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Pharmacology Flashcards

1
Q

Iron oral therapy

A

Ferrous sulphate
Ferrous Gluconate
Ferrous fumarate
السجف من حديد

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2
Q

Blocker of Platelet ADP receptor

A

Ticlopedine
Clopidogrel
prasugrel

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3
Q

mechanism of action of clopidogrel

A

irreversibly inhibit the binding of ADP to its receptors thereby inhibit the activation of glycoprotein IIb/IIIa receptors required for platelets to bing to fibrinogen and to each other

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4
Q

use of clopidogrel

A

prophylaxis of thrombosis in both cerebrovascular and cardiovascular disease

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5
Q

side effects of ticlopedine

A

neutropenia and bleeding

b

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6
Q

blockers of platelet glycoproteins IIb/IIIa receptors

A

Abciximab, eptifibatide, tirofiban

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7
Q

is a Fab fragment of monoclonal antibody that binds to gp IIb/IIIa and blocks binding of platelets to fibrinogen

A

abciximab

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8
Q

is a small synthetic peptide that competitively blocks gp IIb/IIIa receoptors

A

Eptifibatide

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9
Q

is a peptide pf low MW that binds to gp IIb/IIIa receptor

A

Tirofiban

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10
Q

Glanzmann’s thrombasthenia

A

Persons lacking gp IIb/IIIa receptors so they have a bleeding disorder

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11
Q

uses of the drugs that block gp IIb/IIIa receptors

A
  1. percutaneous coronary intervention
  2. unstable angina
  3. post myocardial infarction
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12
Q

mechanism of action of Dipyridamole

A

inhibits phosphodiesterase enzyme —- increase cGMP— VD and inhibition of platelet activity
it also inhibts the uptake of adenosine by platelets and RBCs to prolong its action

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13
Q

uses of Dipyridamole

A

Prophylaxis combined with Warfarin in patients with prosthetic heart valves

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14
Q

the factors that inhibited by antithrombin

A

2, 9, 10, 11, 12

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15
Q

major anticoagulant drugs

A

heparin and warfarin

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16
Q

plasma protien that can dissolve blood clot

A

plasmin

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17
Q

drugs that activate plasminogen to plasmin and enhance fibrinolysis

A

streptokinase
urokinase

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18
Q

inhibitor of fibrinolysis

A

Aminocaproic acid

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19
Q

vitamin K-dependent clotting factors

A

(II, VII, IX, and X)

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20
Q

sources of heparin

A

Natural sulphated polysacchride present in mast cells & carries -ve charge

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21
Q

source of warfarin

A

synthetic coumarin compound

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22
Q

from anticoagulant that can be given orally

A

warfarin

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23
Q

from anticoagulant that pass BBB and placenta

A

Warfarin

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24
Q

MoA of heparin

A

activation of antithrombin III cofactor leading to inhibition of several clotting factors X & thrombin factor II

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25
Q

MoA of Warfarin

A

inhibition of vit K epoxide reductase enzyme

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26
Q

location and function of

vit K epoxide reductase enzyme

A
  1. in liver
  2. reduces the epoxide form of vit K to the reduced form to have a role in synthesis of cofactors 2,7,9,10
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27
Q

onset and duration of heparin and warfarin

A

heparin: immediate and short (2-4 h)
warfarin: delayed and long

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28
Q

meaning of vivo and vitro

A

vivo: on animal
vitro: in lab

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29
Q

Pharmacological effects of heparin

A
  • anticoagulant in vivo and in vitro
  • stimulates lipoprotein lipase&raquo_space; decrease serum triglycerides
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30
Q

Pharmacological effects of warfarin

A

anticoagulant in vivo

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31
Q

monitoring of therapy of

  1. heparin
  2. warfarin
A
  1. activated partial thromboplastin time (APTT)
  2. prothrombin time (PT) or International Normalized Ratio w(INR)
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32
Q

common side effect of anticoagulant drugs

A

Bleeding is the most common and dangerous SE

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33
Q

treat the bleeding resulted from heparin

A

Protamine sulfate (Protam)

