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BVMS 2 > Module 10 Wk 2 > Flashcards

Module 10 Wk 2 Flashcards

1
Q

(The equine vet and the cardiovascular system)

Report the vet’s role in assisting owners with purchasing a horse including knowledge of the pre-purchase examination

A

Vets role is to do a Pre-purchase examination.

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2
Q

Recall a detailed approach to auscultation of the horse’s heart and relate this to cardiac anatomy and physiology

A
  • palpate left apex beat
  • place steth on this point and establish heart sounds, rate and rhythm (remember this si where mitral valve is)
  • move steth radially around here
  • Then move steth cm by cm in cranial direction towards heart base and underneath triceps muscle for semilunar valves (outflow valves - aortic and pulmonary)
  • move steth radially around here
  • palpate right side for apex beat (this is hard to find btw lol)
  • auscultate as far cranial as possible (triscuspid valve here)
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3
Q

Describe the vet’s role regarding aspects of horse insurance

A

Vets role is to do a pre- insurence examination which allows insurence company to asses risk and relate to level of cover

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4
Q

There are two types of insurence covers what are these and describe ther difference in examinations needed for each?

A
  • all-risk mortality - stage 1 and 2 examination (preliminary exam and walk and trot in hand)
  • Loss of Use - Stage 1 to 5 examination (preliminary exam, walk and trot, exercise phase, period of rest and re-exam, second trot up)
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5
Q

State examples of conditions affecting a range of body systems that may lead to poor performance in the equine athlete

A
  • Upper resp system - dorsal displacement of the soft palate
  • Lower resp system - mild to mod equine asthma
  • Cardiovascular system - irregularly, irregular heart rhythm
  • Musculoskeletal system - reccurrent external rhabdomyolysis, hock asteoarthritis
  • Gastrointestinal system - Equine gastric ulceration syndrome, equine squamous gastric disease
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6
Q

Describe what reccurrent external rhabdomyolysis is

A
  • It is a clinical syndrome characterized by painful muscle contractures with exercise and skeletal muscle fiber necrosis
  • you should perform an exercise test and take blood samples pre and 2 post to measure creatine kinase and aspartate aminotransferase (muscle enzymes)
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7
Q

Equine Gastric Ulceration Syndrome

A
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8
Q

what are the squamous ulceration due to in Equine Squamous Gastric Disease?

A
  • The typical race horse diet - lack of fibre to buffer acid dispersal, large quantities of concentrates which causes rapid gastric empytying leading to increased acidity
  • acid splashing during exercise
  • sustained high speed work
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9
Q

(Cardiovascular infections - bacterial and viral)

To define infective endocarditis

A
  • Endocarditis is a bacterial infection of the mural endocardium and heart valves
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10
Q

Describe the pathogenesis of infective endocarditis

A

COME BACK TO THIS
Damage to the endothelial surface of the heart or blood vessels induces platelet and fibrin deposition, producing a sterile thrombotic vegetation
Infective endocarditis is initiated by the binding of microbes, discharged into the general circulation from a peripheral site, to these vegetations
These microbes become encased in further depositions of platelets and fibrin and multiply - BIOFILM
Biofilm - This is where you get Extremely high concentrations of bacteria in the vegetation (109-1011/gram of tissue)
Impotansts as antibiotics find it difficult to penetrate - Hinders antibiotic penetration
Organisms may stop multiplying – less susceptible to Beta lactams
Bacterial enzymes destroy valve tissue, rupture chordae and produce aortic root abscess

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11
Q

Outline the bacterial causes of infective endocarditis in common domestic species

A
  • Streptococci and coagulase positive staphylococci - is half of cases of dogs, they originate in the mouth or gut
  • Rarely due to Gram negatives as they dont have as many bacteria proteins that bind
  • Bartonella
  • Fungi rare in dogs and cats (<5%)
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12
Q

Describe the laboratory diagnosis of infective endocarditis

A

T identify bacteraenia blood culture is needed - ideally three blood cultures obtained from seperate sites and test for pathogens.

