Pharmacology Flashcards
(184 cards)
1
Q
Iron oral therapy
A
Ferrous sulphate
Ferrous Gluconate
Ferrous fumarate
السجف من حديد
2
Q
Blocker of Platelet ADP receptor
A
Ticlopedine
Clopidogrel
prasugrel
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
4
Q
use of clopidogrel
A
prophylaxis of thrombosis in both cerebrovascular and cardiovascular disease
5
Q
side effects of ticlopedine
A
neutropenia and bleeding
b
6
Q
blockers of platelet glycoproteins IIb/IIIa receptors
A
Abciximab, eptifibatide, tirofiban
7
Q
is a Fab fragment of monoclonal antibody that binds to gp IIb/IIIa and blocks binding of platelets to fibrinogen
A
abciximab
8
Q
is a small synthetic peptide that competitively blocks gp IIb/IIIa receoptors
A
Eptifibatide
9
Q
is a peptide pf low MW that binds to gp IIb/IIIa receptor
A
Tirofiban
10
Q
Glanzmann’s thrombasthenia
A
Persons lacking gp IIb/IIIa receptors so they have a bleeding disorder
11
Q
uses of the drugs that block gp IIb/IIIa receptors
A
- percutaneous coronary intervention
- unstable angina
- post myocardial infarction
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
13
Q
uses of Dipyridamole
A
Prophylaxis combined with Warfarin in patients with prosthetic heart valves
14
Q
the factors that inhibited by antithrombin
A
2, 9, 10, 11, 12
15
Q
major anticoagulant drugs
A
heparin and warfarin
16
Q
plasma protien that can dissolve blood clot
A
plasmin
17
Q
drugs that activate plasminogen to plasmin and enhance fibrinolysis
A
streptokinase
urokinase
18
Q
inhibitor of fibrinolysis
A
Aminocaproic acid
19
Q
vitamin K-dependent clotting factors
A
(II, VII, IX, and X)
20
Q
sources of heparin
A
Natural sulphated polysacchride present in mast cells & carries -ve charge
21
Q
source of warfarin
A
synthetic coumarin compound
22
Q
from anticoagulant that can be given orally
A
warfarin
23
Q
from anticoagulant that pass BBB and placenta
A
Warfarin
24
Q
MoA of heparin
A
activation of antithrombin III cofactor leading to inhibition of several clotting factors X & thrombin factor II
25
MoA of Warfarin
inhibition of vit K epoxide reductase enzyme
26
# location and function of
vit K epoxide reductase enzyme
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
27
onset and duration of heparin and warfarin
heparin: immediate and short (2-4 h)
warfarin: delayed and long
28
meaning of vivo and vitro
vivo: on animal
vitro: in lab
29
Pharmacological effects of heparin
* anticoagulant in vivo and in vitro
* stimulates lipoprotein lipase >> decrease serum triglycerides
30
Pharmacological effects of warfarin
anticoagulant in vivo
31
# monitoring of therapy of
1. heparin
2. warfarin
1. activated partial thromboplastin time (APTT)
2. prothrombin time (PT) or International Normalized Ratio w(INR)
32
common side effect of anticoagulant drugs
Bleeding is the most common and dangerous SE
33
treat the bleeding resulted from heparin
Protamine sulfate (Protam)
34
treat the bleeding resulted from warfarin
Vitamin K1
35
side effects of heparin
hematoma if given IM
Thrombocytopenia
osteoporosis
Alopecia and dermatitis
36
side effects of warfarin
* 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
37
Contraindications of anticoagulant therapy
**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.
38
tyrosine synthesis inhibitors
Carbimazole, Methimazole, Propylthiouracil
39
tyrosine release inhibitors
Iodine , Na and K Iodide
40
medication that destruct Radioactive iodine
Radioactive Iodine
41
Inhibit ionic trapping (inhibit Iodide ion uptake by thyroid gland)
Thiocyanates and
perchlorates
42
mechanism of action of propylthiouracil,Carbimazole and methimazole
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
43
# comparison btw carpimazole-methimazole and propyrthiouracil in
1. potency
2. Absorption
3. pregnancy
p. 6 lec 2
44
mechanism of action of Iodine and Iodide salts
* 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
45
used before thyriodectomy and why?
Iodine and Iodide salts because they Decrease size and vascularity of hyperplastic thyroid gland
46
duration of action of Iodine and Iodide salts
2-7 days
47
Iodine and Iodide salts found in
Lugol’s solution
48
name of solution that contain Iodine and Iodide salts
Lugol's solution
49
uses of Iodine and Iodide salts
1- thyroid storm (sever thyrotoxicosis)
2- Prepare the patient for surgical resection of hyperactive thyroid gland
50
use of Radioactive Iodine I 131
Concentrated in thyroid tissue and destruct thyroid tissue
51
duration of action of Radioactive I 131
2 weeks
51
duration of action of Radioactive I 131
2 weeks
52
Inhibit Iodide ion uptake by thyroid gland
thiocynates and perchlorates
53
mechanism of action of Thiocynates and perchlorates
* Inhibit Iodide ion uptake by thyroid gland
* Inhibit proteolysis of thyroglobulin inhibit release of T3 and T4
54
uses of B blockers
1- thyrotoxic crisis
2-while waiting response to propylthiouracil and Carbimazole
3- used with Iodide for preoperative preparation before subtotal thyroidectomy
55
Mechanism of action of insulin
* -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).
56
Preparation of insulin
* Highly purified pork and beef insulin
* Recombinant human insulin
57
Rapid acting insulin
Aspart and Lispro
58
What is aspart?
* Modified human insulin
* Proline at B28 replaced by aspartic acid
59
What is Lispro
* Modified human insulin
B28 lysine
B29 Proline
60
O and D of rapid acting insulin
15 min
2-4 h
61
O and D of short acting
30-60 min
6-8 h
62
short acting insulin
Regular unmodified insulin
63
intermediate acting insulin
Isophane (NPH):
Lente:
Suspensions of zinc –insulin
64
Onset and Duration of intermediate acting of insulin
Onset: 1-2 hours. Duration 10-16 hours
65
long acting insulin
Glargine
Ultralente
66
indication of insulin administration
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)
67
side effects of insulin adminstratiion
1. hypoglycemia
2. Lipodystrophy
3. Allergy
68
causes of hypoglycemia resulted from insulin
overdose
missed meal after injection
vigurous exercises
69
clinical picture of hypoglycemia
* Headache, sweating and palpitation (due to sympathetic overactivity)
* Headache, dizziness and confusion (due to brain deprivation from its main nutrient glucose
70
managment of hypogllycemia caused by insulin
* Simple glucose syrup
* Honey in buccal cavity
* S.C glucagon
* Sever hypoglycemia:
* I.v glucose
71
what is lypodystrophy?
side effect caused by insulin which is the destruction of subcutaneous fat at repeated injection site
72
methods of administration of insulin
* S.c injection
* Potable pen injector
* CSII. (Continous subcutaneous Insulin infusion)
73
mechanism of action of Sulfonylureas
* 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
first generation of sulfonylureas
* Tolbutamide
* Chloropropamide
75
second generation of sulfonylureas
* Gliclazide
* Glipizide
* Glipenclamide
76
which better first or second generation of sulfonylureas
Second generation more potent and efficacy
long Duration of action
fewer side effects
77
uses of sulfonylureas
* 1-type 2 D.M alone or in combination with other Antidiabetics
* 2-type 1 D.M with insulin
78
Side effects of sulfonylureas
* Hypoglycemia
* Weight gain
* Cholestatic jaundice
* anorexia nausea vomiting
79
contraindication of sulfonylureas
Containdications:
* In cardiac, hepatic, renal patients.
* Pregnancy: cross placenta causing fetal hypoglycemia.
80
what are the common Glitinides?
Repaglinide and Nateglinide
81
mechanism of action of Glitinides
Same mechanism of action of sulfonylureas
82
used to decrease postprandial hyperglycemia
Glitinides
83
can be used in diabetic patients with impaired renal function
Glitinides
84
side effects of glitinides
hypoglycemia
cross placenta causing fetal hypoglycemia
85
what are the common gliptins
Vildagliptin and sitagliptin
86
mechanism of action of gliptins
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
mechanism of action of metformin
* Decrease hepatic glucose production
* Decrease glucose absorption from GIT
* Increase up take and utilization of glucose by muscles (increase
insulin sensitivity)
88
which antidiapetic that has antihyperlipidic effect
Metformin
89
used in PCO polycystic ovary syndrome
Metformin
90
uses of metformin
type 2 D.M
PCO polycystic ovary syndrome
91
side effects of metformin
1-loss of appatite (weight loss)
2-lactic acidosis
3-vit B12 deficiency
92
what are the thiazolidindiones
Glitazones (pioglitazone , rosiglitazone)
93
mechanism of action of Thiazolidindiones
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
side effects of Thiazolidindiones
Weight gain
95
what are the Alfa glucosidase inhibitors
Acarbose, Miglitol
96
mechanism of alfa glucosidase inhibitors
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
side effects of alfa glucosidase inhibitors
flatulence, diarrhea, abdominal pain
98
Act on nuclear receptor (PPAR) peroxisome proliferator activated receptor
Thiazolidindiones
* Glitazones (pioglitazone , rosiglitazone)
99
are Dipeptidyl peptidase 4 inhibitors?
Gliptins
100
which drug causes cholestatic jandice
sulfonylureas
101
drugs causes hypoglycemia
insulin
sulfonylureas
Glitinides
102
antidiabetic that don't cause hypoglycemia
Metformin
alfa glucosidase inhibitors
103
drug cause weight loss
Metformin
104
drugs cause weight gain
sulfonylureas
thiazolidinediones
105
oral antidiabetics can't be used in pregnancy
sulfonylureas
glitinides
| insulin is the only safe to use in pregnancy
106
stimulte iron absorption
Ascorpic acid (vit C): increases reduction from ferric iron to ferrous
taken iron with meat: increase gastric acidity
107
Side effects of oral iron
1. GIT irritation: heart burn, vomiting, constipation.
2. Black discoloration of stool.
3. Transient staining of teeth with liquid iron.
108
Parenteral Iron is taken in which conditions
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
preparation of parenteral iron
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
Side effects of Parenteral iron
1. i.v route: headache, fever, urticarial, lymphsdenopathy and anaphylactic shock.
2. i.m. route: local pain and staining at site of injection
110
Side effects of Parenteral iron
1. i.v route: headache, fever, urticarial, lymphsdenopathy and anaphylactic shock.
2. i.m. route: local pain and staining at site of injection
111
Stimulate lipoprotein lipase causing decrease in serum TGA
Heparin
112
Anticoagulant in vitro
Heparin
113
Anticoagulant in vivo only
Warfarin
114
Uses of heparin
Established thrombosis and prevention of thrombosis
115
Administration of warfarin
Orally
116
Uses of warfarin
Prevention and treatment of:
Deep vein thrombosis
Postoperative thrombosis
Cerebral venous thrombosis
Coronary thrombosis
Acute arterial & pulmonary embolism
AF and artificial heart valves
117
Treat the bleeding of heparin by?
protamine sulphate (protam)
118
Treat bleeding caused by warfarin by?
Vitamin K
119
Recommended anticoagulant drugs in pregnancy
LMWH until week 13
Warfarin until week 34
LMWH until delivery
120
Drugs decrease absorption and effect of folic acid
Methotrexate, sulfasalazine, anticonvulsants, cotrimoxazole (metho sulfa anti contrimo)
121
Treatment of B12 deficiency
cyanocobolamine & hydroxcobolamine
122
Administration of treatment of B12
Orally and parentally
123
Treatment of folic acid deficiency
1. Folic acid (orally).
2. Leucovorin (folinic acid) orally and parenterally
124
Leucovorin used for
Folic acid deficiency treatment
125
Therapeutic uses of folic or folinic acid
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
Used for prevention of toxicity of trimethoprim
Folic acid and folinic acid
127
Folic acid is used in prevention of toxicity of which drugs
trimethoprime, proguanil, pyrimethamine
128
Therapeutic uses of Erythropoietin
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
Mechanism of action of aspirin in inhibiting platelet aggregation
* 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
Prophylaxis of thrombosis in both cerebrovascular and cardiovascular disease
Clopidogrel
131
Uses of ACTH therapy
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
What are the common glucocorticoids
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
Glucocorticoid given by inhalation on bronchial asthma
Beclomethasone, Betamethasone(more potent
134
What are the fluorinated corticosteroids
a- Betamethasone is like Beclomethasone but more potent
b- Triamcinolone and Dexamethasone have Pure Potent Glucocorticoid without
mineralocorticoid action
135
have Pure Potent Glucocorticoid without mineralocorticoid action
Triamcinolone and Dexamethasone
136
Glucocorticoids Given IM & IV
Cortisol Na+ Succinate, Cortisol Na+ Phosphate and Prednisolone 21-
Phosphate
137
Glucocorticoids Used in Emergency as acute Addisonian crisis
Cortisol Na+ Succinate, Cortisol Na+ Phosphate and Prednisolone 21-
Phosphate
138
Mineralocorticoids
1- Des-oxy-corticosterone Acetate (DOCA).
2- Des-oxy-corticosterone Trimethyl Acetate.
3- Fludrocortisone acetate.
139
Glucocorticoids that Active & effective after systemic & local administration
Prednisolone
140
The common plasma binding protein of corticosteroids
Corticosteroid binding globulin
141
Mechanism of action of cortisol
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
Pharmacological actions of cortisol
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
Metabolic action of cortisol on glucose concentration
Stimulate gluconeogenesis
inhibit Glycolysis
Stimulate Glycogenolysis
Prevent Glucose output
Results in hyperglycemia and glucosuria (Glucose intolerance
144
Causes Glucose intolerance
Cortisol
145
Metabolic action of cortisol on protein concentration
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
Causes negative nitrogen balance
Glucocorticoids
147
Metabolic action of cortisol on fat metabolism
* 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
Causes Fat Redistribution
Glucocorticoids
149
Causes moon face and buffalo humps
Glucocorticoids
150
Causes Lipemia and lipolysis in limps, thighs, and buttocks
Glucocorticoids
151
Metabolic action of cortisol in SIADH
Cortisol decreases permeability of D.C.T. to free water that maintains the ability of kidney to excrete water load.
152
Effect of lack of cortisol on water in Addison’s disease
Water intoxication
153
Metabolic action of glucocorticoids on calcium
decrease Ca2+ absorption from GIT and increase Ca2+ excretion by the kidney,
leading to Hypocalcemia (negative calcium balance)
154
Action of Glucocorticoids on inflammation
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
Are non-specific anti-inflammatory drugs
Glucocorticoids
156
Described as a deceiver
Glucocorticoids as it masks the signs of infection and inflammation without treating the cause
157
Action of Glucocorticoids on GIT
inhibiting synthesis of cytoprotective PGE2 and PGI2 and
accordingly increase HCl and decrease mucus leading to peptic ulcer.
158
The iatrogenic ulcer is best prevented and treated by
misoprostol
159
Action of Cortisol on uric Acid
Uricosuric action and decrease serum uric acid
160
Action of Cortisol on blood
Polycythemia, neutrophilia, thrombocytosis, increased coagulation, Lymphopenia, Eosinopenia
161
Action of cortisol on CVS and blood pressure
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
Action of cortisol on Respiratory system
* 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
Effect of glucocorticoids on CNS
Causes Euphoria and lead to psychosis
164
Action of glucocorticoids on immunity
inhibition of antibody (immunoglobulins) formation, inhibition of antigen antibody reaction, and reduces tissue response to inflammatory mediators
165
Action of glucocorticoids on inflammation
* 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
Action of glucocorticoids in stress and shock
Anti-stress and anti-shock by increasing Blood volume and blood pressure by hypernatremia, by increasing blood sugar, and by CNS action
167
Stimulate production of surfactant in neonates
Glucocorticoids
168
Treatment of acute Addisonian crisis
Hydrocortisone sodium succinate IV + NaCl IV infusion + glucose IV infusion
169
Treatment of Primary Addison disease
oral steroids having both gluco- and mineralocorticoid actions as cortisol or fludrocortisone
170
Treatment of secondary Addisonian disease
oral steroids having only glucocorticoid
action. (Oral cortisone acetate)
171
Glucocorticoid treats bronchial asthma
Beclomethasone
172
Treatment of status asthmatics
hydrocortisone sodium succinate IV
173
Side effects of Glucocorticoids from sudden withdrawal
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
Side effects of Glucocorticoids due to continued use of large doses
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
Contraindications of Cortisol therapy
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
Synthesis and release of aldosterone is controlled by
1. Renin-Angiotensin system.
2. Low Na+ and high K+ stimulate aldosterone release directly.
177
What augmented and what inhibited action of Aldosterone
Action of aldosterone is augmented by cortisol and estrogen and inhibited by spironolactone and progesterone.
178
Site of action of aldosterone
DCT
179
Aldosterone agonist used in treatment of peptic ulcer
carbenoxolone
180
What are common mineralocorticoids
1- Aldosterone
2- Des-oxy- corticosterone acetate (DOCA)
3- Fludrocortisone Acetate
181
Effect of Aldosterone
Hypervolemia and hypernatremia leads to an increase in blood pressure and then increase RBF and GFR leads to inhibition of renin system
182
What is escape phenomenon of aldosterone
Prolonged hypervolemia decreases sensitivity of D.C.T. to the effect of Aldosterone causes no Na+ & water retention but still K+ excretion.
