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PHA 332 > Corticosteroids 3&4 > Flashcards

Corticosteroids 3&4 Flashcards

1
Q

what hormones does the hypothalamus produce?

A

oxycontocin

ADH

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2
Q

where are hormones from the hypothalamus transported and stored? what happens after?

A

hormones are transported and stored to the posterior pituitary for storage
this directcs the posterior pituitary to release hormones

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3
Q

what controls the pituitary gland?

A

controlled by the hypothalamus

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4
Q

where is the pituitary gland?

A

•Located at the base of the brain–Protected by a bony structure called the sella turcica
–The optic chiasmis located just above the pituitary gland

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5
Q

what are the two lobes of the pituitary gland?

A

anterior lobe

posterior lobe

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6
Q

what is the function of the anterior lobe in the pituitary gland?

A

GH- stimulates increase in size of muscles and bones
luteinzing hormone- females stimulates ovulation and oestrogen production
males-stim testosterone production
adrenocorticotropic-stim the adrenal cortex to release its hormones
prolactin-stimulates milk production
thyroid stim -stimulates the thyroid gland to release its hormones
follicle stimulation
females: stim oestrogen production and maturation of the ova
males-stimulates sperm production

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7
Q

how much do the human adrenals weigh?

A

8-10g

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8
Q

what does the adernal gland comprise of?

A

outer cortex with 3 zones (reticularis, fasciculta and glomerulosa) producing steroids
-inner medulla that synthesizes, and secretes catecholamines

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9
Q

what are the basal daily secretions of the glucocorticoids?

A

cocrtisol 5-30mg

corticosterone 2-5mg

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10
Q

what are the basal daily secretions of mineralocorticoids?

A

aldosterone 5-150mcg

11-deoxycorticosterone trace

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11
Q

what are the basal daily secretions of the sex hormones?

A

androgen-DHEA- 15-30mg
progestogen-progesterone 0.4-0.8mg
oestrogen-oestradiol-trace

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12
Q

what is the pre cursor of all adrenal steroids?

A

cholesterol metabolism

cholesterol and its metabolites are the substrates for multiple enzymes

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13
Q

what are the critical targets in cholesterol metabolism?

A

Cholesterol desmolasen and the17α-and 11β-hydroxylases are critical pharmacologic targets.

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14
Q

what is cholesterol the precursor of?

A

vitamin D and bile acids

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15
Q

what are the 14 pharmacological actions of corticosteroids?

A
  1. Carbohydrate
  2. Protein
  3. Lipid
  4. Electrolyte & water
  5. CVS
  6. Sk. Muscle
  7. CNS
  8. Stomach
  9. Blood
  10. Anti-inflammatory
  11. immunosuppressant
  12. Respiratory system
  13. Growth & Cell Division
  14. Calcium metabolism
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16
Q

what are the main metabolic effects of glucorticosteroids?

A

carbohydrate and protein metabolism

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17
Q

what happens in carb and protein metabolism due to steroids?

A 
• INC Gluconeogenesis
–Peripheral actions (mobilize AA &  glucose and glycogen)
–Hepatic actions
Tendancy for hyperglycaemia
•DEC Peripheral utilization of glucose
• INC Glycogen deposition in liver
overall dec in protein synthesis
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18
Q

what may a decrease in protein synthesis cause?

A

increased protein breakdown, particularly in the muscle

this can lead to tissue wasting

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19
Q

what effect does glucocorticoids hae on the cAMP-dependent lipplytic response?

A

such hormones cause lipase activation through a cAMP dependent kinase

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20
Q

what effect is seen when large doses of glucocorticoids are given over a long period of time?

A

redistribution of fat
-buffalo hump
moon face
these are characterictics of cushing’s syndrome

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21
Q

what does lipid metabolism also promote?

A

promotes adipokinetic agents activity

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22
Q

how is the electrolyte and water balance affected by glucocortcoids?

