cardiovascular 4

Question 1

describe the following results from a left to right shunt: bounding pulse, continuous murmur, mitral valve leak

Answer 1

Bounding pulse - Increase in systolic and decrease in diastolic resulting in increased pulse pressure
- Increase systolic pressure - ejection of blood from the heart - stroke volume increased as increase end diastolic volume (more blood going around lungs back into left atrium and ventricle)
- Decrease diastolic pressure - blood volume and arteriolar resistance - blood volume is decreased as leakage of blood into the PDA - loss of pressure
Continuous murmur - cannot hear S1 and S2 heart sounds - generally caused by PDA
Mitral valve leak - compensatory method for increased volume is eccentric hypertrophy resulting in stretched heart which can pull apart the mitral valve causing incompetence

Question 2

What are the consequences of a patent ductus arteriosus

Answer 2

1) left to right shunt - more blood being pumped around pulmonary circulation
2) eccentric hypertrophy of left ventricle due to increase in volume
3) can result in increase resistance in pulmonary system - cor pulmonale due to remodelling of the vessels
4) changes the shunt to right to left
5) differential cyanosis - PDA after brachiocephalic and left subclavian therefore they are getting oxygenated blood (cranial body) while caudal body gets mixture of oxgenated and deoxygenated blood as bypassing the lungs

Question 3

What are the 4 clinical signs of right to left shunt

Answer 3

1) Red mucus membrane - differential cyanosis results in increase red blood cell production resulting in increased PCV and therefore more intense red in cranial mucus membranes
2) Blue mucus membrane in caudal areas - differential cyanosis results in deoxygenated blood within the caudal area
3) Weakness hind-limbs - differential cyanosis results in deoxygenated blood in the caudal area
4) Seizures - differential cyanosis results in increase red blood cell production (explained above) resulting in increased viscosity of the blood and therefore decrease flow within the brain as increase resistance - resulting in hypoxic damage to areas of the brain - seizures

Question 4

what are the 2 treatment options for right to left shunts and what wouldn’t you do

Answer 4

Cannot undergo surgery as permanent remodelling of the pulmonary vessels has already occurred and therefore closing the PDA will only increase the resistance in the pulmonary system which will lead to right sided congestive heart failure

1) Chemotherapeutic drugs to suppress red blood cell production
- Body is responding to hypoxia from low circulating blood volume by increasing red blood cell production resulting in increased viscosity which in turn leads to seizures therefore to reduce seizures decrease red blood cells
2) Blood letting
- Need to be careful about how much blood you take out of the animal as taking out red blood cells that are already deoxygenated
- Remove blood to decrease blood volume - this will activate RAAS which increases water retention and therefore helps counteract the increase in red blood cells - reducing the viscosity and therefore decreasing the seizures

Question 5

What are the possible adverse effects of myocardial degeneration, necrosis, inflammation or neoplasia on cardiac function

Answer 5

• if animals survive the initial phase the damaged areas will undergo reparative fibrosis
• neoplasm - intra-pericardial haemorrhage (with risk of cardiac tamponade), impairment of chamber filling or emptying, valvular insufficiency, intra-cardiac thrombosis and hence thromboembolism, and/or metastasis to other sites

Question 6

what is the common cause of arrhythmia/dysrhythmia

Answer 6

secondary to myocardial damage rather than to primary lesions of the cardiac conduction system
- - injuried myocadrium may depolarise repeatedly independent on conduction tissue

Question 7

What are potnetial causes of hydropic or fatty degeneration of cardiac myofibres

Answer 7

hydropic - problems with Na+/K+ pump - hypoxia

fatty degeneration - hepatic insufficiency - increase fatty acids in the blood

Question 8

What is brown atrophy of the heart, In which species is it most commonly seen and when

Answer 8

• atrophy is often accompanied by gross dark brown discolouration of the myocardium (“brown atrophy”) due to severe intra-cellular accumulation of golden-brown lipofuscin pigment (“wear-and- tear pigment”) caused by cumulative peroxidative injury to phospholipids of cell and organelle membranes
• high-producing dairy cows, particularly Ayrshire cows (in which there may be a genetic predisposition

Question 9

What are the two main forms of tissue mineralisation and for each describe a cause

Answer 9

Dystrophic mineralisation
- white muscle disease (due to vitamin E or selenium deficiency
Metastatic minearlisation -
may be prominent grossly in such conditions as vitamin D toxicity and vitamin D analogue poisoning

