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1
Q

PNS mechanism

A

Ach from CNS/brain neurons - on Nicotinic receptors N - postganglionic fiber release Ach - M3 on exocrine glands & M3 smooth muscle & M2 heart/ muscarinic receptor

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2
Q

Muscarinic receptor

A

M2 on heart - G-protein coupled receptor -for Ach

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3
Q

cholinergic synapse

A

Ach release

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4
Q

SNS mechanism

A

Ach from CNS/ spinal cord neurons -
neuronal Nicotinic Nn receptors on post ganglion - release NE - on the Alpha-1 R on smooth muscle & beta-1 R on heart

N R on adrenal medulla - releasing N and NE in blood

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5
Q

NE = NA

A

NorEpinephrine = NorAdrenaline

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6
Q

Nicotinic receptors subtypes

A

Nn - nicotinic subtype - the postganglionic neuron - SNS &

Nm - muscle subtype -somatic

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7
Q

autonomic nervous system

A

Ach from pre-synaptic - cholinergic - on Nn & muscarinic R & AChe & presynaptic autoreceptor

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8
Q

somatic nervous system

A

spinal cord - somatic nerves - Ach - Nm on skeletal muscle

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9
Q

AChe

A

primary Ach break down = acetate + choline

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10
Q

cholinergic synapse

A

where the Ach is released

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11
Q

primary breakdown methods -

A 
NE = uptake to presynaptic neuron - Catechol-O-methyl-transferase 
ACh = AChE - enzyme
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12
Q

adrenergic transmission

A

alpha-beta R

presynaptic autoreceptors

primary -reuptake into nerve terminal - catechol-o-methyl-transferase

uptake to tissue - monoamine oxidase MAO

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13
Q

NE making

A

Tyrosine - DOPA -dopamine - NE

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14
Q

ANS tone

A

basal level of activity (basic life function) - parasympathetic or sympathetic

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15
Q

organs with single system control - SNS

A

adrenal gland- release EP

blood vessels - vasoconstriction - gut, skin - Alpha 1 R

blood vessel - vasodilation - skeletal muscle - beta 2 R

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16
Q

heart rate PNS vs SNS

A

inc - SNP - beta 1 R by NE

dec - PNS - muscarinic M2 R by Ach

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17
Q

respiratory bronchi SNS vs PNS

A

SNS - bronchodilation - beta 2 R

PNS - bronchoconstriction -

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18
Q

beta 2 receptor

A

SNS - dilation of vessel and bronchi

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19
Q

drugs used for myasthenia gravis and Alzheimers

A

cholinesterase inhibitors

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20
Q

ATROPINE

A

non-selectiv muscarinic antagonist

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21
Q

M2 receptor

A

GCPR - activates Gi [inhibitory G protein] - dec cAMP

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22
Q

nicotinic antagonist use

A

in surgery - intubation - relaxing muscle

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23
Q

beta2-Receptor

A

treating asthma - dilate bronchi

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24
Q

alpha 2 receptor

A

feedback inhibition - dec NE release

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25
Q

alpha 1 R

A

GPCR - acting through Gq - inc Ca - vasoconstriction - inc BP

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26
Q

beta 1 R

A

GPCR - Gs - inc cAMP - inc Ca - inc Heart force rate

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27
Q

alpha 1 agonist

A

vasoconstriction - inc BP

dilate pupil

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28
Q

COCAINE

A

blocking NE reuptake

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29
Q

AMPHETAMINE

A

release NE from terminal

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30
Q

PRAZOSIN

A

alpha 1 antagonist - dec BP

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31
Q

propranolol

A

beta 1, 2 antagonist - hypertension, angima, arrhythmia, heart failure

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32
Q

lipoprotein[lipid protein complex] classes

A 
chylomicron 
VLDL
LDL 
HDL
(high-low size / triglyceride trend)
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33
Q

highest TG

A

chylomicrons

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34
Q

highest CHOL

how

A

LDL
get most of CHOL of VLDL
bad cholesterol

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35
Q

hepatic cholesterol
biosynthesis
catabolism

A 
Acetyl CoA - HMG-CoA - HMG-CoA reductase/rate limiting - cholesterol (can also be secret to bile as cholesterol)
bile acid  (secreted to bile)
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36
Q

chylomicrons mechanism

A

intestine - dietary lipid - LPL / capillary endothelial cells lipolysis – Fas - tissue - energy utilization / oxidation & energy storage / triglyceride biosynthesis
remnants - liver endocytosis