A

aldosterone is important
act on the distal tubule and collecting duct of the kidney
-increase na+ reabs
- increase urinary excretion of k+ and h+

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23
Q

how does glucocorticoids affect the cardiovascular system?

A
  • Restrict capillary permeability
  • Maintain tone of arterioles
  • Myocardial contractility
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24
Q

what is the effect on skeletal muscles?

A

it is needed for maintaining the normal function of skeletal muscle
addison’s disease: weakness and fatigue- inadequacy of circulatory system
prolonged use: skeletal muscle wasting system- steroid myopathy

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25
Q

what is the effect on the CNS?

A

direct effect on mood, behavior and brain excitability

indirect effect on glucose maintenance, circulation and electrolyte balance

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26
Q

what is the release of glucocrticoids dependent on?

A

the amount of circulating ACTH

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27
Q

when is the plasma cortisol levels highest?

A

in the morning

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28
Q

what effects does glucocortcoids have on the stomach?

A

aggravate peptic ulcer
this may be due to:
-increase in acids and pepsin secretion
-decrease in immune response to h.pylori

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29
Q

what effects do steroids have on the blood?

A

RBC: Hb & RBC content (erythrophagocytosis)
WBC: decrease Lymphocytes, eosinophils, monocytes, basophils
increase Polymorphonuc leocytes

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30
Q

what are the anti-inflamatory and immunosuppressive effects of glucortcoids?

A

suppresses all types of h y persensitivity and allergic phenomeon

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31
Q

what happens with a high dose for the anti-inflam and immunosuppressive effects?

A

interferes with all steps of the immunological response
causes greater suppression of CMI
transplant rejection

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32
Q

what are the action on inflam cells?

A

dec egress of neutrophils from blood vessels
•activation of neutrophils, macrophages and mast cellssecondary to decreased transcription of the genes forcell adhesion factors and cytokines
•decreased overall activation of T-helper (Th) cells
•dec clonal proliferation of T cells, and a ‘switch’ from theTh1 to the Th2 immune response
•decreased fibroblast function, less production of collagen and glycosaminoglycans, and, under some circumstances, reduced healing and repair.

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33
Q

what are the actions on the mediators of inflam and immune responses?

A

• DEC Production of prostanoids through reduced expression of cyclo-oxygenase-2
• DEC Generation of many cytokines, including IL-1, IL-2, IL-3,IL-4, IL-5, IL-6, IL-8, TNF-α, cell adhesion factors and granulocyte–macrophage colony-stimulating factor.These are largely secondary to inhibition of genetranscription
• DEC In the concentration of complement components inthe plasma
• DEC Generation of induced nitric oxide by nitric oxidesynthase 2 (NOS2
DEC Histamine release from basophils and mast cells
• DEC Immunoglobulin G (IgG) production
• INC Synthesis of anti-inflammatory factors such as IL-10, IL-1-soluble receptor and annexin-1

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34
Q

How is calcium metabolism affected?

A

DEC Intestinal absorption
• INC Renal excretion
•Excessive loss of calcium fromspongy bones

35
Q

How is the respiratory system affected?

A
  • Notbronchodilators
  • Most potent and most effective anti-inflammatory
  • Effects not seen immediately (delay 6 or morehrs.)
  • Inhaled corticosteroids are used for long term control
36
Q

what are the major actions of glucocorticoids?

A

increased/stimulated:
gluconeogenesis, glycogen deposition, protein catcbolism, fat deposition, sodium retention, potassium loss, free water clearance, uric acid production, circulating neutrophils

dec/inhibited: protein synth, host response to infection, lymphocyte transformation, delayed hypersensitivity, circulating lymphocytes, circulating eosinophils

37
Q

how does the potency vary for the glucocorticoid vs mineralocorticoid effect?

A 
hydrocortisone 1v1
prednisolone 4 v 0.7
dexamethasone 40 v 2
aldosterone 0.1 v 400
fludroxortisone 10 v 4000
38
Q

how does the short acting preperations vary with anti- inflam effects, salt retention and topical/

A

cortisol 1v1v1

cortisone 0.8 v0.8v0

39
Q

how do the intermediate acting prep vary with anti-inflam,salt retaining and topical effects?