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34
Q

treat the bleeding resulted from warfarin

A

Vitamin K1

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35
Q

side effects of heparin

A

hematoma if given IM
Thrombocytopenia
osteoporosis
Alopecia and dermatitis

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36
Q

side effects of warfarin

A
  • Hemorrhagic skin necrosis due to inhibition of synthesis of protein C
  • Teratogenicity fetal warfarin syndrome if given in early pregnancy
  • CNS Hemorrhage in the fetus if given in late preganancy
  • Sudden withdrawal may lead to thrombotic catastrophes
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37
Q

Contraindications of anticoagulant therapy

A

Neurological: – Recent hemorrhagic stroke within 3 weeks.
– Recent brain or eye surgery.

Hematological: – Hemorrhagic blood diseases e.g. hemophilia & thrombocytopenia.

CVS: – Subacute bacterial endocarditis (SBE).
– Uncontrolled hypertension (→ risk of cerebral bleeding).

GIT: – Active PU, esophageal varices, and hemorrhagic pancreatitis
– Active inflammatory bowel disease (ulcerative colitis).

Liver:– Liver failure (this patient has bleeding tendency)

Renal: – Renal failure.

Gynecological: – Threatened abortion.

– Warfarin is not given in the first timester.

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38
Q

tyrosine synthesis inhibitors

A

Carbimazole, Methimazole, Propylthiouracil

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39
Q

tyrosine release inhibitors

A

Iodine , Na and K Iodide

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40
Q

medication that destruct Radioactive iodine

A

Radioactive Iodine

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41
Q

Inhibit ionic trapping (inhibit Iodide ion uptake by thyroid gland)

A

Thiocyanates and
perchlorates

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42
Q

mechanism of action of propylthiouracil,Carbimazole and methimazole

A
  1. inhibit thyroid peroxidase inhibit oxidation of iodide
  2. inhibit iodination of tyrosine residues
  3. inhibit coupling of MIT and DIT
  4. inhibit peripheral conversion of T4 to T3
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43
Q

comparison btw carpimazole-methimazole and propyrthiouracil in

  1. potency
  2. Absorption
  3. pregnancy
A

p. 6 lec 2

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44
Q

mechanism of action of Iodine and Iodide salts

A
  • Inhibit iodination of tyrosine and thyroid hormone release
  • Decrease size and vascularity of hyperplastic thyroid gland
  • Inhibit synthesis and release of thyroid hormone by inhibition of proteolytic enzymes
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45
Q

used before thyriodectomy and why?

A

Iodine and Iodide salts because they Decrease size and vascularity of hyperplastic thyroid gland

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46
Q

duration of action of Iodine and Iodide salts

A

2-7 days

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47
Q

Iodine and Iodide salts found in

A

Lugol’s solution

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48
Q

name of solution that contain Iodine and Iodide salts

A

Lugol’s solution

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49
Q

uses of Iodine and Iodide salts

A

1- thyroid storm (sever thyrotoxicosis)
2- Prepare the patient for surgical resection of hyperactive thyroid gland

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50
Q

use of Radioactive Iodine I 131

A

Concentrated in thyroid tissue and destruct thyroid tissue

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51
Q

duration of action of Radioactive I 131

A

2 weeks

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51
Q

duration of action of Radioactive I 131

A

2 weeks

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52
Q

Inhibit Iodide ion uptake by thyroid gland

A

thiocynates and perchlorates

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53
Q

mechanism of action of Thiocynates and perchlorates

A
  • Inhibit Iodide ion uptake by thyroid gland
  • Inhibit proteolysis of thyroglobulin inhibit release of T3 and T4
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54
Q

uses of B blockers

A

1- thyrotoxic crisis
2-while waiting response to propylthiouracil and Carbimazole
3- used with Iodide for preoperative preparation before subtotal thyroidectomy

