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Pharma From Sure Success > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Insulin was discovered by …..
Secretion and structure of insulin

A

Banning and best in 1921.

Prepoinsulin (86 aa)
|
Proinsulin
| cleave
C peptide.
Human insulin- 51aa: 21A chain 30Bchain

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2
Q

What are the insulin preparations?

A
  1. Conventional preparation
  2. Highly purified preparation
  3. Human insulin
  4. Insulin analogues
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3
Q

What are the conventional insulin preparations?

A

Beef insulin: 3 aa
Pork insulin: 1 aa
Difference:
Pork: 30B chain : Ala instead of thre
Beef: A chain: 8th: Ala
10th: Val
B chain: 30: ALA

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4
Q

OHA that elevate both C peptide and Human insulin.
Importance of C peptide

A

Sulfonylureas

Insulinomas: both rise
Factious hypoglycemia: only insulin rise
Factious hypoglycemia + sulfonylureas: dx with high index of suspicion + drug level in plasma / urine .

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5
Q

Hormone that inhibits both insulin and glucagon

Hormone that evokes release of insulin + somatostatin

A

Somatostatin

Glucagon

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6
Q

Insulin receptor is …..
B subunit has…..activity

A

Tetrameric glycoproteins containing A and B chain attached together with disulphide bonds.

Tyrosine kinase activity.

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7
Q

How is highly purified forms of insulin made? (2)

A

From gel filtration
Ion exchange chromatography

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8
Q

Human insulin is produced by …..how?

A

Recombinant DNA technology
Isolate insulin gene from human DNA by restriction endonuclease.
Take a vector and cut it -also with same enzyme.- plasmid
Insulin + plasmid —-> inject it into Ecoli/yeast (transformation)
This will multiply to form more human insulin genes.

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9
Q

Benefits of human insulin (3)

A
  1. Rapidly absorbed
  2. Shorter duration of action
  3. Earlier and more defined peak
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10
Q

Insulin analogues on basis of onset and duration of action

A

Rapid : onset: 10mins, DOA: 3-5hrs
Short: onset: 30min-1hr DOA: 6-8 hrs
Intermediate : onset: 1-2hrs DOA: 20hrs
Long acting : onset: 2-4 hrs DOA: >24hrs

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11
Q

What are the rapid acting insulin analogues ? Structure differences

A

Lispro: B chain 28,29
lys, proline-interchanged

Aspart: 28 : lys-> aspartic acid

Glulisine: 23,29 :
Asparate—>lysine
Lys—>glutamic acid

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12
Q

Short acting: is …..
Structure

A

Regular insulin given iv & s/c
Small amount of zinc added to hexameric structure.

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13
Q

Disadvantages of regular insulin
So remedy?

A

Should be taken 1/2-1hr before meals and it’s tiresome.
To overcome that: intermediate acting :

Lente:
ultralente: large crystalline particle,insoluble, longer duration of a action
Semilente: smaller , shorter duration.
Together given in ratio : 7:3.

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14
Q

Structure of glargine
Disadvantages

A

B chain: 2 more aa is added
A chain: aspargine—->glycine at 21.

Provide background insulin coverage but not for meal time insulin spikes

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15
Q

Structure of insulin determir

Longest acting insulin

A

On B chain at 29aa, fatty acid myristol is added.

Degludec- >40hrs
Can be mixed with other insulin as it’s at neutral ph.

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16
Q

All insulin preparations are hexameric except?

All insulin prep is at neutral ph except

A

Aspart, lispro, glulisine- monomeric

Insulin glargine-thus can’t be combined with other insulins

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17
Q

All insulin contains phosphate buffer except ….(3)

A

Regular
Glargine
Glulisine

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18
Q

Regular insulin + lente =…….disadvantage
Shortest acting insulin ….

A

Lose rapidity of action
Aspart- resemble physiological insulin activity

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19
Q

Disadvantage of rapid acting insulin

Use of Glulisine

A

Injected 2-3 times a day.

