Cardio Week 6 Flashcards

1
Q

What is contained in the posterior mediastinum?

A

Oesophagus descending thoracic aorta Thoracic duct sympathetic trunks

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1
Q

In which type of valvular disease is it possible to wait until the appearance of symptoms to intervene?

A

Aortic stenosis

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1
Q

What are some common causes of haemorrhagic necrosis?

A
  1. Venous occlusion
  2. Reperfusion of necrotic tissue
  3. Dual circulation or natural collateral circulation
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2
Q

What are aminoglycosides?

A

Antibiotics they target protein synthesis by binding to and distorting the codon reading frame on the ribosome.

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4
Q

Usually the appearance of symptoms in valvular disease indicates the progression of irreversible, pathological changes to the heart. In which type is this not the case?

A

Aortic stenosis - and LVH can regress.

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5
Q

What are some side effects of ACE inhibitor and angiotensin receptor blockers?

A

Dry cough

First use hypotension

Loss of appetite

Hyperkalaemia

Acute renal failure

Foetal malformations

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5
Q

Why is warfarin described as a “moody” drug?

A
  1. Short half-life
  2. Binds to plasma protein
  3. Highly dependent on dietary vitamin K
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6
Q

What is an example of antimicrobial resistance via drug inactivation due to convalent modification

A

Gentamicin (an aminoglycoside) acetyltransferase - acetylates the gentamicin

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7
Q

What are examples of antimicrobial resistance mediated by altering of target?

A
  1. Alternate PBP (mecA) - methicillin doesn’t recognise
  2. Switch terminal D-ala with monosaccaride to prevent vancomycin blocking cell wall synthesis (VRE)
  3. VISA - vancomycin intermediate resistant Staphlococcus aureus. Over produces peptidoglycan to soak up vancomycin
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8
Q

Why can’t you treat Pseudomonas aeruginosa with co-amoxyclav?

A

Because P. aeruginosa has a chromosomally encoded beta-lactamase that clavulanic acid can’t inhibit and therefore it goes on to hydrolyse the amoxycillin. However you can use Ticarcillin + clavulanic acid as Ticarcillin is resistant to P. aeruginosa’s chromosomal beta-lactamase (you also need clavulanic acid because Ticarcillin is susceptible to plasmid encoded beta-lactamases which clavulanic acid will inhibit).

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9
Q

What does damage to blood vessels lead to in the clotting cascade?

A
  1. Vasocontriction
  2. Platelet adhesion and activation
  3. Fibrin formation
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9
Q

What is the end result of the coagulation cascade

A

Activation of thrombin from prothrombin which cleaves fibrinogen into fibrin

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11
Q

What is the function of clavulanic acid?

A

It is a suicide inhibitor of plasmid encoded beta-lactamases

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12
Q

How is vitamin K relevant to coagulation?

A

Vitamin K is a substrate for Vitamin K reductase that is essential for the formation of coagulation factors II, VII, IX and X.

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13
Q

What is an example of a platelet inhibitor?

A

Aspirin - inhibits cyclo-oxygenase to prevent thromboxane production (thromboxane is a potent activator of platelets)

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14
Q

What are some drug actions that will decrease preload?

A

Diuretics

Venodilators - nitrates

Aldosterone receptor antagonists

Aquaretics

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15
Q

What are some fibrinolytic drugs?

A

Streptokinase, alteplase

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15
Q

Rheumatic fever almost always causes this type of valvular disease…

A

Mitral stenosis

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16
Q

What are some drug actions that will decrease afterload?

A

Angiotensin receptor antagonists

Beta-adrenoceptor antagonist

Arterial vasodilator

ACE inhibitor

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16
Q

How does valve stenosis cause a pressure difference across valves?

A

Narrower space for blood to travel through therefore it requires greater pressure to get the blood through

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17
Q

Bowel infarcts are usually haemorrhage T/F? Why?

A

True, commonly due to venous occlusion

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19
Q

What is an examples of antimicrobial resistance via drug inactivation via hydrolysis

A

Chromosomal encoded beta-lactamase in P. aeruginosa hydrolyases beta-lactams

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21
Q

What is the mecA protein?

A

An altered penicillin binding protein that isn’t recognised by beta-lactams therefore affording resistance to penicillin/methicillin to the pathogens that have it. This is the mechanism in methicillin resistance and the protein is called mecA.

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23
Q

Define Thrombosis

A

Pathological haemostatic plug formation in the absence of blood loss

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24
Q

At what level does the superior vena cava enter the right atrium?

A

Posterior to the 3rd costal cartilage

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26
Q

What causes the 4th heart sound?

A

Forceful atrial contraction to overcome stiff ventricle, occurs during diastole due

27
Q

Describe the action of heparin

A
  • Anti-coagulant
  • Enhances activity of antithrombin III which inactivates Factor Xa and thrombin
  • Injectable
28
Q

What are some stimuli for platelet activation?

A
  1. Collagen 2. Thrombin 3. Thromboxane 4. ADP
29
Q

Why is Amrinone useful when beta1-adrenoceptors are desensitised due to over activation?

A

Amrinone mechanism to increase intracellular Ca is not mediated via those receptors. Rather it inhibits phosphodiesterases > less cAMP to AMP > more active PKA > more phosphorylation of Ca channels > more intracellular Ca.

30
Q

What is the ligamentum arteriosum?

A

Connects the aorta to the pulmonary trunk - remanence of shunt that allowed blood to bypass the pulmonary circulation in utero.

31
Q

At what level to the left and right brachiocephalic veins meet?