A 
prednisone: 4v0.8v0
prednisolone 5v0.3v4
methylprednisolone 5v0.3v4
methylprednisolone 5v0v5
triamcinolone 5v0v5
paramethasone 10v 0
fluprednisolone 15v0v7
40
Q

how do the long acting prep vary with anti-inflam, salt retaining and topical effects?

A 
betamethasone 25-40 v 0v 10
dexamethasone 30v0v10
mineralcorticoids:
fludrocortisone:10v250v10
DOCA 0c20v0
41
Q

what are the different types of glucorticoids?

A

short acting
intermediate acting
long acting

42
Q

whatare the different corticosteroids preperations?

A

glucocorticoids
mineralocorticoids
inhalant steroids
topical steroids

43
Q

what prep can you have IM?

A

cortisone
desoxycorticosterone
triamcinone

44
Q

what prep can you have IM and IV?

A

dexamethasone
hydrocortisone
methylprednisolone
prednisolone

45
Q

what prep can you have as an aerosol?

A

beclomethasone
flunisolide
fluticasone
triamcinolone

46
Q

what prep can you have topically?

A

beclomethasone
dexamethasone
hydrocortisone
triamclinolone

47
Q

how would you investigate glucocortoicoid abnormalities?

A

basal levels

ACTH and cortisol are released epsodically and in response to stress

48
Q

how should you take a blood sample?

A

–Sampling time should be recorded accurately.–Conventionally, basal levels are obtained at between 0800 h and 0900 h near the peak of the circadian variation.–Stress should be minimized
.–Appropriate reference ranges (for time and assay method) should be used.

49
Q

what is the dexamethasone suppression test?

A

•Administration of a synthetic glucocorticoid to a normal subject produces prompt feedback suppression of CRH and ACTH levels

50
Q

how does the ACTH stimulation test work?

A

•Synthetic ACTH (tetracosactide, which

consists of the first 24 amino acids of human ACTH) is given to stimulate adrenal cortisol production.

51
Q

how is dexamethasone used for the diagnosis of cushing’s syndrome

A

low dose- 0.5mg 6 hourly
eight doses
plasma cortisol at 900h on days 0 and 2+
plasma cortisol< 50 mmol/L on second sample
high dose 2mg to 6 hourly
eight doses
plasma cortisol on day 2+ less than 50% of that on day 0 suggests pituitary dependent disease

52
Q

how is ACTH used for the diagnosis of addisons?

A

short- 250ug tetracosactide iv or im- 0,+30 min plasma and cortisol at 30+ min> 600mmol/l
>if unclear use long test to differeciate

long
depot tetracosactide 1mg im 
plasma 0,1,2,3,4,8,24hr
max >1000nmol/l
rise>550nmol/l
53
Q

what is the pathophisology of addison’s disease?

A
  • Destruction of the entire adrenal cortex.
  • Glucocorticoid, mineralocorticoid and sexsteroid production are therefore all reduced.
  • Reduced cortisol levels lead, throughfeedback, to increased CRH and ACTHproduction, the latter being directlyresponsible for the hyperpigmentation.
54
Q

who is primary hypoadrenalism most common in?

A

female preponderance and is most often caused by auto-immune disease rather than TB

55
Q

what are the causes of addison’s diesase? ( primary)

A 
Autoimmune disease (approx. 90% in UK)
Tuberculosis (< 10% in UK)
Surgical removal
Haemorrhage/infarction
Meningococcal septicaemia
Venography
Infiltration
Malignant destruction
Amyloid
Schilder's disease (adrenal leucodystrophy)
56
Q

what is the peak age that addison’s disease occurs at?

A

between 30-50

57
Q

who are more likely to develop addisons disease?