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13
Q

Define myocarditis caused by infectious agents

A

Inflammation of heart muscle

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14
Q

Describe the pathogenesis myocarditis

A

Infectious myocarditis in dogs and cats usually results from haematogenous spread of microorganisms to the myocardium or extension of endocarditis lesions to the myocardium.

(Viruses, bacteria, protozoa, or fungi may be involved)

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15
Q

Describe infectious agents causing pericarditis

A
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16
Q

( Cardiovascular-related physiological adaptation to disease)

How do different components coordinate in response to different challenges?

A

Each major adaptation is through integration of several smaller responses

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17
Q

With a significant haemorrhage what are all reduced?

A

Arterial pressure
Systolic pressure
pulse pressure

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18
Q

what are the clinical signs of a heamorrhage?

A
  • Pulse is rapid and weak
  • Mucous membranes are pale as to drive up blood pressure it decreases blood pressure in areas that is not needed at that moment
  • Respiration is rapid
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19
Q

Due to heamorrhage there is a drop of CO, what does this cause?

A

A sudden drop in blood pressure - this can reciver over a few hours others begin to decline and BP drops till death.

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20
Q

Describe the heamorrhage recovary method 1 - baroreceptor relfex

A
  • Where a reduction in BP leads to decreased baroreceptor stimulation this leads to increased sympathetic, decreased parasympathetic stimulation.

This causes
- tachycardia
- increased contractibility
- increased vasodilation - leads to increased CVP

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21
Q

T/F arterial vasoconstriction leads to increased TPR?

A

True

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22
Q

What will sustained vasoconstriction lead to?

A

Kidney damage and sloughing of mucosa in intestine

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23
Q

Describe how the chemoreceptor reflex aids heamorrhage recovary

A

If BP does go very low the baroreceptor reflex is no longer sensitive and chemoreceptor will aid baroreceptor reflex

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24
Q

What will occur in heamorrhage recovary if BP drops too low?

A

Cerebral ischemia - this sets off sympathetic discharges as reflex response

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25
Q

What is another relfex that adds to increases sympathetic activity?

A

Atrial Volume receptor reflex

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26
Q

Reabsorbtion of fluid is also key to heamorrhage recovery, decribe how increased sympathetic actvity plays a role in this

A
  • Increased sympathetic activity is an increased renin secretion.
  • Through action of angiotension II and aldosterone there is decreased Na+ excretion.
  • Also there is a reflexes to increase ADH release which reduces water loss

Both of these act to conserve fluid.

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27
Q

Reabsorbtion of fluid is also key to heamorrhage recovery, decribe how baroreceptor reflex plays a role in this

A

The baroreceptor reflex acts through the hypothalamus to induce the sensation of thirst and water intake increases

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28
Q

How is cardiac railure a decompensatory mechanism of heamorrhage?

A
  • Hypotension reduces coronary blood flow
  • depresses ventricular function,
  • reduces CO
  • reduces pressure
  • reduces blood flow
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29
Q

How is Acidosis a decompensatory mechanism of heamorrhage?

A
  • reduced blood flow so not getting enough oxygen leading to production of energy anaerobically
  • This increases lactic acid and reduces hydrogen production so blood becomes more acidic
  • The body needs to respond to catecholamines but the acididity reduces this ability
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30
Q

How is CNS depression a decompensatory mechanism of heamorrhage?

A
  • Blood flow to CNS drops too much leads to increased symapthetic output
  • If it falls further the cardiac and vasomotor centres become depressed leading to loss of sympathetic tone
  • This reduces cardiac output to heart and CNS
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31
Q

How is Changes in clotting a decompensatory mechanism of heamorrhage?

A
  • Initially there is an increase in clotting but eventually clotting time is prolonged
  • This aggravates haemorrhage
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32
Q

How is Inhibition of the immune system a decompensatory mechanism of heamorrhage?

A
  • Leads to invasion of endotoxins into systemic circulation inducing a form of shock
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33
Q

Whether an animal will recover or decompensate will depend on what?

A

The degree of haemorrhage and
Individual variation

(More severe the blood loss the greater the chance of going into decompensation)

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34
Q

COMPENSATION FOR HEAMORRHAGE CHART (go look babe)

A
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35
Q

Heart failure is?

