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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5337_Библиотеки_им_академика_М_И_Перельмана.pdf
146. Antidote of atropine is:
A. Neostigmine B. Pralidoxime
C. Physostigmine D. None of these
147. Atropine blocks the muscarinic actions of
acetylcholine by:
Inhibiting synthesis of ACH
A.
B. Inhibiting release from storage sites
C. Competing at receptor sites
D. All
148. Sweating is inhibited by:
A. Atropine B. Phenothiazines
C. Scopolamines D. All
149. Beta agonist used in bronchial asthma exert action
by
Blocking B1 receptor
A.
B. Blocking B2 receptor
C. Stimulating B1 receptor
D. Stimulating B2 receptor
150. Which of the following agent irreversibly bound
with acetyl cholinesterase:
Dispropylfluorophosphate
A.
B. Ecothiopate
C. Both a and b
D. None of these
151. Neostigmine effectively antagonizes skeletal
muscle relaxation produced by:
Tubocurarine B. Gallamine
A.
C. Pancuronium D. All
152. For glycogenolysis in liver one of the following
adrenoreceptor is responsible:
Alpha-1 receptor B. Alpha-2 receptor
A.
C. Beta-1 receptor D. Beta-2 receptor
153. Alcuronium is a semisynthetic derivative with
similar properties of:
Gallamine B. Pancuronium
A.
C. Succinylcholine D. D-tubocurarine
154. Example of a directly acting sympathomimetic
agent is:
Ephedrine B. Amphetamine
A.
C. Dopamine D. All
155. Gingival hyperplasia is an oral condition possible
in using:
Phenobarbital B. Phenytoin
A.
C. Pentobarbital D. Valproic acid
156. Tachyphylaxis is an unwanted effect of:
A. Methohexamine
B. Methylphenidate
C. Ephedrine
D. Methamphetamine
157. Activation of alpha-2 receptors in the pancreatic
islets causes
Suppression of insulin secretion
A.
B. Stimulation of insulin release
C. Suppression of glucagon secretion
D. None
158. Mass discharge of the sympathetic nervous system
is:
A.
Regulated by the centre in the thoracic and
lumber segments of spinal cord
B. Initiated and coordinated by higher centres in
the hypothalamus
C. Associated with increased activity of the
gastrointestinal tract
D. Harmful and may cause failure of the
cardiovascular and respiratory system
159. Darifenacin is a:
A. M1 antagonist B. M2 antagonist
C. M3 agonist D. M3 antagonist
160. Which of the following muscle relaxant has
peripheral action?
A.
Diazepam B. Mephenesin
C. D-Tubocurarine D. Orphenadrine
161. Cardiac effects of epinephrine include all except:
A. Act on B-receptor of myocardium
B. Induced cardiac arrhythmias are blocked by
propranolol
C. Prolong refractory period of AV nodes
D. Decrease the amplitude of the T-waves of ECG
162. Which of the following agent is a cholinesterase
re-activator?
A.
Pilocarpine B. Pralidoxime
C. Neostigmine D. Physostigmine
163. Pilocarpine is best used in:
A. Congential glaucoma
B. Open angle glaucoma
C. Secondary glaucoma
D. All
164. Timolol reduces the intraocular pressure by which
mechanism of action?
A.
Muscarinic agonist
B. Anticholinestarase
C. Carbonic anhydrase inhibitor
D. Beta-adrenoceptor antagonist
165. Serious unwanted effect of epinephrine is:
A. Respiratory difficulty
B. Palpitation
C. Cerebral heamorrhage
D. Tremor
166. ……………….. is the bundle axons in the PNS.
A. Tract. B. Nerve
C. Nucleus D. Ganglion
167. A bundle of neuron axons called the ………………..
which connect the right and left halves of the
cerebral hemispheres?
A.
Thalamus
B. Insula
C. Corpus cavernosum.
D. Corpus callosum.
168. Major adverse effect of clonidine is:
A. Bradycardia B. Tachycardia
C. Sexual dysfunction D. Dry mouth
Section 1 Pharmacology
29
169. Choose the drug which inhibits the acetylcholine
synthesis?