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55
Q

Mechanism of action of insulin

A
  • -facilitate glucose transport across cell membrane in liver, muscles,
    adipose tissue facilitate glucose uptake and utilization
  • -stimulate enzyme glycogen synthase facilitate glycogen synthesis
    from glucose in liver, muscles and adipose tissues.
  • -inhibit gluconeogenesis( glucose synthesis from non carbohydrate
    precursors in liver from protein and fatty acids).
  • -facilitate glucose transport across cell membrane in liver, muscles,
    adipose tissue facilitate glucose uptake and utilization
  • -stimulate enzyme glycogen synthase facilitate glycogen synthesis
    from glucose in liver, muscles and adipose tissues.
  • -inhibit gluconeogenesis( glucose synthesis from non carbohydrate
    precursors in liver from protein and fatty acids).
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56
Q

Preparation of insulin

A
  • Highly purified pork and beef insulin
  • Recombinant human insulin
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57
Q

Rapid acting insulin

A

Aspart and Lispro

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58
Q

What is aspart?

A
  • Modified human insulin
  • Proline at B28 replaced by aspartic acid
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59
Q

What is Lispro

A
  • Modified human insulin
    B28 lysine
    B29 Proline
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60
Q

O and D of rapid acting insulin

A

15 min
2-4 h

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61
Q

O and D of short acting

A

30-60 min
6-8 h

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62
Q

short acting insulin

A

Regular unmodified insulin

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63
Q

intermediate acting insulin

A

Isophane (NPH):
Lente:
Suspensions of zinc –insulin

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64
Q

Onset and Duration of intermediate acting of insulin

A

Onset: 1-2 hours. Duration 10-16 hours

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65
Q

long acting insulin

A

Glargine
Ultralente

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66
Q

indication of insulin administration

A

1_ type 1 D.M
2_ type 2 D.Mbin cases of
A- Failure to control by oral Antidiabetics
B- Hyperglycemic coma and diabetic ketoacidosis
C- pregnancy
D- sever stressful conditions ( severe infection, burns accidents)

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67
Q

side effects of insulin adminstratiion

A
  1. hypoglycemia
  2. Lipodystrophy
  3. Allergy
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68
Q

causes of hypoglycemia resulted from insulin

A

overdose
missed meal after injection
vigurous exercises

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69
Q

clinical picture of hypoglycemia

A
  • Headache, sweating and palpitation (due to sympathetic overactivity)
  • Headache, dizziness and confusion (due to brain deprivation from its main nutrient glucose
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70
Q

managment of hypogllycemia caused by insulin

A
  • Simple glucose syrup
  • Honey in buccal cavity
  • S.C glucagon
  • Sever hypoglycemia:
  • I.v glucose
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71
Q

what is lypodystrophy?

A

side effect caused by insulin which is the destruction of subcutaneous fat at repeated injection site

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72
Q

methods of administration of insulin

A
  • S.c injection
  • Potable pen injector
  • CSII. (Continous subcutaneous Insulin infusion)
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73
Q

mechanism of action of Sulfonylureas

A
  • Block ATP sensitive k channels in pancreatic beta cells.
  • Inhibit k efflux
  • Depolarization open voltage gated calcium-channels
  • Increase Ca entery increase intracellular calcium causes exocytosis of granules
  • Releaee of performed insulin into circulation
74
Q

first generation of sulfonylureas

A
  • Tolbutamide
  • Chloropropamide
75
Q

second generation of sulfonylureas

A
  • Gliclazide
  • Glipizide
  • Glipenclamide
76
Q

which better first or second generation of sulfonylureas

A

Second generation more potent and efficacy
long Duration of action
fewer side effects

77
Q

uses of sulfonylureas

A
  • 1-type 2 D.M alone or in combination with other Antidiabetics
  • 2-type 1 D.M with insulin
78
Q

Side effects of sulfonylureas

A
  • Hypoglycemia
  • Weight gain
  • Cholestatic jaundice
  • anorexia nausea vomiting
79
Q

contraindication of sulfonylureas

A

Containdications:
* In cardiac, hepatic, renal patients.
* Pregnancy: cross placenta causing fetal hypoglycemia.

