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My1 Cardiology > pharmacology > Flashcards

pharmacology Flashcards

(113 cards)

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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

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2
Q

what happens in phase 4 of ventricular myocytes

A

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

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3
Q

what happens in phase 0 ventricular myocytes

A

v fast influx of Na

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4
Q

what happens in phase 1 of ventricular myocytes

A

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

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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

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6
Q

what happens in phase 3 of ventricular myocytes

A

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

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7
Q

what happens in the fast response in atrial AP

A

phase 2 less developed so phase 3 accelerated

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8
Q

what is the AP phases in the SA node

A

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

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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)

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10
Q

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

A

noradrenaline and B1 receptors

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11
Q

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

A

Gs alpha subunit, increases cAMP

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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)

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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

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14
Q

cAMP phosphorylates calcium L type channels causing..

A

an influx of ca

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15
Q

explain CICR from sarcoplasmic reticulum

A

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

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16
Q

how does calcium increase contractility

A

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

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17
Q

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

A

ATP (and ADP)

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18
Q

what protein does cAMP also activate

A

protein kinase A (PKA)

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19
Q

PKA phosphorylates ___ which then activates ____

A

phospholambam, SERCA

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20
Q

what is the function of SERCA

A

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

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21
Q

what inactivates cAMP, breaking it down into what

A

PDE, turns it into 5AMP

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22
Q

name a drug that can inhibit PDE, therefore increasing contractility

A

milrinone

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23
Q

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

A

Acetylcholine and M2

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24
Q

once activated, what does the Gi alpha subunit do

A

inhibits adenylyl cyclase, reducing cAMP

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25
what does reduced cAMP do
reduces pacemaker slope, (decreased If and Ical), slower conduction. little effect on contractility
26
once activated, what does the Gi beta receptor do
activates GIRK channels which allow K to leave the cell making it more negative. This increases the reach to the AP threshold.
27
what type of channels are involved in funny current and what activates them
HCN (influx of Na), hyperpolarisation
28
what happens when you block the funny current HCN channels? name a drug that can do this
decreases pacemaker slope and slows HR, ivabradine for angina
29
in relaxation of cardiac cells, what happens to calcium? (4 things)
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.
30
name a b1 adrenoreceptor agonist used for heart failure
dubatamine
31
name a b1 adrenoreceptor agonist used for heart cardiac failure and anaphylactic shock
adrenaline
32
what do beta blockers do
stop NA binding Beta receptors, reducing heart rte and contractility
33
name a non selective beta blocker
propanolol
34
name a selective b1 blocker
atenolol, metoprolol
35
what can b blockers be used for
arrhythmias, angina, hypertension, heart failure (at low dose)
36
what are adverse effects of b blockers
bronchospasm (asthma), bradycardia, cold extremities, aggravated heart failure, fatigue
37
name a muscarinic ACh receptor antagonist and what it is used for
atroprine, bradycardia
38
what does digoxin do, what's it used for
increases activity of heart an slows HR. heart failure and fibrillation
39
why is digoxin dangerous
low therapeutic ratio so can be toxic
40
what does levosimendan do
increases contractility by increasing troponin affinity for Ca
41
in vascular smooth muscle, ___ binds to ___, forming ___ to regulate myosin binding
calcium, calmodium, Ca-CaM
42
Ca-CaM then activates what
myosin light chain kinase (MLCK)
43
MLCK then activates ___ by ___
myosin-LC by phosphorylation
44
what dephosphorylates MLCK
myosin-LC phosphotase
45
in smooth muscle what ca cause relaxation
nitric oxide
46
what are the substrates for NO and the enzyme