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37
Q

lipoprotein with;
majority of serum triglyceride
most TG

A

VLDL

Chylomicron

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38
Q

VLDL mechanism

A

liver - LPL lipolysis / capillary peripheral tissue - Fas - tissue - energy storage and utilization
remanent VHDL = IDL - removal of apolipoprotein & lipolysis of triglyceride - LDL / blood

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39
Q

intermediate density lipoprotein

A

IDL is the VLDL remanent

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40
Q

LDL

A

from the IDL - LDL - peripheral tissue + 50% liver /endocytosis

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41
Q

immature HDL

A

apolipoproteins [ApoAI, ApoAll] + phospholipids

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42
Q

HDL

A

liver - HDL immature - during VLDL & chylomicrons lipolysis get lipid/cholesterol + get cholesterol from peripheral tissue - uptake by SR-BI - liver - bile acid - bile / or can directly from cholesterol add to bile - excursion

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43
Q

bad
good
cholesterol

A

LDL

HDL

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44
Q

hyperlipoproteinemias

A

heterogenous group of disorders
can be monogenic , polygenic/common,
differ based on cause, lipoprotein affected, cholesterol and most important their CVD risk increase

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45
Q

hyperlipoproteinemias

A

based on the lipoprotein affected determine which lipid will elevate in blood

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46
Q

hypercholesterolemia
hypertriglyceridemia
mixed hyperlipidemia

A

major inc in;
LDL
VLDL
VLDL + LDL

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47
Q

disease associated with high cholesterol = high CVD

bad cholesterol = LDL

A

hypercholesterolemia

hyperlipidemia

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48
Q

treatments for the CVD

A

achieve lower LDL cholesterol l

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49
Q

atherosclerosis

A

red blood flow
CVD, stroke, kidney failure
severity with again genetic
high LDL - primary risk factor

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50
Q

atherosclerosis risk relation

A

+ LDL:HDL, total cholesterol, LDL

- HDL / inverse cholesterol transport mechanism

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51
Q

TLC

A

Therapeutic life style change

10-30% LDL red

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52
Q

statin

A

open lactose ring
competitive inhibitor of HMG CoA reductase
primary action = inc hepatocyte LDL receptors -

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53
Q

statin use

A

most effective for dec LDL
primary prevention of CVD
anti-inflammation - anti-coagulant

54
Q

statin adverse effects

A

muscle pain
reversible liver toxicity
cardiomyopathy
drug interaction

55
Q

bile acid binding resins

A

anion exchange resins

in small intestine

56
Q

resin bile acid function

A
  • excreted in feces
  • red intestinal-bile acid reabsorption & return to liver
  • red liver bile acid - inc Bile acid biosynthesis in liver - dec hepatic cholesterol
  • inc LDL receptor - inc hepatic LDL uptake
  • lower blood LDL
  • dec plasma total cholesterol and LDL
57
Q

resin side effect

A

diarrhea, constipation, irritation

58
Q

resins inc chol in liver

A

1- inc LDL R on liver

2- inc biosynthesis of cholesterol - so statin is used with resin to inhibit HMG CoA - cholesterol biosynthesis

59
Q

cholesterol absorption inhibitor

A

inhibit internalization of sterol-bound NPC1L1

60
Q

NPC1L1

A

Niemann-Pick C1-Like 1

on luminal face of enterocyte - bind& internalize sterol in small intestine - absorption of CHOL

61
Q

EZETIMIBE

A

cholesterol absorption inhibitor drug

62
Q

ezetimibe mechanism

A

red cholesterol-chylomicron delivery to liver - red hepatic chol -inc LDL R - inc LDL uptake to liver - dec total and LDL chol-

63
Q

ezetimibe function benefits

A

primary; dec LDL cholesterol
dec TG
in HDL cholesterol

64
Q

ezetimibe adverse effect - rare

A

reversible impaired liver function

myositis/muscle inflammation

65
Q

PCSK9 inhibitor

A

newest LDL lowering drug
monoclonal antibodies - injection
second line medication - narrow usage indication
with diet & max statin therapy

66
Q

PCSK9 inhibitor usage

A

sever hypercholesterolemia

atherosclerotic CVD - max statin used but need further LDL lowering

67
Q

PCSK9

A

Proprotein Convertase Substilisin/Kexin type 9

enzyme

68
Q

PCSK9 -inhibitor mechanism

A

monoclonal antibodies - bind to PCSK9 - inhibit PCSK9 attach to LDL receptor - LDL R internalized & not degrade - LDL degraded - inc LDL R on hepatocyte - Inc LDL uptake from blood

