Cardiovascular Flashcards
(178 cards)
1
Q
Ach agonists
A
Ach (M and N)
Bethanechol (M)
Nicotine (N)
Pilocarpine (M)
2
Q
Ach Agonist, which ones go to CNS? And why ?
A
Nicotine and pilocarpine, not an ester
3
Q
Ach agonist, whcih one resistant to breakdown of Ach E
A
Bethanechol (M) because it is a choline ester
4
Q
Indirect Ach agonist?
A
Ach E inhibitor, only works where Ach is present, no selective for M or N
5
Q
Neostigmine, what? enter CNS? use?
A
Indirect Ach agonist, AchE inhibitor
synthetic carbamate, no CNS entry
Used in myesthesia gravis
6
Q
Parathion? enter CNS?
Source?
A
Source: insecticide
Indirect Ach agonist, AchE inhibitor
Synthetic organophosphate, CNS entry
7
Q
Ach R found in 3 locations?
A
- Ganglia of ANS (Nn)
- PANS (M) and SANS sweatgland (M)
- NMJ (Nm)
8
Q
3 types of Ach M R? location? which one has inhibitory effect?
A
M1: nerve ending
M2: Heart - Inhibitory
M3: Smooth muscle
9
Q
Clinical use of Bethanecol?
A
Activation of bowel and bladder smooth muscle
10
Q
Use of pilocarpine
A
Glaucoma, Xerostomia
11
Q
Use of Neostigmine
A
Activation of bowel and bladder smooth muscle, myasthenia gravis
12
Q
AchE inhibitor poisoning symptoms
Treatment?
A
DUMBBELS: diarrhea, Urination, Miosis, Brachycardia, Bronchioconstriction, Excitation, lacrimation, Salivation
Treatments: Atropine (M antagonist) And pralidoxime (AchE activator)
13
Q
Atropine? Use?
What is atropine fever
A
M Antagonist
Use in insecticide poisoning, eye exam (mydriasis)
Hyperthermia; block sweating
14
Q
Glycopyrrolate
A
M Antagonist
Gi Gu muscle relaxation to reduce motility or spasm
15
Q
CO? how to calculate
A
CO: mL/min
CO = HR * SV
16
Q
3 functions of artery?
A
- deliver blood
- convert pulsatile output to continuous flow
- small high-energy resevoir of blood
17
Q
Mean Arterial Pressure (Pa) formula?
A
Pa = Pdias +1/3 Ppulse
18
Q
Aterial baroR? location?
A
- carotid sinus and arch of aorta
19
Q
Relationship between R and radius
A
R ~ 1/r^4
20
Q
Causes of shock
A
NACHOS
Neurogenic, Anaphylactic, Cardiogenic, Hypovolemic, Obstructive, Sepsis
21
Q
Arteriosclerosis. Types? What affect mortality more?
A
hardening of the arteries, less complicance
Atherosclerosis: involves the intima of muscular and elastic arteries.
Monckeberg Sclerosis: media
Ateriolosclerosis: degenerative change in the arterioles
Atherosclerosis affect mortality
22
Q
Two Immune cytokines responsible for endotoxic sptic shock
A
TNF and IL1
23
Q
Aneurysm, when it happens
A
localized dilation of the blood vessel wall, happens when the wall thinner/ higher compliance
24
Q
Diseases of veins
A
Varicose veins
Phlebothrombosis and Thrombophlebitis
25
Angioma?
Tumor of blood vessel, head and neck is common place because highly vacularized
26
consequence of developing Atherosclerosis, up to what point is stil reversible?
Fatty streaks > Atheromas > fibrous plaques> atheromas
| up to step 2
27
Risks factors of atheosclerosis
Diabetes, hyperlipidemia, hypertension, smoking, obesity
28
what initiates atherosclerosis leision?
M, inflammation disease
29
The leading cause to infarction?
atheorosclerosis
30
most common complication of myocardial infarction?
Arrhythmia (90%)
31
Rheumatic Heart disease
hypersensitivity type II
due to beta hemolytic Group A Strep
fibrosis of heart valve
32
Congestive Heart failure
heart is unable to pump an adequate amount of blood or meet the metabolic needs of the body
33
K channel
slightly open at resting
pen gradually when depolarization
delayed outward recifier
34
K1 channel
Open: resting
Close depolarization
Also called inward recifier
35
K to channel
Close: resting
opens rapidly and trasiently at depolarization
Trasient outward recifier
36
Fast opening Na channel:
Activating gate: close at resting, open at depolarization
Inactivating gate: close at depolarization, open at resting
but inactivating gate close much slower>> leave small opning time
37
Slow opening Ca
Inactivation and activation gate
| but activation close slower
38
what happen during plateau of cardiac AP?