Question 10

when is the capacity of mitotic division of cardiac myofribres lost

Answer 10

decreases in late foetal life and is lost in the early neonatal period

Question 11

Where are foci of myocardial necrosis most likely to be found in the heart and why

Answer 11

left ventricle, especially in the subendocardial myocardium of the interventricular septum and in the papillary muscles (these are the sites of greatest chamber wall tension development during systole)

Question 12

How long must a patient survive after necrosis of cardiac myofibres before the lesions are likely to become grossly obvious and what gross lesions might you see

Answer 12

4-12 hours post-injury when subtle pallor may emerge
18-24 hours - necrotic zone is pale maybe dystrophic mineralisation
2-4 days - necrotic foci become more prominent due to reactive hyperaemia with neutrophil and macrophages
7 days - fibroplasia

Question 13

list 4 causes of mycardial necrosis and what do they attack

Answer 13

1) ischaemia/hypoxia - shock
2) excess catecholamines - overdose of synpathomimetric drugs
3) nutritional deficiencies - vitamin E/selenium deficiency - white muscle disease
4) drugs and chemical toxins - fluoroactetate 1080
Attack cardiac and skeletal myofibres

Question 14

how long can cardiac myofibres tolerate hypoxic conditions and why common in humans

Answer 14

20-30 minutes of hypoxia - necrosis of cardiac myofibres

consequence of atherosclerosis of the coronary arteries with thrombosis +/- thromboembolism

Question 15

List 3 causes of myocardial ischaemic/hypoxic injury

Answer 15

1) thrombosis/thromboembolism of coronary arterial branches
2) aged animals - lumina of coronary arteries and arterioles may decrease because of arteriosclerosis/arteriolosclerosis
3) dilated and hypertrophied hearts

Question 16

What are the circumstances in domestic animals in which β-adrenergic stimulation of the myocardium can result in myocardial necrosis

Answer 16

overdose with negative inotropic drugs (e.g. β-adrenergic blockers such as propanolol

Question 17

List 4 plants that contain toxins capable of causing myocardial necrosis and what species most likely to be intoxicated

Answer 17

1) Avocado leaves - horses, birds
2) phalaris - sheep
3) fluoroacetate containing plants - ruminants
4) canola oil

Question 18

What is the aetiopathogenesis of white muscle disease (nutritional myopathy) and which
animals are most likely to be affected?

Answer 18

Most likely effect domestic ruminants such as lambs and calves
- highly unpredictable occurrence, with triggering factors including rapid growth in juvenile animals, unaccustomed exercise, cold weather, dietary factors (e.g. high intake of unsaturated fatty acids from pasture plants), iron injections that increase demand for anti-oxidants etc

Question 19

what gross lesions would you expect to find in a lamb or beef calf that has died from white muscle disease

Answer 19

mineralisation on major skeletal muscles of the shoulder, myocardium (right ventricle lambs, left ventricle calves)

Question 20

What is the aetiopathogenesis of mulberry heart disease in young pigs

Answer 20

excellent nutritional condition at 2-4 months of age

- sudden death is due to acute right- and/or left-sided congestive heart failure +/- ventricular arrhythmia

Question 21

What cardiac lesions might you expect to find in a pig that has died from mulberry heart
disease

Answer 21

multifocal to diffuse haemorrhage in the epicardium, myocardium and subendocardium and patchy myocardial pallor due to multifocal necrosis
usually only minor dystrophic mineralisation of the affected myocardium

Question 22

List 4 large groups of causes of myocarditis and examples within

Answer 22

1) viruses - canine parvovirus
2) protozoa - toxoplasma gondii
3) helminths - nematodes
4) bacteria - clostridium

Question 23

How do you reach a diagnosis of

cardiomyopathy

Answer 23

Always by exclusion of other possible causes - further down the diagnosis steps

Question 24

what are the gross characteristics of hypertrophic cardiomyopathy what common in and what effect on function

Answer 24

• cardiomegaly with prominent concentric hypertrophy of the LV and IV septum
• common in cats
• myocardial contractility is usually increased or normal but diastolic filling of the ventricles is decreased (i.e. diastolic failure)

Question 25

What are the 3 major forms of cardiomyopathy

Answer 25

1) hypertrophic cardiomyopathy 2) dilated cardiomyopathy 3) restrictive cardiomyopathy

Question 26

what are the gross characteristics of dilated cardiomyopathy, what major effect does it have on cardiac function and which species most common in

