Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

My1 Cardiology > pharmacology > Flashcards

pharmacology Flashcards

1
Q

what are the phases of fast AP’s in ventricular muscle cells

A

phase 4: resting potential, Phase 0: upstroke, phase 1: early repolarisation, phase 2: plateau, phase 3: final repolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what happens in phase 4 of ventricular myocytes

A

resting potential -90mv, K efflux (Ik1), small Na influx balanced by NaKATPase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what happens in phase 0 ventricular myocytes

A

v fast influx of Na

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what happens in phase 1 of ventricular myocytes

A

rapid inactivation of Na (Ina), transient K efflux (IKt0)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what happens in phase 2 of ventricular myocytes

A

plateau due to influx of calcium and slow efflux of K. l gated ca channels open (Ica), IKto decreases and IK increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what happens in phase 3 of ventricular myocytes

A

outward K current overtakes calcium influx. Ikr, Iks and Ik1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what happens in the fast response in atrial AP

A

phase 2 less developed so phase 3 accelerated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the AP phases in the SA node

A

phase 0: upstroke, phase 3: repolarisation, phase 4: gradual depolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what happens in phase 4 of SA node AP

A

activation of L gated ca channels (ca influx), decreased K efflux (reduced IK), funny current (Na influx activated by hyperpolarisation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the neurotransmitter and receptor of sympathetic nerve activity of the heart

A

noradrenaline and B1 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

once B1 is activated, what subunit activates adenylyl cyclase? what does this do

A

Gs alpha subunit, increases cAMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what does increased cAMP do

A

increased AP potential frequency by acting on funny current and L type ca channels (HR), increased ca influx (force), decreases systole (HR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the sequence of events in ventricular excitation contraction (5)

A

ventricular AP, L-type channels open, Calcium imduced calcium release, calcium binds to myosin head, actin-myosin cross bridge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

cAMP phosphorylates calcium L type channels causing..

A

an influx of ca

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

explain CICR from sarcoplasmic reticulum

A

calcium binds to RyR2 on sarcoplasmic reticulum and calcium is released.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how does calcium increase contractility

A

binds to troponin C on myosin head which allows the myosin actin cross bridge to form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

apart from calcium, what is needed for activation of myosin and actin

A

ATP (and ADP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what protein does cAMP also activate

A

protein kinase A (PKA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

PKA phosphorylates ___ which then activates ____

A

phospholambam, SERCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is the function of SERCA

A

to pump calcium back into the SR to reduce systole (increases HR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what inactivates cAMP, breaking it down into what

A

PDE, turns it into 5AMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

name a drug that can inhibit PDE, therefore increasing contractility

A

milrinone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

In the parasympathetic chain on the heart, what is the neurotransmitter and receptor

A

Acetylcholine and M2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

once activated, what does the Gi alpha subunit do

A

inhibits adenylyl cyclase, reducing cAMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what does reduced cAMP do

A

reduces pacemaker slope, (decreased If and Ical), slower conduction. little effect on contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

once activated, what does the Gi beta receptor do

A

activates GIRK channels which allow K to leave the cell making it more negative. This increases the reach to the AP threshold.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what type of channels are involved in funny current and what activates them

A

HCN (influx of Na), hyperpolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what happens when you block the funny current HCN channels? name a drug that can do this

A

decreases pacemaker slope and slows HR, ivabradine for angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

in relaxation of cardiac cells, what happens to calcium? (4 things)

A

Ca influx stops from L-gated channels, ca dissociates from troponin C, SERCA pumps ca to SR, sodium-calcium pump pumps Ca out of cell.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

name a b1 adrenoreceptor agonist used for heart failure

A

dubatamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

name a b1 adrenoreceptor agonist used for heart cardiac failure and anaphylactic shock

A

adrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what do beta blockers do

A

stop NA binding Beta receptors, reducing heart rte and contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

name a non selective beta blocker

A

propanolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

name a selective b1 blocker

A

atenolol, metoprolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what can b blockers be used for

