RBF Flashcards

Question

What are the pros and cons and uses of LMWH compared to UF heparin

Answer 1

Pros are improved pharmacokinetics, less monitoring requirement, as well as less risk of thrombocytopenia and osteoporosis Cons are that APTT cannot be used to monitor it, it cannot be reversed by protamine, and it is harder in renal failure as LMWH are cleared by kidneys while UF heparin is cleared by reticuloendothelial system Both are used in stemi, initial DVT/PE, and as a warfarin alternative. LMWH is also used for catheterisation and nstemis.

Answer 2

It is a vitamin K antagonist, with S isoforms more active than R It inhibits synthesis of coagulation factors VII, IX, X and II, but has a slow onset- so while it is waiting to kick in, heparin is used It is metabolised by CYP450 and crosses the placenta

Answer 3

It is used for thrombses, and for preventing these in cases of mechanical heart valves and atrial fibrillation (lifelong) In terms of warfarin duration of treatment in DVT, it used for months for risk factors or first DVT. It is used lifelong in thrombophilia and potentially cancer cases

Answer 4

Intracrainal or GI haemorrhage (more likely in oder age groups, those with cerebrovascular disease, previous GI ulcer/bleed, liver/renal damage, and high target INR Contraindicated by pregnancy, high risk of haemorrhage (uncontrolled alcohol, dementia, high falls)

Answer 5

By INR: Ratio of patient's PT to mean normal PT. Those with prosthetics and recurrent thromboses have a higher target INR than those with a single venous thrombosis episode

Answer 6

Most increase effect of warfarin's effect by inhibiting CYP450 Eg. intermittent alcohol, analgesics, amiodarone Some inhibit warfarin by increasing P450- eg. prolonged alcohol, barbituates

Answer 7

``` Giving vitamin K if bleeding is not severe Giving prothrombinex (concentrate containing vitamin K dependent factors) if lifethreatening ```

Answer 8

Narrow therapeutic window Lifetime risk of haemorrhage increases Drug interactions Needs regular INR

Answer 9

It's a prodrug that is converted to an inhibitor of coagulation by gut, plasma and liver esterases It isn't P450 dependent, but is excreted renally It is used to treat and prevent VTE, for atrial fibrillation, but NOT for mechanical valves Bleeding can be managed by monoclonal IV antibody idarucizumab

Answer 10

VQ mismatch is a ratio of the perfusion of alveoli to their ventilation An alveolus that is ventilated but not perfused has a ratio of infinity, and can be considered dead space as it does not affect gas exchange at all An alveolus that is perfused and ventilated has a ratio of 1, and gives a normal CO2 and CCO2. An alveolus that is perfused but not ventilated has a ratio of 0, and is called venous admixture, as the blood being combined in later circulation is technically venous. It has a low CO2 and high CCO2. Overall, this has the effect of slightly lowering CO2 and keeping CCO2 normal (due to the shape of its dissociation curve). However, this regulation is decreased in a loss of competence or introduction of an abnormal load.

Answer 11

It is characterised by airflow obstruction that is not fully reversible It is progressive, related to an abnormal inflammatory response Symptoms include chronic mucus hypersecretion, emphysema and small airway inflammation, with increased and hypertrophied goblet cells and destruction of lung parenchyma

Answer 12

PaCO2 will increase, causing a loss of CO2 drive and respiration to depend on hypoxic drive If O2 is administered due to SOB, it will cause loss of drive, causing reduced ventilation, hypercapia, and potentially respiratory and metabolic acidosis. CO2 increases can show intracellular acidosis, hypoxia, and sleep depravation.

Answer 13

Reduced cardiac and respiratory muscle contractility, reduced endurance time, arterial vasodilation, increased cerebral blood flow, arrhythmias etc.

Answer 14

Oxygen's dissociation is sigmoidal, but normally CO2 is on the high side, so when hyperventilating, the Co2 only moves along the flat part of the curve CCO2 is diagonal, so when PCO2 decreases during hyperventilation, CCO2 also decreases

Answer 15

It is an anatomical abnormality shnting blood from the RHS to LHS of the heart Distinguished from VQ mismatch b administering 100% O2- VQ mismatch will always increase with 100% O2, while a shunt increases much less as it worsens This is because the shunted blood does not see the added O2, and so depresses the arterial PO2- however, it can still help by increasing the dissolved oxygen content, . Shunting will show cyanosis due to desaturated Hb and ruddiness due to increased Hb concentration due to chronic hypoxaemia

Answer 16

The highest proportion of smooth muscle in the vessel walls is located in the small arteries and arterioles, while the postcapillary vessels have the smallest The microcirculation is in intimate contact with the tissue it supplies

Answer 17

Sympathetic adrenergic nerves supply all vascular beds in the body. However, its extent varies widely, with arteries and arterioles directly innervated, and veins more sparsely (increasing with size), and no direct capillary innervation. Parasympathetic cholinergic innervation of precapillary vessels exists in some organs.

Answer 18

The small arteries and arterioles are the site of the largest pressure change across the whole vasculature. Therefore they contribute the most to resistance Vasodilation of these precapillary vessels reduces resistance and increases blood flow, and vice versa. Constriction means that energy dissipated as blood flows through the small arteries and arterioles is increased, resulting in a reduction in mean hydrostatic pressure. Precapillary dilation leads to extrusion of fluid, and vice versa

Answer 19

The organ has an intrinsic tendencey to maintain constant blood flow despite change in perfusion pressure As perfusion pressure increases, there is an increase in blood flow that then returns to the previous level, often within a few seconds and vice versa. This varies however- cutaneous circulation exhibits almost no autoregulation, while the cerebral circulation is tightly maintained

Answer 20

After a short period of blood vessel occlusion, blood flow rises above the level of flow before the occlusion, for a period proportional to the duration of the occlusion

Answer 21

An increase in transmural pressure on a blood vessel results in increased vascular contraction and vice versa Responses of this nature are most potent in medium arterioles and small to medium veins. This is done as the pressure increase distends the vessel walls, depolarising the vascular smooth muscle cells and causing contraction

Answer 22

Local vascular contraction is dependent on the perivascular concentration of metabolites. This is determined by the rate at which they are produced compared to the rate at which they are washed out. More active cells produce more adenosine, etc, which stimulates contraction of nearby smooth muscle cells

Answer 23

The endothelium releases nitric oxide, which acts on VSM to increase intracellular cGMP, causing relaxation. It can also release endothelin, which causes Ca2+ channel agonism and vasoconstriction

Answer 24

There are three options for its binding to the VSM membrane channels 1. A1 receptors. This is linked to the G protein Gq, which activates phospholipase, increasing IP3 and DAG. This causes increased Ca2+ and vasocontstriction 2. A2 receptors. These are linked to Gi proteins, which inhibit adenylate cyclase, decreasing cAMP, increasing Ca2+ extrusion and sequestering it intracellularly. This leads to vasodilation

Answer 25

Excitatory: Ang II, adrenaline | Inhibitory" ACh adenosine, dopamine, histamine, PGE1/2

Answer 26

Activation releases ACh, binding the the M3 receptors in vascular endothelium, stimulating NO synthesis. However, if it binds to M2, it causes vasodilation Sympathetic cholinergic nerves are similar, but innervate precapillary vessels in skeletal muscles and sweat glands, leading to vasodilation and sweating

Answer 27

NA causes widespread vasoconstriction excep for the coronary and cerebral circulations A causes this as well as vasodilation in skeletal muscles and splanchnic circuits This is done as B2 receptors (which stimulate cAMP to do vasodilation) have a higher affinity for adrenaline than noradrenaline. These receptors are located only in skeletal and splanchnic circuits

Answer 28

At moderate and high exercise levels, sympathetic stimulation is ineffective, as the concentrations of extracellular metabolite become so high in the working tissue that they cause vasodilation as well as inhibiting sympathetic transmission There may also be action of sympathetic nerves on B2 receptors The metabolites don't really affect postcapillary vessels The speed and magnitude of hyperaemia is not totally explained by these mechanisms!

Answer 29

The skin has low capillary density and lots of shunting. Blood flow at rest is even greater than requirements. only a receptors are present, and therefore is powerfully influenced by sympathetic innervation Affinity of a receptors for NA decreases as skin temperature rising, leading directly to increased cutaneous blood flow The sweat glands also activate the kinin cascade, increasing blood flow and improving heat loss

Answer 30

Total blood flow remains very constant, but regional variations may be marked. Perivascular pH and CO2, O2, K+ are used in matching the two. High PaCO2 causes increased flow and vice versa. Catecholamines have little effect as they cannot penetrate the BBB. Sympathetic innervation provokes only transient results Interstitial fluid volume and intracranial pressure can also cause alterations in flow- similarly to compartment syndrome

Answer 31

Associated with prolonged vasoconstriction of digital arteries of the hand when exposed to cold stimulus Due to inappropriate responsiveness of a adrenergic receptors In chronic disease, skin ulcers and bone necrosis may occur due to abnormal vessel structure

Answer 32

Initially it goes up, as sympathetic stimulation bronchodilates the airways Then there is a massive drop in FEV1 as airway hyperresponsiveness causes histamine and leukotrine release, resulting in airway narrowing. This can be mediated by smooth muscle contraction or by increased thickening of mucus

Answer 33

This occurs because when an asthma attack occurs, flow becomes proportional to elastic pressure over resistance. The pleural pressure must increase as expiration is more and more forced, until the point at which pleural pressure equals the pressure within the airway- this then forces the airway to collapse, and expiration becomes effort independent as changing the force no longer increases the flow

Answer 34

Flow is on the y axis, volume on the x axis Expiratory flow sees the graph peak upwards sharply to PEF, and then decrease through FEV1 and to minimum. Inspiration has less flow peak, but just a curve underneath. Tidal breathing tends to be within the middle of this graph. The first half of the Fexpiratory descent line is effort dependent, while the lower part is effort independent.

Answer 35

A reduced PF Reduced FEV1 Reduced FVC, but FEV1 reduced to a greater extent Increase in residual volume Tidal breathing occurs at higher lung volumes, esp in emphysema as it allows the airways to stretch, increasing use of elastic pressure to drive outflow

Answer 36

FEV1: Much better for distinguishing abnormality and relatively effort independent PEF is simple and cheap, but there is a wide normal range and it is relatively effort dependent.

Answer 37

Normally we breathe in the steep part of the sigmoidal pressure volume curve, but at high lung volumes this is flatter, indicating lower compliance. This means it takes more generation of pressure to maintain the same lung volumes in pathology

Answer 38

Normally due to extrathoracic limitation, as both the elastic recoil must be overcome as well as the airflow limitation.

Answer 39

Due to thickened interstitial barrier between alveloli capillaries- the basal airways close off during tidal breathing, and must be 'popped' open once the lung reaches a certain pressure. The noncompliant airways all open together, causing a crackle

Answer 40

SOB mostly correlates with increased work of breathing, rather than actual hypoxaemia Normally, tidal volume and pressure has an increasing slope. In fibrosis, this slope is flatter, meaning there is increased elastic work of breathing that needs to be overcome as the lung is less compliant. When exercising, this increases work of breathing markedly, so resp rate increases as it is easier to maintain adequate breathing in this way.

Answer 41

The wavefront spreads from endocardium to epicardium and from apex to base It moves from SA node to atria, to AV node, to bundle branches to purkinje fibres

Answer 42

- Suppression of lower frequency pacemakers. While AV cells have an unstable membrane potential and could act as pacemakers, the SA node drives them because it has the fastest spontaneous rate. This suppresses the automaticity of lower pacemakers. - Programmed excitation via the conduction system - A prolonged refractory period in the myocardium

Answer 43

Arrhythmia is defined as any deviation from normal sinus rhythm. It may be caused by early pacemaker discharge or activity triggered by an unstable RMP. This is caused by delayed or early afterdepolarisations. These tend to occur in the relative and supernormal refractory periods, though these are poorly conducted. Ectopic beats must be generated by numerous cells synchronously It can also be due to impulse conduction, such as AV/bundle branch block (slowed heart rate) or reentry (altered time course of spatial or temporal repolarization)

Answer 44

Caused by a single atrial reentry circuit and assoc with fast atrial rate, increasing the likelihood of partial AV block It shows sawtoothed waves between QRS complexes

Answer 45

Rapid disorganised atrial activation, with not all being conducted to ventricles and so causing a disordered ventricular rhythm. It is more common after lesions, CHF or in the elderly. Significant risk of clots and PE/Stroke

Answer 46

Can occur in myocardial ischaemia, due to remodelling after healed infarction, heart failure or due to hereditary ion channel mutations. It is associated with rapid ventricular activation and impaired mechanical function

Answer 47

Sodium and calcium are higher outside than within the cell, while potassium is higher intracellularly When MP is brought to threshold, rapid transient openings of sodium channels carry the fast sodium current in and cause depolarization. This reduces the permeability of the potassium channel, preventing it at first from removing K+ ions. This depolarization also causes slow calcium channels to open, allowing Ca2+ in. this remains in balance for a plateau phase, before the K_ ion current increase due to fast and slow delayed rectifiers, returning levels to normal

Answer 48

These are gates that may be open or closed depending on the voltage status of the cell. Eg. fast sodium channels have their gates shut at RMP, but open quickly with depolarization. Inactivation gates are open at rest, but shut as depolarization occurs. This means there is a brief delay between activation and inactivation, so allows a short transient sodium current, and is responsible for the prolonged refractory period of the AP. The gates progressively reset during repolarization

Answer 49

It is due to propagation of a current around a region in which activation is blocked due to refractoriness or injury. If only one side allows propogation, the wave will move around the region of block, and pass retrogradely up the other side. This means it is able to reactivate tissue and generate sustained activation around the entry circuit, if the time of propgation is the same as the effective refractory period of tissue (when reactivation cannot occur). This means it requires a circuit, a unidirectional block, slow conduction or short ERP, and a trigger. Vulnerability increases with decreased conduction velocity and refractory periods. In ventricular myocardium, this is most probably when repolarization is not spatially homogeneous

Answer 50

The bundle of kent is present, proving an accessory pathway for propogation to move between atria and ventricles. Normally, the early activation collides with normal activation via the slower AV node current. This gives a wide QRS with slurred delta wave beginning, and short PR interval It becomes an issue if ectopic activation occurs in the atria or ventricles which tissue in one of the pathways is refractory. This can cause rapid tachycardia, ventricular fibrillation and death

Answer 51

The wavelength for a reentrant arrhythmia depends on conduction velocity and effective refractory period. Factors reducing the velocity increase the probability of this. It is influenced by cell dimension, gap junction density, and status of the membrane sodium channels In the vulnerable period, the myocardium has a medium low MP, meaning few inactivation gates have rest- this means the number of sodium channels able to open is small, giving a slow depolarising current and non-uniform repolarization

Answer 52

ATP decreases, so sodium potassium ATPase is inhibited, raising K+o and Na+i. This causes - Slow conduction - Reduced AP duration with nonuniform repolarization - After-depolarizations

Answer 53

Increased Extracellular potassium reduces the RMP, inactivating Na+ channels as the gates are partially closed already, and slowing conduction. Acidosis leads to decoupling of gap junctions, increasing electrical resistance and further reducing conduction velocity

Answer 54

Kyperkalaemia reduces AP duration via the rectifier and the APT dependent currents. This reduces AP duration in the ischaemic region, leading to nonuniform current

Answer 55

The reduction of ATP means Ca2+i rises, and spontaneous release of oversoaded SR generates calcium transients, and increased extrusion of Ca2+ via the Na+/Ca2+ exchanger. This generates a depolarizing current. Typically these occur as DADs

Answer 56

Onset of VT can cause positive feedback, where increased HR increases O2 demand and reduces diastolic perfusion. Increased HR can also impair ventricular performance further, increasing the extent of the ischaemic region and making VF more likely. Tissue heterogeneity as a result can lead to disordered structure and electrical coupling, allowing a potential reentry arrhythmia to occur

Answer 57

Cellular and structural changes occur, with dilated atria (increasing reentrant path length and stimulating stretch activated ion channels) . It also causes atrial fibrosis, resulting in region dependent slowing of conduction Changes in sodium calcium exchangers can also cause DADs and trigger reentrant arrhythmia There is also remodelling of ANS inputs to the atria in a heterogeneous way, influencing its electrical properties Similar processes occur in the ventricles

Answer 58

Ventricular arrhythmias that are triggered by exertion or emotional excitement, leading to fainting and sudden death This is due to prolonged APDs, and generation of APs late in the plateau or early in repolarization. EADs can result from prolonged APs, allowing Ca2+ channels to resent and reactivate. These channels are sensitive to adrenergic stimulation, explaining the reason for the occurrences. Reentrant arrhythmia is a great risk due to increased non uniformity of repolarization

Answer 59

May be diet or drug induced - Hypokalaemia - Amiodarone (prolongs QT interval) - Hereditary membrane ion channel issues

Answer 60

LQT1: Most common, due to mutation in delayed slow K+ rectifier channel, reducing repolarization and increasing APD LQT2: Mutation of the rapid K+ rectifier channel, increasing APD LQT3: Mutation in the sodium channel, causing failure to maintain INa inactivation later in the action potential. This allows late inward current, delaying repolarisation and increasing APD

Answer 61

A long QT interval If VT results, it shows continuously varying polymorphic VT, named Torsade de Pointes. It may resolve spontaneously or progress to VF

Answer 62