A. Neomycin
B. Vasamicol
C. Botulinum toxin
170. Ganglionic blocking agents may cause except
A. Mydriasis
B. Loss of accommodation
C. Reduced sweating is reduced
D. Inhibit erection and ejaculation
D. Atropine
ANSWER KEY
1. B 2. C 3. C 4. C 5. A 6. B 7. A 8. C 9. D 10. B 11. D 12. C 13. C 14. C
15. B 16. B 17. B 18. B 19. C 20. B 21. B 22. D 23. D 24. A 25. C 26. A 27. D 28. B
29. C 30. B 31. C 32. B 33. C 34. B 35. D 36. B 37. B 38. A 39. C 40. D 41. C 42. B
43. B 44. C 45. C 46. C 47. B 48. C 49. D 50. C 51. A 52. B 53. C 54. C 55. B 56. B
57. B 58. D 59. A 60. C 61. A 62. C 63. D 64. A 65. C 66. B 67. B 68. D 69. C 70. D
71. D 72. C 73. C 74. D 75. B 76. A 77. D 78. C 79. C 80. D 81. D 82. A 83. A 84. D
85. D 86. B 87. D 88. C 89. D 90. C 91. A 92. C 93. C 94. B 95. C 96. D 97. C 98. C
99. D 100. D 101. B 102. B 103. D 104. D 105. A 106. C 107. B 108. C 109. D 110. D 111. C 112. A
113. B 114. B 115. A 116. A 117. D 118. B 119. A 120. B 121. D 122. B 123. A 124. A 125. D 126. A
127. D 128. C 129. B 130. D 131. B 132. C 133. A 134. D 135. B 136. C 137. C 138. B 139. A 140. D
141. C 142. C 143. D 144. D 145. A 146. C 147. D 148. D 149. D 150. C 151. D 152. A 153. D 154. C
155. B 156. C 157. A 158. B 159. D 160. C 161. C 162. B 163. B 164. D 165. C 166. B 167. D 168. D
169. B 170. D
3. Pharmacology of Cardiovascular System
Anatomy and physiology of heart
The heart is a muscular organ that acts like a pump to
continuously send blood throughout body.
The heart is at the center of the circulatory system. This
system consists of a network of blood vessels, such as
arteries, veins and capillaries.
These blood vessels carry blood to and from all areas of
the body. Blood carries the oxygen and nutrients that
your organs need to work normally.
Blood also carries carbon dioxide, a waste product, to
your lungs to be passed out of the body and into the air.
Size and Shape of the Heart
The heart is located underneath the sternum in a thoracic
compartment called the mediastinum, which occupies the
space between the lungs.
It is approximately the size of a man’s fist (250-350
grams) and is shaped like an inverted cone.
The Chambers of the Hearts
The heart is made up of four chambers. The superior
chamber consists of the right atrium and the left atrium,
which lie primarily on the posterior side of the heart.
Extending anteriorly from each thin walled atrium is a
small, ear-shaped appendage called auricle that expands
Section 1 Pharmacology
the volume of the chamber.
Blood drains into the atria from the pulmonary and
30
systemic circulatory system. Composing the lower
chambers are the right ventricle and left ventricle, which
are much larger than the atria.
The right ventricle pumps blood through the pulmonary
circulatory system and the thicker walled left ventricle
pumps blood through the longer systemic circulatory
system. Internally, the two ventricles are separated by a
thick myocardial wall called the interventricular septum.
Definition of BP
It is the lateral pressure exerted by the blood on the vessel
wall perpendicularly while flowing through it.
Types
1. Systolic pressure: Pressure exerted during contraction
(systole) of the heart.
2. Diastolic pressure: Pressure exerted during relaxation
(diastole) of the heart.
3. Pulse pressure: It is the difference between systolic and
diastolic pressure.
4. Mean pressure: It is the diastolic pressure + one-third
of pulse pressure.
Blood pressure is directly equal or proportional to the
product of cardiac output and the peripheral vascular
resistance.
Blood pressure = Cardiac output × Peripheral resistance.
Control Mechanism
There are two ways of blood pressure control. These are
as follows.
1. Baroreceptor mechanism
2. Renin angiotensin aldosterone system.
Anti-hypertensive drugs
Hypertension
It is a condition where BP values are over 140/90 mm Hg.
Types
Primary or essential—where cause is unknown
(incidence 95%)
Secondary—where cause is known (Incidence 5%).
Causes
1. Renal cause—renal artery stenosis, glomerulonephritis,
polycystic kidney, diabetic nephropathy.
2. CVS cause—coarctation of aorta.
3. Endocrine cause—pheochromocytoma, Cushing
syndrome, thyrotoxicosis.