Answer 26

- heart appears flabby and the chambers thin-walled - characterised by decreased myocardial contractility, increased end-diastolic volume of the ventricles and decreased ventricular ejection (i.e. systolic failure) - common in dogs

Question 27

what was previously an important cause for cardiomypoathy in cats

Answer 27

causal association with taurine deficiency was recognised in the late 1980s and the taurine content of commercial diets was increased accordingly

Question 28

what effect does restrictive cardiomyopathy have on cardiac function, which species common

Answer 28

- stiffness, reduced ventricular compliance and impaired diastolic filling of especially the LV - myocardial contractility is usually normal - mainly seen in middle-aged or older cats

Question 29

what is a common consequence of cardiomyopathy in cats and what clinical signs would alert you to this

Answer 29

intra-cardiac thrombosis and thromboembolism - typically see sudden onset of bilateral or unilateral hindlimb paresis, with absence of femoral pulses, cool hindlimbs, cyanotic nail beds and firm painful hindlimb muscles - the ischaemic hindlimb muscles undergo dry gangrene

Question 30

what neoplasm can involve the heart in dogs, what is the most common form and where does it arise and how behave

Answer 30

metastases from malignancies arising elsewhere but some may be primary haemangiosarcoma - arises as a red-black haemorrhagic mass subepicardially in the wall of the right atrium or at the entrance to the right auricle ○ tends to metastasise widely, often as “cannonball” metastases to the lungs

Question 31

what is the tumour that commonly involve heart in ruminants

Answer 31

Peripheral nerve sheath tumour

Question 32

List some differentials for gross appearance of small cream-white foci randomly scattered in the heart

Answer 32

1) dystrophic or metastatic minearlisation - white muscle disease 2) fluid fluid parasitic cysts 3) multifocal myocarditis from bacteia, virus, parasite 4) causes of myocardial necrosis such as ischaemia/hypoxia, plant toxins

Question 33

what 4 sympathetic compensatory effects of heart failure and negatives

Answer 33

1) vasoconstriction - increase TRP and maintain BP but increase afterload 2) increase HR and SV so increase in CO but increase work 3) renal effects - increase BP by retention of H2O and Na - increase preload increased TRP to maintain BP - increase afterload 4) cardiac hypertrophy to increase SV - increase work of contraction

Question 34

What occurs with chronic activation of sympathetic nervous system

Answer 34

1) Reduced baroreceptor sensitivity--> maintained sympathetic drive even when MAP is appropriate 2) Down regulation of beta receptors in the heart--> reduced capacity of heart to respond to sympathetic stimulation Chronic activation of RAAS • Persistent vasoconstriction --> increased pre load and afterload • Increased blood volume--> increased preload • Increased angiotensin--> decreased baroreceptor sensitivity myocardial toxicity

Question 35

What are the 3 downsides of cardiac hypertrophy

Answer 35

1) Decreased capillary and mitochondrial density --> decreased energy supply 2) Decreased inotropy and lusitropy - decreased inotropy--> “weak” heart (systolic heart failure) - decreased lusitropy--> “stiff” heart (diastolic heart failure) 3) Increased risk of arrythmias - Poor supply of oxygen to cardiac myocytes

Question 36

What are the 5 main groups of drugs to treat heart failure

Answer 36

1) positive inotropes 2) negative inotropes 3) diuretics 4) vasodilators 5) antiarrythmics

Question 37

what do positive ionotropes do, how problematic and list the 4 classes

Answer 37

- increases cardiac contractility by increasing intracellular calcium - increase workload on heart - may be bad 1) Cardiac glycosides 2) B adrenoceptor agonists (mimic adrenalin and noradrenalin) 3) Phosphodiesterase inhibitors 4) Calcium sensitisers

Question 38

Cardiac glycosides what class of drug, example and mechanism of action

Answer 38

positive iontropes - digoxin - Inhibit Na/K ATPase pump - Increased intracellular Na - Decreased Na movement into cell - Decreased exchange of calcium out of cell - increase intracellular concentration - increase contractility

Question 39

explain the effects Cardiac glycosides have on the heart

Answer 39

positive iontrope - Direct effect on the myocardium: ○ Shortened refractory period in atria & ventricles - Vagal effects on pacemaker tissues: ○ Slowed AV conduction ○ Vagal effect on SA and AV nodes (slowing of HR) - increase vagal tone - Decreased sympathetic drive- mediated from medullary cardiovascular centre