``` CO = HR x SV SV = EDV - ESV ```

Answer 63

Preload (Increased preload increases SV) Afterload (Increased afterload decreases SV) HR Inotropic state

Answer 64

Depolarization opens L type Ca2+ channels in the T tubules, allowing Ca2+ to enter the cell and bind to RyR2 receptors on the SR, opening calcium release channels. Therefore, Ca2+ conc rises rapidly in the cytoplasm. Ca2+ then binds to regularatory protein TnC, allowing active sites on the thin filaments to be expose and allowing cross bridge formation.

Answer 65

SERCA pumps transfer Ca2+ into the SR, where it is stored. | Also some extrusion by Na/Ca exchangers

Answer 66

Magnitude and rate of SR calcium release | Affinity of TnC for Ca2+ ions

Answer 67

The adenylate cyclase system is the most important Gs stimulates adenylate cyclase, increasing cAMP, more protein kinase A and phosphorylation of L-type Ca2_ channels, phospholamban, ryanodine receptors and TnI. This leads to opening of L type calcium channels, SR stimulation, faster Ca2+ kinetics and faster X bridges Therefore- faster Ca2+ release and reuptake, increasing inotropy

Answer 68

Noradrenaline and adrenaline act via B1 receptors to cause Gs activation ACh from the PNS acts on M2 receptors, which activates Gi, which inhibits adenylate cyclase and increases K+ reuptake, shortening APs

Answer 69

There is both passive force and active force. Passive force is related to the stretch acting on resting muscle, and active is that generated at a given sarcomere length. Passive force limits sarcomere length to less that 2.4um The force length relationship is much steeper in cardiac than in non cardiac contraction- this is due to the length dependent affinity of TnC for Ca2+

Answer 70

If oxygen supply is reduced relative to demand, ATP stores quickly become depleted and pump operation is impaired. Ca2+ in diastole is therefore elevatd, causing reduced relaxation, impacting electrical function and filling. Acidosis can also set in, impacting mechanical function as H+ competes with Ca2+ for TnC binding. There is also increased extracellular K+, affecting AP duration, as the speed of depolarization is reduced.