A

Acondition of depressed contractility and an inability of the heart to provide the metabolic requirements of the body.

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36
Q

T/F heart failure can be restricted to one side?

A

True

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37
Q

What are the two respones to heart failure

A
  • Starling mechanism: If LV fails and SV goes down there is an accumulation of blood in the LA and pulmonary veins – leads to increased preload and greater SV.
  • The drop in BP induces a baroreceptor reflex increase in sympathetic activity. This increases HR and contractility
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38
Q

Describe how oedema is a complication in heart failure

A
  • Accumulation of blood in veins, increases hydrostatic pressure:
  • LV failure – pulmonary oedema - what comes prior too it rather than where its going
  • RV failure – systemic oedema - liver oedema and swelling in the periphery
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39
Q

Describe how Exercise intolerance is a complication in heart failure

A
  • In heart failure (HF) if sympathetic system is already active so individual is unable to cope with increased demand from skeletal muscle.

(Get a big drop in BP and inadequate Q – leads to rapid exhaustion)

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40
Q

(Diagnostic Imaging of the Heart)

Recognise the normal anatomy of the heart as seen using radiography and echocardiography

A
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41
Q

Understand the use of these imaging modalities in the investigation of cardiac disease

A
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42
Q

What type of imaging would you use to see overal size, shape and location of the heart?

A

radiography

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43
Q

What does radiography not show?

A

Internal structures of heart (valve leaflets, vetricular septum, etc)
Myocardial function
Valve incompetence

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44
Q

whats the word for ultrasound when it comes to imaging the heart?

A

echocardiography

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45
Q

What does a echocardiography allow you to asses?

A
  • Chamber size
  • Myocardial Function
  • Direction and velocity of blood flow
  • Blood flow and leakage through valves
  • Disease of internal cardiac structures
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46
Q

What imaging modality is best evidence of congestive failure?

A

radiography

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47
Q

What is the normal intercostal space the heart takes up in cats and dogs?

A

dogs is 3-3.5
cats is 2-3

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48
Q

T/F Degree of sternal contact partially depends on breed

A

True

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49
Q

Describe Cardiomegaly

A
  • Enlargement of the heart
  • elavated trachea
  • increased contact with the sternum and diaphragm
  • spread over more intercostal spaces
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50
Q

apart from measureing intercostal spaces taken up and how much thoracic cavity the heart takes up what is another way to asses size?

A

The Vertebral Heart Score

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51
Q

what does B mode show?

A

slice of anatomy

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52
Q

what does m mode show?

A
  • Shows movement or contraction of structures over time
  • Allows measurement of myocardial contractility – assessment of myocardial function
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53
Q

what does doppler imaging show?

A
  • Allows measurement of blood flow
  • This is via Colour-flow - Qualitative and BART (Blue Away, Red Towards)
  • Pulsed-wave & Continuous-wave - Quantitative and Shows the velocity increasing and decreasing
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54
Q

what is the most widely used scanning approach?

A

Right Parasternal Approach - Place transducer on apex beat of heart on right thoracic wall

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55
Q

What info does right parasternal approach of imaging heart give?

A

Chamber sizes
Myocardiac function
Valve function

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56
Q

What is Left apical view position?

A

Patient in left lateral recumbency, scan from dependent left thoracic wall

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57
Q

what is left apical view good for?

A
  • Mitral and tricuspid valves (four chamber)
  • Aortic outflow (five chamber)
  • Good for accurate measurements of blood flow velocities
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58
Q

What are common cardiac disease?

A
  • myocardial - dilated and hypertrophic cardiomyopathy
  • valvular disease
  • pericardial disease
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59
Q

(Haemostasis)

What does normal heamostasis result from?

A

Result of tightly regulated processes that accomplishes two important functions

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60
Q

Describe the normal heamostatic process

A
  • After vascular injury
    platlets attach to the site
  • they start to secrete ADP and thromboxane which attracts more platelets
  • coagulation cascade starts over these platelets
  • fibrin which is formed due to cascade anchors platlets inplace
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61
Q

what sytstem is also activated when coagulation cascade activated?