80
Q

what are the common Glitinides?

A

Repaglinide and Nateglinide

81
Q

mechanism of action of Glitinides

A

Same mechanism of action of sulfonylureas

82
Q

used to decrease postprandial hyperglycemia

A

Glitinides

83
Q

can be used in diabetic patients with impaired renal function

A

Glitinides

84
Q

side effects of glitinides

A

hypoglycemia
cross placenta causing fetal hypoglycemia

85
Q

what are the common gliptins

A

Vildagliptin and sitagliptin

86
Q

mechanism of action of gliptins

A

inhibit Dipeptidyl peptidase 4 that break GLP-1 (glucagon like peptide 1) and GIP(Glucose insulinotropic polypeptide) hormones secreted from small intestine

these enzyme stimulate secretion of insulin by B cells of pancreas

Gliptins loves GLP

87
Q

mechanism of action of metformin

A
  • Decrease hepatic glucose production
  • Decrease glucose absorption from GIT
  • Increase up take and utilization of glucose by muscles (increase
    insulin sensitivity)
88
Q

which antidiapetic that has antihyperlipidic effect

89
Q

used in PCO polycystic ovary syndrome

90
Q

uses of metformin

A

type 2 D.M
PCO polycystic ovary syndrome

91
Q

side effects of metformin

A

1-loss of appatite (weight loss)
2-lactic acidosis
3-vit B12 deficiency

92
Q

what are the thiazolidindiones

A

Glitazones (pioglitazone , rosiglitazone)

93
Q

mechanism of action of Thiazolidindiones

A

Act on nuclear receptor (PPAR) peroxisome proliferator activated
receptor affect insulin expressive genes increase transcription of
insulin sensitive genes and decrease transcription of resisting genes
genes cause insulin Resistance

94
Q

side effects of Thiazolidindiones

A

Weight gain

95
Q

what are the Alfa glucosidase inhibitors

A

Acarbose, Miglitol

96
Q

mechanism of alfa glucosidase inhibitors

A

Inhibit intestinal brush border enzyme alfa glucosidase which break
down starch carbohydrate starch into smaller particles to be absorbed
Inhibition of this enzyme inhibit glucose absorption from GIT

97
Q

side effects of alfa glucosidase inhibitors

A

flatulence, diarrhea, abdominal pain

98
Q

Act on nuclear receptor (PPAR) peroxisome proliferator activated receptor

A

Thiazolidindiones
* Glitazones (pioglitazone , rosiglitazone)

99
Q

are Dipeptidyl peptidase 4 inhibitors?

100
Q

which drug causes cholestatic jandice

A

sulfonylureas

101
Q

drugs causes hypoglycemia

A

insulin
sulfonylureas
Glitinides

102
Q

antidiabetic that don’t cause hypoglycemia

A

Metformin
alfa glucosidase inhibitors

103
Q

drug cause weight loss

104
Q

drugs cause weight gain

A

sulfonylureas
thiazolidinediones

105
Q

oral antidiabetics can’t be used in pregnancy

A

sulfonylureas
glitinides

insulin is the only safe to use in pregnancy

106
Q

stimulte iron absorption

A

Ascorpic acid (vit C): increases reduction from ferric iron to ferrous
taken iron with meat: increase gastric acidity

107
Q

Side effects of oral iron

A
  1. GIT irritation: heart burn, vomiting, constipation.
  2. Black discoloration of stool.
  3. Transient staining of teeth with liquid iron.
108
Q