Answer 71

Myocytes have a principal orientation, defined by the organization of collagen. When the heart beats, most of the pump function is performed by wall thickening, rather than any real change to the diameter of the heart.

Answer 72

- There is cifcumerential and longitudinal shortening, as well as wall thickening- changes are greatest endocardially Circumferential shortening is greater than longitudinal. Some torsion occurs as the apex twists counter-clockwise Some shear deformations involve movement of cells relative to one another. This is reversed in diastole

Answer 73

Myocyte hypertrophy and wall thickening Increased LV collagen density and stiffness Circumferential and longitudinal shortening decrease EF is generally mainttained initially by increased torsion Eventual enlargement of ventricular cavity ad reduction of ejection fraction

Answer 74

Pre-ganglionic sympathetic fibres come from upper thoracic segments of the spinal cord, ascending in the paravertebral chain to synapse with postganglionic neurons in the sup, middle and stellate cervical ganglia. Preganglionic vagal neurons come from the medulla oblongata and course down the neck and chest as branches of the vagus nerve.

Answer 75

Parasymp innervation of the SA and AV node, and atrial myocardium, is dense. The ventricles are less densely innervated Sympathetic innervation is relatively homogenous The right fibres innervate the SA, while the left do the AV node

Answer 76

Through norepi acting on B1 receptors in the myocardium. This causes phosphorylation of If, allowing more Ca2+ in and more reuptake into the SR to shorten AP duration causes- increased rate Reduced AP duration, so acceleration of impulse propagation through the AV node Increased inotropic state

Answer 77

Left- it predominantly innervates the AV node so we see less HR change but greater systolic pressure If we stimulate the RHS it targets the SA node so we see a large change in HR but reduced systolic pressure change.

Answer 78

Pressure of atrial and LV contractions are increased Initial blood ejection speed and max ejection speeds are greater SV increases due to reduced ESV Filling occurs faster, despite the reduction in diastolic interval

Answer 79

Mediated by ACh, which binds to M2 receptors to turn off the Gs pathway, increasing K+ extrusion and reducing AP duration It reduces HR Also causes deceleration of impulse propagation through the AV node (and may cause block)

Answer 80

PNS stimulation is instant, SNS is slower, so respiratory sinus arrest is due to PNS stimulation/ this is because ACh has lots of sites and esterases, unlike epi/norepi The PNS dominates short term heart rate control, and normally checks resting heart rate. When it's active, the vagus is turned down

Answer 81

Interruption to blood supply leads to decline in ventricular performance, with prolonged underperfusion leading to irreversible cell damage. Function is dependent on aerobic metabolism Determinants include basal mechanism- the metabolic cost of maintaining organelle systems Wall force development is related to pressure generated and dependent on the geometry of the ventricle- eg. a dilated heart requires more wall force development for a given LV pressure, both in terms of magnitude and time Also inotropy and heart rate

Answer 82

Aortic pressure, extravascular compression (ie as the heart contracts the vessels get squished) and local regulation This has impacts on perfusion pressure, impedance, and the need for CaO2, O2 extraction and vessel flow MVO2 = Q x (CaO2 - CvO2) Note that there is a capillary for each myocyte!

Answer 83

Coronary blood vessels are compressed during isovolumetric conraction, with some small recovery during systole. It then relaxes and allows full flow. Normally, Diastolic pressure time index should be greater than tension time index, but an loss of health can change this. Vascular resistance is mainly controlled by local factors The SNS causes vasoconstriction of these vessels, resulting in vasoconstrictor tone under normal situations It is often overridden by a concurrent increase in oxygen demand during times of stress.

Answer 84

The afferent blood supply goes to the glomerulus, which has the glomerular filtration basement- fenestrated endothelium, basement membrane and podocytes. Prourine is produced by fluid's movement through these layers

Answer 85

Elimination of waste products Control of fluid balance Regulation of acid-base balance Production of hormones

Answer 86

The rate at which the blood is cleared is defined as the GFR, which is normally >120mL/min

Answer 87

AKI is acute kidney injury, and occurs over hours to days | CKD is chronic kidney disease, and occurs over weeks, months or years. It is progressive but irreversible

Answer 88

It can have multiple aetiologies, and is assoc with many preventable hospital deaths. It is defined in 3 stages, with 3 being worse, and assoc with increased risk of death

Answer 89

Pre renal Renal Post renal

Answer 90

Identify high risk patients and optimise their care Stop nephrotoxic agents Assess and optimise volume status Monitor creatinine and urine output

Answer 91

``` CKD patients Those over 75 HF patients Liver disease CVD DM Polypharmacy ```

Answer 92

NSAIDs Gentamicin Anti-hypertensive Meds that are renally excreted should be revised

Answer 93

Check for dry mucous membranes JVP Oedema Sunken eyes

Answer 94

``` Strep serology Antibodies Hepatitis Coagulation Biopsy Ultrasound ```

Answer 95

GFR will be very low- can be measured with Cr clearance or by clearance of injected substances eg. insulin, isotopes

Answer 96

It is secreted in small amounts by the tubules, and so using creatinine tends to overestimate the GFR Moderate and severe CKD also confounds the interpretation of creatinine clearance. As filtration decreases, extrarenal excretion of creatinine increases and muscle mass decreases, resulting in an overestimation in end-stage patients

Answer 97

5 stages for GFR going from >90, 60, 30, 15 and <15 | Albuminuria has 3 stages of <30, <300 and >300

Answer 98

Diabetic nephropathy Glomerulonephritis Hypertensive nephrosclerosis PKD

Answer 99

``` Systemic hypertension Intraglomerular hypertension Glomerular hypertrophy Ca and P Dyslipidaemia Proteinuria Tubulo-interstitial fibrosis Toxicity of iron, ammonia and/or middle molecules ```

Answer 100

Progression of CKD is linked to HT, and lowering it can slow the speed of progression

Answer 101

It's important for prognostics. Reducing proteinuria improves outcomes It can be modified with weight loss, ACEi/ARB, statins, moderate protein restrictions, alowering BP

Answer 102

Ca and P content of the kidney is increased in CDK, assoc with progressive decline in renal function. it gets deposited within the kidney, but its reduction can be assoc with reduction in rate of decline This is managed by limiting dietary phosphate, or giving phosphate binders so that phosphate is not absorbed.

Answer 103

CDK patients are more prone to either dehydration or volume overload.

Answer 104

Reduced EPO, vitamin D, RAA etc Issues with Na, P regulation Typically develops metabolic acidosis due to lack of non-organic acid excretion- may need to add oral sodium bicarbonate

Answer 105

Manifestation of organ dysfunction typically seen in CDK 4/5 | No single compound is solely responsible

Answer 106

Neuro- fatigue, sleep, headache, seizures, paralysis Haem- anaemia, easy bleeding, platelet dysfunction, infection CV- pericarditis, HT, HF, IHD, PVD Pulmonary- Pleuritis, uraemic lung GI- anorexia, N&V, bleeds Metabolic- glucose intolerance, hyperlipidaemia, malnutrition, sex dysfunction, infertility, osteodysplasia Skin- pigmentation, easy bruising, uraemic frost, pruritis Psych- depression, anxiety, denial, psychosis

Answer 107

Treat the primary disease, secondary factors Avoid nephrotoxins Correct abnormalities Renal replacement therapy

Answer 108

Conservatively if not indicated for other treatment Dialysis (can be peritoneal or haemodialysis) Renal transplant (can be cadaveric or living)

Answer 109

Activated by SNS activity, low BP or low Na/K+ passing the JG cells Causes vasoconstriction, formation of angII, and secretion of aldosterone.

Answer 110

It can increase activity is CCF and hypertension as it works in harmony with the SNS It's involved with CHF progression Can have adverse CV effects including hypertrophy, atherosclerosis development, and pro-inflammatory conditions

Answer 111

ACEs act on angiotensin converting enzyme, which changes Ang 1 to Ang2. However, blocking this also breaks down bradykinin and increases levels of Ang9 and heptopeptide concentrations increase. This means it has multiple benefits for blood vessels. However, other pathways can be used instead, to increase Ang II over time Ang II antagonists- inhibit angiotensin II type 1 receptors

Answer 112

Phospholipase C GPCRs

Answer 113

Type I receptors- affect the kidney, heart, VSM, Brain, adrenal glands, adipocytes and placenta. Main target of ARBs Type II receptors- affect the heart, adrenals, CNS, kidneys Also counterbalance some type I effects and cause cell proliferation & apoptosis. These are allowed to exert their beneficial effects when type I receptors are blocked

Answer 114

Cardiac myocytes: Cause hypertrophy, apoptosis, cell sliding, wall stress, increased O2 consumption and impaired relaxation Fibrobasts: Cause hyperplasia, collagen synthesis and fibrosis Peripheral artery: Cause vasoconstriction, endothelial dysfunction, hypertrophy and decreased compliance Coronary artery: Cause vasoconstriction, endothelial dysfunction atherosclerosis, and thrombosis.

Answer 115

Causes hypertrophy and Ne in cardiac myocytes Hyperplasia, collagen synthesis, fibrosis in fibroblasts Vasocnstriction, endothelial dysfunction, hypertrophy and decreased compliance in peripheral arteries Potassium loss and sodium retention in the kidney

Answer 116

Benefits are reduced ang II concentration, reduced aldosterone concentration, and potentially increased Ang 9. Also, bradykinin levels rise, causing vasorelaxation and increased endothelial function However, eventually aII and also begin to increase, due to chymase activity

Answer 117

Ace inhibitors are most common, especially cilazapril. All others end in 'pril' ARBs include candesartan. All others end in sartan ACEs are given as prodrugs and hydrolysed int he liver. They are excreted mostly renally ARBs have variable excretion

Answer 118

They cause vasodilation, lowering arterial and venous pressure, and reducing preload and afterload They decrease blood volume, causing natriuresis an diuresis. Decrease sympathetic activity Decrease cardiac and vascular hypertrophy

Answer 119

ACEs: Hypertension, either monotheraphy or combination with a diuretic Also CCF as part of multiple treatments with a diuretic, B blocker or aldosterone antagonist ARBs: Used in ACE inhibitor intolerant patients, hypertension and heart failure NEVER USE THE TWO TOGETHER

Answer 120

ACE: Produce a dry cough due to bradykinin increases, as well as hyperkalaemia, decreasd renal function (initial), hypotension and angioedema due to vasodilation ARBs show dry cough in small amount of people, hyperkalaemia, renal deterioration, hypotension and angioedema, though less than ACEis They are both contraindicated in pregnancy

Answer 121

In hyperkalemic patients Renally impaired patients Volume depeted or diurised patients, as they are dependent on RAAS to overcome their dehydration

Answer 122

Pregnancy Bilateral renal artery stenosis, as they have narrowing proximal to the glomerulus They need ang II to constrict the efferent arteriole to maintain glomerular pressure. If it is not present, it can reduce perfusion across the glomerulus and cause AKI. Therefore, you need to watch creatinine for the first few weeks when going on the drug.

Answer 123

Can get renin inhibitors potentially | Also vasopeptidase inhibitors which block the breakdown of 'good' things like bradykinin and substance P.

Answer 124

A1 (post-synaptic): They cause vasoconstriction and increase BP (A1a in the prostate) A2 (pre and post synaptic): Inhibit release of norepi and insulin

Answer 125

They act on alpha 1 receptors to block noradrenaline landing (alpha 2 antagonism isn't used clinically)

Answer 126

Doxazosin- blocks all a1 subtypes for causing vasodilation | Tamsulosin- specific to a1a so useful for prostatic profile but with little effect on BP

Answer 127

Essential hypertension. However, they don't tend to be first- line therapy and are used in combination with diuretics and ace inhibitors to acheive targets. Also useful for prostatism as they improve tone of vessels can can reduce symptoms. They can also be used to block norepi effects postoperatively

Answer 128

A reversible alpha blocker with greater affinity for 1 than 2 Blocks all a1 subtypes for vasodilation It can also reduce prostatic symptoms Given once daily, starting with a low dose and titrating uo

Answer 129