Question 40

Explain the possible toxic effects of cardiac glycosides

Answer 40

``` Low therapeutic index (TI = max non toxic dose/minimum effective dose • Na/K ATPase pumps are everywhere! - Myocardial effects--> arrhythmias - G-I signs - CNS signs - Ototoxicity • Hypokalaemia exacerbates toxicities… Digoxin competes with K+ for the Na/K ATPase pump so decrease retention of K+ in kidneys - hypokalaemia - also occurs with diuretics so could be an issue if use together ```

Question 41

Beta adrenoreceptor agonists what type of drug in heart failure, effects, adverse effects and examples

Answer 41

positive inotropes - use in severe acute heart failure - increase HR adverse effects - arrhythmias, increase work load on heart 1) dobutamine - beta 1 specific 2) adrenaline - beta 1 and 2 - trachycardia

Question 42

Phosphodiesterase inhibitors what type of drug in heart failure and effects

Answer 42

``` positive inotrope Inhibition of phosphodiesterase - Less b’down of cAMP - Higher cAMP--> - Increased Ca influx --> - Increased cardiac contractility ```

Question 43

Calcium sensitisers what type of drug in heart failure, example, effect and how does it work

Answer 43

Pimobendan • Similar mechanism to other PDE inhibitors ( increased Ca (intracellular) through increased cAMP) - potent vasodilatory - reduce pre and afterload - don't know how it works

Question 44

negative inotropes how work and the 2 classes

Answer 44

- To reduce the work load on a failing heart 1) Beta adrenergic antagonists 2) Calcium channel blockers

Question 45

Beta antagonists what type of drug in heart failure, effect and side effects

Answer 45

negative inotropes Decreased cardiotoxic effects of excessive sympathetic drive - improving beta receptor expression • Decreased activation of RAAS so decreased afterload and preload - decreased HR and contractility - Increased ‘window’ for coronary perfusion Side effects - Some animals relying on sympathetic drive to survive in this state and therefore may push animal into decompensatory heart failure so need to consider whether have the proper reserve - Broncho constriction in asthmatics (more humans) - Hypoglycaemia in diabetics - Bradycardia and heart block - Fatigue - Cold extremities - Heart failure at higher doses

Question 46

what type of vessels are most vunreable to compression, occlusion, neoplastic invasion by extension of inflammation from adjacent tissues

Answer 46

veins and lymphatics due to narrower walls than arteries and arterioles

Question 47

how is the inner and outer half of the wall of a blood vessel suppplied with oxygen

Answer 47

- vasa vasorum supply the tunica adventitia and outer half of the tunica media - the tunica intima and inner half of the tunica media are avascular and rely on oxygen and nutrient diffusion from the vessel lumen

Question 48

How do vascular smooth muscle cells respond to sustained increase in blood volume or pressure

Answer 48

by undergoing hypertrophy and, to a lesser extent, hyperplasia

Question 49

what causes hypertrophy of the smooth muscle cells of arterioles and what are possible consequences

Answer 49

- sustained hypertension (increased blood pressure) or hyperperfusion (increase blood flow) - consequence is further hypertension as lumen decreases - increasing resistance to flow

Question 50

what circumstances does sustained arteriolar vasoconstriction occur and what is the possible consequence

Answer 50

1) sustained vasoconstrction in cold climates - frost bite 2) mycotoxins consequence - sustained arteriolar vasoconstriction - exacerbation of the hypertension (due to increased vascular resistance) +/- downstream ischaemic tissue injury

Question 51

What does arteriosclerosis look like grossly, what is the clinical significance and is it common

Answer 51

- may not be grossly obvious, slightly raised, thickened, wrinkled intima - rarely clinical significance - common in older domestic animals

Question 52

what are the characteristic lesions of atherosclerosis, when is it likely to develop and what is the clinical significance

Answer 52

1) atheroma (fibrofatty plaque) - core of lipid covered by fibrous cap 2) fatty streak - soft, smooth, lipid-rich - myocardial infarction, and ischaemic injury in peripheral tissues - generally not clinically significant

Question 53

list 5 circumstances in which fiibrinoid change develop in domestic animals

Answer 53

1) renal failure 2) system hypertension 3) vasculitis 4) selenium/vitamin E deficiency 5) oedema disease in pigs