Parenteral Iron is taken in which conditions

A
  1. Severe anemia Hb < 8 -7g/dl.
  2. In the presence of factors that decrease iron absorption e.g. malabsorption syndrome.
  3. If oral therapy is not tolerated (severe GIT disturbance).
109
Q

preparation of parenteral iron

A
  1. Iron sorbitol: suitable for i.m. injection and not for i.v.
  2. Iron dextran: suitable for i.v. injection and not for i.m. because of pain and local staining at site of injection
110
Q

Side effects of Parenteral iron

A
  1. i.v route: headache, fever, urticarial, lymphsdenopathy and anaphylactic shock.
  2. i.m. route: local pain and staining at site of injection
110
Q

Side effects of Parenteral iron

A
  1. i.v route: headache, fever, urticarial, lymphsdenopathy and anaphylactic shock.
  2. i.m. route: local pain and staining at site of injection
111
Q

Stimulate lipoprotein lipase causing decrease in serum TGA

112
Q

Anticoagulant in vitro

113
Q

Anticoagulant in vivo only

114
Q

Uses of heparin

A

Established thrombosis and prevention of thrombosis

115
Q

Administration of warfarin

116
Q

Uses of warfarin

A

Prevention and treatment of:
Deep vein thrombosis
Postoperative thrombosis
Cerebral venous thrombosis
Coronary thrombosis
Acute arterial & pulmonary embolism
AF and artificial heart valves

117
Q

Treat the bleeding of heparin by?

A

protamine sulphate (protam)

118
Q

Treat bleeding caused by warfarin by?

119
Q

Recommended anticoagulant drugs in pregnancy

A

LMWH until week 13
Warfarin until week 34
LMWH until delivery

120
Q

Drugs decrease absorption and effect of folic acid

A

Methotrexate, sulfasalazine, anticonvulsants, cotrimoxazole (metho sulfa anti contrimo)

121
Q

Treatment of B12 deficiency

A

cyanocobolamine & hydroxcobolamine

122
Q

Administration of treatment of B12

A

Orally and parentally

123
Q

Treatment of folic acid deficiency

A
  1. Folic acid (orally).
  2. Leucovorin (folinic acid) orally and parenterally
124
Q

Leucovorin used for

A

Folic acid deficiency treatment

125
Q

Therapeutic uses of folic or folinic acid

A
  1. Treatment of megaloblastic anaemia due to folic acid deficency.
  2. Prophylaxis in pregnant, lactating woman.
  3. Treatment of or prevention of toxicities of trimethoprime, proguanil, pyrimethamine
126
Q

Used for prevention of toxicity of trimethoprim

A

Folic acid and folinic acid

127
Q

Folic acid is used in prevention of toxicity of which drugs

A

trimethoprime, proguanil, pyrimethamine

128
Q

Therapeutic uses of Erythropoietin

A
  1. End stage renal disease
  2. Bone marrow failure due to cancer.
  3. In premature infants (prophylaxis).
  4. Anaemia of chronic inflammation e.g. rheumatoid arthritis.
129
Q

Mechanism of action of aspirin in inhibiting platelet aggregation

A
  • Irreversible inhibition of COX enzyme»decrease thromboxane synthesis»decrease platelet aggregation
  • Irreversible acetylation of platelet cell membranes»decrease platelet adhesion
  • Decrease platelet ADP synthesis» decrease platelets accumulation
130
Q

Prophylaxis of thrombosis in both cerebrovascular and cardiovascular disease

A

Clopidogrel

131
Q

Uses of ACTH therapy

A
  1. Diagnostic: diagnosis of adrenocortical function: ACTH releases cortisol from cortex → eosinopenia and increases metabolites as 17-keto-steroids in urine.
  2. Therapeutic: same indications as cortisol with the advantage of less catabolic effect in old patients and less growth retardation in children.
  3. During gradual withdrawal of steroids after long use to avoid acute Addisonian insufficiency
132
Q