Given s/c via continuous pump.

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20
Q

Sites of insulin administration (4)
How to give insulin ?

A

Abdomen
Arms
Thigh
Flanks

Massage the s/c area to increase blood flow and give it s/c.

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21
Q

Sms of hypoglycaemia

A
  1. Sweating, anxiety ,palpitation, tremor
  2. Decrease glucose in brain: dizziness,headache,fatigue ,weakness,behavioural changes
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22
Q

Hypoglycaemic unawareness

A

30% lose adrenergic stimulation after some time .
Due to diabetic neuropathy, which abolishes the nerves,they are unable to recognise the hypoglycaemic changes.

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23
Q

Rx of hypoglycaemia in insulin rx

A
  1. Glucose
  2. Glucagon=0.5-1mg / adrenaline =0.2mg s/c where glucose is n/a.
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24
Q

Local reactions of insulin

A

Sweating,stinging,erythema
Lipodystrophy -multiple inj on same site

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25
Q

Allergy reaction of insulin injection (3)

A

Urticaria
Angioedema
Anaphylaxis

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26
Q

When does Edema occur?

A

Short lived, due to Na+ retention in early insulin rx.

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27
Q

What is NPH?

A

Isophane/ neutral protamine hagedorn
Instead of zinc, protamine is added 1:1 with regular insulin.

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28
Q

Interactions of insulin (4)

A
  1. B2 receptor blocker- masks warning signs, only rise in BP due to a stimulation by ADR.
  2. Thiazide,furosemide ,CS, OCP, salbutamol, nifedipine
  3. Acute ingestion of alcohol
  4. Lithium, aspirin,theophylline.
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29
Q

Regimen of insulin (2)

A
  1. Split mixed regimen:
    Regular + lente=30:70
    Bbf, before dinner
  2. Basal bolus regimen
    3-4 inj rapid acting daily + glargine
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30
Q

Isophane insulin has ……structure

Cloudy insulin is …..

A

6 molecules of insulin with 1 protamine

NPH insulin

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31
Q

Afreeza was used for …..

A

Rx of only post prandial hyperglycaemia - 30mins before meal.

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32
Q

Pharmacodynamics of afreeza
Mc side effect is ……

A

Absorption rapid
Peak insulin level- 15 mins
Declines to baseline after 3 hrs

Cough

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33
Q

C/I of afreeza (3)

A

Smokers
Asthma
Copd

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34
Q

Define term insulin’s resistance

A

When >100 units insulin is needed to keep blood glucose within normal limits

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35
Q

Causes of insulin resistance (14)

A

LOW PRACs
Leprechaunism
Lipodystrophy

Obesity
Werger syndrome

PCOD
Pineal hyperplasia

Rabson Mendenhall syndrome
Acute and chronic Renal failure

Anti insulin Ab
Acromegaly
Asian origin
Alstrom syndrome
Ataxia telangiectasia

Cystic fibrosis

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36
Q

Clinical markers of insulin resistance (6)

A
  1. Acanthosis nigricans
  2. Multiple skin tags- acrochordons
  3. Acromegaloid features
  4. Hyperandrogenism-acne,hirsuitism,oligomenorrhoea
  5. Central obesity: high waist-hip ratio
  6. High BMI >30kg/m2.
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37
Q

Functions of insulin anabolic hormone (8)

A

Decrease gluconeogesis
Increase glycogenesis
Increase glucose transport in muscle,ad tis
Increase glycolysis
Increase lipogenesis (TG,cholesterol)
Increase protein synthesis
Increase sodium retension in kidney
Increase cellular uptake of K+

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38
Q

Functions of glucose as catabolic hormone (4)

A

Increase glycogenolysis
Increase gluconeogenesis
Increase ketogenesis
Increase lipolysis

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39
Q

Organs that don’t need insulin for glucose uptake

A

L-BRICK
Liver
Brain
RBC
Intestine
Cornea
Kidney

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40
Q

Insulin physiology

A

Blood glucose increases >70mg/dl—> goes to beta cells of pancreas-> enter via GLUT2, glucose —>g6p by enzyme Glucokinase
1atp is released—> inhibits K+ channel —> membrane depolarizes—> calcium channel open, calcium comes in, and throws out insulin from the cell.