``` Orthostatic hypotension causing dizziness- can just give the first dose at night Feeling tired Nasal stuffiness Dry mouth Urinary incontinence in women ```

Answer 130

Irreversible alpha blocker used in phaeocrhomocytoma (eg. for sympathetic tumours) or preoperatively Gives postural hypotension, tachycardia, nasal stuffiness and CNS symptoms

Answer 131

Lebetalol- used in pregnant women hypertension Carvedilol- used in CCF These are B1 = B2 > a1 >a2

Answer 132

An oral alpha blocker than blocks a1a receptors,causing a relief from prostatism and less postural hypertension

Answer 133

Hypertension, angina, arrhythmias and vasospasm | This is because it causes vasodilation, reduced cardiac work, affect supraventricular tachyarrhythmias (good for AF)

Answer 134

They block voltage-operated L type Ca2+ channels in cardiac tissue and smooth muscle. They do have some selectivity for resistance vessels, the myocardium, and conducting tissue. In vascular smooth muscle, they decrease arteriolar tone, PVR, BP and afterload In cardiac cells they decrease contractility, sinus node rate and AV node transmission

Answer 135

Dihydropyridines like Nifedipine and Amlodipine. These affect resistance vessels with little cardiac effect, causing flushing, headache and oedema Phanylalkylamines like verapamil act on cardiac tissue to cause heart block, negative inotropy and constipation- so they're not for heart failure Bezothiazepines like diltiazem are in the middle of both

Answer 136

They are all oral but can be made IV They have significant first pass metabolism with CYP450 They have a variable half life but those with short T1/2 may come in slow release capsules

Answer 137

Used for hypertension and vasospasm Main side effect is oedema, probably due to precapillary arteriole relaxation and potential block of lymphatic peristalsis This type of oedema is resistant to diuretics

Answer 138

Used for angina, hypertension and tachyarrhythmias | Can be used with beta blockers as it isn't the most potent B blocker

Answer 139

Used for tachyarrhythmias and hypertension. Can cause bradycardia and negative inotrope Never used with beta blockers, and needs care with statins

Answer 140

Flushing Headache Oedema Negatively inotropic and constipation (verapamil)

Answer 141

You would use diltiazem | Normally you would use a B blocker, but this is contraindicated by asthma

Answer 142

Diretuc, ACEi, and a vasodilator as well as a statin

Answer 143

Alpha blockers: 3rd line for hypertensio, used in combo with ACEis and diuretics. Consider if concurrent prostatism CCB: 2nd or 3rd line for hypertension. Combined with ACEis and diuretics. Use if concurrent angina, for rate control and SVT control

Answer 144

Hypertension Angina, as they reduce cardiac work Heart failure Arrhythmias, as they are god for AF and SVT as they block reentry currents

Answer 145

B1 cause tachycardia, vasoconstriction and renin release B2 cause bronchorelaxation and renin release Therefore blocking them can reduce heart rate and contractility, but can have an adverse effect for asthmatics

Answer 146

They change beta adrenergic receptor kinases to decrease cAMP They vary in their selectivity Metoprolol has much more B1 sensitivity than B2, while propanolol has similar between the two. Mixed antagonists between a and b are the ones indicated in pregnancy

Answer 147

Selectivity Elimination may be renal or liver Half life Water soluble (excreted renally, long T1/2, caution with impaired renal Fx) Lipid soluble (liver excreted, rapid absorption and metabolism, short T1/2 but cross BBB)

Answer 148

They are well absorbed orally Can come in sustained release forms (esp liver solubles) They also have some iv preparations (Esmolol is only given IV as it is rapidly absorbed by plasma esterases (only for ICU patients, eg in aortic dissection)

Answer 149

``` BP lowering through unclear mechanisms Less HR and decreased cardiac work Reduced renin and SNS activity Reduce Norepi release Negative chronotropy at SA and AV nodes Negative inotropy in the short term, but positive in the long term Thyrotoxicosis Reduced aqueous humour production Decreased glycogenolysis (can reduce gypoglycaemic symptoms in diabetics making it more dangerous) ```

Answer 150

Asthma exacerbation Hypotension, bradycardia and acute CCF exacerbation due to negative inotropy Incometence nightmares masking of hypoglycaemia Drug withdrawal as long term post synaptic receptors go up- if stopped immediately, see tachycardia, sweating, angina

Answer 151

Verapamil is a contraindication as there is negative chronotropy there too, increasing risk of heart block Diltiazem is acceptable Other BP lowering drugs Diabetics

Answer 152

Angina Most MI to decrease arrhythmia, ventricular rupture and cardiac remodelling Heart failure

Answer 153

Normally there is mainly B1, with some B2 and a little A1 | In a failing heart, this changes to 50% B1, 25% B2 and 25% A1

Answer 154

``` Decrease HR and O2 consumption, Increase filling Upregulate B receptors Attenuate apoptosis Improve baroreceptor functioning Improve LV remodelling ```

Answer 155

Mechanism unclear but used in 2nd or 3rd line therapy

Answer 156

Initially: Diuretics, O2, ACEi LOW DOSE B blocker due to not wanting to slow heart further Titrate up when his condition is stable

Answer 157

Add a B blocker once daily for 'anxiety' and HR Warn about fatigue, dizziness, erectile dysfunction Enquire about asthma

Answer 158

A drug that changes the force of cardiac muscle contraction- can be positive or negative

Answer 159

Shock is characterised by inadequate organ perfusion to meet the tissue's O2 demand, leading to organ dysfunction Can be hypovolemic- due to haemorrhage or dehydration Cardiogenic- HF Distributive- sepsis or anaphylaxis Obstructive- tamponade, PE

Answer 160

Tend to be given via continuous infusion into a large vein | This is because peripheral drugs may take some time to deliver drugs centrally, and may risk phlebitis due to toxicity

Answer 161

Goal is to restore BP and ensure euvolaemia Normalise systemic perfusion to preserve organ function, and then treat the underlying cause Shock has a high risk of death

Answer 162

Caused by ischaemic disease, valve dysfunction, acute VSD | Shows high systemic resistance due to symp activity, and low cardiac output

Answer 163

The goal is to get preload as high as ideal as possible depending on the inotropy. Inotropic agents can be used to return the heart to normal, augmenting contractility after preload has been established, improving cardiac output and global perfusion HOWEVER they do increase the risk of tachycardia, MI, arrhythmia, and increase myocardial oxygen consumption

Answer 164

``` Alpha and beta adrenoreceptor agonists to increase tone, vasoconstriction, and cardiac contractility Include Norepi Epi Dobutamine Dopamine ```

Answer 165

It is a very pure B agonist, but can cause vasodilation Positive inotrope but variable chronotrope Caution in hypotension as may worsen it or precipitate tachycardia

Answer 166

First choice vasopressor as it's a potent a agonist Minimal B adrenergic effects so little inotropy and chronotropy Causes increased PVR and BP Short T1/2 due to reuptake by uptake I channels at nerve terminals

Answer 167

Mixed A and B agonist depending on whether an organ has more alpha or beta receptors. Can vasoconstrict and vasodilate Potent inotrope and chronotrope so used in cardiac arrest Increased myocardial O2 consumption Retaken up by postsynaptic cells at uptake 2 channels so needs continuous IV infusion Useful in anaphylaxis as causes BP increase and dilates bronchi

Answer 168

