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MODA > Cardiovascular and Renal > Flashcards

Cardiovascular and Renal Flashcards

1
Q

What does PKA phosphorylate in the heart?

A

SERCA2 and phospholamban

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2
Q

Which heart fibres are fastest?

A

SAN

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3
Q

What is Wolff-Parkinson-White syndrome?

A

Abnormal conducting fibres so A>V is too fast

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4
Q

How do inodilators act?

A

Inhibit PDE (mimic sympathetic stimulation)

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5
Q

How do methylxanthines act?

A

Non-specific PDE inhibitors and A1 and A2 agonists

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6
Q

What causes phospholamban to inhibit SERCA2?

A

Sympathetic via B receptors and PKA

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7
Q

Which factors does plasmin cause breakdown of?

A

II, V, VII

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8
Q

What is glyciproteins IIB/IIIa receptor needed for?

A

Fibrinogen binding between platelets that causes aggregation

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9
Q

Where does ATIII act and what does it affect?

A

The brain affecting ADH release

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10
Q

What does adenosine acting on A1 receptors inhibit?

A

Rise in intracellular cAMP

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11
Q

What does ANP via cGMP inhibit?

A

Renin release

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12
Q

What are the ATII receptors?

A

AT1 and AT2

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13
Q

What converts ATII to ATIII?

A

Brain aminopeptidase A

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14
Q

What converts ATIII to ATIV?

A

Aminopeptidase-N

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15
Q

Which tubule has peptidases to metabolise bradykinin?

A

Proximal

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16
Q

Which receptors does the collecting duct have?

A

Kininogen and bradykinin B2

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17
Q

What converts kininogen to bradykinin?

A

Killikrein

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18
Q

How do loop diuretics work?

A

Block Na-K-Cl transport in apical membrane of thick ascending limb

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19
Q

How do thiazide diuretics work?

A

Block Na-Cl cotransport in cortical thick ascending limb and distal tubule, also some CA inhibition

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20
Q

How do K+-sparing diuretics work?

A

Block apical Na+ channels OR aldosterone antagonists

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21
Q

How do CA inhibitors work?

A

Inhibit bicarb reabsorption and decrease H+ availability so there is less to exchange with Na

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22
Q

Which PDE is Ca2+/calmodulin-dependent?

A

I

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23
Q

Which PDE is cGMP-stimualted?

A

II

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24
Q

Which PDE is cGMP-specific?

A

V

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25
Q

Which PDE is cGMP-inhibited?

A

III

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26
Q

Which PDE is cAMP-specific?

A

IV

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27
Q

Which inodilator is used for heart failure and which PDE does in inhibit?

A

Milrinone - type III

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28
Q

Which two drugs inhibit PDE type V?

A

Dipyridamole and sildenafil

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29
Q

Where is I Ca-L found and what is it for?

A

Everywhere for plateau phase

30
Q

Where is I Ca-T found?

A

Nodal/conductive

31
Q

Where is I Na-Ca found?

A

Everywhere

32
Q

Which Na sites can be glycosylated?

A

All

33
Q

Which subunits are linked by a disulphide bridge and are from the same gene?

A

ALpha2 and delta

34
Q

Which Ca drugs don’t show use dependence?

A

DHPs

35
Q

How many phosphorylation sites do L type Ca2+ channels have?

A

Two phosphorylation sites on cytoplasmic domain

36
Q

Where are T type Ca2+ channels found?

A

Heart conductive tissue

37
Q

Where are the two DHP binding sites?

A

S6 and S5-6 loop in domain III and S5-6 loop in domain IV

38
Q

Where is benzothiazepine binding site?

A

Outside

39
Q

What is N type K+ channel inactivation?

A

Ball and chain

40
Q

What is C type K+ inactivation?

A

Residues near the extracellular surface moving

41
Q

What regulates Kirs?

A

Phosphorylation, Ca2+ or ATP

42
Q

Which Gi subunit opens I K-ACh channel?

A

Beta-gamma

43
Q

In what conditions do ATP-sensitive Kir channels open?

A

Low intracellular ATP

44
Q

What are HCN channels permeable to?

A

Na and K

45
Q

What do catecholamines do to RyRs?

A

Sensitize

46
Q

What are cells like in ischaemic heart disease?

A

Partly depolarised and liable to inappropriate action

47
Q

Which dysrhytmias are class III used for?

A

Ventricular and re-entrant

48
Q

Which tissue do class IV antidysrhytmics act on?

A

Nodal

49
Q

What causes dilated cardiomyopathy in cats?

A

Taurine or carnitine deficiency

50
Q

Which receptors are upregulated when using beta blockers?

A

Alpha1

51
Q

Which PDE is it in heart failure

A

III

52
Q

How do Ca sensitizers cause peripheral vasodilation?

A

Inhibit PDEIII

53
Q

What converts kininogen into bradykinin?

A

Kallikrein

54
Q

How do AT2 receptors cause vasodilation?

A

Use NO which raises cGMP

55
Q

When is the AT2 receptor present?

A

Brain and adrenal medulla, fetal development

56
Q

How do ACE inhibitors affect pre and afterload?

A

Increase

57
Q

How do ACE inhibitors affect vascular resistance and blood pressure?

A

Decrease vascular resistance not blood pressure

58
Q

How does ANP inhibit renin release?

A

Via cGMP

59
Q

How does Angiotensin II inhibit renin release?

A

IP3 mediated -ve feedback

60
Q

How does adenosine increase cAMP?

A

AT1 receptors

61
Q

What is the structure of angiotensin I?

A

Decapaptide

62
Q

What is the structure of angiotensin II?

A

Octapeptide

63
Q

How is blood pressure maintained when using an ACE inhibitor?

A

CO increases

64
Q

What is angiotensin IV for?

A

Learning, memory, LTP

65
Q

Where is AT4 receptor located?

A

Widely

66
Q

What is the structure of the AT4 receptor?

A

Transmembrane, insulin regulated

67
Q

Where are peptidases which produce bradykinin?

A

Proximal tubule

68
Q

Where are the kininogen and bradykinin B2 receptors?

A

Collecting duct

69
Q

Where is HCN1 found?

A

Heart and brain

70
Q

Where is HCN2 found?

A

Throughout heart

71
Q

Where is HCN4 found?

A

Pacemaker region and Purkinje fibres

72
Q

Which factors does warfarin inhibit synthesis of?

A

II, VII, IX, X, C, X, Z

MODA (10 decks)

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