69
Q

niacin mechanism

A

in adipose tissue - niacin bind niacin receptor - inhibit hormone-sensitive lipase = lipolysis of TG- dec plasma fas - dec hepatic triglyceride synthesis - red VLDL synthesis - red plasma LDL

red apoA-1 clearance from plasma = inc apolipoprotein - inc HDL - inc reverse cholesterol transport = cholesterol excursion in bile

70
Q

niacin function

A

inc HDL

dec LDL & total chol

71
Q

niacin usage

A

niacin + other drugs = hyperlipidemia

72
Q

niacin adverse effect

A

high does

flushing, hot flush, GIT irritation, hepatotoxicity

73
Q

fibrates

A

used for;

high TG and low HDL

74
Q

vibrates are

A

PPAR alpha

75
Q

PPAR alpha

A

Peroxisome Proliferator Activated Receptor Alpha

76
Q

fibrates

A

PPAR alpha agonist

77
Q

PPAR Alpha

A

ligand activated transcription factor

78
Q

PPAR alpha function

A

inc expression gene involved in lipid metabolism;
endothelial lipoprotein lipase;
hepatic and muscle fas oxidation enzyme ;
hepatic apo A-I & apo A-II;

79
Q

Fibrate - inc Endothelial Lipoprotein Lipase

A

inc clearance chylomicrons/VLDL;

  • dec TG plasma
  • inc Fas - uptake and oxidation in muscle
80
Q

fibrate - inc hepatic fas oxidation enzyme

A

dec TG biosynthesis - dec VLDL secretion -

dec plasma TG

81
Q

fibrate - inc hepatic apo A-I and apo A-II

A

inc plasma HDL

82
Q

treatments;
hypercholesterolemia; high LDL
hyperglyceridemia; high VLDL
hyperlipidemia; LDL+ VLDL

A
  • TLC, niacin, resin, statin, ezetimide, PCSK9-inhibitor
  • TLC, niacin, fibrate
  • TLC, niacin, fibrate, resin, statin, PCSK9 inhibitor
83
Q

homozygote hypercholesterolemia

A

min effect to resin, statin or combination

TLC+Niacin - effective

84
Q

hypertension

High BP

A

systolic BP > 140 mmHg

diastolic BP > 90 mmHg

85
Q

RAS

A

Renin Angiotensin System

86
Q

RAS mechanism

A

Angiotensinogen - Renin - angiotensin I - ACE -Angiotensin II - receptors on;
vascular - vasoconstriction
adrenal glands - aldosterone - inc NA H2O - inc blood volume

87
Q

diuretics

A

naturiesis + diuresis

88
Q

loop and thiazide diuretics

A

loss of NA and K /excretion

hypokalemia

89
Q

K sparing diuretics

A

loss of Na
gain of K in blood - less excretion
hyperkalemia

90
Q

diuretics for diseases;
thiazide
k sparing
Loop

A

hypertension
CHF
CHF

91
Q

CHF

A

Congestive Heart Failure

92
Q

sympatholytic drugs

not first line drugs

A

centrally-acting; dec SNS, central vasometer centre in brain, dec BP
beta-blockers;
short term, beta 1 blockers in heart, dec HR, contraction, CO, BP
long term, beta 1 blocker in kidney, vasodilation, dec renin, aldosterone, NA+H2O, BP
alpha1-blocker; blocking SNS acting on vascular smooth muscles, vasodilation, red BP

93
Q

orthostatic hypertension is

A

adverse effect of alpha 1 blocker

94
Q

angiotensin inhibitors RAS

first line drugs

A

1- ACE inhibitor ACE-I ; dec AI to AII - dec AII - vasodilation, dec BP, Na
2- All(angiotensin II) antagonist;
block AII R on vessel, vasodilation, dec BP
block AII R on adrenal gland, dec aldosterone, NA, BP
3- direct renin inhibitor; dec AI or AII

95
Q

vasodilator

first line drug

A

Ca channel blocker; CCB
Nifedipine; act on blood vessel
diltiazem & verapamil; act on blood vessel and heart
dec ca, dec contraction, vasodilation - dec BP
heart - dec HR, CO = dec BP

96
Q

first line drugs - commonly used

A

Thiazide, ACE-I, ARB, CCB

97
Q

Orthostatic hyportension

A

head rush

alpha 1 blocker

98
Q

ACE Inhibitor = ACE-I

A

cough, teratogenic

99
Q

AII antagonist ARB

A

no cough, teratogenic

100
Q

MI

A

myocardial infraction

101
Q

coronary arteries diseases treatment

A

aspirin ; red clot

statin ; red LDL

102
Q

ASA

A

Aspirin - red platelet aggregation

anti-thrombotic

103
Q

vasodilator

A

organic nitrates

104
Q

NITROGLYCERIN

A

organic nitrate for vasodilation

105
Q

nitrate/nitroglycerin mechanism

A

nitrate, nitric oxide in VSM, activate enzyme Guanylyl cyclase, convent GTP to CGMP, dec phosphorylation of myofilament, relax blood vessel