Insulin binds on a subunit of insulin receptor found on the target cell—> b subunit gets activated—>TK released. Series of phosphorylation takes place inside the cell , GLUT4 is expressed on the surface of target cell, and glucose gets inside.

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41
Q

Classification of OHA

A
  1. Enhance insulin secretion from pancreas
    a. K+ channel inhibitors:
    Sulfonylureas, meglinitide
    b. GLP-1 agonist
    c. DDP4 inhibitor
  2. Decrease insulin resistance
    Biguanides
    Thiazolidindiones
  3. Miscellaneous
    a. A-glucosidase inhibitors
    b. Amylin analogue
    c. DA against
    d. SGLT2 antagonist
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42
Q

MOA of sulfonylureas
Extrapancreatic action of sulfonylureas

A

Similar to release by normal glucose, they inhibit K+ channel activity
At least 30% fn cells should be present for its action to take place.

When the insulin releasing activity from pancreas is decreases , they synthesize target tissues to increase action of insulin.
Due to increase sensitivity of insulin receptors

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43
Q

Advantages of repaglinide, nateglinide
Shortest acting miglitol

A

Decrease post prandial hypoglycemia as they are short acting.

Nateglinide

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44
Q

S/e of miglitol (4)

A

Headache, dyspepsia, arthralgias, weight gain

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45
Q

S/e of chlorpropamide (3)

A
  1. Cholestasis
  2. Dilutional hyponatremia -ADH like
  3. Intolerance to alcohol-disulfiram like
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46
Q

Longest acting sulfonylureas
Drugs that displace sulfonylureas from protein binding (4)

A

Chlorpropamide

  1. Phenylbutazone
  2. Sulfinpyrazone
  3. Salicylates
  4. Sulfonamides
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47
Q

Drugs that prolong sulfonylureas actions (5)

A

1 salicylates
2. Propanolol
3. Lithium
4. Theophylline
5. Alcohol

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48
Q

Hypoglycemia is most with ….sulfonylureas

Lowest risk,low potency sulfonylureas

A

Chlorpropamide

Tolbutamide

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49
Q

Non specific symptoms of sulfonylureas (5)

A

N/V
Flatulence
Constipation
Diarrhea
Headache

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50
Q

Max insulinotropic action of Su
T1/2 of glyburide
Lowest hypoglycemia with su is with …

Approved in Japan

A

Glyburide

1-2hrs

Glimepride

Mitiglinide

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51
Q

Drug that binds to SUR-1 receptor binder and beta cell sequestration

A

Glyburide

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52
Q

What are the egs of incretins?

A

2 types :
GIP: present on K cells of prox intestine
GLP-1: present on L cells of terminal ileum and colon.

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53
Q

MOA of incretins

A

food into stomach —-> glucose into blood—> directly stimulate pancreatic cells to release insulin.
—> decrease glucagon
—-> delay emptying
Thus there is a feeling of satiety.

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54
Q

What inhibits incretins ?
DDP4 resistant incretins
Disadvantage

Long acting GLP-1 against

A

DDP4— degrade the incretins.

Exenatide
Coz it’s
peptide, can’t be taken orally .

Liraglutide

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55
Q

S/e of GLP-1 agonist
DPP4 inhibitors are ……
S/e…..

A

Nausea

Competitive and selective

Nasopharyngitis
Cough
URTI
—due to inhibition of substance P degradation.

