithyroid Peroxidase (anti-TPO) Antibodies are usually present in

A

Grave’s Disease and Hashimoto’s Thyroiditis

307
Q

antithyroglobulin antibodies are usually present in

A

Grave’s Disease, Hashimoto’s Thyroiditis and thyroid cancer.

308
Q

TSH Receptor Antibodies are usually cause

A

Grave’s Disease

309
Q

radioisotope scan with iodine in Grave’s disease will show

A

Diffuse high uptake

310
Q

radioisotope scan with iodine in toxic multinodular goitre and adenomas will show

A

focal high uptake

311
Q

radioisotope scan with iodine will show cold areas

A

thyroid cancer

312
Q

commonest cause of hyperthyroidism is

A

Grave’s disease

313
Q

toxic multinodular goitre causes

A

hyperthyroidism

314
Q

Exopthalmos refers too

A

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
Q

Pretibial Myxoedema refers too

A

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
Q

features of hyperthyroidism

A 
Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss
Fatigue
Frequent loose stools
Sexual dysfunction
317
Q

features specific to grave’s disease

A

Diffuse Goitre (without nodules)
Graves Eye Disease
Bilateral Exopthalmos
Pretibial Myxoedema

318
Q

features specific to toxic multinodular goitre

A

Goitre with firm nodules
Most patients are aged over 50
Second most common cause of thyrotoxicosis (after Grave’s)

319
Q

De Quervain’s Thyroiditis describes

A

presentation of a viral infection with fever, neck pain and tenderness, dysphagia and features of hyperthyroidism. This progresses to hypothyroid phase

320
Q

De Quervain’s thyroiditis Tx

A

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
Q

thyroid storm presentation

A

severe presentation of hyperthyroidism with pyrexia, tachycardia and delirium

322
Q

first line for hyperthyroidism

A

carbimazole

323
Q

two therapies for carbimazole treatment of hyperthyroidism

A

titration-block or block and replace

324
Q

second line drug for hyperthyroidism

A

Propylthiouracil

325
Q

other treatments for hyperthyroidism include

A

radioactive iodine, beta blockers, and surgery.

326
Q

common cause of hypothyroidism in the developed world is

A

hashimoto’s thyroiditis

327
Q

common cause of hypothyroidism in the developing world is

A

iodine deficiency

328
Q

secondary causes of hypothyroidism

A 
Carbimazole
Prophylthiouracil
Radioactive iodine
Thyroid surgery
lithium and amiodarone
329
Q

presentation of hypothyroidism

A 
Weight gain
Fatigue
Dry skin
Coarse hair and hair loss
Fluid retention (oedema, pleural effusions, ascites)
Heavy or irregular periods
Constipation
330
Q

Tx of hypothyroidism

A

levothyroxine which is synthetic T4 that metabolises into T3

331
Q

ideal blood glucose level

A

between 4.4. and 6.1 mmol/l.

332
Q

insulin is produced by

A

beta cells in the islets of langerhans in the pancreas

333
Q

glucagon is produced by

A

alpha cells in the islets of langerhans in the pancreas

334
Q

glucagon role

A

glycogenolysis and gluconeogenesis

335
Q

glycogenolysis refers too

A

the liver to break down stored glycogen into glucose

336
Q

gluconeogenesis refers too

A

liver to convert proteins and fats into glucose.

337
Q

triad of DKA

A

dehydration, potassium imbalance, ketoacidosis

338
Q

why dehydration in DKA?

A

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
Q

excessive thirst is called

A

polydipsia

340
Q

why potassium imbalance in DKA

A

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
Q

presentation of DKA

A 
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
Q

diagnosing DKA is through

A

Hyperglycaemia (i.e. blood glucose > 11 mmol/l)
Ketosis (i.e. blood ketones > 3 mmol/l)
Acidosis (i.e. pH < 7.3)

343
Q

DKA TX

A

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
Q

long term complications of hyperglycaemia

A

macrovascular, microvascular and infection

345
Q

macrovascular complications of hyperglycaemia

A

Coronary artery disease is a major cause of death in diabetics
Peripheral ischaemia causes poor healing, ulcers and “diabetic foot”
Stroke
Hypertension

346
Q

microvascular complications of hyperglycaemia

A

Peripheral neuropathy
Retinopathy
Kidney disease, particularly glomerulosclerosis

347
Q

monitoring of glucose can be conducted via

A

HBA1c, capillary blood glucose, flash glucose monitoring

348
Q

presentation of type 2 diabetes

A 
Fatigue
Polydipsia and polyuria (thirsty and urinating a lot)
Unintentional weight loss
Opportunistic infections
Slow healing
Glucose in urine (on dipstick)
349
Q

oral glucose tolerance test method

A

involves taking a baseline fasting plasma glucose result, giving a 75g glucose drink and then measuring plasma glucose 2 hours later.