106
Q

nitroglycerin & sildenafil drug interaction

A

sildenafil; inhibit CGMP to GMP conversion by phosphodiesterase PDE = inc CGMP, - high dec in BP

107
Q

calcium channel blockers CCB

A

nifedipine; in VSM, dilate vessel, dec vasospasm = inc o2 supply- dilate arteries, dec afterload = dec o2 demand
verapamil & diltiazem;
dec O2 demand and Inc O2 supply; in VSM -
in heart;
dec contraction =dec work, dec HR =dec O2 demand

108
Q

beta blocker

A

dec O2 demand;

dec HR, contraction, after load (RAS), work of heart

109
Q

SNS and RAS remodelling

A

hypertrophy
apoptosis
fibrosis
dilation

110
Q

CHF drugs

A

positive inotropic drugs; inc contraction, CO

inhibit RAS; ARBs & ACEIs; red remodelling
inhibit SNS; beta-blocker; red remodelling

aldosterone antagonists/K sparing & other diuretics/loop; red pulmonary & systemic congestion

vasodilator; dec pre-load & after-load

111
Q

carvedilol

A

beta1,2 - alpha 1 blocker
beta1 blocker= dec HR, renin
beta 2 blocker = asthma not good
alpha 1 blocker =vasodilation - dec after load

112
Q

ICD

A

Implantable Cardioverter-Defibrillator

113
Q

drugs classes fro tachycardias

A 
class I; Na channel blocker 
Class II; Beta blocker
class III; K channel  blocker
class IV; Ca channel blocker = diltiazem, verapamil 
other;     digoxin
114
Q

tachycardias drugs with similar effect

A

class II, IV, other like adenosine and digoxin

115
Q

synthesis;
Ach
NE

A

acetyl coa + choline = Ach

tyrosine- dopa - dopamine- NE

116
Q

NE degradation adrenergic

A

uptake to pre-synapse; catechol-O-methyl-transferase

uptake to post-synapse; monoamine oxidase

117
Q

indirect agonist of Ach cholinergic

A

for Alzheimer and myasthenia gravis

118
Q

agonists;
cholinergic
adrenergic

A

indirect;
inhibit AChE
inhibit NE reuptake & inc NE release

119
Q

alpha 1 R

A

vasoconstriction - inc BP

dilate pupil

120
Q 
drugs;
atropine 
cocaine 
amphetamine 
prazosin 
propranolol
A

muscarininc antagonist -non-selettive - cholinergic antagonist

inhibit NE reuptake - adrenergic indirect agonist
amphetamine - inc NE secretion - indirect adrenergic agonist
alpha-1 antagonist - red BP - adrenergic antagonist -selective
beta antagonists - non-selective - adrenergic antagonist

121
Q

HDL

A

liver -immature; Apolipoproteins [apoAl, appall] + phospholipid
acquire cholesterol;
-during lipolysis of chylomicrons & VLDL
-from peripheral tissue

122
Q

statin mechanism

A

for high LDL patients;

  • inhibitor of HMG CoA reductase
  • so the hepatic cholestrol drops
  • liver makes more LDL receptors - dec LDL blood
123
Q

statin drug

A

best for LDL lowering

primary prevention of CVD

124
Q

resin combination

A

with statin

to dec the cholesterol biosynthesis

125
Q

ezetimibe

A

cholesterol absorption inhibitor

inhibit internalization of sterol-bound NPC1L1

126
Q

PCSK9 inhibitor

A

new for LDL lowering - severe heterozygous hypercholesterolemia
combine with max statin and diet
monoclonal antibodies
second line

127
Q

niacin mechanism

A

inhibit TG lipolysis - dec Fas, hepatic TG, VLDL, LDL

red apoA-I clearance - inc HDL

128
Q

fibrate

A

best for high TG & red HDL

PPARalpha agonists

129
Q

PPARalpha

A

transcription factor - inc gene expression for lipid metabolism;
endothelial lipoprotein lipase
fatty acid oxidation
apo A-I apo A-II

130
Q

RAS renin angiotensin system

A

angiotensinogen
Renin
AI
Angiotensin-Converting Enzyme ACE
All
1- AII R on the vessel - vasoconstriction
2-AII R on adrenal gland - aldosterone - inc Na + H2O - inc Blood volume

131
Q

k sparing diuretic

A

aldosterone antagonist

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