A

Fibrinolytic system

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62
Q

Fibrinolytic system generates what and how does this effect coagulation?

A

plasmin which breaks down fibrin and interferes with its polymerisation

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63
Q

What is thrombocytopenia and describe the clinical presentation?

A
  • Decreased circulating platelets in the peripheral circulation
  • Epistaxis, Ecchymoses, Petechiae, heamaturia, heamatochezia, melaena and hyphaema
64
Q

How would you evalulate for thrombocytopenia in lab?

A
  • CBC
  • Smear examination – check for platelet aggregates, morphology and size
  • Manual platelet count – if numbers fall below the sensitivity of the automated machine
65
Q

What are the causes of thrombocytopenia?

A
  • Increased destruction
  • Decreased production
  • Increased consumption
  • Increased sequestration
66
Q

What is VIII-von Willebrand factor (vWF) complex?

A

Sticky Protein that helps the platelets stick down to the damaged area

67
Q

what is Von Willebrands disease?

A

An inherited bleeding disorder caused by lack of von Willebrand factor protein (vWF)

68
Q

what are the three types of von willebrands disease?

A

I partial quantitative disorder
II loss of large molecular weight multimers
III absence

69
Q

what is Thrombocytosis?

A

Blood platelet concentration above reference interval

70
Q

What are the causes of thrombocytosis

A

Reactive thrombocytosis
-Increased production (Inflammation, Iron deficiency, Blood loss, Nonhemic neoplasia)

  • Redistribution - Physiologic (exercise, epinephrine)

Haemic neoplasia
- Primary essential thrombocythemia
- Acute megakaryocytic leukaemia

71
Q

T/F clotting disorders can be Acquired and hereditary

A

True

72
Q

What are the two hereditary clotting disorders?

A
  • Haemophilia A (FVIII)
  • Haemophilia B (FIX) (X-linked recessive traits; males affected. Present clinically with haemarthrosis, haematomas)
73
Q

what are the two acquired clotting disorders?

A
  • Vitamin K deficiency (Biliary obstruction, Infiltrative bowel disease)
  • Vitamin K antagonism (Coumadin (warfarin), 2nd generation anticoagulant rodenticides)
74
Q

How is fibrinogen measured?

A

Measurement by the modified Claus method (thrombin initiated clotting rate) - Rate of clot formation in diluted citrated plasma with addition of high concentration thrombin solution

75
Q

What is Disseminated intravascular coagulation?

A

“An acquired syndrome characterised by the intravascular activation of coagulation with loss of localisation resulting from different causes. It can originate from and cause damage to the microvasculature, which if sufficiently severe can produce organ dysfunction”.

76
Q

T/F DIC is always a secondary phenomenon, there is always a primary issue

A

True - so can only be resolved if primary issue resolved first

77
Q

What are the primary disease condition to DIC

A

Neoplasia
Systemic infammation
Endotoxaemia
Sepsis

78
Q

After the primary cause how is DIC initiated?

A

Massive tissue trauma causes exposure of huge amounts of tissue factor
Some conditions can induce TF expression
Aberrant expression of TF by intravascular cells (monocytes, tumour cells)

79
Q

(Pharmacological Options in Heart)

Describe the mechanism of action of the sympathomimetics in terms of their cardiac action

A
  • They mimic the sympathetic nervous system
  • beta 1 agonsists stimulate adenylate cyclase via a G protein which increases cAMP, Ca2+ and ultimatly contraction
80
Q

T/F sympathomimetics just stimulate beta receptors

A

False also stimulate alpha receptors therefore side effects all over body

81
Q

When are Sympathomimetic drugs used?

A

Used in resuscitation (emergency), not for heart failure

82
Q

Describe the mechanism of action diuretics

A
  • Shows how much capacity to influence
  • 100%- large capacity to have an effect
  • 10%- restricts influence of total volume of urine
83
Q

What does diuretics cause?

A

Increased urine flow (diuresis)
Increased Na+ excretion (natriuresis)

84
Q

When would you use diuretics?