4. Pregnancy—preeclampsia, eclampsia.
Fig. 3.2: Mechanism of action of methyldopa
7. Antihypertensive effectdevelopsover 4–6 hours andlasts
12–24 hours.
8. Circulating levels of NA and renin tend to fall due to
reduction in sympathetic tone.
9. Inhibition of postural reflexes is mild.
Fig. 3.1: Antihypertensive drugs
CENTRALLY ACTING ANTIHYPERTENSIVES
METHYLDOPA, CLONIDINE
Adverse actions
1. Drowsiness, sedation
2. Fatigue, nightmares
3. Fever, GIT upset, dry mouth
4. Parkinsonism, nasal congestion
5. Failure of ejaculation, hemolytic anemia
6. Gynecomastia, impaired lactation
7. Thrombocytopenia and rarely lupus
8. Fluid retention and weight gain.
CALCIUM CHANNEL BLOCKERS (CCBS)
Properties
1. a-methyldopa is chemically related to dopa.
2. It is a prodrug.
3. It is converted to methyl noradrenaline.
4. Its acts as agonist of a2-adrenergic receptors in the
brainstem.
5. Methyldopa is a moderate efficacy antihypertensive.
6. Methyldopa had been a widely used antihypertensive
for mild to moderate cases, especially in combination
with a diuretic.
Fig. 3.3: Mechanism of action
Section 1 Pharmacology
31
β-BLOCKER
a-RECEPTOR BLOCKER
Fig. 3.6: Mechanism of action
Fig. 3.4: β-Blockers
ANTIHYPERTENSIVE ACTION: ACE INHIBITORS
Section 1 Pharmacology
32
Fig. 3.5: Antihypertensive action: ACE inhibitors
VASODILATORS
Fig. 3.7: Diuretics
attack. The whole phenomenon is often viewed as a balance
supply and O2 demand.
of O
2
Antianginal drugs: angina pain is a pain in chest due to
decrease in oxygen supply, there is a two type of angina
1. Classical or Stable
2. Variant/Prinzmetal/Unstable.
1. Classical or Stable angina: attack increase by exercise
emotions, eating decrease by rest.
2. Variant/ Prinzmetal/ Unstable angina: Attack
occurs at rest, sleep, sexual intercourse, eating,
unpredictable. they are due to recurrent localized
coronary vasospasm.
Classification
Nitrate: Glyceryl trinitrate, isosorbide dinitrate
Beta blocker: Propanolol, atenolol.
Calcium channel blocker: Niphidipin, amlodipine,
verapamil
Potassium channel opener: Nicorandil, pinacidil.
Fig. 3.8: Mechanism of action
Fig. 3.9: Nonreceptor adrenergic inhibitors
ANTIANGINAL DRUGS
Angina (pain) pectoris (chest) is a very common disease,
mostly affecting middle-aged persons usually men. Angina
is caused by myocardial ischemia. Basically, there are two
factors to be considered (i) the requirement (the demand)
of the heart; and (ii) the O
flow. Obviously, fail of O
combination of both the factors can precipitate an anginal
supply, via the coronary blood
2
supply or rise of O2 demand or
2
Fig 3.10: Classication of antianginal drugs
Fig. 3.11: Nitrates: Mechanism of action
1. Nitrates reduce the O2 demand by venodilatation (i.e.
by reducing the preload of the heart).
2. The Ca+2 channel blockers by reducing BP (i.e. the
afterload, i.e. the systemic arteriolar dilation as well as
epicardial ones).
3. The β-blockers by reducing the tachycardia + contractility
(work done by the heart).
Section 1 Pharmacology
33
Uses of Nitrates
1. Angina pectoris
2. Heart failure
3. Acute hypertension
4. Acute myocardial infarction.
+2
Ca
CHANNEL BLOCKER
Fig. 3.12: Mechanism of action angina
3. They slow down the heart rate
4. They reduce myocardial contractility both (3 and 4)
reduce of development of angina.
β-BLOCKERS
Mechanism of Action in Angina
1. They reduce myocardial oxygen demand by reducing—
a. Heart rate
b. Myocardial contractility
c. BP.
2. They also increase diastolic period.
Effects of β-Blockers in Angina
1. It prevents development of exertional angina
2. It increases the duration of exercise tolerance
3. By opposing the injurious effects of CA, it reduces the
reach of angina during emotional outbursts (e.g. ragepanic)
4. It reduces the chance of mortality in IHD
5. In silent ischemia (where pain is absent but ECG signs
of ischemia are present) β-blockers are helpful.