Ca in balance K out
39
Pacemaker AP
depolarized spontaneously toward the threshold
Lack K1 channel (repolarization activated)
mmb potential never become as negative as other cells
Resting potential >. max diastolic potential
inactivating gate of Na channel never open (no hyperpolarization)
Has pacemaker/ funny current (Na leak)
40
Why there is plateau in placemake potential?
still K out, Ca in , but because depolarization was relative slow, repolarization begins immediately.
41
Signal conduction across theheart
gap junction
intercalated disk
functional syncytium
42
Functional Syncytium
the heart behaves as if the indivivdual cells were fused into one giant cell. Intercalated disk
43
conduction sequence
SA> Atria> across atrium from R to L, top to bottom> AV node (slow propagation allow nodal delay) > bundle of His > punrkinje > ventricular muscle
44
Types of pacemaker, and their conductant rate
SA: 75 beats/min
AV: 40-60 beats/mins (reversed pacemaker), slow-opening Ca channel> nodal delay
Purkinje; 15-40 beats/min, 2nd reversed, fast, fast opening Na channel
45
PANS on heart
Vagus nerve, Mreceptor
Increase permeability K
Na funny channel delayed
decrease Ca influx
46
SANS on heart
Beta 1, NE, increase cAMP
increase Ca open
increase funny channel
47
P wave of ECG
atrial depolarization (R> L)
48
is the depolarization in AN node shown on ECG?
No, amount of tissue in AV nose is small. the net dipole is small and is not projected on ECG
49
PQ interval
AV node delay
50
Q wave
1. depolarization from left Purkinje into interventricular septum (L>R)
downward deflection
2. also repolarization of atria from R > L> downward
51
R wave
AP move from Purkinje to right and left ventricle muscle,
however, left ventricle muscel is much greater > greater net dipole
upward defleciton
52
S wave
depolarization the basal part of the L ventricle (may or may not show)
53
Unusual prolongation of QRS?
depolarization moves sloW in the ventricle, block in purkinje
54
T wave
Ventricular repolarization from left to right
55
ST segment
```
ventricular depolarized ( no net dipoles)
Plateau phase 2
```
56
Stenotic valve
valve that fails to open completely
57
Diastasis
period of reduced ventricular filling
58
Atrioventricular valves
R: Tricuspid
L: mitral
59
Semilunar valves
Aortic valve
| Semilunar valve
60
T/F: end diastolic = mitral close = frist heart sound
T
61
Isovolumetric contraction: how is P aorta compared to
Paorta> P Ventricle
62
Rapid ejection vs. Reduce ejection
Rapid: when aortic valve just open
Reduced: blood flow in arteries falls below blood flow out of arteries.
T wave is recorded - ventricular repolarizing
2nd heart sound
63
Isovolumic relaxation
| What is dicrotic notch?
Aortic valve closes. recoil in aorta causes a slight increase in aortic pressure
64
End systolic volume
volume remain in ventricle when aortic valve is closed, about 40% od end diastolic Vol
65
Elastance, formula
the ability to return to its original shape
| E = delta P/ delta V
66
compliance, formula
How stretchable
| C = delta V/ delta P
67
Increase ventricular contraction (increase/decrease) elastance? what does it mean?
increase
| require a greater pressure to add a certain volume at a high volume
68
Higher E max, greater contractilty (T/F)
T
69
Preload
the level muscle stretches when it starts to contracts, more blood flow itno ventricle during diastole
70
afterload
pressure muscle musr generate ro push blood into aorta
71
Starling law of the heart
Venous rerun increases, Sv will increase by the same amount >> so CO = VR
72
T/F: end diastolic = mitral close = frist heart sound
T
73
Isovolumetric contraction: how is P aorta compared to
Paorta> P Ventricle
74
Rapid ejection vs. Reduce ejection
What feature shown in ECG?
any heart sound?
Rapid: when aortic valve just open
Reduced: blood flow in arteries falls below blood flow out of arteries.
T wave is recorded - ventricular repolarizing
2nd heart sound
75
Isovolumic relaxation
| What is dicrotic notch?