``` Precursor of norepi Taken up by uptake 1 and 2 so short T1/2 Given low dose, can cause increased renal blood flow At moderate doses it shows B effects At high doses it shows a effects ```

Answer 169

Sympathetic activity is already high in shock Shows vasoconstriction, potentially causing ischaemia in the heart, limbs, gut or brain Increases cardiac work, potentially causing cardiac work and ischaemia

Answer 170

Amrinone/Milrinone They cause vasodilation and positive inotropy by preventing cAMP breakdown by phosphodiesterase III They are often added to dobutamine in intensive care settings

Answer 171

Thrombocytopenia Hypotension Arrhythmias due to increased cAMP Mortality

Answer 172

Levosimendan - Enhances Tn sensitivity to Ca2+ to increase inotropy Can cause arrhythmia or death

Answer 173

Atrial fibrillation and rate control as it slows HR, improves cardiac work and can help in acute or chronic heart failure Has no effect on mortality, but reduces symptoms and hospital admissions

Answer 174

1.6 day T1/2 so needs a loading dose for quick effects | Kidney elimination so care in renal patients

Answer 175

Blocks Na+ extrusion so that Na+ rises To compensate, a sodium/calcium exchanger activates, bringing more Ca2+ into the cell. But this is dangerous in hypokalemic patients as it can exacerbate digoxin toxicity as it binds competitively with the receptor It also augments vagal tone at the AV node, slowing AV conduction and ventricular rate

Answer 176

Acute heart failure with fast AF | Third line for rate control behind B blockers and diltiazem

Answer 177

``` Arrhythmias ECG changes (increased PR interval, LQTS, reverse tick sign during the ST segment) NV Abdo pain Fatigue Visual complaints Muscular weakness Dizziness ```

Answer 178

Hypokalemic patients increase digoxin effect side effects so care must be taken when given to a diuresed patient Also interacts with Quinidine, amiodarone, verapamil, diltiazem etc, resulting in increased plasma levels PGP inhibitors also reduce its excretion

Answer 179

Blood pressure above 140/90- mainly used for trials

Answer 180

It's a major risk factor for stroke, coronary artery disease and renal disease CVS death risk doubles for ever 20mmHg systolic and 10mmHg diastolic It is common, esp over 65, but poorly diagnosed and treated, esp in developing countries

Answer 181

Reduction in stroke, MI and mortality

Answer 182

Lifestyle changes, including diet (esp sodium), weight loss, exercise and alcohol reduction Drug therapy- mainly polypharmacy

Answer 183

It's a lifelong condition, assoc with concurrent disease, and often asymptomatic Therapy must be daily, and has side effects

Answer 184

``` Think ABCD Ace inhibitors/ARBs (first line) Beta blockers Calcium channel blockers Diuretics ```

Answer 185

Includes bendrofluazide, etc. Inhibits Na/Cl exchanger in DCT to decrease BP. They can also vasodilate as they open vascular K+ channels While plasma volume and CO return to normal after about a week due to the activation of RAAS, BP doesn't increase due to the action on blood vessels

Answer 186

``` Increase glucose, reducing tolerance Increase urate, precipitating gout Decrease potassium, sodium, MG++ Diuresis Erectile dysfunction ```

Answer 187

Frusemide Inhibits Na+/K+/Cl- cotransporter in the aschending LoH Potent diuretic with little antihypertensive effect alone Can cause dehydration and polyuria Used with ACEi for potent effect

Answer 188

Spironolactone (aldosterone antagonist) Inhibits distal Na+/C+ exchange Can cause hyperkalaemia as it blocks K+ wasting Used for people with resitant hypertension

Answer 189

Vasodilators like minoxidil that open K+ channels | Ones that act on the medulla to decrease sympathetic tone like methyldopa ad clonidine

Answer 190

Younger patients: Start with A or B Older: Start with C or D. (This is because young people have high renin hypertension whereas older people have low renin hypertension) Then: Add an A/B or C/D (whatever is opposite) Then: A or B + C AND D Then: Add alpha blocker, spirolactone or other diuretic

Answer 191

ACEi or diuretics

Answer 192

Alpha blocker

Answer 193

``` Can cause maternal and fetal complications, like abruption, IUGR and prematurity Can give central agents Labetalol Ca channel blockers Vasodilators STAY AWAY FROM ACEi Diuretics Atenolol ```

Answer 194

One pill with small doses of all classes of hypertensive medication (ABCD) All are sub-therapeutic so don't tend to give side effects, but they act synergistically to have a good effect

Answer 195

Intracellular fluid within cell membranes Extracellular fluid outside of cell membranes - Can be interstitial- found in the interstices, and the medium between which molecules travel between the ICF and intravascular space - Can be transcellular- formed from transportation activities of cells. Includes CSF, joint fluid, pericardial fluid. ECF: High sodium, low K ICF: Low sodium, high K Maintained by the na/K ATPase

Answer 196

Occurs in the kidney. GFR is approx 120mL.min The proximal tubule reabsorbs 2/3-3/4 of the salt and water The LoH reabsorbs water across the descending loop, and ascending loop reabsorbs 15-20% of sodium. Some sodium is reabsorbed in the DCT and CD

Answer 197

It is produced in the hypothalamus and released from the post pituitary when BP falls or osmolarity increases. It causes increased reabsorption of water to increase BP and reduce osmolarity

Answer 198

It is a mineralocorticoid stimulated by high potassium or Ang II It acts on the DCT and CD to increase sodium reabsorption and potassium excretion

Answer 199

``` Impaired thirst or consciousness No water access Burns Diarrhoea Blood loss Solute diuresis- HONK, DKA, drug overdose ```

Answer 200

A reduction in the amount or efficacy of ADH (central or nephrogenic) Presents with polyuria and water loss, with dilute urine Patient can't drink enough to keep up with losses, showing elevated plasma osmolality, hypernatremia and dehydration

Answer 201

Central: Pituitary not producing enough ADH due to brain injury etc Nephrogenic: Genetic issue with aquaporin channels, with partial or complete ADH resistance

Answer 202

Increased solutes in the tubules that cannot be reabsorbed causing increased urination When drinking can't keep up it leads to dehydration

Answer 203

Excessive sodium loss or excessive water retention (or both)

Answer 204

Presents with normal serum osmolarity as some other solute may be making the ICF volume higher For example, hyperglycaemia causes water to move into the ECF

Answer 205

Check urine osmolarity If low- consistent with water intoxication, psychotropic drugs Check volume status of patient - Hypovolemia- dehydration, with sodium loss but relatively less water loss. Due to diarrhoea, vomiting, bowel obstruction, burn, sweating, diuresis, addison's disease, ketonuria, osmotic diuresis or RTA Hypervolemia- fluid overload, with sodium retention but relatively more water retention. Due to cirrhosis or nephrotic syndrome Euvolaemic- due to SIADH, endocrinopathies like hypothyroid or low cortisol.

Answer 206

Inappropriate ADH is produced in the absence of normal stimuli such as a low BP. The body accumulates too much water, but this is stored in cells to the patient doesn't appear overloaded. Urine osmolality isn't low, and neither is urine sodium. Causes can be trauma, surgery, tumours, chronic lung disease or head injury

Answer 207

If slow onset- brain may adapt, so just confusion and 'not being themselves' If rapid onset- cerebral oedema leads to confusion, seizures and coma, requiring more vigorous treatment

Answer 208

If it is treated too quickly, it can cause central pontine myelinosis. This compresses myelin sheaths, causing spastic paralysis, quadraparesis, pseudobulbar palsy and irreversible locked-in syndrome

Answer 209

If slow onset: Generally just fluid restriction | If fast onset- normal saline slowly in the ICU

Answer 210

Carbonic anhydrase inhibitors- PCT Loop diuretics- LOH Thiazide diuretics- DCT K+ sparing diuretics- CD

Answer 211

It has a role in bone formation Co-factor in enzymatic reactions like ATP metabolism, muscle contraction/relaxation, normal neurological function, release of neurotransmitters Regulation of vascular tone Cardiac rhythm Platelet-activated thrombosis Stored in bone, muscle and soft tissue. Only 1% is extracellular When dissolved, it attracts water molecules, expanding its physical volume (active transport required to carry it across membranes)

Answer 212

Mainly by the kidney Some is reabsorbed in the PCT by the paracellular pathway Most is reabsorbed in the thick ascending limb of the LoH, moving paracellularly with Claudin 16/19 channel There is active reabsorption in the DCT

Answer 213

Hypermagnesurea, and hypomagnesaemia with potential stone formation Assessment by serum Mg, red cell Mg, 24h excretion, Mg retention test and isotope analysis Total body Mg can be low even if serum Mg is normal

Answer 214

Due to decreased dietary intake, GI malabsorption, diabetes, hyperaldosteronism, SIADH or renal loss (congenital, acuired or drug induced by aminoglycosides, amphotericin, omeprazole) Symptoms include weakness, fatigue, fasciculations, cramps, tetany, numbness, paraesthesia, seizures and arrhythmia Treated with oral or IV Mg

Answer 215

Hypermagnesaemia can be due to advanced CKD as compensatory mechanisms may be inadequate (or drug induced) Shows weakness, N&V, impaired breathing, heart arrhythmias

Answer 216

Mainly comes from fruit and vegetables. It has a high intracellular concentration and a low extracellular concentration

Answer 217

Immediate buffering occurs regulated by insulin (hyperglycaemia leads to K+ efflux from cell in exchange for glucose, causing hyperkalaemia) Acidosis can drive K+ in a similar away

Answer 218

K+ filters freely across the GBM, mainly reabsorbed by Na/K ATPase in the PCD, with some paracellular movement In the LoH it is absorbed by ROMK channels, the Na/K/Cl pump, and the Na/K pump Aldosterone regulates collecting tubule action

Answer 219

``` Muscle weakness Paralysis Cardiac conduction abnormalities Cramps Constipation ```