Myocardial infarction (MI)
Myocardial infarction (MI): it is an ischaemic necrosis
of portion of myocardium due to sudden occlusion of
coronary artery.
Treatment
Pain anxiety: Opium analgesic/diazepam.
Oxygenation
Maintenance of microcirculation: slow i/v.
Correction of acidosis: As lots of lactic acid is produced,
sodium bicarbonate is giving in IV infusion
Prevention and treatment of arrhythmia: Beta blocker
Pump failure: So, we have to increase cardiac output by
a) Inotropic agent (increase concentration) by Dopamine
or Dobutamine b) Vasodilator
Prevention of thrombus extension: Heparin
(only injected subcutaneously) followed by oral
anticoagulant
Thrombolysis: Streptokinase, urokinase, alteplase.
Prevention of future attack: Aspirin (it has platelet
aggregation inhibition factor).
Control of hyperlipidemia: Diet control, hypolipidemic
drugs
Anti-arrhythmic Drugs
Arrhythmias are dysfunction in impulse formation and
conduction in the myocardium. Cardiac arrhythmias may
cause the heart—
1. To beat too slowly (sinus bradycardia).
2. To beat too rapidly (sinus or ventricular tachycardia,
atrial or ventricular premature depolarization, or atrial
flutter).
3. To respond to impulses originating from sites otherthan
the SA node.
4. To respond to impulses traveling along accessory (extra)
pathways that lead to deviant depolarizations (AV
reentry, Wolff-Parkinson-White syndrome).
Section 1 Pharmacology
34
Fig. 3.13.: Classication of antiarrhythmic drugs
Arrhythmias: These are the drugs used to prevent or treat
irregularities of cardiac rhythm.
For supraventricular arrhythmia: Propanol
For ventricular arrhythmia: Lignocaine
For AV block and bradycardia: Atropine
Anti-arrhythmic drugs:
Class 1— sodium channel blocker
Class 2— beta blocker-propanol
Class 3— bretylium
Class 4— calcium channel blocker, nefedipine, verapamil
SITE OF ACTION OF DRUGS (WITH DIAGRAM) AND
MECHANISM OF ACTION
Phase 0: It is due to explosive Na+ entry from ECF to
ICF (Na
Phase 1: It is due to stoppage of Na+ and entry of Cl– ions
Phase 2: It continued entry of Na+ stoppage + beginning
of exit of K
Phase 3: It is due to stoppage of Na+ + exit of K
of Ca
Phase 4: Finally develops.
Treatment of cardiac heart failure when cardiac output
is insufficient to meet the demand of God acres cardiac
heart failure.
3D: Diuretics, Dilators, Digitalis
+2
+
influx)
++
influx of Ca
+
++
stoppage
potassium ATPase of myocardial fibre and inhibit this
enzyme.
It results in increase of sodium Ion intracellularly witch
indirectly results in increase in calcium ion accumulation
by sodium ion, calcium exchange.
The excess calcium ion in cytosol is taken up into
sarcoplasmic reticulum which progressively get loaded
with more calcium Ion. This trigger release of calcium
ions stored in sarcoplasmic reticulum cytosolic calcium
iron increases triggers contraction.
Ca2+ is then activity taken up by sarcoplasmic reticulum
and fraction is extracted by three sodium Ion or calcium
Ion exchange.
Pharmacological action
1. Heart
z
increase force of contraction have inotropic effect so
cardiac output increase.
z
Heart rate decrease which is more in cardiac heart
failure by this the circulation improved.
2. Blood vessels
z
Digoxin has no prominent action
3. Kidney
z
Diuresis is needed specially in cardiac heart failure; no
diuresis node occurs in normal individual
4. CNS
z
No effect in lower doors, with higher dose it causes
CTZ activation results in nausea vomiting.
z
Still higher dose causes mental confusion
disorientation.
Fig. 3.14: Site of action of antiarrhythmic drugs
Diuretics:
It decreases preload and improve ventricular efficiency
by decrease circulatory volume.
It removes peripheral edema and pulmonary congestion.
Dilators:
Arterial Dilator: Hydralazine, calcium channel blocker
and potassium channel opener
Venodilator: Nitrate, it decreases preload.