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56
Q

MOA of biguanides

A

Metformin—> enters target cell via Oct-1 channel—-> inhibit mitochondrial ATP. AMP activated —> activated AMPk —> more vesicles to enter the cell, decreasing insulin resistance.

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57
Q

Action of metformin
Intestine
Liver
Skeletal muscle

A
  1. Increase glycolysis
  2. Inhibit gluconeogenesis
    Increase lipogenesis -> decrease hyperlipidemia
  3. Increase glucogenesis
58
Q

Advantages of metformin. (4)

A

Non hypoglycemic
Reduces both macro and micro vascular complications
Weight loss
Combined with other drugs

59
Q

C/I of metformin.

A
  1. Hypotension
  2. Heart failure , renal failure,liver failure
  3. Alcoholics
60
Q

MOA of TZD

A

Glitazones—> go to nuclear PPAR gamma of target cell—> enhance transcription of insulin responsive gene —> increase GLUT-4 expression to the surface of the cell.

61
Q

OHA safer in renal disease, but c/I in ….
Rosiglitazone was banned because….

A

TZD

Liver disease

MI/stroke

62
Q

S/e of TZD

A

Weight gain , pedal edema , macular edema, hepatotoxicity

63
Q

MOA of Acarbose

A

Food —> intestine —>polysaccharide—> monosaccharides by enzyme a glucosidase and is absorbed.

Acarbose blocks a glucosidase. Polysaccharide goes into the large intestine, acted upon by bacteria and cause bloating, flatulence.

64
Q

……strong inhibitor of sucrose

MOA of pramlintide

A

Miglitol

It’s an amylin analogue
Causes : 1. Decrease glucagon from pancreas
2. Acts on the brain , cause satiety
3. Delays gastric emptying

65
Q

Only drug other than insulin that can be given for type 1 and type 2 DM

A

Pramlintide

66
Q

MOA of SGLT2 inhibitors

S/e

A

All the glucose that is filtered from the bowman’s capsule is absorbed in the PCT via SGLT2 .
Glifloxcins inhibit SGLT2 transporter.

Vaginal candidiasis
UTI

67
Q

Leg and foot amputations seen with ……OHA

Breast and bladder cancer seen with ….

A

Canagliflozin

Dapagliflozin

68
Q

Drug that can decrease TG

Type 2 DM regimen

A

Dual PPAR agonist -Saroglitazar

Type 1: insulin
Type 2: diet, exercise , metformin
If uncontrolled = metformin + add 1 drug
If uncontrolled = metformin + 2 drugs
If uncontrolled = metformin + 3 drugs / insulin + metformin .
Pregnant: insulin +_ metformin

69
Q

OHA with max decrease in HbA1C
OHA with min decrease in HbA1C

A

Sulfonylureas

Acarbose

70
Q

Essential meds of WHO list

Shortest acting SU
Longest acting SU

Shortest acting OHA

A

Metformin, glimenclamide
Tolbutamide

Chlorpropamide

Nateglinide

71
Q

Eg of Aldose reductase inhibitor MOA

A

Epalrestat
Delay sorbitol accumulation in sciatic and other nerves
Delay progression of Diabetic neuropathy

72
Q

GLP2 agonist Eg
Use

A

Teduglutide

Rx of short bowel syndrome

73
Q

Main source of GLP-1 in the body is …

Hormone that remain stable with aging

A

Intestinal L cells - secrete GLP-1 as gut hormone

GLP.

74
Q

Insulin analogue that changes both A and B chains

Antidiabetic drug with insulin independent action …..

A

Glargine

SGLT2 inhibitor

75
Q

S/e of SGLT2 inhibitors (6)

A
  1. Vaginal Candida
  2. UTI
  3. Hypotension
  4. Weight loss
  5. Fourniers gangrene
  6. DKA
76
Q

OHA causing weight loss, weight gain and neutral

A

Weight loss: GSP
GLP-1 agonist
SGLT2 inhibitor
Pramlintide

Weight gain: SIT
SU, Insulin, TZD

Weight neutral: DPP4 inhibitor, Metformin

77
Q

OHA that decrease ASCVD mortality (3)

A
  1. Metformin
  2. SGLT2 inhibitor
  3. GLP-1 agonist
78
Q

Rx of hypothyroidism
Difference between T3 , T4. (3)

A

Levothyroxine T4.