What are the common glucocorticoids

A

Cortisone (inactive): activated in liver to hydrocortisone or cortisol
Cortisone acetate suspension: like cortisone with longer duration.
Cortisol acetate suspension: like cortisol with longer duration
Prednisone: stronger and longer than cortisone must be activated to prednisolone.
Methyl prednisolone:

133
Q

Glucocorticoid given by inhalation on bronchial asthma

A

Beclomethasone, Betamethasone(more potent

134
Q

What are the fluorinated corticosteroids

A

a- Betamethasone is like Beclomethasone but more potent
b- Triamcinolone and Dexamethasone have Pure Potent Glucocorticoid without
mineralocorticoid action

135
Q

have Pure Potent Glucocorticoid without mineralocorticoid action

A

Triamcinolone and Dexamethasone

136
Q

Glucocorticoids Given IM & IV

A

Cortisol Na+ Succinate, Cortisol Na+ Phosphate and Prednisolone 21-
Phosphate

137
Q

Glucocorticoids Used in Emergency as acute Addisonian crisis

A

Cortisol Na+ Succinate, Cortisol Na+ Phosphate and Prednisolone 21-
Phosphate

138
Q

Mineralocorticoids

A

1- Des-oxy-corticosterone Acetate (DOCA).
2- Des-oxy-corticosterone Trimethyl Acetate.
3- Fludrocortisone acetate.

139
Q

Glucocorticoids that Active & effective after systemic & local administration

A

Prednisolone

140
Q

The common plasma binding protein of corticosteroids

A

Corticosteroid binding globulin

141
Q

Mechanism of action of cortisol

A

Cortisol easily passes the cell
membrane by simple diffusion being lipophilic, then binds to cytoplasmic receptors
forming hormone-receptor complex which enters the nucleus and binds to nuclear
receptors (a specific site on DNA strands) leads to:
a. Gene expression: synthesis of m-RNA (transcription) leads to synthesis of
specific proteins as Lipocortin I (Annexin 1) and catabolic enzymes.
b. Gene repression: inhibition of synthesis of certain proteins as COX-II, Nitric
oxide synthase (NOS), and antibodies (immunoglobulins).
2- Non-genomic mechanism: (Rapid onset of action) few actions of cortisol are
due to stimulation membrane receptors, such as the action on HPA axis.

142
Q

Pharmacological actions of cortisol

A
  1. Negative feed-back inhibition of HPA axis
  2. Metabolic Actions (Carbohydrates, proteins, fat)
  3. Mineralocorticoid action
  4. Free Water Clearance: “Occurs in SIADH
  5. Vitamin D and Ca2+
  6. Anti-inflammatory action
  7. Immunosuppression and Anti-allergic actions
  8. Anti-stress and Anti-shock
  9. Action on CNS
  10. Antiemetic action
  11. Action on Respiratory system
  12. Action on CVS
  13. Actions on blood
  14. Action on GIT
  15. Action on uric Acid
143
Q

Metabolic action of cortisol on glucose concentration

A

Stimulate gluconeogenesis
inhibit Glycolysis
Stimulate Glycogenolysis
Prevent Glucose output
Results in hyperglycemia and glucosuria (Glucose intolerance

144
Q

Causes Glucose intolerance

145
Q

Metabolic action of cortisol on protein concentration

A

Causes protein catabolism in most tissues skeletal muscles, bone, lymphoid tissue, and connective tissue leading to muscle wasting and myopathy,
osteoporosis, growth retardation in children, and delayed wound healing without affecting protein in liver
Amino acids are converted into urea, which is excreted in urine
Known as negative nitrogen balance