Answer 220

Mutation of K+ channels on cell membranes, triggered by high carb meals (insulin) or SNS activation causing periodic weakness

Answer 221

Renal losses - Aldosterone based, eg a tumour. Conns syndrome has an adrenal adenoma secreting aldosterone, presenting with hypokalaemia and hypertension - Licuorice - Diuretics Gut losses - K+ loss from diarrhoea or vomit Treated by treating underlying condition and replacing K+ orally or IV if severe

Answer 222

``` Fatigue Weakness Paraesthesia N&V Dyspnoea Palpitations Emergency as it causes PR prolongation, wide QRS and peaked T waves Can cause cardiac arrest and VF ```

Answer 223

Addison's disease Increased intake Disruption of cell intake (B blockers, acidosis, rhabdomyolysis) Decreased excretion- renal failure, hypoaldosteronism, ACEis/ARBs Pseudohyperkalaemia- due to a haemolysed blood sample due to blood cells being left long enough (give repeat test and ECG)

Answer 224

Decreased cortisol and aldosterone secretion, with high K+, low BP, weight loss, lethargy, and pigmentation due to excessive ACTH that crosses onto melanocytes Diagnosed on short synacthen test Treated with adrenal replacement

Answer 225

- Stabilization of AP with Ca2+ - B agonists and Insulin push K+ into cells, but give glucose concurrently Treat acidosis with oral/IV bicarbonate Reduce absorption with cation exchange products, binding to K+ in the gut and increasing fecal elimination Increased renal elimination with dialysis or a K+ wasting diuretic (Fruzemide)

Answer 226

The sympathetic and parasympathetic outflow from the ANS to the heart and blood vessels Components of the neuroendocrine system, including catecholamines, from adrenal medulla, RAAS, ADH and natriuretic peptides

Answer 227

Mechanoreceptors in the walls of blood vessels or cardiac chambers- contain stretch sensitive ion channels, and are activated by distension. Activation is therefore dependent on transmural pressure and the distensibility of the chamber in question

Answer 228

These are found in the carotid sinus (CNIX) and aortic arch (CNX). They give rise to myelinated and unmyelinated afferents, and also receive efferent innervation. Their threshold for activity is 30-50mmHg, and saturation is 150-180mmHg. Rate of firing is greater for pulsatile pressure than for steady pressure, even if the mean pressure is the same. They are also adaptive- if sustained high pressure occurs, they will fall back to control levels after a few hours to days. This is because they become less sensitive after activation.

Answer 229

It is affected by pressure, as well as being modulated by external neural factors and local paracrine effects NO and prostacyclin also increase baroreceptor sensitivity, while endothelin reduces it.

Answer 230

When arterial pressure falls, baroreceptors decrease their firing, resulting in augmented sympathetic outflow to the heart and vessels, reduced cardiac vagal activity, and increased catecholamine secretion from the adrenal muscle. This causes increased HR and inotropy, and constriction of precapillary sphincters And vice versa. Additionally, it causes changes in metabolism of ADH (and ang II more slowly)

Answer 231

Cardiac receptors have myelinated vagal afferents They are located in subendocardial tissue, mainly in the veno-atrial junctions. The atrial receptors are sensitive to the filling of highly compliant antrial chambers. The receptors emit bursts of firing synchronous with atrial contraction (a wave) or ate in ventricular systole, when atrial filling is most complete (v wave) They function to provide afferent information on the extent of cardiac filling They are directly influenced by changes in venous return and blood volume- considered to be low pressure/volume receptors

Answer 232

Unmyelinated C fibre afferents have greater density than the myelinated ones. Their output increases markedly when cardiac filling goes up. This causes reduced sympathetic outlfow to the heart and vessels, increased vagal activity, reduced catecholamine secretion, and decreased ADH and AngII

Answer 233

They are found in the supraoptic and paraventircular nuclei of the hypothalamus. They are stretch sensitive cells that detect changes in effective plasma osmolality by altering their volume They increase secretion and release of ADH in response to high plasma osmolality, and vice versa

Answer 234

There are peripheral chemoreceptors in the aortic and carotid bodies, and there are central chemoreceptors in the hindbrain They respond to increased PaCO2 and H+, and reduced levels of PaO2. For the peripheral chemoreceptors, the latter response is the most important. Increased discharge of peripheral chemoreceptors (due to reduced paO2, stimulates increased sympathetic drive to heart and blood vessels. This can cause some patients to be resistant to blood pressure drugs.

Answer 235

There are discrete groups of neurons in the ventrolateral medulla oblongata that are responsible for the tonic activity and reflex control of the autonomic nerves supplying the heart and vessels Preganglionic sympathetic neurons in the intermediolateral column of the thoracic spinal cord are the common pathway for sympathetic heart drive. Their activity is driven by cell bodies in the rostral ventrolateral medulla (RVLM) (stroke here causes poor BP control) Another neuron pool in the ventrolateral medula called the caudal ventrolateral medulla inhibits the RVLM activity The nucleus tractus solitarius is the initial processing and relay centre for sensory info from systemic arterial baroreceptors and cardiac/respiratory receptors Afferents enter the hindbrain in nerves IX and X, and synapse within the NTS. This is relayed to regions in the ventrolateral medulla for CV control Cardiac vagal nuclei (CVN) is the centre for cardiac parasympathetic vagal activity

Answer 236

Excitatory connections between NTS and CVN and NTS and CVLM Inhibitory between CVLM and RVLM Excitatory connection between RVLM and preganglionic sympathetic neurons

Answer 237

Lost by sweating, diuresis, diarrhoea, blood loss, vomiting | Gained through diet

Answer 238

There is a porous membrane between the plasma and ISF, so fluid and electrolyte are able to freely diffuse, with proteins being held back to form a pressure gradient The ISF/ECF barrier is fairly solid, so only H2O is able to diffuse freely

Answer 239

Osmotic gradients and hydrostatic pressure | Net water movement: K[Pc-Pt]-[Opl-Oif]

Answer 240

ICF volume will not alter, but plasma volume will increase. This increases blood volume, filling pressure of the heart, and cardiac output. If TPR is unchanged, this also increases BP.

Answer 241

This will reduce the osmolality of the ECF, causing water to flow into the ECF. At equilibrium, the volumes of both compartments will be increased

Answer 242

It tends to stay low until the threshold, when it increases linearly. However, after it reaches a max effective conc it increases in concentration, but has no further physiological increase

Answer 243

Decreased intrathoracic blood volume causes reduced cardiothoracic receptor firing, causing an increase in ADH quickly, stimulating thirst and water retention It also causes a slightly slower increase in sympathetic activity, and RAAS, causing sodium retention, and reduced capillary bed filtration pressure. This causes water to move from the ISF to plasma, called an internal transfusion

Answer 244

Operates over a period of days to weeks Immediately after acute loss, small preformed albumin are transferred into circulation Bulk is restored by hepatic synthesis over 3-4 days. Red cell is stimulated by EPO from the kidney as a response to low O2 tension.

Answer 245

10% or less: MAP normally unchanged, but pulse pressure declines (nonhypotensive haemorrhage). This is because the neurally mediated reflex mechanisms are enough to maintain homeostasis There is also no change in baroreceptor firing, but there is a significant decrease in firing of cardiac receptors, causing aldo and ADH to increase substantially, as well as HR and inotropy

Answer 246

Fall in systempic MAP, causing reduced baroreceptor firing, aldo and ADH increase, and HR and inotropy increase Resistance and capacitance vessels constrict Sometimes, organ beds may be shut down In extreme and uncompensated loss for long periods, haemorrhagic shock occurs and replacement may not be able to restore health.

Answer 247

Most cardiac filling occurs while lying down. Then standing, the blood has higher hydrostatic in the lower extremities, so Stroke volume drops as the blood moves into the ISF due to increased pressure

Answer 248

Baroreceptors buffer short term changes in pressure around a set point Cardiac receptors are not involved in beat to beat regulation of pressure, and contribute to setting the set point that baroreceptors work around

Answer 249

Transcellular gradients- fast, rapid equilibration | Renal excretion and tubular buffering, reabsorption in the DCT and CD- slow

Answer 250

``` Promotes: - Glucose uptake in muscle and adipose tissue - Glycolysis - Glycogen synthesis - Protein synthesis - Uptake of ions (potassium and phosphate) Reduces: - Ketogenesis - Proteolysis - Lipolysis - Glyconeolysis - Gluconeogenesis ```

Answer 251

Insulin Counterregulatory- glucagon, adrenalline and catecholamines, HGH, cortisol

Answer 252

At night, our insulin levels are very low. Steroid levels are highest just before we wake, and lowest in the middle of the night We still increase our blood sugar after eating, and reduce it afterwards- we can't trigger insulin before the glucose is absorbed (though this practice works well in treatment) Insulin concentration gradient is greatest after a meal.

Answer 253

It binds to its receptor and stimulates the GLUT4 transporter to move glucose into the cell

Answer 254

We transform triglycerides from fat into non-esterified fatty acids and glycerol (done with lipase, but inhibited by insulin). We then stimulate B-oxidation (done by glucagon) to form ketones using Acetyl CoA via the krebs cycle.

Answer 255

Lack of insulin | Excess glucagon

Answer 256

Acetoacetate Beta Hydroxybutyrate Acetone Acetoacetate and B are in an equilibrium- B is stimulated when there is more free H+ present, so is often there in acidosis.