Question 54

in what disease states is arterial mineralisation occur

Answer 54

areas of vasculitis, arteriosclerosis, atherosclerosis or thrombosis

Question 55

Apart from trauma, what are potential causes of arterial rupture in domestic animals

Answer 55

- spontaneous rupture pf uterine artery, internal carotid artery, aorta - tears in ascending aorta, pulmonary artery (less common)

Question 56

What are the potential consequences of vasculitis

Answer 56

- depend on the size, number and type of vessels involved, the degree of associated thrombosis, haemorrhage and oedema, presence of collateral circulation etc - vessel wall damage

Question 57

what is the usual cause of lymphoedema and what is the difference between primary and secondary lymphoedema

Answer 57

Primary - results from anomalous development of lymphatic system inadequate formation of lymphatic channels secondary - obstruction of previously normal efferent lymphatics

Question 58

what are the two main tumors arising from vascular endothelium in domestic animals

Answer 58

1) Haemangioma - benign tumor - blood filled spaces | 2) haemangiosarcoma - malignant neoplasm, older dogs and german shepherds common

Question 59

Antiarrythmics what is important to remember and how

Answer 59

remember to treat the patient – not the arrhythmia 1) Direct damage to the heart- - eg chamber enlargement, cardiomyopathy, myocarditis, myocardial ischaemia 2) Systemic abnormalities - Eg electrolyte or acid-base imbalances , toxicity – drugs,uraemia, septicaemia, pyometra, hypoxia, fever, endocrine disorders e.g. hyperthyroidism, autonomic activity- pain, gastric dilatation/ volvulus

Question 60

what are some clinical signs of arrhythmias and mechanism

Answer 60

1) Lack of substrate delivery due to inadequate cardiac output - exercise intolerance - weakness, syncopal episodes - chest pain/ angina : difficult to document in animals 2) Electrical instability - syncope, sudden death - ventricular fibrillation 3) Refractory or worsening heart failure - sudden development of dysarrythmia (e.g. atrial fibrillation or ventricular tachycardia) may lead to decompensation of previous stable congestive signs

Question 61

How to diagnose arrhythmias

Answer 61

ECG | -normal heart rate, regular rhythm, P wave for every QRS

Question 62

what are the 5 classes/drugs of antiarhymtic drugs

Answer 62

1) Sodium channel blockers 2) Beta blockers 3) Potassium (outward) channel blockers 4) Calcium channel blockers 5) Other drugs eg digoxin

Question 63

Sodium channel blockers what type of drug mechanism of action, special characteristic and therefore when most useful

Answer 63

Mechanism of Action: - block movement of Na+ which myocytes need to contract however pacemaker cells do not Use dependence - more active sodium channels have a greater likelihood of being blocked herefore more excitable ( eg ectopic) cells are more likely to be blocked Rogue pacemaker cells that are spontaneously depolarising - sodium channel blockers can stop this by allowing SA node to reset

Question 64

sodium channel blockers side effects

Answer 64

1) can promote arrhythmia | 2) wrong dose can have effect on nervous tissue

Question 65

beta blockers effects

Answer 65

- Inhibit sympathetic stimulation to heart - Control dysrhythmias driven by excessive sympathetic tone - Used in atrial tachycardias - Slow sinus (SA) rate - effect the pacemaker cells - driven by SA node ○ Slow AV conduction

Question 66

beta blockers uses and example

Answer 66

- Use in patient that is dependent on sympathetic drive can be lethal - decompensate patient and push into heart failure - Used in humans to treat stress induced tachycardia - Used in dogs to treat fear related behaviours - behavioural specialist • Examples: propranolol

Question 67

calcium channel blockers what used for with heart. mechanism of action, when used

Answer 67

arrythmias L-­‐Type Calcium Channel Blockers - Bind to Calcium channel from inside - Use dependence again - Render channel inactive - Cells dependent on these channels for depolarisation are more likely to be affected ie NODAL tissues - Useful in atrial tachycardias- ventricular tachycardias are not responsive

Question 68

Calcium channel blockers effects and the selectivity

Answer 68

Effects - Nodal /conducting tissue--> decreased heart rate, & AV conduction (pacemaker tissue) - Myocardium --> decreased force of contraction - Vascular smooth muscle --> relaxation Vascular: myocardial selectivity: - Verapamil 1:1 therefore more use in arrhythmia - Diltiazem 7:1 some vascular effects - Amlodipine 14:1 vascular ( antihypertensive)