350
Q

pre diabetes Dx

A

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
Q

diabetes Dx

A

HbA1c > 48 mmol/mol
Random Glucose > 11 mmol/l
Fasting Glucose > 7 mmol/l
OGTT 2 hour result > 11 mmol/l

352
Q

HBA1c target for new type 2 diabetics

A

48 mmol/mol for new type 2 diabetics

353
Q

first line for type 2 diabetes

A

metformin titrated from initially 500mg once daily as tolerated.

354
Q

second therapy for t2dm

A

sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor.

355
Q

T2dm + CV consider

A

SGLT-2 inhibitors and GLP-1 inhibitors

356
Q

metformin mechanism

A

biguanide”. It increases insulin sensitivity and decreases liver production of glucose. It is considered to be “weight neutral”

357
Q

metformin SE

A

Diarrhoea and abdominal pain. This is dose dependent and reducing the dose often resolves the symptoms
Lactic acidosis

358
Q

pioglitazone mechanism

A

“thiazolidinedione”. It increases insulin sensitivity and decreases liver production of glucose.

359
Q

pioglitazone SE

A 
Weight gain
Fluid retention
Anaemia
Heart failure
Extended use may increase the risk of bladder cancer
360
Q

sulfonylurea mechanism

A

The most common sulfonyluria is “gliclazide”. Sulfonylureas stimulate insulin release from the pancreas.

361
Q

sulfonylurea SE

A

Weight gain
Hypoglycaemia
Increased risk of cardiovascular disease and myocardial infarction when used as monotherapy

362
Q

incretins are

A

hormones produced by the GI tract. They are secreted in response to large meals and act to reduce blood sugar.

363
Q

incretins role

A

Increase insulin secretions
Inhibit glucagon production
Slow absorption by the GI tract

364
Q

main incretin is

A

glucagon-like peptide-1” (GLP-1).

365
Q

incretins are inhibited by

A

dipeptidyl peptidase-4” (DPP-4).

366
Q

GLP-1 mimetic example

A

exenatide

367
Q

SE of GLP-1 mimetic

A

GI tract upset
Weight loss
Dizziness
Low risk of hypoglycaemia

368
Q

SGLT-2 inhibitor examples

A

-gliflozin”, such as empagliflozin, canagliflozin and dapagliflozin.

369
Q

SGLT-2 inhibitor mechanism

A

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
Q

SE of SGLT-2 inhibitors

A

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
Q

rapid acting insulin examples

A

Novorapid
Humalog
Apidra

372
Q

short acting insulin examples

A

Actrapid
Humulin S
Insuman Rapid

373
Q

intermediate acting insulin examples

A

Insulatard
Humulin I
Insuman Basal

374
Q

long acting insulin examples

A

Lantus
Levemir
Degludec (lasts over 40 hours)

375
Q

combination insulins

A 
Humalog 25 (25:75)
Humalog 50 (50:50)
Novomix 30 (30:70)
376
Q

commonest cause of acromegaly is

A

pituitary adenoma

377
Q

visual problem associated with acromegaly is

A

bitemporal hemianopia (loss of vision of outer half)

378
Q

space occupying lesion symptoms of acromegaly

A

Headaches

Visual field defect (“bitemporal hemianopia”)

379
Q

overgrowth of tissues symptoms in acromegaly

A

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
Q

GH organ dysfunction

A

Hypertrophic heart
Hypertension
Type 2 diabetes
Colorectal cancer

381
Q

other symptoms that may suggest acromegaly

A

Development of new skin tags

Profuse sweating

382
Q

Ix for acromegaly

A

IGF-1 screening, OGTT, MRI, ophthalmology referral

383
Q

surgical Tx for acromegaly

A

trans sphenoidal resection

384
Q

medical Tx for acromegaly

A

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
Q

what cells specifically produce PTH

A

chief cells

386
Q

PTH raises calcium by

A

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
Q

primary hyperparathyroidism is

A

excess PTH from tumour leading to hypercalcaemia

388
Q

secondary hyperparathyroidism is caused by

A

lack of vit D or CKD leads to low calcium. the glands react by producing PTH and undergo hyperplasia.

389
Q

tertiary hyperparathyroidism is caused by

A

chronic secondary hyperparathyroidism leading to hypercalcaemia even post treatment of underlying cause

390
Q

high PTH and high calcium may be

A

primary or tertiary

391
Q

high PTH low/normal calcium may be

A

secondary

392
Q

Conn’s syndrome (primary hyperaldosteronism) pathology

A

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
Q

causes of conn’s include

A 
An adrenal adenoma secreting aldosterone (most common)
Bilateral adrenal hyperplasia
Familial hyperaldosteronism type 1 and type 2 (rare)
Adrenal carcinoma (rare)
394
Q

secondary hyperaldosteronism is caused by

A

excessive renin stimulating the adrenal glands to produce more aldosterone. Serum renin will be high.