Aortic valve closes. recoil in aorta causes a slight increase in aortic pressure
76
End systolic volume
volume remain in ventricle when aortic valve is closed, about 40% od end diastolic Vol
77
Elastance, formula
the ability to return to its original shape
| E = delta P/ delta V
78
compliance, formula
How stretchable
| C = delta V/ delta P
79
Increase ventricular contraction (increase/decrease) elastance? what does it mean?
increase
| require a greater pressure to add a certain volume at a high volume
80
Higher E max, greater contractilty (T/F)
T
81
Preload
the level muscle stretches when it starts to contracts, more blood flow itno ventricle during diastole
82
afterload
pressure muscle musr generate ro push blood into aorta
83
Starling law of the heart
Venous rerun increases, Sv will increase by the same amount >> so CO = VR
84
venous resevoir
short term correction of blood vol.
| Reduce unstressed vol (Vo), but does not change venous compliance
85
increase in aortic pressure, what happen to SV right after and after awhile
Immediately, SV reduces
| later, has new end-diastolic volume to maintain SV
86
posiive inotropic effect
increase contractility
87
Epinephrine
activate a1,a2,b1,b2 (all adreR)
BP increase slightly, increase HR
used with local anesthesia
88
Cocaine
block NE reuptake, activate all adreno R
89
Amphetamines (methylphenidate)
stim NE release, activate all adrenoR
| attention deficit disorder
90
NE
activate alpha 1,2,b1
| vasoconstriction, bradycardia (?)
91
Phenylephrine
activate a1
| increase Bp, slow HR
92
clonidine
activate a2
93
isoproterenol
b1,2 activation
| vasodilation, decrease BP, tachycardia
94
dobutamine
beta 1 activation
95
allbuterol
beta 2 activation
| asthma
96
effect of alpha 1, beta 1
alpha 1: increase BP, vasoconstriction
| beta 1: increase BP, CO
97
Prazosin, terazosin
alpha 1 blocker:
Terazosin has longer half life
treat hypertension
Adverse: postural hypertention
98
Propanolol
beta 1,2 (non selective)
| Adverse: hypotension, bradycardia
99
metoprolol
beta 1 only
| safe for patient with asthma, diabetes
100
carvedilol
beta& alpha (mixed antagonist)
101
labetalol
beta & alpha 9mixed antagonist)
102
Postural hypertension
when we stand up suddenly, alpha 1 R activated to maintain BP
103
why should not stop Beta blocker suddenly
prolonged blockade of beta blocker will result upregulate Beta R at cell surface.
removal of beta blocker will cause an overshoot effect
104
pulse pressure
the difference between diastolic and systolic pressure
| proportional to SV
105
mean arterial Pa as function of CO and TPR
Pa = CO* TPR
106
Why faint from heat?
heat> vasodilator> TPR decreases>Pa decrease
107
poiseuille's law
R = 8nL/Pi (r^4)
108
SANS control resistance
| Rceptor conc in the body
SANS releases NE, Adrenal Epi
High conc of Receptor in skin and kidney
Low in cardiac and cerebral arteries
no Receptor in placenta
109
local control resistance mechanism (3)
1. autoregulation (myogenic)
2. metabolic regulation (O2, CO2)
3. locally release messenger
110
favorable conditions for exchange in the capillarity
large surface/volume ratio
low flow velocity
thin leaky wall
111
Pinocytotic vescicle
shuttle large -lipid-insoluble molecules through the mmb
112
Rate of diffusion depends on
1. permeability to the subtance
2. concentration gradient
3. SA
113
Flitration
flow of fluid between plasma and ISF
114
Rate of filtration depends on
1. permeability of water
| 2. pressure gradient
115
Pressure Gradient formula
P gradient = P outward - P inward
| = (Pcap+ Oisf) - (Pisf + Ocap)
116
Edema
accumulation of ISF
117
Causes of edema
```
1. Increase cap BP
> HF: low contractility> increase preload> increase vR
> pregnacy: increase Blood vol
2. decrease plasma protein conc
3. blocked lymphatics
4. leaky cap (inflam)
```
118
Causes of Arrythmias
1. Abnormal impulse initiation ( sinus nose abnormality, ectopic pacemaker, trigger rhythms)
2. Abnormal conduction (simple block, reentry)
119
Why are arrythmias bad?
1. mirror arryth > major one
2. Decrease CO
3. embolus formation (stroke)
120
How to treat arrythmia, abnormal pacemaker
HypoK > setum K
Digitalis toxic> reduce digitalis dose
imcease SANS> use a beta blocker?