Mixed Dilator (decrease preload and afterload): ACE
inhibitor, prazosin, Na nitropruside, losartan
Digitalis: Digoxin
Mechanism of action:
Digitalis increase force of contraction. It selectively binds
to extracellular face of membrane associated sodium
Uses
1. CHF
z
Slow digitalization: 0.25 mg/day for five days
z
it may cause bradycardia, so we need to stop digital
z
Rapid digitalization—digitoxin is effective within few
hours.
z
0.5–1.0 mg state followed by 0.25 mg every 6 hours.
z
Many mild-to-moderate cases of CHF can be treated
with diuretics and vasodilators only if not relieved
then digoxin is added.
2. Cardiac arrhythmia
z
Atrial fibrillation: Drug of choice for control ventricular
rate.it increases effective refractive period of AV node.
Atrial rate is 200 /min.
z
Atrial flutter: at real rate is 250 per minute
Side effect:
Extracardiac: Nausea, vomiting, abdominal pain due to
gastric irritation and CTZ stimulation, headache, mental
confusion, disorientation.
Cardiac: Every type of arrhythmia is produced by digitalis,
pulses bigeminus Ventricular extrasystoles, ventricular
tachycardia and fibrillation, partial to complete AV block,
severe bradycardia, atrial extrasystole, atrial fibrillation
and atrial flutter.
Treatment:
For ventricular arrhythmia: Lignocaine
For supraventricular arrhythmia: Propranolol
For a β block and bradycardia: Atropine.
Section 1 Pharmacology
35
Contraindication
Hypokalaemia— increased digitoxin toxicity
In elderly causes renal or severe hepatic disease
Partial A V block—may be converted to complete A V
Block
Ventricular tachycardia—Digoxin may precipitate
ventricular failure
Acute myocarditis—response of digoxin is very poor.
Beta blockers
Beta blockers
The drugs inhibit
adrenergic response mediated through the beta receptor
All beta blockers are competitive antagonist.
Classification
Nonselective— Propranolol, sotalol, timolol, labetalol
(drug of choice in pregnancy)
Selective β1-atenolol, Acebutolol.
Selective β2-butaxamine
Pharmacological action
1. Heart—decrease heart rate, decrease force of contraction
and cardiac output decrease blood vessels
2. Vasodilation—decrease in BP
3. Respiratory—bronchoconstriction
4. CNS- no effect
5. Local anaesthesia—potent local anaesthetic but not used
because its irritant property
6. Metabolic—lipolysis, free fatty acid, inhibit
glycogenolysis in heart, liver, skeleton muscle.
7. Skeletal muscle—inhibits trimmer
8. Eye—miotic
9. Uterus—contraction.
Side effect and contraindication:
Bradycardia—pulse rate decrease
Contraindication in bronchial asthma
Exacubate variant angina (prinzmetal)
Carbohydrate tolerance maybe impaired in prediabetic
Total triglyceride and LDL cholesterol tend to increase
Can precipitate bronchial asthma
Can precipitate and attack of CHF
Contraindication in partial and complete heart block
Tiredness and reduce exercise capacity.
Uses:
Hypertension
Angina pectoris
Arrhythmia
Myocardial infarction
Migraine
Essential tremor
CHF
Glaucoma
Dissecting aortic aneurysm
Section 1 Pharmacology
Pheochromocytoma
Thyrotoxycrosis
36
Increases thyroid.
Antihypertensive drugs
ACE Inhibitor (angiotensin converting enzyme): They
1.
decrease preload and afterload in congestive heart
failure.
z
Captopril
z
Enalapril
z
Lisinopril
z
Ramipril
2. Angiotensin antagonist
z
Losartan
3. Blocker
z
β blocker: Propanolol, atenolol
z
a blocker: Prazosin, terazosin, phentolamine
4. Calcium channel blocker— they are useful in angina
pectoris
z
Virapamil
z
Nefidipine
z
Diltiazen
z
Amlodipine
z
They are also used in arrhythmia, Raynaud’s disease
and prevention of neurological damage.
5. Central sympatholytic
z
Clonidine
z
Methyldopa.
6. Diuretic
z
High ceiling: Furosemide
z
Thiazides: Hydrochlorothiazide
z
K Sparing: Spironolactone, amiloride.
7. Dilator
z
Hydralazine (arteriolar)
z
Minoxidil (arteriolar+venous)
z
Na nitroprusside
z
Pinacidil
Hypertensives in pregnancy
z
Methyldopa
z
Selective β-blocker (labetalol)
Contraindications drugs
z
ACE inhibitor
z
Diuretics.