146
Q

Causes negative nitrogen balance

A

Glucocorticoids

147
Q

Metabolic action of cortisol on fat metabolism

A
  • Lipolysis of fats in limbs, thighs, and buttocks.
  • Lipemia: cortisol increases free fatty acids in blood.
  • Lipogenesis in face, back, and trunk leading to “moon face”, “buffalo hump”, and
    truncal obesity. This is known as Fat Redistribution.
148
Q

Causes Fat Redistribution

A

Glucocorticoids

149
Q

Causes moon face and buffalo humps

A

Glucocorticoids

150
Q

Causes Lipemia and lipolysis in limps, thighs, and buttocks

A

Glucocorticoids

151
Q

Metabolic action of cortisol in SIADH

A

Cortisol decreases permeability of D.C.T. to free water that maintains the ability of kidney to excrete water load.

152
Q

Effect of lack of cortisol on water in Addison’s disease

A

Water intoxication

153
Q

Metabolic action of glucocorticoids on calcium

A

decrease Ca2+ absorption from GIT and increase Ca2+ excretion by the kidney,
leading to Hypocalcemia (negative calcium balance)

154
Q

Action of Glucocorticoids on inflammation

A

Stimulate the synthesis of lipocortin 1 which inhibits phospholipase A2 produced bt neutrophils and macrophages leading to inhibition of synthesis of inflammatory mediators : PGs, leukotrienes, and platelet activating factor (PAF)

Inhibit synthesis of COX-II, NOS, adhesion molecules, and complement components

155
Q

Are non-specific anti-inflammatory drugs

A

Glucocorticoids

156
Q

Described as a deceiver

A

Glucocorticoids as it masks the signs of infection and inflammation without treating the cause

157
Q

Action of Glucocorticoids on GIT

A

inhibiting synthesis of cytoprotective PGE2 and PGI2 and
accordingly increase HCl and decrease mucus leading to peptic ulcer.

158
Q

The iatrogenic ulcer is best prevented and treated by

A

misoprostol

159
Q

Action of Cortisol on uric Acid

A

Uricosuric action and decrease serum uric acid

160
Q

Action of Cortisol on blood

A

Polycythemia, neutrophilia, thrombocytosis, increased coagulation, Lymphopenia, Eosinopenia

161
Q

Action of cortisol on CVS and blood pressure

A

Glucocorticoids elevate blood pressure
1. Sodium and water retention by its mineralocorticoid action which increases cardiac output
2. Potentiation of the vasoconstrictor action of noradrenaline and angiotensin II, which increases total peripheral resistance
3. Decrease in capillary permeability thus maintaining blood volume

162
Q

Action of cortisol on Respiratory system

A
  • Stabilization of mast cells membrane to prevent the release of “allergotoxins” in bronchial asthma.
  • Increase number of β2-receptors thus prevents down regulation by β2-agonists as salbutamol.
  • Stimulate production of surfactant in neonates.
163
Q

Effect of glucocorticoids on CNS

A

Causes Euphoria and lead to psychosis

164
Q

Action of glucocorticoids on immunity

A

inhibition of antibody (immunoglobulins) formation, inhibition of antigen antibody reaction, and reduces tissue response to inflammatory mediators

165
Q

Action of glucocorticoids on inflammation

A
  • Glucocorticoids stimulate synthesis of lipocortin I which inhibits phospholipase A2
    produced by neutrophils and macrophages leading to inhibition of synthesis of
    inflammatory mediators: PGs, leukotrienes, and platelet activating factor (PAF).
  • Inhibit synthesis of COX-II, NOS, adhesion molecules, and complement
    components.
  • Inhibit migration of neutrophils.
  • Decrease circulating lymphocytes, eosinophils, monocytes, basophils.
  • Decrease synthesis of inflammatory cytokines as interleukins, TNFα, and colony
    stimulating factor (CSF).
  • Stabilize lysosomal membrane and inhibit release of lysosomal enzymes thus preventing cell death and tissue destruction.
  • Decrease capillary permeability thus decreasing inflammatory edema and joint effusion.
166
Q