121
Arrythmia> how to treat abnormal conduction
make the sick tissue sicker ( no conduct at all)
| blocking specific channels
122
State-dependent block in Arryth drug
drug binds strongly to open/inactivatedand only weakly to the resting state
123
4 major groups of Arryth drugs
| Which group are nodal, which are non-nodal
```
1. Group 1: suppress conduction by blocking Na channel
Group II: beta blocker
Group III: Blocking K channel
Group IV: blocking Ca channel
Group 1, 3 are non-nodal
Group 2,4: nodal
```
124
Arrythmias drug: group I A, MOA, problem
decrease Na current > decrease conduction velocity
decrease K> increase AP duration
Problem: non selective, can block healthy tissue
Ex: Procainamide, Quinidine, Disopyramide, Amiodarone
125
Amiodarone
Arryth drug, blocking Na, Ca, K channel and beta R
Very effective for a variety of atrial and ventricular arryth
Eliminate slowly (3months)
Accumulate in skin cause discoloration
Hypo or Hyperthyroid
Pumonary fibrosis
126
Lidocaine in treating arrythmias
| Group IB
Block Na
Selective for sick tissue
Only for ventricular arryth
Tocxicity affects CNS
127
Group IC Drug Arryth Flecainide
Block Na but recovery very slow
Non-selective (prolong QRS)
Vetricular
Toxicity: dose dependent blurring of vision
128
Group II Beta blocker Arrythmia
AP: reduce plateau and slope
Supress ectopic pacemarker
Reduce HR, slow AV conduction (long PR)
Ex: propanolol, metoprolol
129
Group III: Arrythmia - K blocker
```
Prototype: Ibutilide, sotalol
both atrial and ventricular arryth
Prolong duration of Ap
ECG: lengthens QT, lengthen PR, no change in QRS
Toxicity:
- Early after depolarization
- Torsades
```
130
Early after depolarization (Arryth druf: K blocker)
Prolong repolarization, allow Ca channels to recover from inactivation and open during plateau (see 2 peaks)
131
Torsedes ( Arryth drug, K blocker)
Type of ventricular fibrillation, reduce CO
132
Group IV Arryth drug: Ca blocker
Ex: Verapamil, Diltiazem
AP: slow conduction of AV nodal, reduce SA rate
ECG: lengthen PR, no change in QRS or QT
Toxicity: Sa nodal depression, Av node block, hypotension, DDI with Digoxin
133
Adenosine
Arryth Drug
| terminate reentrant Supreventricular Tachycardias, hyperpolarization
134
class of hypertension drug
Diuretics
Sympatholytic
Vasodilator
Anti Renin-Ang
135
cause of hypertension
Primary: unknown
Secondary: renal, coartation of aorta, cushing 's disease
136
Diuretics drug treating hypertension
| K wasting
control volume
| Ex: hydrochlorothiazide, furosemide
137
Thiazide
treating Hypertension (hydrochlorothiazide
maz efficacy small (10 mmHg) (10% Na)
long half life
PO
max out on BP effect nefore the diuretics effect
Adverse effect:HypoK
138
Furosemide
Loop diuretics treating Hypertension
strong iduretic (40% Na), better efficacy than thiazide
short half life, more toxicity
Adverse: HypoK
139
Diuetics (K sparing)
```
Ex: Spironolactone, Eplerenone
Max efficacy small: 10mmHg)
Collecting duct
inhibit Na take up at collecting duct, no need to exchange with K
Adverse: HyPER K,
```
140
Spironolactone
K sparing diuretic drug: Hypertension
block aldosterone R prevent Na take up in collecting duct
Adverst effect: KyperK, Anti androgen effects
141
Sympatholytics Hypertension drug
Ex: clonidine, Beta blocker, alpha blocker
142
Clonidine, methyl dopa
alpha 2 agonist in brain stem
Reduce SANS
Advers: sedation, sleep disturbances, dry mouth, postural hypotension
Methyldopa does not cause the overshoot in bp when stop using like clonidine
143
Clonidine and the overshoot when stopping suddenly
when on clinidine, alpha 2 R is down regulated in response to constant stimulus
Now stop suddenly: less alpha 2 to handle negative FB> NE increase> B increase
PO,
144
Methyldopa
transform to alpha Mel-NE stored in vescicles
does not cause over shoot high BP because conc decrease slowly , allow time for desensitized R to resume their normal function
Pregnancy approved
145
Propanolol for hypertension
b blocker, nonselective
reduce CO, reduce renin released, CNS effect
Adverse: astha (B2 blocked), heart block, sleep alteration, depression, alterations in lipids
146
Beta blocker to treat hypertension
Propanolol, metoprolol
| carvedilol, labetalol
147
Alpha blocker to treat hypertension
MOA: vessel relaxation (PVR)
Adverse: postual hypertensio, first dose affect, tachycardia
Ex: Prazosin
148
Vasodilator in treating hypertension
MOA: reduce depolarization, block Ca channel > reduce contraction of smooth muscle
Types:
K channel opener
Ca blocker
149
K channel opener to treat hypertension
Vasodiator
Hyperpolarization
Ex: monoxidil, PO,
Adverse: hair growth
150
Ca blocker to treat hypertension
Ex: Nifedipine, amplodipine
can combine poly RX for severe case
Adverse: Nifedipine selective for vessel> heart
posture hypotension
151
Angina Pectoris: definition?