A
  • Treatment & control of systemic oedema
  • ALL patients with signs of congestive heart failure should receive a diuretic (the only exception to the use of diuretics in CHF is cardiac tamponade)
85
Q

what are loop diuretics?

A
  • They have High capacity for diuresis
  • Inhibits Na+/K+/2Cl- carrier in the luminal membrane by combining with the Cl- binding site causing loss of these ions, with water, in the urine
86
Q

Describe the pharmakokenetics of loop diuretics?

A
  • Potent, “high ceiling” drugs
  • Can increase Na+ excretion from ~1% to >15-25%- therefore dose control essential
  • Rapid in onset of action
  • 10-20min i/v, 1-1.5hrs PO (well absorbed); last 4-6hrs
87
Q

What if any side effets does loop diuretics cause?

A

Dehydration, pre-renal azotaemia, electrolyte disturbances, esp. K+ Na+ Mg++, ototoxicity

88
Q

What is the mechanism of action of the diuretic thiazides?

A

They are secreted into PCT, act in DCT to block Na+/Cl- reabsorption causing loss of Na+, H+, K+, Mg++, Cl-, with water, in the urine

(Mechanism dependent on renal PG production)

89
Q

Describe the pharmokenetics of Thiazides?

A
  • Mild to moderate potency
  • Ineffective if renal blood flow is low (can’t be used as the sole drug)
  • Slower onset, longer acting than furosemide
  • Good oral absorption
90
Q

What are the two K+ sparing diuretics used in vet med?

A
  • Amiloride
  • Spiromolactone
91
Q

Describe the mech of action of Amiloride?

A

Block luminal sodium channel and indirectly decreasing K+ loss

92
Q

Why is Amiloride used in combo with others?

A

To reduce hypokalaemia

93
Q

What is the mechanism of action of Spironolactone?

A

Aldosterone antagonist

94
Q

What are Spirolactones used for?

A

To counter aldosterone escape

95
Q

What is the main aim of Vasodilators?

A

aims to decrease preload and afterload

96
Q

Whata are the main classes of vasodilators?

A

Calcium channel blockers
Alpha1 adrenoceptor antagonists
Nitrates
Angiotensin inhibitors

97
Q

What is the mechanism of action of Ca channel blocker?

A

block L-type Calcium channels which allow calcium to enter the cell during depolarization

98
Q

An example of a Dilhydropyridines ca channal blocker is Amlodipine, what is its pharmacokenetics?

A
  • 90% bioavailability
  • Extensive metabolism but slowly
  • Long t½
  • High Vd- 25l/Kg due to high affinity for the Ca+ channels
  • Good safety profile- dosed 1 or 2 times a day
99
Q

What is Amlodipine used for?

A

Used for systemic hypertension in cats and heart failure in dogs

100
Q

What is the mech of action of alpha 1-adrenoreceptor antagonist?

A

Non-selective aplha 1-antagonist

101
Q

What are alpha1-adrenoreceptor antagonist pharmacokenetics?

A
  • Well absorbed
  • t½ 3-4 hours
  • Hypotensive effect prolonged
  • Tolerance is not permanent (cells will revert to normal once stimulant is removed)
102
Q

Is there side effects of alpha 1-antagonist?

A

Yes - hypotension and syncope

103
Q

What is the mechanism of action of Nitrovasodilators?

A
  • Nitrates act as donors of nitric oxide (NO)
  • Mimic endogenous system
  • Friction of blood flowing over endo cell which stimulates it to produce eNOS which produces NO- autoregulatory system (greater friction shows that the vessel is constricted, the NO that is produced by this regulates this contraction)
  • NO diffuses and stimulates Guanylate cyclase to produce cAMP and leads to relaxation
  • Nitrates bypass the endothelial cell layer, it circulates into the vessels where it is spontaneously broken down and relaxes the constricted vessels
104
Q

what are the side effects of nitrovasodilators?

A

Hypotension

105
Q

What caustion should you take when using nitrovasodilators?

A

Application- ointment on hairless portion of body, person applying needs to be careful as it can cause their own BP to drop

106
Q

What are ACE’s?