A

arrhythmias, angina, hypertension, heart failure (at low dose)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what are adverse effects of b blockers

A

bronchospasm (asthma), bradycardia, cold extremities, aggravated heart failure, fatigue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

name a muscarinic ACh receptor antagonist and what it is used for

A

atroprine, bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what does digoxin do, what’s it used for

A

increases activity of heart an slows HR. heart failure and fibrillation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

why is digoxin dangerous

A

low therapeutic ratio so can be toxic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what does levosimendan do

A

increases contractility by increasing troponin affinity for Ca

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

in vascular smooth muscle, ___ binds to ___, forming ___ to regulate myosin binding

A

calcium, calmodium, Ca-CaM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Ca-CaM then activates what

A

myosin light chain kinase (MLCK)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

MLCK then activates ___ by ___

A

myosin-LC by phosphorylation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what dephosphorylates MLCK

A

myosin-LC phosphotase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

in smooth muscle what ca cause relaxation

A

nitric oxide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what are the substrates for NO and the enzyme

A

l-argenine and O2, NOS

47
Q

where is NO produced

A

endothelial cells

48
Q

what does NO stimulate guanylate cyclase to do

A

covert GTP –> cGMP

49
Q

what does cGMP do

A

activates PKG which causes relaxation by increasing SERCA activity

50
Q

what organic nitrates can be used for angina

A

GTN spray fro instant release and isosorbide mononitrtate (ISMN) for prophylaxis

51
Q

high doses of nitrates are needed for what?

A

arterial dilation

52
Q

why is it important to have nitrate low periods

A

to avoid becoming resistant

53
Q

what do calcium channel blockers (CCB) do

A

prevent opening of L type channels, reduce force and rate

54
Q

name 3 calcium channel blockers

A

verapamil (cardiac cells), amlodipine (smooth muscle), diltiazem

55
Q

when can CCB’s be used

A

hypertension, angina

56
Q

what are the main side effects of CBB’s

A

ankle oedema

57
Q

what does renin do and where is it produced

A

produced in kidneys, coverts angiotensinogen (from liver) to angiotensin 1

58
Q

what converts angiotensin 1 –> angiotensin 2

A

ACE in lungs

59
Q

angiotensin II causes what to be released from adrenal cortex

A

aldosterone

60
Q

what receptors to angiotensin II act on

A

AT1

61
Q

what does ACE inhibit

A

bradykinin (dilation)

62
Q

name an ACE inhibitor

A

lisinopril

63
Q

what do ARBS block, name one

A

AT1, losartan

64
Q

what effects to ACEi and ARBs have on the heart

A

decrease venous dilation, preload, afterload and resistance

65
Q

what can a1 adrenoreceptor antagonists treat

A

high BP

66
Q

what do a1 adrenoreceptor antagonists act on

A

block a1 in arteries to cause dilation

67
Q

name 2 a1 adrenoreceptor antagonists

A

prazosin and dixazosin

68
Q

what do K channel openers act on (cause hyperpolarisation)

A

arterial smooth muscle

69
Q

name 2 k channel openers

A

minoxidil and nicroandil

70
Q

what is the overall action of diuretics

A

increase Na, Cl and water excretion

71
Q

what is an undesirable effect of diuretics

A

loss of K+

72
Q

Name a thiazide diuretic and conditions it is used in

A

Bendroflumethazide

Mild heart failure, hypertension

73
Q

Name a loop diuretic and conditions it is used in

A

Furosemide

Chronic heart failure, acute pulmonary oedema

74
Q

when should ACEi and ARBs never be used

A

pregnancy

75
Q

CVD is associated with what type of lipid

A

low density lipids (LDLs)