Action of glucocorticoids in stress and shock

A

Anti-stress and anti-shock by increasing Blood volume and blood pressure by hypernatremia, by increasing blood sugar, and by CNS action

167
Q

Stimulate production of surfactant in neonates

A

Glucocorticoids

168
Q

Treatment of acute Addisonian crisis

A

Hydrocortisone sodium succinate IV + NaCl IV infusion + glucose IV infusion

169
Q

Treatment of Primary Addison disease

A

oral steroids having both gluco- and mineralocorticoid actions as cortisol or fludrocortisone

170
Q

Treatment of secondary Addisonian disease

A

oral steroids having only glucocorticoid
action. (Oral cortisone acetate)

171
Q

Glucocorticoid treats bronchial asthma

A

Beclomethasone

172
Q

Treatment of status asthmatics

A

hydrocortisone sodium succinate IV

173
Q

Side effects of Glucocorticoids from sudden withdrawal

A
  1. Suppression of HPA axis and adrenal atrophy which leads to acute adrenocortical
    insufficiency if exogenous steroids are suddenly stopped after prolonged therapy.
  2. Corticosterone withdrawal syndrome: fever, myalgia, arthralgia, and malaise
174
Q

Side effects of Glucocorticoids due to continued use of large doses

A
  1. Iatrogenic Cushing syndrome: moon face, buffalo-hump, truncal obesity and wasting of limbs.
  2. Iatrogenic peptic ulcer and acute pancreatitis.
  3. Hyperglycemia and glucosuria.
  4. Skeletal muscle wasting and myopathy, osteoporosis, sub laxation of joints, delayed wound healing-growth retardation in children.
  5. Na+ and water retention leading to edema and weight gain, elevation of ABP, and may cause HF.
  6. Hypokalemia.
  7. Hypocalcemia.
  8. Immunosuppression and masking of inflammation leading to infection by T.B., viral and fungal infections (candidiasis). Inhaled steroids cause oropharyngeal candidiasis and dysphonia.
  9. Increased blood coagulability and thrombo-embolic manifestations.
  10. Cataract and glaucoma.
  11. Hirsutism and menstrual disturbances. (Lowers estrogen levels).
  12. Psychosis.
  13. Teratogenicity.
175
Q

Contraindications of Cortisol therapy

A
  1. Sudden withdrawal of glucocorticoids after prolonged use.
  2. Cushing syndrome.
  3. Peptic ulcer.
  4. Diabetes mellitus.
  5. Osteoporosis.
  6. Repeated intra-articular injections lead to sub laxation of joints.
  7. Hypertension.
  8. CHF.
  9. In digitalis toxicity and with K+ losing diuretics.
    10.Uncontrolled infections.
    11.Thrombo-embolic diseases.
    12.Glaucoma and cataract.
    13.Psychotic patients.
    14.Pregnancy.
176
Q

Synthesis and release of aldosterone is controlled by

A
  1. Renin-Angiotensin system.
  2. Low Na+ and high K+ stimulate aldosterone release directly.
177
Q

What augmented and what inhibited action of Aldosterone

A

Action of aldosterone is augmented by cortisol and estrogen and inhibited by spironolactone and progesterone.

178
Q

Site of action of aldosterone

179
Q

Aldosterone agonist used in treatment of peptic ulcer

A

carbenoxolone

180
Q

What are common mineralocorticoids

A

1- Aldosterone
2- Des-oxy- corticosterone acetate (DOCA)
3- Fludrocortisone Acetate

181
Q

Effect of Aldosterone

A

Hypervolemia and hypernatremia leads to an increase in blood pressure and then increase RBF and GFR leads to inhibition of renin system

182
Q

What is escape phenomenon of aldosterone

A

Prolonged hypervolemia decreases sensitivity of D.C.T. to the effect of Aldosterone causes no Na+ & water retention but still K+ excretion.

HEN (8 decks)

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