HT urgency (due to severe elevated BP i.e. 200/120):
When 2.4 hr
z
Can be allowed for reduction.
z
Nifidipine
z
Captopril
z
Hydralazine
HT emergency: When BP must have to be decrease
within seconds.
z
Na nitropruside (I/V)
z
Nitroglycerine.
Hyperlipidemic drugs
These are the drugs which lower the level of lipids and
lipoproteins in blood.
These drugs have potential to prevent cardiovascular
disease by retarding accelerated atherosclerosis in
hypolipidemic individuals.
Increase LDL—cholesterol leads to atherogenic (harmful)
and increase HDL—cholesterol indicates low atherogenic
state(protective).
Classification
1. HMG—coenzyme a reductase inhibitor(statins)—
lovastatin, simvastatin, pravastatin, atorvastatin and
rosuvastatin.
2. Bile acid sequestrants(resins)—cholestyramine,
colestipol.
3. Lipoprotein lipase activators (bric acid derivatives)—
clofibrate, gemfibrozil, benzafibrate, finofibrate.
4. Inhibitor of triglyceride synthesis and lipolysis—
nicotinic acid.
5. Miscellaneous—ezetimibe.
HMG-CoA reductase inhibitors(statins)-
Most efficacious and best tolerated hypolipidemic drugs.
Mechanism of action
They inhibit conversion of 3-hydroxy 3-methyl glutaryl
coenzyme A (HMG-COA) to mevalonate,
The rate limiting step in cholesterol synthesis by enzyme,
HMG coenzyme a reductase.
Therapeutic drug dose reduces Cholestrol synthesis by
22–50%.
Thus, results in compensatory increases in LDL receptors
on liver cells thus increase uptakes and catabolism of
intermediate density lipoprotein. Hence, they cause dose
dependent lowering of IDL—Ch level.
Side effect: All statins are well tolerated but do make side
effects:
Headache, nausea, bowel upset, rashes, sleep
disturbances.
Rise in serum transaminase but liver damage is rare.
Muscle tenderness
Myopathy is only serious reaction, but is rare
Ezetimibe
1.
2. Ezetimibe is weak hypocholesterolemic drug but
energise with statins.
3. Ezetimibe + statins (low dose)—cause much LDLcholesterol lowering.
4. Ezetimibe is well tolerated.
In-situ, these materials are absorbed in one to four weak
and generally cause no foreign body reaction.
Thrombin obtained from bovine plasma may be applied
as dry powder or freshly prepared solution.
Adrenaline solution as vasoconstrictor.
Astringents like tannic acid or metallic salt used for
bleeding gums bleeding piles.
C/N of drug—angel, etc.
Hematinic
Hematinic: Substances used in anemia condition and
necessary for blood formation.
Anemia: Anemia is a condition that develops when no
of red blood cells or amount of hemoglobin in the red
blood cells decreased which results into fatigue and lack
of energy state.
Normal range of hemoglobin:
For men, 13.5 to 17.5 grams per deciliter.
For women, 12.0 to 15.5 grams per deciliter
Coagulants
These are the substances which promote coagulation and
indicated in haemorrhagic states.
Drugs: Used to restore hemostasis used to stop bleeding.
1. Vitamin K-
z
K1: Phytonadion (natural)
z
K3: Menadione (synthetic)
2. Fibrinogen
3. Antihemophilic factor
4. Ethamsylate 99% used.
Vitamin K
It is fat soluble vitamin, required for synthesis of clotting
factors.
Fat soluble forms of vitamin K are observed from
intestine via lymph and requires bile salt for absorption
whereas water soluble form is absorbed directly into
portal blood.
Deficiency
Liver disease
Obstructive jaundice
Mall absorption syndrome
Long term antimicrobial therapy with disturbs the
microbial flora.
Bleeding tendency increased.
Symptoms
Bleeding tendency
Haematuria blood in urine (first to occur)
Local haemostatics
These are the substances used to stop bleeding from local
and approachable side particularly from tooth sockets
oozing.
Surface abrasions.
Absorbable materials like (fibrin prepared from human
plasma and dried as sheet of foam) gelatin foam, oxidized
cellulose (as stripe with can be cut off and placed in the
socket) provides a meshwork and activated clotting
mechanism.
Uses
1. Only use is in prophylaxis and treatment of bleeding
due to deficiency of clotting factor.