Answer 257

In acidoses, there is more H+ in the circulation, forming CO2 and H2O and lessening HCO3-. The ketone bodies then circulate as anions, increasing the anion gap. In DKA, bicarbonate is replaced by B and acetoacetic acid, with the decrease in HCO3- approximating the increase in anion gap

Answer 258

If the acidosis is reduced, and the H+ is converted to CO2 and H2O, we have NaB and Cl- left over. Ketones are excreted as their salt. Cl- shows none of this loss We normally replace volume loss with 0.9% NaCl to salt load, but end up with hyperchloraemia after treating DKA- fixable by the kidneys (Note that treatment with insulin reduces B)

Answer 259

Measured using acetoacetate, as B cannot be detected, and the two are normally equal (note that in acidosis B increases to 3-5:1, meaning that urine ketones underestimate the severity of ketonaemia

Answer 260

Hyperglycaemia Acidosis below 7.3/bicarbonate <15 Presence of ketonaemia or ketouria (proposed change replaces last point with "serum B level of more than 3)

Answer 261

Lack of insulin plus physical stressor (illness, UTI etc) due to overstimulation of counterregulatory hormones that promote ketone formation

Answer 262

98% is intracellular

Answer 263

In potassium intake, extra potassium is shifted into cells, and then slowly removed and excreted This means we have feedforward control, which is rapid and anticipatory. This allows K to begin to be excreted before we see an increase in plasma ECF (the sensors are located in the gut)

Answer 264

Insulin causes upregulation of Na/K ATPase, resulting in increased K uptake (can be used to treat hyperkalaemia!) Consumption of a glucose rich meal therefore stimulates K shift independently of K content. Some evidence for glucagon and cAMP, meaning a protein rich meal increases these, causing glucagon release into the portal vein, increasing the transtubular potassium gradient, GFR and doubling potassium excretion

Answer 265

This is a backup for any major changes. It is mainly done using aldosterone, which increases uptake by cells throughout the body, as well as stimulating renal excretion

Answer 266

B2 adrenergic stimulation with epi and norepi. This causes K shift from ECF to ICF. Continuous contraction and relaxation of muscles causes extrusion of K from the cells, and these shift the K to be taken back up afterwards Acidosis increases K loss from cells, likely by inhibition of Na/K ATPase exchanger Cell lysis causes ICF K to be released into the ECF Increased ECF osmolarity causes water to be pulled rom cells, increasing relative ICF K conc, causing it to diffuse down its conc gradient into the ECF (and vice versa). This extra potassium tends to be excreted by the kidneys, thanks to aldosterone, causing a net whole body loss of potassium

Answer 267

It is reabsorbed early on in the nephron, and secreted later on Reabsorption happens mostly in the PCT, some in ascending thick LoH by N/L/2Cl channel. Secretion occurs through the DCT and collecting duct- where most of the variation occurs. About 4% remains by the time the DCT is reached, though due to excretion the body can secrete more than initially filtered out by the GFR The kidney is slow to conserve K+ K+ depletion and hypokalaemia can result if K+ intake is restricted

Answer 268

- Activity of Na/K ATPase on basolateral membranes of intercalated cells - Permeability of the luminal membrane - Electrochemical gradient from lumen to blood (Aldosterone works on the principal cells of the CD and causes changes here slowly)

Answer 269

Increased serum K+ - Over 4.1, there is a steep nonlinear effect on K+ secretion Distal tubular flow rate - Increased distal flow increases secretion, as if you have a higher flow rate, there is less reabsorption time, and an increased gradient between the lumen and the blood Decreased flow increases serum potassium as in severe renal impairment (Diuretics increase flow and decrease serum potassium- similar to diabetes effects) Aldosterone

Answer 270

Acidosis decreases K+ secretion due to effects on Na/K ATPase Alkalosis increases secretion

Answer 271

Plasma lipids include cholesterol, found in membranes, bile salts and as steroid precursors, as well as triglycerides, fatty acids and phospholipids

Answer 272

LDL- adverse effects. Transport from liver to peripheral tissues. Predisposes atherosclerosis HDL- beneficial effects- delivery from periphery to liver. Good prognostic sign. Slows atherosclerosis Triglycerides- adverse vascular effects and pancreatitis

Answer 273

Primary prevention: Reduction in vascular events, but small effect on mortality Secondary prevention: Large beneficial effects, reduced CVS mortality and morbidity (Total cholesterol 1mmol/L reduction causes a 25% decrease in vascular effects) Different risk factors also synergize, so all need to be targeted

Answer 274

History- look for signs of end organ damage Exam- check BP, xanthoma, xanthelasmata Investigations- urea, electrolytes, fasting cholesterol, LDL, HDL, Trigs Glucose and ECG

Answer 275

In secondary prevention in those post angina, MI, CVA, PVD, or diabetics Also in primary prevention for those with CVS risk >30%/10 years

Answer 276

Lifestyle changes Drugs - Statins (lower total, LDL chol, trigs. Increase HDL). Eg. simvastatin - Fibrates (lower trigs lots, increase HDL) eg. bezabifrate - Exetimibe (decrease TC and LDL) - Nicotinic acid (lower trigs only)

Answer 277

Used in high CVS risk patients, diabetics, and for familial hypercholesterolaemia Also used in secondary prevention after MI, angina, VCA, PVD, TIA. They competitively inhibit HMG CoA reductase, causing reduced cholesterol synthesis, as well as stimulating hepatocytes to increase LDL receptors on their surface, stimulating uptake of circulating LDL Metabolized by CYP3A4, so can interact with drugs

Answer 278

Myalgia Myositis (stop if creatinine kinase increases markedly) Rhabdomyolysis Deranged LFTs (Stop when ALT at 3x) Fibrate, amiodarone, verapamil, diltiazem, erythromycin interaction Teratogenic Rarely causes diabetes

Answer 279

Occurs in 1/10000 per years | Related to statin concentration

Answer 280

They are also anti-thrombotic and anti-inflammatory | They modulate the immune system, and have some benefits occurring even before cholesterol decreases

Answer 281

Eg Bezafibrate Indicated for isolated hypertriglyceridaemia (as well as diet, exercise, weigh loss, alcohol and diabetes interventions) Also for combined therapy with statins for resistant hypercholesterolaemia It is a PPARa agonist, which causes reduced VLDL production, and increased clearance as well as increased skeletal muscle fatty acid storage. It also causes lipoprotein lipase to break down triglycerides

Answer 282

GI upset Deranged LFTs Myositis (risk increases with concurrent statins)

Answer 283

Low efficacy as monotherapy, but used with statins It reduces cholesterol absorption, delivery of cholesterol to the liver, increases LDL receptor expression in the liver, and affects enterohepatic circulation It blocks a channel bringing cholesterol in from the gut

Answer 284

Abdominal pain | Diarrhoea

Answer 285

Also known as vitamin B3 very rarely used unless in combination therapy Causes reduced fatty acid mobilisation from the periphery, reduced TG/VLDL production, and reduced HDL degradation

Answer 286

GI intolerance Flushing Dry skin

Answer 287

Now uncommonly used Drugs such as cholestyramine bind bile acids, stopping enterohepatic circulation, reducing exogenous cholesterol absorption, increasing conversion of endogenous cholesterol to bile acids, and increasing hepatic LDL receptor expression

Answer 288

Many GI side effects | Impairment of ADEK absorption and absorption of other drugs like digoxin, warfarin, thiazides etc

Answer 289

Often lifelong, with side effects There is lots of evidence of CV benefit However, detection and active treatment needs to be improved

Answer 290

PCSK 9 inhibitors- decrease LDL by prolonging the life of the LDL receptor Also monoclonal antibodies (evolocumab) and an RNA inhibitor (inclisiran)

Answer 291

as it moves through the capillaries, it collects co2, causing it to become more acidic the more capillaries it has passed. This is done by pushing equilibrium towards bicarbonate

Answer 292

pH = 6.2 + log10[HCO3-]/[0.03xPCO2] | PCO2 is proportional to VCO2/VA.

Answer 293

Arterial PCO2 and pH are sensed by chemoreceptors in the brain and aortic/carotid bodies Centrally, increased pCO2 and pH stimulate ventilatory drive and vice versa, via the ventrolateral medulla Hypoxia is sensed peripherally and also stimulated ventilatory drive As hydrogen ions don't cross the BBB, central chemoreceptors actually sense CO2 and other secondary changes in pH due to metabolism/resp changes Increased CO2 is the main driver of respiration

Answer 294

PO2 is a nonlinear stimulus of ventilation, with a great increase in drive only occurring at PaO2 at 60 or lower- not potent PCO2 is linear and potent

Answer 295

Requires: - Reabsorption of all HCO3- - Regeneration of all HCO3- lost in the buffering of nonvolatile acids - Removal of fixed acids incorporated into the non-bicarbonate buffer systems Done in the PCT

Answer 296

The Na/KATPase causes exchange of 3 sodium into the blood for 2K+ into the cell/. There is therefore a built in gradient of sodium- high outside the cell, low inside. This causes a negative cell potential. The Na/H Antiporter causes H+ to be secreted into the lumen of the tubule in exchange for Na+. The H+ joins with the HCO3- to cause H2CO3. Carbonic anhydrase on the luminal surface of the cells cases it to form CO2 and H2O, which are then freely diffused into the cell This then reacts again to form H+ and HCO3-. The bicarbonates then move down the electrical gradient to outside the cell. However, this also causes some sodium to be moved with it

Answer 297

Glutamine is converted by a dehydrogenase into glutarate. This is then released as glucose and bicarbonate. It also produces ammonium, which is exchanged for sodium to move the NH3 into the tubular lumen, where it joins with H+ to form NH4+. Cl- also joins on to this, allowing the whole molecule to be excreted

Answer 298

It joins with NH3 as well as HPO42- to excrete these acids

Answer 299

Secretion of H+ by the nephron is increased, and nearly all HCO3- is reabsorbed. Alkalosis: vice versa HCO3- is inversely related to plasma Cl- as they share the same electrical gradient. A loss of Cl- means bicarb has to be reabsorbed, causing alkalosis