A

Posterior to the 1st costal cartilage

32
Q

Which vitamin is important in coagulation?

A

K

33
Q

Who is the co-ordinator of secondary haemostasis

A

Thrombin - cleaves fibrinogen to fibrin

34
Q

What is the course of the vagus nerve in the mediastinum?

A

-Descending in the carotid sheath, posterorlateral to common carotid artery -R: Along trachea L: Lateral aortic arch -Posterior to lung root -Along ant. of oesophagus where L & R join to form the oesophageal plexus

35
Q

What does the descending aorta supply in the thoracic cavity?

A

Intercostal space (posterior intercostal arteries)

Bronchial arteries

Pericardium

36
Q

Volume overload is caused by what?

A

Valve regurgitation

37
Q

What is the course of the phrenic nerve in the mediastinum?

A

Descending on the scalenus anterior Passes between the subclavian artery and vein Passes anterior to the lung root Pierces the diaphragm

38
Q

What are some examples of emboli?

A
  1. Thrombus 2. Atherosclerotic rupture 3. Gas 4. Vegetative mass from bacteria aka septic emboli 5. Tumour emboli 6. Fat emboli
39
Q

What are examples of antimicrobial resistance mediated by prevent drug getting to its target?

A

Reduced entry into cell - eg modification of outer membrane in gram -ve to prevent entry of aminoglycosides

Increase efflux of drug from cell

40
Q

How long can neurones survive without blood supply?

A

3-4 minutes

41
Q

How does valve stenosis cause a pressure difference across valves?

A

Narrower space for blood to travel through therefore it requires greater pressure to get the blood through

42
Q

In which type of valvular disease do you hear no second heart sound but murmur instead?

A

Aortic regurgitation

43
Q

What are some side effects of heparin?

A

Haemorrhage, thrombocytopaenia and osteoporosis

44
Q

How long can cardiac muscle survive without blood supply?

A

20 minutes

45
Q

An inhibitor of vitamin K reductase is?

A

Warfarin

46
Q

What are the goals of treatment for cardiac failure?

A
  1. Decrease cardiac work and improve cardiac function 2. Decrease signs and symptoms 3. Increase survival
47
Q

What is the mechanism of vasoconstriction in response to blood vessel damage?

A

Platelets adhere to the damaged wall and are activated and release ADP and 5-HT - potent vasoconstrictors

48
Q

What is the mechanism of glycosides on the heart?

A

Increase contractility by increase intracellular Ca by inhibiting ATPase which reduces the amount of Ca pumped out of the cell.

49
Q

What does Amrinone do?

A

Inhibits phosphodiesterases that break down cAMP therefore Ca channels are more activated = increased intracellular Ca = Increased contractility

50
Q

What can you use to reduce preload?

A

Diuretics

Venodilators

Aldosterone inhibitors

Angiotensin Receptor Antagonists

ACE inhitiors

51
Q

What are the 3 essential features of accurate clinical trials?

A
  1. Randomisation (reduce compounding error)
  2. Blinding (reduce observational bias/error)
  3. Intention to treat (reduce selection error) - treat people like they’re still in their original group (control or treatment) regardles of whether they stick with it.
52
Q

What are they four functions of the kidneys?

A
  1. Regulate electrolyte and water volume
  2. Endocrine production
  3. Exogenous waste excretion
  4. Endogenous waste excretion
53
Q

What are the structural components of the kidney?

A
  1. Glomerulus
  2. Proximal tubule
    - 60-70% of water and NaCl reabsorbed
  3. Loop of Henle
    - water, K+ and 20-30% of NaCl reabsorbed
  4. Distal tubule
    - 5-10% of NaCl reabsorbed and K+ secreted
  5. Collecting ducts
    - K+ secreted and rest of NaCl is reabsorbed
54
Q

What is the significance of probenecid?

A

It is a drug that prevents to secretion of banned substances used by unethical athletes.

55
Q

What are diuretics?

A

Drugs that decrease NaCl reabsorbion thereby increase its secretion and water’s secretion.

56
Q

What are the 4 classes of diuretics?

A

Loop diuretics

Thiazide diuretics

Potassium-sparing diuretics

Osmotic diuretics

57
Q

What is the mechanism of action of loop diuretics?

A

They inhibit Na/Cl/K carriers into the cell in the loop of Henle. Leads to reduced water reabsorption due to reduction of hypertonicity in interstitum and greater [Na] in the distal tubule.

58
Q

What is the duration of action of loop diuretics? What are some side effects?

A

3-6 hours.

Hypokalaemia (due to increased Na+ in distal tubule = more Na reabsorbed and more K+ secreted via Na/K ATPase)

Hypovolaemia

59
Q

Why are thiazide diuretics less potent than loop diuretics when they both act on Na/Cl co-transport?

A

Because thiazide diuretics act in the distal tubule where less Na/Cl is reabsorbed.

60
Q

Thiazide diuretics have a slower, less urgeny effect compared to loop diuretics T/F?

A

True

The duration is 8-12 hours

61
Q

When are K sparing diuretics mainly used?

A

With loop or thiazide diuretics to prevent hypokalaemia

62
Q

What is spironolactone? What is its mechanism of action?

A

It is a K-sparing diuretic and a aldosterone receptor antagonist - stops stimulation of Na reabsorption thereby preventing K secretion.

63
Q

Why is the kidney susceptible to toxins?

A
  1. Toxins can be at a high concentration
  2. The kidney filters 25% of blood
  3. The kidney can metabolise
  4. Contribution from extrarenal events.