l-argenine and O2, NOS
47
where is NO produced
endothelial cells
48
what does NO stimulate guanylate cyclase to do
covert GTP --> cGMP
49
what does cGMP do
activates PKG which causes relaxation by increasing SERCA activity
50
what organic nitrates can be used for angina
GTN spray fro instant release and isosorbide mononitrtate (ISMN) for prophylaxis
51
high doses of nitrates are needed for what?
arterial dilation
52
why is it important to have nitrate low periods
to avoid becoming resistant
53
what do calcium channel blockers (CCB) do
prevent opening of L type channels, reduce force and rate
54
name 3 calcium channel blockers
verapamil (cardiac cells), amlodipine (smooth muscle), diltiazem
55
when can CCB's be used
hypertension, angina
56
what are the main side effects of CBB's
ankle oedema
57
what does renin do and where is it produced
produced in kidneys, coverts angiotensinogen (from liver) to angiotensin 1
58
what converts angiotensin 1 --> angiotensin 2
ACE in lungs
59
angiotensin II causes what to be released from adrenal cortex
aldosterone
60
what receptors to angiotensin II act on
AT1
61
what does ACE inhibit
bradykinin (dilation)
62
name an ACE inhibitor
lisinopril
63
what do ARBS block, name one
AT1, losartan
64
what effects to ACEi and ARBs have on the heart
decrease venous dilation, preload, afterload and resistance
65
what can a1 adrenoreceptor antagonists treat
high BP
66
what do a1 adrenoreceptor antagonists act on
block a1 in arteries to cause dilation
67
name 2 a1 adrenoreceptor antagonists
prazosin and dixazosin
68
what do K channel openers act on (cause hyperpolarisation)
arterial smooth muscle
69
name 2 k channel openers
minoxidil and nicroandil
70
what is the overall action of diuretics
increase Na, Cl and water excretion
71
what is an undesirable effect of diuretics
loss of K+
72
Name a thiazide diuretic and conditions it is used in
Bendroflumethazide | Mild heart failure, hypertension
73
Name a loop diuretic and conditions it is used in
Furosemide | Chronic heart failure, acute pulmonary oedema
74
when should ACEi and ARBs never be used
pregnancy
75
CVD is associated with what type of lipid
low density lipids (LDLs)
76
what is the main component of a lipoprotein
hydrophobic core and hydrophillic coat
77
what is the hydrophobic core made up of
cholesterol esters and triglycerides
78
what makes up hydrophillic coat
apoproteins, phospholipids
79
name the 4 major lipoproteins
HDL, LDL, VDLD and chylomicrons
80
what apoproteins are associated with liproteins
HDL: apoA1+A2 LDL: apoB100 VLDL: apoB100 chylomicrons: apoB48
81
what do apoB lipoproteins do
transfer triglycerides to muscles for ATP biogenesis and to adipocytes for storage
82
what do chylomicrons do in exogenous pathway
formed in intestinal cells and transport dietary triglycerides
83
what do VLDL's do, what pathway is this
formed in liver and transport triglycerides endogenous
84
what is the life cycle of apoB containing proteins
assembly, | intravascular metabolism, receptor mediated clearance
85
where are chylomicrons formed
gut
86
where are VLDLs formed and how
liver, from free fatty acids from adipose tissue and de novo synthesis
87
what are triglycerides made from
3 fatty acids and monoglyceride
88
why do triglycerides need to be broken down, what enzyme does this
can't be absorbed else wise, pancreatic lipase
89
what protein allows cholesterol to enter a cell by making it esterified
NPC1L1
90
what needs to be added to a chylomicron so it can leave cell and enter lymphatic system
apoA1
91
how are chylomicrons and VLDL particles activated
transfer of apoCII by HDL, needed so LDL can bind
92
what enzyme hydrolyses apoB proteins
lipoprotein lipase (LPL)
93
what does hydrolysis of apoB proteins allow
free fatty acids and glycerol to enter cell
94
what do chylomicron and VLDL remnants contain
cholesteryl ester
95
apoCII is returned to HDL for the exchange of what apoprotein and why
apoE, so they can be cleared
96
what percentage of VLDL and chylomicron remnants are cleared via liver in receptor-mediated clearance.
50%
97
what happens to remaining remnants
become LDL
98
what receptors are needed for LDL clearance and where are they
LDL receptors in liver
99
how does cholesterol in liver affect cholesterol synthesis
more cholesterol returned by LDL the less is produced by liver hepatocytes
100
how does cholesterol release inhibit cholesterol release by liver hepatocytes
inhibits HMG-CoA reductase which downregulates LDL production
101
why is LDL bad cholesterol and cause atherosclerosis
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
why is HDL good cholesterol
access extra cholesterol and delivers it to liver. enables scavenger receptors to uptake cholesterol
103
how do statins work
inhibit HMG-CoA which is rate limiting step in de novo synthesis of cholesterol. increases LDL receptor action for LDL clearance
104
how are statins administered
taken orally at night
105
name 2 statins
simvastatin and atorvastatin
106
what do fibrates do
decrease triglycerides
107
how do fibrates work
inhibit PPAR alpha which allows increased LPL transcription
108
name some fibrates
bezafibrate, gemifibrozil
109
when should fibrates be avoided
alcoholics
110
what do bile acting resins do
cause bile salts to be excreted so more cholesterol is converted to bile salts
111
name some bile acting resins
cholestyramine, colestipol, colsevelam
112
what is a side effect of bile acting resins
GI irritation
113
what does Ezetimibe do
inhibits NPCL1L, decreases LDL's

My1 Cardiology (16 decks)

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