T4: levothyroxine. T3: liothyronine 1. Less potent. More potent
2. Longer DOA. Less plasma t1/2
3. Decrease arrhythmias. More

79
Q

Rx for myxedema coma

A
  1. T4
    2 T3- add on drug
80
Q

Drugs for hyperthyroidism (4)

A
  1. Damage NIS
  2. TPO inhibitors
  3. Inhibit Iodine release
  4. Radioactive I 131
81
Q

Actions where TPO is required (3)

A

Oxidation : I - to I+
Organification: I+ + TG —> MIT/DIT
Uncoupling: T3,T4 bound to TG- release

82
Q

Difference between methimazole and PTU (5)

A

Methimazole. PTU
1. More potent. Less potent
2. More plasma t1/2. Less plasma t1/2
Sustained action
3. Teratogenic. Less placental tx
4. More PC. Less peripheral C
5. Less problem. Increased S/e

83
Q

Action of iodide (3)

A
  1. Fast acting anti thyroid drug
    Inhibit T3,T4 release -thyroid constipation
    Rx: thyroid storm
  2. Decrease blood flow to gland-shrink size, used before thyroid surgery
  3. High dose/ chronically
    Inhibit proteolysis/organification. Inhibit thyroid synthesis.
84
Q

S/e of action of iodide (3)

A
  1. Fetal goiter
  2. Iodism = mucosal I.F -> conjunctivitis,
    Painful swollen parotid gland
85
Q

Beta blocker use.

Drugs that decrease peripheral conversion of T4——>T3 (5)

A

Given as add on rx, symptomatic Rx:
Tremor, arrhythmia

  1. PTU
  2. Propanolol
  3. Prednisolone
  4. Amiodarone
  5. Lithium.
86
Q

What is thyroid storm? DOC

A

Life threatening condition. Cause seizures,arrhythmias—> death.

DOC:
1. PTU
2. Iodide (given 1-2hrs after PTU)
3. Beta blocker-propanolol

87
Q

DOC for hyperthyroidism
What is carbimazole?

A

Methimazole

Prodrug—>methimazole

88
Q

Where is PTU useful?

A
  1. Pregnancy
  2. Thyroid storm
89
Q

S/e of PTU
Carbimazole causes ……s/e (3)

A

Hepatotoxicity
Agranulocytosis

  1. Aplasia cutis
  2. Choanal atresia
  3. Fetal goiter
90
Q

Drugs that inhibit iodide trapping ? (2)
……..contains thiocyanate,avoid in patients with thyroid disease

A

Percholates
Thiocyanates
Inhibit sodium iodide cosymporter

Cabbage 🥬

91
Q

Drugs that inhibit hormone release? (2)

A
  1. Lugol’s iodine
  2. Potassium iodide
92
Q

What is lugol’s iodine?
Use.

A

5% iodine + 10% potassium iodide
Used in thyroid storm- as it causes decrease T3,T4 release—>thyroid constipation.

93
Q

T1/2 of radioactive I 131.
Indication

A

8 days

Elderly,unfit for surgery coz of Mi/stroke

94
Q

Uses of various rays of
radioactive I 131. (2)

A
  1. Gamma rays - thyroid scan
  2. Beta particles- destroy thyroid gland.
    Slow acting -3 weeks
    Until then, give methimazole,or beta blocker.
95
Q

Contraindications of radioactive iodine. (3)

A

Pregnancy
<25 years
Graves opthalmopathy

96
Q

Drugs causing hypothyroidism (8)

A

Lithium
Amiodarone
Sulfonamides
Phenobarbitone
Phenytoin
Para-amino salicylic acid
Carbamazepine
Rifampin

97
Q

What is dronedarone?