Answer 300

HCO3- is inversely related to plasma K+. This is increased by corticosteroids like in cushing- high levels of aldo lead to high ECF HCO3- This is because aldo cause Na sparing and K and H+ wasting via the Na/H antiporter. H loss is matched by increased HCO3- reabsorption, causing metabolic alkalosis with hypochloraemia and hypokalaemia, often with expanded ECF volume

Answer 301

Decrease secretion of hydrogen ions Reduce reabsorption of HCO3- Reduce renal net acid excretion to restore pH, but reduces HCO3- reabsorption

Answer 302

Increase ventilation to induce slight hypocapnia We know it's chronic when a small amount of acid is being produced to try to compensate- resulting in a smaller than expected base excess

Answer 303

Through oxidative metabolism, which produced CO2 | Protein catabolism

Answer 304

``` Via buffering (transient, so short term) Excretion (regulates long-term) This is done either in the lungs (CO2 removed via gas exchange) or in the kidneys (acid from proteins catabolism) ```

Answer 305

Carbonic acid | H2O + CO2 H2CO3 H+ + HCO3-

Answer 306

Those produced by protein catabolism, eg. H2SO4 Doesn't equilibrate, and therefore is excreted in the kidneys Increases in ischaema or extreme exercise (lactic acid) or DKA (B hydroxybutyric acid)

Answer 307

For a given pH, as CO2 increases, bicarbonate also increases. This is because the CO2 is beginning to be converted to HCO3- to buffer it out. As H+ increases, pH drops, and we get acid combining with bicarbonate, causing it to drop again

Answer 308

Bicarbonate is the main extracellular buffer, and so blood and ECF is good for short term buffering H+ combines with intracellular proteins/organic phosphates in tissue and bone They are transported across the cell membrane in exchange for Na+ and H+. This is a slow process Ultimately, fixed acids are excreted by the kidney

Answer 309

Bicarbonate, phosphate and protein buffer systems all use the ka = [H+][HCO3-]/[H2CO3] style system However this is not good for calculating intracellular pH, as it isn't homogenous with the ecf

Answer 310

If CO2 is added, the bicarbonate increases, and pH decreases due to acidity In the plasma, it is buffered by non-bicarbonate buffers, such as phosphate and acid proteins In The RBCs it is buffered to produce HCO3-, as well as being used to bind to amino groups attached to the Hb. It forms an equilibrium with carbamino Hb This causes red cells to swell slightly, as well as causing the Hb to release O2

Answer 311

Carbamino Hb is responsible for 30% of the CO2 eliminated from the lungs As O2 falls, the Hb becomes reduced in capillaries, making it a better base and therefore a better buffer

Answer 312

An increased ability of the blood to carry CO2 when oxyHb is decreased. This is because DeoxyHb is more effective than oxy at forming carbamino compouds

Answer 313

Chloride shift accounts for 60% of CO2 carriage, as it enters the cell, causing a switch with bicarbonate exiting the cell. This attaches to CO2 in the plasma, carrying it out towards the lungs 10% dissolves H+ is also buffered by histidine

Answer 314

Base excess appears in metabolic acidosis, and is measured by titiration of a blood sample with a strong acid to pH 7.4 at a standard PCO2 and temp Base defecit is there reverse

Answer 315

Inadequate ventilation to clear enough CO2

Answer 316

Overventilation relative to degree of CO2- like anxiety, or overbreathing Causes lightheaddness, limb tingling- need to place bag over nose and mouth

Answer 317

Excess acid production due to ischaemia, DKA or reduced excretion by kidneys or loss of bicarbonate (due to tubulopathy in PCT, bicarbonate wasting, congenital issue, diarrhoea)

Answer 318

Vomiting, loss of acid production

Answer 319

Metabolic alkalosis- loss of HCl from the stomach if severe and recurrent

Answer 320

Mild acidosis, normal CO2 and low bicarbonate due to potassium and bicarbonate loss

Answer 321

Respiratory alkalosis

Answer 322

Mild acidosis, high CO2 and a base excess

Answer 323

If plasma bicarbonate is more than 24mmol/L it is excreted by the kidney. Anything under this promotes reabsorption and regeneration of all filtered HCO3-, and excretion of filtered fixed acid

Answer 324

There needs to be both an initiator as well as an impaired renal correction mechanism

Answer 325

A gain of alkali in the ECF May be exogenous (IV infusion, citrate in transfused blood). May be endogenous (metabolism of ketoanions to produce bicarbonate) May be a loss of H+ from the ECF. May be from kidneys (diuretics) or gut (vomiting of gastric fluid, NG suction, infant pyloric stenosis)

Answer 326

A lack of chloride increased HCO3- reabsorption. This because Cl- and HCO2- are the only anions present in appreciable concentrations in the ECF. Due to Na+ and K+ reabsorption we need to reabsorb some balancing anions to maintain electroneutrality- deficiency of one increases reabsorption of the other.

Answer 327

If the person is volume depleted due to a diuretic, they will increase their aldosterone levels and losing NaCl, causing increased bicarb reabsorption. A low salt diet can also do this

Answer 328

Rare but important Can be due to hyperaldosteronism- either primary or secondary Increased distal tubular sodium reabsorption increases K and H loss. Increased HCO3- reabsorption matches the increased loss of H+, so you shift electroneutrality further in favour of K and H loss This can happen in 2 ways Indirect: Increased Na reabsorption causes increased negative cell voltage promoting H+ secretion Direct: Stimulation of H+ ATPase, upregulating the anion exchanger and facilitating HCO3-/Cl exchange

Answer 329

It is the difference between the concs of major cation (Na+) and anions (HCO3-, Cl-). iF the anion of the nonvolatile acid is not Cl- (eg. lactate or B hydroxybutyrate) the anion gap will increase, suggesting that acid is being produced in the body.

Answer 330

We can use the alveolar arterial gradient: PAO2 = 150-PACO2/0.8 +2 Substract PaO2 from this. Over 25mmHg difference in elderly or 12 in young indicates impaired lung diffusion

Answer 331

The compensation is metabolic alkalosis due to increased CO2 retention- HCO3- will elevate in response and pH will drop Note that if there iw an ongoing metabolic acidosis the HCO3- may be normal, and pH may be slightly lower than expected.

Answer 332

If there is limited O2 delivery to the tissues, lactic acidosis may develop due to ischaemia Can be determined with an anion gap

Answer 333

Normal- involves ectopics Bradycardias- involves AV or SN conduction disorders Tachycardias- includes automaticity and triggered activity issues as well as reentrant mechanisms

Answer 334

Bradycardias: Physiological from the sinus node, AV node, or neurally mediated Tachycardias: Can be atrial, junctional (supraventricular tachycardia) or ventricular due to a scar

Answer 335

``` Single chamber: AAI/VVI Dual chamber (DDD) Pacemaker or ICD (Implantable cardiac defibrillator ```

Answer 336

Helps with rate support, AV synchrony, VV synchrone, monitoring, syncope etc Good for those at risk of sudden cardiac failure

Answer 337

Pacemaker: - Used in high grade AV block (second, third or complete) - Symptomatic sinus node disease ICD: Used for people who have had aborted sudden cardiac death - Sustained VT in structural heart disease CRT: - Used for cardiomypoathy and Left bundle branch block

Answer 338

A common condition, but the majority are benign- Assessment can be examination and an ECG/echo Treat either with reassurance, or with suppressive drugs such as B blockers and class 1 agents. Can also withdraw responsible drugs, manage the underlying condition, or insert a device/perform a surgery.

Answer 339

Sodium channel agents (mostly blockers) 1A reduce Vmax and prolong APs by decreasing conduction velocity and prolonging refractoriness- eg. quinidine, procainamide 1B shorten AP without affecting Vmax by decreasing the refractory period- phenytoin, lidocaine 1C reduce Vmax and slow conduction but don't affect the refractory period

Answer 340

Beta blockers, such as metoprolol, atenolol etc Blocks the B adrenergic system, decreasing sympathetic tone Can result in fatigue and bradycardia- so start low, go slow Contraindicated for asthma but not COPD Prescribed for atrial and ventricular arrhythmias

Answer 341

Potassium channel blockers to increase repolarisation - Sotalol, amiodarone Can affect defibrillation thresholds- amiodarone increases, sotalol decreases. Reduce digoxin with amiodarone Toxic levels may build up

Answer 342

Slow calcium channel blockers | - Verapamil, diltiazem, nifedipine

Answer 343

They affect the cell membranes, ANS and vagal tone Increased vagal tone decreases HR, slows AV node conduction and decreases SA node automaticity Cell membrane activity affects the conduction velocity, length of the refractory period, and automaticity of the SA or AV node.

Answer 344

Digoxin: Increases PNS activity to slow atrial rate and AV nodal conduction Adenosine- typically IV bolus. Causes AV node block

Answer 345

Can do medical therapy (adenosine when needed) | Or ablation therapy

Answer 346

Common with varying symptoms. Need to aim for either rhythm (sotalol) or rate (AV node slowing) control. Issues with anticoagulation

Answer 347

Can be reentrant or an automatic trigger around or in scar tissue VT invades the rest of the ventricles with a broad complex, activating the whole chamber through cell to cell contact rather than the fast conduction His Purkinje network The atria contract and activate independently

Answer 348

VF- emergency resuscitation Need to treat underlying pathology- ischaemia, bradycardia, structural, metabolic or drug causes Give anti ischaemic and ACEi drugs, antiarrhythmics (Class II/III), potentially implant an ICD or pacemaker, and potentially surgery

Answer 349

Side effect profile is large- myalgia, gait disturbance, insomnia, interaction with warfarin Issues with loading doses Toxicity can cause pulmonary fibrosis, hypo/hyperthyroidism, liver failure, bone marrow suppression, renal failure, photosensitivity, and corneal deposits

RBF Flashcards

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