2. All newborns have no level of prothrombin and clotting
factor so vitamin K 1 mg intramuscular is used
3. It reserves the effect of overdose of anticoagulants K1 is
used.
Test to be given is an appropriate amount
a) International normalised ratio (INR),
prothrombin (PT)
Section 1 Pharmacology
37
b) Pregnancy induced hypertension eclampsia patient
may under (DIC) disseminated intravascular
coagulation.
Ethamsylate
It reduces the capillary bleeding when platelets are
adequate.
Improves capillary wall stability.
Use
Menorrhagia— increased menstrual blood after abortion.
Epistaxis nasal bleeding.
Malena stool bleeding.
Hematuria blood in urine.
After tooth extraction.
Side effect
Nausea
Rash
Headache
Falling BP only after I/V infection
Anticoagulants
These drugs used to reduce the coagulability of blood, they
may be classified into: -
1.Used in vivo:
A. Parenteral anticoagulant
Heparin
Low molecular weight heparin
Heparin sulphate
B. Oral anticoagulants
i. Coumarin derivatives
Dicumarol
Warfarin sodium
Nicoumalone
ii. Indandione derivative
Phenindione
2. Used in vitro:
A. Heparin
B. Calcium complexing agent.
z
Sodium citrate
z
Sodium oxalate
z
Sodium edetate
Management of a case of anaphylactic shock
Summon ambulance.
Always check respiratory distress is due to other cause.
Assess the degree of cardiovascular collapse by checking
pulse and blood pressure.
Assess the degree of airway obstruction.
Stop administration of drug.
Patient should be kept supine.
Assess breathing difficulty by checking for stridor.
Administer oxygen to patient by face mask.
Administer hydrocortisone 20 milligram.
Section 1 Pharmacology
Monitor consciousness, airway, breathing, circulation,
pulse and blood pressure.
38
Raise legs if blood pressure is low.
Adrenaline 1: 1000, 0.5 ml intramuscular is given
immediately.
Repeat intramuscular adrenaline every 5 minute while
waiting for ambulance.
Administered 100% oxygen.
CPR if cardiac arrest occurs.
If blood pressure fall is rapid 1:10000
Adrenaline maybe infused IV slowly.
Drugs used in hypotensive states and shock
Antihypotensive drugs or agents are used to elevate a
low blood pressure and may be classified as follows:
I. Agents intended to increase the volume of blood in
active circulation. These include intravenous fluids such
as whole blood, plasma, plasma components, plasma
substitutes and solution of crystalloids
II. Vasoconstrictor drugs these include: • Peripherally
acting vasoconstrictors which are further divided into
sympathomimetic drugs and direct vasoconstrictors.
Sympathomimetics used to elevate the blood pressure
include adrenaline, noradrenaline, methoxamine,
phenylephrine, mephentermine and ephedrine.
Direct vasoconstrictors include vasopressin and
angiotensin.
Treatment of shock
Shock is a clinical syndrome characterized by decreased
blood supply to tissues. Common signs and symptoms
include oliguria, heart failure, disorientation, mental
confusion, seizures, cold extremities, and comma.
Most, but not all people in shock are hypotensive.
The treatment varies with type of shock. The choice
of drug depends primarily on the pathophysiology
involved.
For cardiogenic shock and decreased cardiac output,
dopamine or other cardiotonic drug is indicated. With
severe CHF characterized by decreased CO and high
PVR, vasodilator drugs (nitropruside, nitroglycerine)
may be given along with the cardiotonic drug. Diuretics
may also be indicated to treat pulmonary congestion if
it occurs.
For anaphylactic shock or neurogenic shock
characterized by severe vasodilation and decreased
PVR, a vasoconstrictor drug (e.g. levarterenol) is the
first drug of choice
For hypovolemic shock, intravenous fluids that replace
the type of fluid lost should be given o For septic shock,
appropriate antibiotic therapy in addition to other
treatment measure
Plasma expanders are agents that have relatively high
molecular weight and boost the plasma volume by
increasing the osmotic pressure. They are used to treat
patients who have suffered hemorrhage or shock. Shock
occurs due to reduced blood volume (usually due to
hemorrhage) and it is necessary to get the blood volume
back to normal as quickly as possible. Major blood loss
entails the danger of life-threatening circulatory failure,
i.e., hypovolemic shock. The immediate threat results
not so much from the loss of erythrocytes, i.e., oxygen
carriers, as from the reduction in volume of circulating
blood.