A

Amiodarone - Iodide = dronedarone
It does not cause thyroid abnormality.

98
Q

Define osteoporosis. (3)

A

Reduction in bone mass
Normal bone mineralization
Sparse trabeculae

99
Q

What are the types of osteoporosis?

A

Type 1: postmenopausal- due to decreased estrogen.

Type 2: senile osteoporosis (>70yrs)

100
Q

Features of vertebral crush fracture (3)

A

Acute back pain
Loss of height
Kyphosis

101
Q

What are the fractures that occur in osteoporosis? (3)

A

Vertebral crush fractures
Colle’s fracture - distal radius fracture
Vertebral wedge fracture

102
Q

Prophylaxis of osteoporosis (3)
ALP is ……..in osteoporosis

A

Exercise
Calcium
Low dose estrogen rx

Normal

103
Q

Dose of calcium and vit d for rx of osteoporosis

A

Calcium : 1200mg/d
Vitamin D: 400-800IU/d

104
Q

MOA of denosumab

A

RANK ligand inhibitor.
Prevents bone resorption

105
Q

MOA of romosozumab

A

Inhibits sclerostin
Increases new bone formation

106
Q

Calcitonin is given as …..route for osteoporosis

MOA of teriparatide
It’s withdrawn from market .why?

A

Nasal spray

Teriparatide,abaloparatide given as PTH analogue
Stimulates formation of new collagen matrix, so mineralized can take place with calcium and vit D supplements.

C/I Paget’s disease and osteosarcoma
Causes hypercalcemia

107
Q

DOC for osteoporosis
MOA

A

Bisphosphonates
Inhibit osteoclast bone resorption by inhibiting farnesyl pyrophosphate synthetase

108
Q

Drugs that decrease bone resorption (3)

A

Denosumab
Bisphosphonates
Calcitonin

109
Q

Drugs that increase bone formation (2)

A

Teriparatide
Romosozumab

110
Q

Dosing frequency of alendronate, risedronate,ibandronate, zolindronate

A

Alendronate,risendronate: once weekly
Ibandronate: once a month
Zolindronate: once a year

111
Q

Most potent bisphosphonates
S/e (4)

A

Zolindronate

S/e:
1. Acute phase reaction-fever,chills,myalgia etc
2. Acute renal failure
3. Atrial fibrillation
4. Uveitis

112
Q

Fracture that occurs with zolendronate
X ray shows:…….

A

Chalk stick fracture of femur -aka insufficiency fracture

Lateral cortical fracture

113
Q

Osteonecrosis of …..take place with bisphosphonates.
Risk of ……..cancer

A

Jaw
Esophageal cancer

114
Q

Bone mineral changes first seen in immobilization osteoporosis is in ….
Immobilization osteoporosis occurs in….&…..patients

A

Proximal humerus

Stroke
Hemiplegic

115
Q

…….bone density is reliable for predicting risk of hip fracture
……….bone density to monitor response to rx .

A

Hip bone density

Spine bone density

116
Q

T score for :
1. Normal bone:
2. Osteopenia
3. Osteoporosis
4. Severe osteoporosis

A
  1. > -1
  2. -1 to -2.5
  3. Less than -2.5
    4 less than -2.5 + presence of non traumatic fracture
117
Q

Mgt of acute hypercalcemia

A
  1. Iv saline + furosemide
  2. Iv pamidronate
  3. Calcitonin iv
    Given last, onset within hrs (fastest acting)
    S/e: tachyphylaxis
118
Q

Vit D synthesis physiology

A

Skin by UV rays —-> cholecalciferol
Cholecalciferol—->liver—-> 1(OH) D3
1(OH)D3——> kidney—-> 1,25(OH) D3