A

membrane bound enzymes converting inactive Ang I to active Ang II and degrade active bradykinin (BK)

107
Q

What are the side effects of ACE

A
  • Hypotension
  • Renal Impairment- Monitor renal function & electrolytes
  • Hyperkalaemia
    (Anorexia, Diarrhoea, Vomiting)
    (Cough – more important in human medicine)
108
Q

what are the pharmocokenetics of ACE

A
  • Administered as pro-drugs - given in inactive form and is metabolised to become active
  • Renal/Hepatic elimination
  • Food can decrease bioavailability so should be given on empty stomach (Enalapril/Imidapril)
109
Q

What is the mech of action of angiotension 2 receptor anatgonist?

A

Direct action at Angiotensin II receptors

110
Q

What is the diff between angiotenssion 2 receptor anatgonist and ACE

A
  • Block AII formed by other routes
  • Do not prevent breakdown of Bradykinin
111
Q
A
112
Q
A
113
Q

(Antiarrhythmic Drugs)

Where do supraventricular arrhythmia originate?

A

Atria

114
Q

Where do the ventricular arrhythmias originate?

A

Ventricles

115
Q

Describe the phases of the cardiac action potential

A

0 - rapid depolarisation: entry of Na
1 - Partial repolaristation
2 - Plateau: net reflux of Ca+
3 - repolarisation
4 - pacemaker depolarisation: efflux of K+

116
Q

What Anti-arrhythmic drugs treat tachyarrythmias?

A
  • Vaughan Willian classification
  • Digoxin
  • Vaughan Williams Classification
117
Q

What Anti-arrhythmic drugs treat bradyarryhtmias

A
  • Muscarinic antagonists
  • Beta antagonists
  • Methylxanthines
118
Q

When treating tachyarrhythmias, describe the mechanism of action of Class 1 AARD’s

A
  • Block Na channels to reduce the rate of depolarisation during phase 0 therefore reducing the slope of phase 0
119
Q

What are the major indication of Class 1a AARD’s?

A
  • Hemodynamically significant or life-threatening ventricular arrhythmias
  • To convert atrial fibrillation to sinus rhythm
120
Q

Are there any side effects of Class 1a AARD’s?

A

Yes - hypotension, increased QRS duration, QT interval, and ventricular tachycardia

121
Q

What are the major indications of Class 1b AARD’s?

A
  • Hemodynamically significant or life-threatening ventricular arrhythmias
  • Lidocaine effective in recent onset arrhythmia in dogs
122
Q

Are there any side effects of Class 1b AARD’s?

A

Yes - tremors, shivering, muscle fasciculations and seizures

123
Q

T/F lidocaine (class 1b AARD) is also a local anasthetic?

A

True bitches

124
Q

T/F Class c AARD’s do not affect Action potential duration?

A

True

125
Q

T/F class 2 AARD’s are beta blockers

A

TRUEEEE slay?

126
Q

What do the Class 2 AARD’s reduce?

A
  • Reduce Sympathetic drive - slow AV node conduction, negative isotropes
  • Reduce O2 consumption leading to imporved oxygenation
127
Q

what are the major indications of Class 2 AARD’s

A
  • Arrhythmias
  • Hypertrophic cardiomyopathy
  • heart failure
128
Q

Is there any side effects of Class 2 AARD’s?

A

aye - worsening CHF, negative inotropy, lethargy (depression), bradycardia and bronchospasm

129
Q

Give three examples of Class 3 AARD’s

A

Amiodarone, sotalol, Bretylium

130
Q

What do class 3 AARD’s do?

A
  • Block outward K+ channels
  • Markedly increase Action potential duration and RP
131
Q

What are the pharmokenetics of class 3 AARD’s ?

A

They have a long half-life and are lipophilic

132
Q

Name the side effects of Class 3 AARD’s

A
  • Elevated liver enzymes
  • GI disturbances
  • Pulmonary fibrosis
  • Thyroid effects
133
Q

T/F class 4 AARD’s are Ca channel blockers?