pain due to myocardial ischemia,
152
types of angina
classic: symptoms is predictable at level of exercise
| Vasopastic Angina: episodic, unpredictable
153
Twp option to treat angina
Surgical
| Pharmaco:
154
4 Pharm approach to treat Angina? which options is the most effective
decrease resting oxygen use
decrease preload
decrease after load
decrease SANs
Decrease preload is the most effective
155
```
3 drugs class to treat angina
Which one cant treat vasospastic angina?
```
Nitrate
Beta blocker
Ca blocker
Beta cannot treat vasospactic angina
156
Nitrates
MOA
Toxicity
Tolerance? DDI
Treat angina: reduce preload
MOA: nitric oxide stimulates Guanylate cyclase> cGMP> inhibit Ca influx and contraction
Dilate Vein >>> Artery
Ex: Nitroglycerin (Sublingual)
Dilate venous vessel
Toxicity: postural hypotension, tachycardia
Tolerance: Monday headache: loss of tolerance over the weekend
DDI: NO + viagra (sildenafil)> +++ hypotension
157
Beta blockers in treating angina
reduce HR, contractility
> decrease PVR, afterload
Use for clinical Angina only
Tpxicity: may worse CHF, athsma, AV block
158
Ca channel blocker in treating Angina
Prototypes: Verapamil
MOA: block L type Ca channel in heart more than in vasculature
Decrease HR and contractility, afterload
Use: vascopastic angina, combination with NO
Toxicities: CHF, AV block, constipation
159
how to combine drug in Agina treatment? No, Beta blocker, Ca blocker
Either Beta or Ca combine with NO
| Beta combine with CA will cause synergic effect
160
Most common cause of CHF
coronary artery disease
161
2 form of CHF
Systolic (60-70%):loss of contraction
| Diastolic: loss of relaxation
162
Digitalis
+ inotropic agent
Toxic: jaundice, yellow vision (xanthopsia), hypoK
MOA: increase Ca storage by blocking Na/KATPAse (Na/Ca exchanger and ATP Ca pumo system)
narrow theurapeutic index
163
Phosphodiesaterase Inhibitor
Treat CHF
Ex: Inamrinone, Milrinone
Prevent cAMP breakdown > increase Ca
164
Isosorbide Dinitrate
Vasodilator to treat CHF
+ Hydralizine = BiDil
African American
do not reduce Na and water retention
165
Beta alpha blocker to treat CHF
Carvedilol
| SANS makes HF worse
166
ACE inhibitor (-April)
treat CHF: block Angio I > Angio II
Reduce both PVR and water retension
Captoapril, Enalapril
Adverse: cough due to build up bradykynin
167
Angiotensin R blocker (losartan)
Lorsatan
| Toxicity: nasal congestion
168
Spironolactone
Aldosterone inhibitor CHF treatment
| HyperK
169
congestion> consequence?
dilated blood vessel >> hpoxia
170
Nutmeg liver
Hypoxia injury of the liver, congestion
171
Hemostasis, define, what component that help
process cause bleeding to stop
| vascular wall, platelets, coagulation
172
what thrombogenic factors in endothelial lining of vascular wall
Potent thrombogenic factor: thromboplastin, von Willebrand, thromboxane A2
Anti-thrombogenic : thrombomodulin,
173
coagulation
intravascular transformation of fluid blood into a get matric entrapped cellulce constituents
174
Intrinsic system coagulation
```
Activated by contact with a foreign surface
Hageman Factor (XII)
```
175
Extrinsic system coagulation
After injury, tissue thromboplastin is released to the blood
VII+ thromboplastin
176
Common pathway of coagulation: which factor
Factor X >> prothrombin> thormbin>>Fibrinogen> fibrin
177
Consequence of hemostasis
1. vasocontriction
2. vWF binding
3. platelet adhesion
4. fibrin mesh formation
178
where all clotting factor are synthsized? which vitamin?
liver, K