Order: skin-liver-kidney

119
Q

Rx for rickets

A

Type 1: deficiency of 1,hydroxylase
Rx: calcitriol
Can also give alpha calcidiol, 1(OH) vit D3—> liver—-> 1,25(OH) vit D3

120
Q

GH effect on blood sugar

A

Via IGF-1: hypoglycemia
Directly via liver: increase gluconeogenesis—> increase RBC

121
Q

Rx for acromegaly (4)

A
  1. Doc: Octreotide
  2. DA agonist : cabergoline
  3. GH antagonist: pegvisomant
  4. Tamoxifen- decrease IGF-1 level
122
Q

Action of DA in normal and acromegaly patients

A

Normal: increase GH
Acromegaly: decrease GH

123
Q

Side effects of GH rx (4)

A
  1. Edema
  2. Slipped capital epiphysis
    Carpal tunnel syndrome
    Scoliosis
  3. Increased ICP
  4. Hypothyroidism-unmask TSH def
124
Q

Long acting analogue of somatostatin is …..
…….times more potent than somatostatin

A

Ocreotide
45

125
Q

Uses of ocreotide (4)

A
  1. Decrease GH: acromegaly
  2. Decrease insulin: insulinomas
  3. Decrease Gi secretion: secretary diarrhoea
  4. Vasoconstriction splanchnic vessels- Rx of bleeding varices
126
Q

S/e of ocreotide (2)

A

Hyperglycemia
Gall stones

127
Q

Somatostatin analogue for Rx thyroid tumors

GH antagonist for rx acromegaly

A

Lanreotide

Pegvisomant

128
Q

Recombinant GH for Rx GH deficiency (2)

A

Somatropin
Somatrem

129
Q

Rx for Laron’s syndrome (2)

A

Dwarfism
Rx: 1. Somatrem (im)
2. No benefit —> rIGF-1 : mecasermin

130
Q

What is mecasermin? Use

A

Recombinant IGF-1 + recombinant IGFBP-3

For rx short stature

131
Q

Define mecamylamine

A

Hexamethionium ganglion blocker

132
Q

DA against drugs (4)

A
  1. Bromocriptine
  2. Cabergoline
  3. Pergolide
  4. Quinagolide
133
Q

Most potent glucocorticoid

Glucocorticoid similar efficacy to prednisone but lesser s/e

A

Dexamethasone

Deflazacort

134
Q

Glucocorticoid antagonist

GC synthesis inhibitors (4)

A

Mifepristone

Metyrapone
Aminogluthimide
Mitotane
Ketoconazole

135
Q

What are anabolic steroids? Eg?
(4)

A

Used to reduce virilization while maintaining anabolic effects.

Eg:
Methandienone
Oxymetholone
Nandrolone
Stanozolol

136
Q

Betamethasone preferred over hydrocortisone why?

A

They have zero mineralocorticoid action

137
Q

Rx for adrenal cortex insufficiency

A

GC+ MC =
hydrocortisone + fludrocortisone

138
Q

Corticosteroid with maximum A/E potential

A

Any CS given long term as it decrease the HPA axis

139
Q

In a patient taking long term CS gets a trauma or stress. Next course of action.

A

Increase the dose of GC.
Chronic use suppresses HPA axis-ongoing dose can’t produce enough cortisol to control the stress related condition.

140
Q

Rx of Cushing syndrome.MOA of drugs

A

11 beta hydroxylase inhibitors—> inhibit formation of CS.
Metyrapone
Ethomidate
Ketoconazole
Mitotane

141
Q

Drug that acts on CS receptor and inhibit it.

CS not suitable for alternate day Rx

A

Mifepristone

Betamethasone t1/2- >36hrs

142
Q

DOC for child born with adrenal cortex hyperplasia

Doc for pregnant female with in utero child with CAH:

A

Hydrocortisone + fludrocortisone

Dexamethasone- prevent virilization of female fetus.
Better placental transfer

Pharma From Sure Success (10 decks)

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