A

True

134
Q

What is class 4 AARD’s mech of action?

A
  • Block L-type Ca channels
  • Profound effect on nodal tissue by reducing AP height and prolong the AP
  • Cardiomyocytes - due to shorter AP negative inotropes and positive lusitropes which help to improve heamodynamics and inprove oxygenation
135
Q

Qhat are the major indications of Class 4 AARD’s ?

A
  • Supraventricular arrhythmias
  • Hypertrophic cardiomyopathy
136
Q

Is Digoxin a Cardiac glycoside class drug?

A

Yes it is maam

137
Q

What do these Cardiac Glycodises have?

A
  • a narrow therapeutic index
  • pro-drug
138
Q

What are the 3 components of cardiac glycosides?

A
  • sugar (hydrolysed)
  • steroid (released)
  • lactone
139
Q

What are the pharmacodynamics of cardiac Glycosides?

A
  • AAR effect
  • Baroreceptor/neuroendocrine effects
  • Positive inotropic effects (increase heart contraction strength so increase CO)
  • diuretic effects
140
Q

Describe Cardiac Glycosides AAR effects

A
  • Increase parasympathetic activity which leads to a decrease in sinus rate.
  • AV node conduction meaning they prolong the refractory phase.
  • Slow ventricular response to arterial fibrillation.
141
Q

Describe Cardiac Glycosides Baroreceptor modulatory effects

A
  • in heart failure baroreceptor function is decreased so Glycosides increase this
  • Do this via decreasing symp activity and circulating catecholamine.
142
Q

What are the positive inotropic effects that Glycosides have?

A
  • Inhibition of the Na/K ATPase which lead to mild positive inotrope (strengthen force of heart beat)
143
Q

What are the Diuretic Effects AARD’s can have?

A
  • Na+/K+ ATPase on the basolateral aspect of renal tubular epithelial cells which promotes tubular reabsorption of Na
144
Q

T/F digoxin has oral administration with 60-70% bioavailability?

A

True ladiessss

145
Q

Does digoxin have a high or low volume of distribution?

A

HighW

146
Q

What causes the high half life of digoxin?

A

Its high affinity for Ca+ binding sites in the skeletal muscle which builds up a reservoir

147
Q

How is digoxin excreted from body?

A

Renal

148
Q

what are signs of toxicity of Glycosides?

A

Excessive borborygmi (mild sign), depression, anorexia, vomiting and diarrhoea, and cardiac arrhythmia

149
Q

How do you prevent the toxicity of Glycosides?

A
  • Start on low dose
  • Dose by body surface area
  • Avoid loading doses
  • Reduce dose if predisposed
  • Check serum level after 7 days
150
Q

How do you deal with Glycoside toxicity?

A
  • Stop for 3-5 days
  • Start again at lower dose
  • Check electrolytes, acid base balance
  • Treat arrhythmias
    Overdose - Activated charcoal/cholestyramine resin, Digibind
151
Q

What is the mechanism of action of Muscarinic antagonists when treating bradyarrhythmias?

A

Antagonism of muscarinic acetylcholine receptors

152
Q

What are the indications of muscarinic antagonists when treating bradyarrhythmias?

A

Bradyarrhythmia’s associated with high vagal tone

153
Q

What are the side effects of muscarinic antagonists when treating bradyarrhythmias?

A

Constipation, sinus tachycardia, urinary retention and dry mucous membranes

154
Q

What is the mechanism of action of Beta agonists when treating bradyarrhythmias?

A

Stimulation of b-adrenergic receptors

155
Q

What are the indications of Beta agonists when treating bradyarrhythmias?

A
  • sinus arrest, AV block
  • bronchodilator
156
Q

What are the side effects of Beta agonists when treating bradyarrhythmias?

A
  • isoprenaline (ventricular arrhythmias)
  • Terbutaline (tremor, tachycardia, hypotension)
157
Q

What are the mech of action of methylxanthines when treating bradyarrhythmias?

A
  • Mild PDE inhibition
  • Enhanced sympathetic drive leading to mild positive inotropic and chronotropic effects

BVMS 2 (18 decks)

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