76
Q

what is the main component of a lipoprotein

A

hydrophobic core and hydrophillic coat

77
Q

what is the hydrophobic core made up of

A

cholesterol esters and triglycerides

78
Q

what makes up hydrophillic coat

A

apoproteins, phospholipids

79
Q

name the 4 major lipoproteins

A

HDL, LDL, VDLD and chylomicrons

80
Q

what apoproteins are associated with liproteins

A

HDL: apoA1+A2
LDL: apoB100
VLDL: apoB100
chylomicrons: apoB48

81
Q

what do apoB lipoproteins do

A

transfer triglycerides to muscles for ATP biogenesis and to adipocytes for storage

82
Q

what do chylomicrons do in exogenous pathway

A

formed in intestinal cells and transport dietary triglycerides

83
Q

what do VLDL’s do, what pathway is this

A

formed in liver and transport triglycerides endogenous

84
Q

what is the life cycle of apoB containing proteins

A

assembly,

intravascular metabolism, receptor mediated clearance

85
Q

where are chylomicrons formed

A

gut

86
Q

where are VLDLs formed and how

A

liver, from free fatty acids from adipose tissue and de novo synthesis

87
Q

what are triglycerides made from

A

3 fatty acids and monoglyceride

88
Q

why do triglycerides need to be broken down, what enzyme does this

A

can’t be absorbed else wise, pancreatic lipase

89
Q

what protein allows cholesterol to enter a cell by making it esterified

A

NPC1L1

90
Q

what needs to be added to a chylomicron so it can leave cell and enter lymphatic system

A

apoA1

91
Q

how are chylomicrons and VLDL particles activated

A

transfer of apoCII by HDL, needed so LDL can bind

92
Q

what enzyme hydrolyses apoB proteins

A

lipoprotein lipase (LPL)

93
Q

what does hydrolysis of apoB proteins allow

A

free fatty acids and glycerol to enter cell

94
Q

what do chylomicron and VLDL remnants contain

A

cholesteryl ester

95
Q

apoCII is returned to HDL for the exchange of what apoprotein and why

A

apoE, so they can be cleared

96
Q

what percentage of VLDL and chylomicron remnants are cleared via liver in receptor-mediated clearance.

A

50%

97
Q

what happens to remaining remnants

A

become LDL

98
Q

what receptors are needed for LDL clearance and where are they

A

LDL receptors in liver

99
Q

how does cholesterol in liver affect cholesterol synthesis

A

more cholesterol returned by LDL the less is produced by liver hepatocytes

100
Q

how does cholesterol release inhibit cholesterol release by liver hepatocytes

A

inhibits HMG-CoA reductase which downregulates LDL production

101
Q

why is LDL bad cholesterol and cause atherosclerosis

A

LDL is taken into tunica intima when endothelial is damaged, it then becomes oxidised to OXLDL. OXLDL is taken up by macrophages causing them to become foam cells that form fatty streaks. this can eventually cause a plaque

102
Q

why is HDL good cholesterol

A

access extra cholesterol and delivers it to liver. enables scavenger receptors to uptake cholesterol

103
Q

how do statins work

A

inhibit HMG-CoA which is rate limiting step in de novo synthesis of cholesterol. increases LDL receptor action for LDL clearance

104
Q

how are statins administered

A

taken orally at night

105
Q

name 2 statins

A

simvastatin and atorvastatin

106
Q

what do fibrates do

A

decrease triglycerides

107
Q

how do fibrates work

A

inhibit PPAR alpha which allows increased LPL transcription

108
Q

name some fibrates

A

bezafibrate, gemifibrozil

109
Q

when should fibrates be avoided

A

alcoholics

110
Q

what do bile acting resins do

A

cause bile salts to be excreted so more cholesterol is converted to bile salts

111
Q

name some bile acting resins

A

cholestyramine, colestipol, colsevelam

112
Q

what is a side effect of bile acting resins

A

GI irritation

113
Q

what does Ezetimibe do

A

inhibits NPCL1L, decreases LDL’s

My1 Cardiology (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions