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Steroidal And NSAIDS Flashcards

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1
Q

Clinical effects of glucocorticoids

A

Decrease glucose utilisation in muscles and adipose tissue, increase blood glucose, decrease protein synthesis in muscle,CT and skin, increase lipolysis and lipogenesis, increase Na and water reabsorption and k excretion, decrease osteoblast formation,enhance bone reabsorption, increase HCL and Pepsin production, decrease tissue inflammatory response, cytokines formation,T lymphocyte activation and proliferation, macrophage phagocytic activity and antibody formation , increase glycogen synthesis in liver

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2
Q

Rheumatoid arthritis

A

Chronic destructive inflammatory disease of joints,can also express extra articular with severity,due to dysregulation of pro-inflammatory cytokines TNF-@,IL-1, inflammatory action through Janus kinase signal transduction cascade

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3
Q

Addison’s disease

A

Caused by primary chronic adrenal cortex deficiency,resulting in partial or total hormone(cortisol , aldosterone ) deficiency

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4
Q

DMARD full form

A

Disease modifying anti-rheumatic drugs

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5
Q

3 groups of DMARDS

A

Synthetic DMARDS, biological DMARDs,JAK I(Janus kinase inhibitors)

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6
Q

Systemic lupus erythematous

A

Chronic, autoimmune disease that affects various organs mainly skin,joints, kidneys, circulatory system,CNS

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7
Q
A
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8
Q

Tertiary chronic adrenal cortex deficiency can be caused by

A

Rapid discontinuation of glucocorticoid after long-term GC administration

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9
Q

Tertiary chronic adrenal cortex deficiency doesn’t cause electrolyte imbalance, because

A

Aldosterone regulation is primarily regulated by RAAS system,not by ACTH

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10
Q

Cushing’s disease (Hypercortisolism)

A

A disease characterized by excessive cortisol production in adrenal gland.eg: pituatry or adrenal cortex tumour

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11
Q

Variants of hypercortisolism

A

Cushing’s disease (ACTH dependent hypercortisolism) and Cushing’s syndrome (ACTH independent hypercortisolism)

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12
Q

Iatrogenic Cushing’s syndrome caused by

A

Prolonged glucocorticoid therapy at supraphysiological doses

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13
Q

Inflammatory bowel diseases

A

Ulcerative colitis and chrons disease ( caused by inflammation of intestinal walls)

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14
Q

Chrons disease

A

Is chronic,can affect any part of digestive tract,can affect entire thickness of intestinal wall,can spread to outside organ, characteristic fragmentary nature of intestinal lesions

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15
Q

Ulcerative colitis

A

Only affect colon and rectal mucosa and only the upper layer of mucosa

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16
Q

Glucocorticoid receptor agonists

A

Hydrocortisone, prednisolone, methylprednisolone, Dexamethasone

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17
Q

Main mechanism of glucocorticoid happens through the receptor in

A

Intracellular,which is stabilized by heat shock protein 90 and immunophilin

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18
Q

Main effect of glucocorticoids that cause the anti inflammatory and immunomodulatory effect are

A

Reduction in the synthesis of inflammatory cytokines and upregulation in the synthesis of annexin 1

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19
Q

Hydrocortisone use

A

Acute and chronic adrenal cortex insufficiency

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20
Q

Prednisolone, methylprednisolone and dexamethasone use

A

Autoimmune diseases(eg:RA), Inflammatory bowel diseases (IBD),Transplantology, allergic conditions ( anaphylactic shock, bronchial asthma)

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21
Q

Prednisolone, methylprednisolone, Dexamethasone action

A

Fast membrane stabilizing effect( decrease vascular permeability, increase adrenoreceptor sensitivity against catecholamines)slow, genomic, intracellular corticosteroid receptor activation,anti inflammatory,anti edema,anti allergic,anti shock, Immunosuppressive, Antiproliferative effect

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22
Q

Iatrogenic Cushing’s syndrome pathway

A

Excessive GC intake- -decrease effect of corticotropin releasing Hormone -decrease ACTH secretion- decrease cortisol secretion and adrenocortical atrophy

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23
Q

Symptoms of Cushing’s syndrome

A

Central obesity (face and torso), osteoporosis,atrophy of lymph muscles, hyperglycaemia, hypertension, abdominal stretches, depressed immunity, Hirsutism in women, ulcerogenic effect, mental disorders ( depression)

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24
Q

Glucocorticoid therapy elimination

A

Do it gradually,not fast as it can cause secondary adrenal insufficiency

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25
Alternative therapy of GC
Double GC dose every second day
26
Topical GC( inhalers, ointment) can be used in
Bronchial asthma, allergic rhinitis, atopic dermatitis
27
Duration of action of hydrocortisone
Short
28
GC s with medium duration of action
Prednisolone and fludrocortisone
29
GC with long duration of action
Dexamethasone
30
Peak conc of cortisol in human body is in
Early in the morning around 6 am
31
Lowest cortisol level.in human body is around
Midnight
32
Mineralocorticoid receptor agonists
Fludrocortisone
33
Fludrocortisone is a
Fluorinated hydrocortisone derivative
34
Use of fludrocortisone
Replacement therapy for Addison's disease ( in combination with GC)
35
SE of fludrocortisone
Hypertension,edema, hypokalemia
36
Fludrocortisone action
Aldosterone receptor agonist in distal renal tubules and Collecting duct,DNA transcription,promotes expression of epithelial Na channels, increase Na reabsorption and water retention - increase BP, promote k excretion and mineralocorticoid substitution
37
Cyclooxygenases are
Intermediate enzymes in the formation of prostaglandins
38
The expression of cox 2 compared to cox 1 can be induced by
Inflammatory stimuli by 10 to 20 times
39
Thromboxane A2 is
A potent vasoconstrictor and platelet agonist present in platelet granules,secreted during platelet activation by various stimuli like epinephrine,thrombin,ADP
40
Arachidonic acid after the intermediate unstable prostaglandin H 3 formation ,after tissue specific isomerases changes to
Prostacyclin( PGI 2),TXA2, prostaglandin E2, prostaglandin F2 alpha
41
Prostacyclin ( PGI 2) present in
Brain, kidney, endothelium
42
TXA2 present in
Platelet, macrophage, kidney,smooth muscles
43
Prostaglandin E2 present in
Brain , kidney,smooth muscle
44
Prostaglandin. F2 alpha present in
Brain kidney ,smooth muscles
45
Prostaglandins present in brain and kidney
Prostacyclin, prostaglandin E2 and F2 alpha
46
Prostaglandin present in smooth muscles
Prostaglandin E2 and F2 alpha
47
Prostaglandins in kidney
Prostacyclin, TXA2, prostaglandin E2 and F2 alpha
48
Selective COX 2 inhibitors are Dev to avoid
GIT side effects of non selective cox inhibitors due to inhibition of prostaglandin synthesis
49
Cox 2 is particularly expressed in
Inflamed tissue
50
Cox 2 is minimally expressed in
GIT
51
Selective COX 2 inhibitors compared to non selective cox 2 inhibitors, exhibits anti inflammatory effects with
Lower incidence of GI side effects
52
Contraindications for selective cox 2 inhibitors are
Coronary heart disease, peripheral artery disease,severe chronic heart failure
53
54
The risk of cardiovascular events of selective cox 2 inhibitors increase with
Increased dose and duration of use
55
NSAIDS examples
Acetylsalicylic acid,diclofenac , ibuprofen
56
Selective COX 2 inhibitors example
Etoricoxib
57
Acetylsalicylic acid (Aspirin) action
Non selective inhibition of cox 2 and 2 in dose dependent manner( inhibition of cox 2- inhibition of prostaglandin synthesis)- antiinflammatory, analgesic and antipyretic. 2)inhibition of cox 1- antiplatelet effect ( irreversible inhibition of cox1)
58
Use of aspirin ( Acetylsalicylic acid)
For temporary treatment of various genesis of mild to moderate acute pain,fever
59
Cox 1 inhibition of aspirin is
170 times more potent than cix 2 inhibition
60
SE of aspirin (Acetylsalicylic acid)
Risk of gastrointestinal bleeding
61
Contraindications for aspirin
Children under age 12 with fever
62
Toxicity of aspirin
Central stimulation of respiratory center causes hyperventilation - respiratory alkalosis- dehydration and compensatory metabolic acidosis,causes central and pulmonary edema,alters platelet function and increase prothrombin time
63
Metabolic acidosis related to aspirin toxicity is caused by
Inhibition of oxidative phosphorylation process and disruption of glucose and fatty acid metabolism
64
T1/2 of aspirin at low dose
2 to 3 hrs
65
T1)2 of aspirin at high dose
Longer than 15 hours
66
Acute intoxication symptoms of aspirin
Vomiting - tachypnea, tinnitus, sweating, headache, dizziness, drowsiness, metabolic acidosis detected in lab
67
Severe acute intoxication of aspirin causes symptoms like
Coma, convulsions, hypoglycemia, hyperthermia, pulmonary edema, children may develop Reyes syndrome
68
Reye's syndrome is
Rapidly progressive toxic encephalopathy
69
Death of patients by aspirin intoxication is caused by
CNS depression and cardiovascular collapse
70
Aspirin intoxication= salicylate intoxication =
Salicylism
71
Chronic aspirin intoxication are non specific like
Disorientation, dehydration, metabolic acidosis which could be associated with sepsis, pneumonia or meningitis
72
73
Fatality in chronic salicylate intoxication is higher than acute overdose and cerebral and pulmonary edema is
More often and severe poisoning with small dose of salicylate
74
Treatment of salicylism
Symptomatic treatment+ sodium bicarbonate iv for metabolic acidosis ,forced alkaline diuresis (,in severe case - hemodialysis)
75
Diclofenac, ibuprofen and etoricoxib use
Musculoskeletal disorders ( rheumatoid arthritis, osteoarthritis), temporary treatment of various genesis,mild to moderate acute pain ( migraine attack, dysmenorrhoea)
76
Diclofenac and ibuprofen action
Inhibition of cox 1 and 2-decrease prostaglandin synthesis - antiinflammatory,analgesic and antipyretic
77
Etoricoxib action
Selective inhibition of cox2 - inhibition of prostaglandin synthesis, doesn't affect cox1( analgesic, antipyretic, antiinflammatory)
78
Etoricoxib compared to other NSAIDS have
Low ulcerogenic potential,have higher risk of prothrombotic or thrombosis,but at same time less risk of bleeding
79
Interactions of diclofenac, ibuprofen and etoricoxib
Increased risk of bleeding when combined with systemic glucocorticoid, antiplatelets and anticoagulants,reduces antihypertensive effect of ACE inhibitor
80
PGE2 and PGI2 activation in macrophages, fibroblasts and endothelial cells by cox2 enzymes cause
Vasodilation, increased vascular permeability, increase cytokine release,increase leukocyte migration,pain
81
In CNS ,PGE 2 is released by both
Cox 1 and 2 and cause fever and pain neurotransmission
82
In lungs / asthma ,LTC4 and LTD4 are released by enzyme
LOX( lipooxygensase)
83
LTC4 and LTD4 action
Bronchoconstriction, mucus secretion,edema, eosinophil migration
84
Analgesic effect
Reduce the sensitisation of nociceptive neurons caused by PGE2
85
PGE2 action in gastrointestinal mucosa
Increase mucus secretion, increase bicarbonate, increase mucosal blood flow
86
PGE 2 and PGI2 action in kidney
Afferent arteriolar vasodilation ( increase GFR),increase Na and water excretion
87
PGI 2 and TXA2 action cardiovascular system
PGI2: Vasodilation,inhibit platelet aggregation TXA2: vasoconstriction and platelet aggregation (Cox2 action by PGI2 greater than Cox1 action by TXA2)
88
NSAIDS action on macrophage, fibroblasts and endothelial cells
Anti inflammatory and anlgesic
89
NSAIDS effect on CNS
Antipyretic ( analgesic)
90
NSAIDS effect on lungs( montelucast)
LOX inhibition and LT receptor antagonism cause decrease bronchoconstriction and antiinflammatory effect
91
NSAIDS effect on GI mucosa
Cause peptic ulcer and bleeding
92
93
NSAIDS effect on kidney
Increase Na and water retention, hypertension, cause hemodynamic acute kidney injury
94
NSAIDS on cardiovascular system effect
Cause stroke and MI
95
Low dose aspirin irreversibly inhibit
Platelet cox1
96
Arachidonic acid on PGI2 of endothelial cells cause
Vasodilation and decrease platelet aggregation
97
Arachidonic acid on TXA2 of platelet
Vasoconstriction, platelet granules release and change in shape of platelet - all these leads to thrombosis
98
Gout
Chronic disease,caused by deposition of urate crystals in joints and tissues,most common in men
99
Uric acid is end product of
Purine metabolism
100
Cascade reaction of uric acid formation
Hypoxanthine - xanthine - uric acid
101
Uric acid formation cascade is catalyzed by the enzyme
Xanthine oxidase
102
Acute gout attack treatment
NSAIDS and Glucocorticoid locally
103
104
Agents influencing uric acid metabolism
Allopurinol and febuxostat
105
Allopurinol is a prodrug which is metabolised to
Alloxanthine
106
Allopurinol is n analogue of
Purine/hypoxanthine
107
Allopurinol action
Alloxanthine is an irreversible xanthine oxidase inhibitor - inhibition of hypoxanthine/xanthine oxidation - blocks uric acid synthesis 2) inhibition of purine synthesis Uricostatic effect
108
Febuxostat action
Selective, reversible xanthine oxidase inhibitor of non purine origin ( uricostatic effect)
109
Clinical use of allopurinol and febuxostat
Chronic hyperuricemia in gout patients ( prevent progression of gouty arthritis and urate nephropathy),prevents complications of chemotherapy by allopurinol
110
SE of allopurinol and febuxostat
Skin rash
111
Skin rash caused by allopurinol is called
Stevens Johnson syndrome

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