395
Q

causes of secondary hyperaldosteronism include

A

Renal artery stenosis
Renal artery obstruction
Heart failure

396
Q

Renal artery stenosis maybe confirmed by

A

doppler ultrasound, CT angiogram or magnetic resonance angiography (MRA).

397
Q

Ix for hyperaldosteronism

A 
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
Q

High aldosterone and low renin indicates

A

primary hyperaldosteronism

399
Q

High aldosterone and high renin indicates

A

secondary hyperaldosteronism

400
Q

aldosterone antagonists include

A

Eplerenone

Spironolactone

401
Q

renal artery stenosis TX

A

Percutaneous renal artery angioplasty via the femoral artery to treat in renal artery stenosis

402
Q

common cause of secondary hypertension is

A

hyperaldosteronism (pot. low K+)

403
Q

ADH is produced by

A

hypothalamus and secreted by the posterior pituitary gland. It is also known as “vasopressin”.

404
Q

ADH role

A

DH stimulates water reabsorption from the collecting ducts in the kidneys.

405
Q

SIADH may be caused by

A

posterior pituitary secreting too much ADH or the ADH may be coming from somewhere else, for example a small cell lung cancer.

406
Q

SIAD commonly causes

A

euvolaemic hyponatraemia”.

407
Q

SIADH euvolaemic hyponatreamia is demonstrated by

A

“high urine osmolality” and “high urine sodium”.

408
Q

symptoms of SIADH

A 
Headache
Fatigue
Muscle aches and cramps
Confusion
Severe hyponatraemia can cause seizures and reduced consciousness
409
Q

rapid correction of serum sodium may cause

A

central pontine myelinolysis.

410
Q

Mx of SIADH

A

Fluid restriction
Tolvaptan. “Vaptans” are ADH receptor blockers.
Demeclocycline is a tetracycline antibiotic that inhibits ADH.

411
Q

first stage of central pontine myelinolysis

A

encephalopathic and confused. They may have a headache or nausea and vomiting.

412
Q

second stage of central pontine myelinolysis

A

occurs few days post correction. This may present as spastic quadriparesis, pseudobulbar palsy and cognitive and behavioural changes

413
Q

Diabetes insipidus is a lack of

A

antidiuretic hormone (ADH) or a lack of response to ADH.

414
Q

Nephrogenic diabetes insipidus is when

A

the collecting ducts of the kidneys do not respond to ADH.

415
Q

causes of nephrogenic diabetes insipidus include

A

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
Q

Cranial diabetes insipidus is when the

A

hypothalamus does not produce ADH

417
Q

cranial diabetes insipidus can be caused by

A 
Brain tumours
Head injury
Brain malformations
Brain infections (meningitis, encephalitis and tuberculosis)
Brain surgery or radiotherapy
418
Q

presentation of cranial diabetes insipidus

A 
Polyuria (excessive urine production)
Polydipsia (excessive thirst)
Dehydration
Postural hypotension
Hypernatraemia
419
Q

Ix for cranial diabetes insipidus

A

Low urine osmolality
High serum osmolality
Water deprivation test

420
Q

water deprivation test method

A

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
Q

after deprivation low urine osmolality and after ADH high points to

A

Cranial Diabetes Insipidus

422
Q

after deprivation high urine osmolality and after ADH high points to

A

Primary Polydipsia

423
Q

after deprivation low urine osmolality low and after ADH urine osmolality low

A

nephrogenic diabetes insipidus

424
Q

Mx of diabetes insipidus is

A

Desmopressin (synthetic ADH) can be used in:

Cranial diabetes insipidus to replace ADH
Nephrogenic diabetes insipidus in higher doses under close monitoring

425
Q

adrenal is produced by what cells

A

chromaffin cells

426
Q

phaeochromocytoma is a tumour of the

A

chromaffin cells

427
Q

adrenaline is an example of

A

catecholamine” hormone

428
Q

what is the genetic association with phaeochromocytoma

A

25% are familial and associated with multiple endocrine neoplasia type 2 (MEN 2).

429
Q

what is the pattern of a phaeochromocytoma

A

10% bilateral
10% cancerous
10% outside the adrenal gland

430
Q

Dx of a phaeochromocytoma is with

A

24 hour urine catecholamines

Plasma free metanephrines

431
Q

presentation of a phaeochromocytoma is

A 
Anxiety
Sweating
Headache
Hypertension
Palpitations, tachycardia and paroxysmal atrial fibrillation
432
Q

Mx of a phaeochromocytoma is with

A 
Alpha blockers (i.e. phenoxybenzamine)
Beta blockers once established on alpha blockers
Adrenalectomy to remove tumour is the definitive management

fourth year (12 decks)

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