Question 69

Digoxin what is the mechanism to help with ventricular arrhythmias

Answer 69

- Vagal effects on pacemaker tissues: - Slowed AV conduction - increase risk of rogue pacemaker establishing itself - direct effect on myocardial NA/K ATPase

Question 70

Atrial fribrillation and ventricular tachycardia what drugs to use

Answer 70

``` Atrial 1) digoxin, beta blocker, calcium channel blocker 2) Na channel blocker Ventricular 1) sodium channel blocker ```

Question 71

what are the following general effects of negative iontropes, positive inotropes, diuretics, vasodilators, antiarrhythmics

Answer 71

Positive inotropes increase cardiac contractility, cardiac output Negative inotropes decrease cardiac contractility, decrease preload Diuretics decrease preload (volume overload) Vasodilators decrease preload, afterload or both Antiarrhythmics increase cardiac output

Question 72

what are the consequences of Mitral Valve Endocardiosis

Answer 72

○ Resulting in left atrial enlargement ○ Results in atrial fibrillation - no obvious P waves, irregular R-R intervals, ○ Also resulting in left-sided cardiac failure resulting in pulmonary oedema

Question 73

why is there an increase in fractional shortening in mitral valve endocardiosis

Answer 73

1) Responding reduced ejection fraction, reduced cardiac out - sympathetic nervous system activation - increase contractility 2) Responding to stretch of the ventricle, increase distance between myofibrils resulting in optimal length-tension relationship

Question 74

Mitral valve endocardiosis list the initial treatment

Answer 74

Restore oxygen supply decrease pulmonary oedema 1) Diuretics - Frusemide - given intravenously until oedema resolves once resolves decrease dose to prevent side effects of acid-base abnormalities, dehydration and electrolyte imbalance 2) Provide an oxygen enriched atmosphere and reduce oxygen demand with rest Reduce preload 1) Diuretics - Frusemide - reduce blood volume to reduce venous return which reduces 2) Pimobendan - peripheral vasodilating to reduce preload (also increases contractility

Question 75

What treatment would you provide after the ascites so once right sided heart failure has developed with mitral valve endocardiosis

Answer 75

1) Spironolactone - add a potassium sparing diuretic as frusemide can decrease potassium which can have an effect on the side effects of digoxin 2) Digoxin - depleted potassium greater effect as digoxin competes with K+ for the active site on the Na+/K+ ATPase and therefore depletion in K+ will result in increased effects of digoxin

Question 76

Mechanism for the development of ascites secondary to congestive heart failure

Answer 76

Stretch of the heart due to increase end diastolic volume resulting from the regurgitation of the mitral valve - pulling apart of the tricuspid valve resulting in tricuspid valve incompetence - increase regurgitation into right atrium - congestion into cranial and caudal vena cava - increase hydrostatic pressure in abdomen - net filtration in venous end of capillary - ASCITES

Question 77

What are the 4 classes of Diuretics and example of each

Answer 77

1) Proximal Convulted Tubule - carbonic anhydrase inhibitor 2) loop diuretics - Frusemide 3) Distal Convoluted Tubule - Thiazides 4) collecting duct - spironolactone

Question 78

Proximal convoluted tubule mechanism of action

Answer 78

Carbonic Anhydrase Inhibitor - Prevents formation of H+ and therefore prevent H+ being exchanged for Na+ at the apical membrane ○ Increase loss of bicarbonate in urine ○ Increase loss of Na+ and water

Question 79

Loop Diuretics mechanism of action and possible problems

Answer 79

Frusemide - Inhibits Na/K/2Cl cotransporter - Most powerful diuretics - May cause ○ Hypokalaemia as K+ is secreted into tubular lumen via channel and reabsorbed via the cotransporter that is inhibit by this diuretic Potentiate toxicity of cardiac glycosides

Question 80

Distal convoluted tubule diuretics mechanism of action and what may cause

Answer 80

Thiazides - Inhibit Na/Cl luminal cotransporter so drop Na+ and Cl- levels - Also cause potassium loss due to increased flow rate through collecting duct ○ Hypokalaemia ○ Hypoantraemia - low Na+ blood levels

Question 81

collecting duct diuretic mechanism of action

Answer 81

- Potassium sparing diuretics 1. Spironolactone: synthetic aldosterone inhibitor - Decreased luminal Na+ channels - Decreased Na/K/ATPase on basal membrane - increase loss of Na+ and decreases loss of K+