A

People with other autoimmune diseases, suchas Graves’ disease, hypothyroidism, type 1diabetes, pernicious anaemia and vitiligo,have agreater risk of also developing autoimmune Addison’s disease.

58
Q

what is dehydroepindrosterone deficiency and who does it occur in?

A

(loss of axillary/pubic hair, absence ofpubarche in children, reduced libido and dryskin).
only in women

59
Q

what happens if patient is seriously ill or hypotensive when addison’s disease is suspected?

A

hydrocortisone100 mg should be given intramuscularly together with intravenous saline (Done immediately after a blood sample is taken for later measurement of plasma cortisol.)
or ACTH stim test preformed

60
Q

what is the regular tests for addisons dieases not in an emergency?

A 
Single cortisol measurements
The short ACTH stimulation test
A 0900 h plasma ACTH level
Electrolytes and urea
Blood glucose
Adrenal antibodies
Chest and abdominal X-rays
Serum aldosterone
Hypercalcaemia and anaemia
61
Q

what lab results would you look for in addison’s disease?

A 
DEC Corticosteroids
INC ACTH
INC K+
DEC Na+
DEC Cl-
DEC HCO3-
DEC Glucose
62
Q

Assuming normal cardiovascular function what is the treatment for addisons disease?

A

1L of 0.9% saline should be given over 30-60 minutes with 100 mg of intravenous bolus hydrocortisone.
Subsequent requirements are several litres of saline within 24 hours(assessing with central venous pressure line if necessary) plushydrocortisone, 100 mg i.m., 6-hourly, until the patient is clinicallystable.
Glucose should be infused if there is hypoglycaemia.
Oral replacement medication is then started, unless unable to take oralmedication, initially hydrocortisone 20 mg, 8-hourly, reducing to 20-30mg in divided doses over a few days
Fludrocortisone is unnecessary acutely as the high cortisol doses provide sufficient mineralocorticoid activity - it should be introduced later.

63
Q

what patient advice should people with addisons know?

A

Patients requiring replacement steroids should:
Know how to ↑steroid replacement dose for intercurrent illness
Carry a ‘Steroid Card‘
Wear a Medic-Alert bracelet (or similar), which gives details of their condition so that emergency replacement therapy can be given if found unconscious
Keep an (up-to-date) ampoule of hydrocortisone at home in case oral therapy is impossible, for administration by self, family or GP.

64
Q

what is the average drug replacement for addison’s disease?

A

hydrocortisone: 20-30mg daily
or prednisolone 7.5mg daily
rarely dexamethasone 0.76mg daily
fludrocortisone 50-300ug daily

65
Q

what is cushing’s syndrome?

A
  • Term used to describe the clinical state of increased free circulating glucocorticoid.
  • Occurs most often following the therapeuticadministration of synthetic steroids or ACTH
66
Q

what causes cushings disease?

A

due to adrenal disease occurs 4times more commonly in women than in men

67
Q

when are the majority of people diagnosed with cushings syndrome?

A

20-50

68
Q

what are the two main causes of cushings syndrome?

A

–↑circulating ACTH from the pituitary (65% ofcases), known as Cushing’s disease–

From an ‘ectopic’, non-pituitary, ACTH-producing tumour elsewhere in the body (10%) with consequential glucocorticoid excess

69
Q

what are the ACTH dependent diseases causes of cushing’s syndrome?

A

Pituitary-dependent (Cushing’s disease)
Ectopic ACTH-producing tumours
ACTH administration

70
Q

what are the non-ACTH dependent causes of cushing’s syndrome?

A

Adrenal adenomas
Adrenal carcinomas
Glucocorticoid administration

71
Q

what is another way that cushing’s syndrome can be induced?

A

Alcohol-induced pseudo-Cushing’s syndrome

72
Q

what are the predominant clinical features of cushing’s syndrome?

A
  • Pigmentation occurs only with ACTH-dependent causes.
  • A cushingoid appearance can be caused by excess alcohol consumption (pseudo-Cushing’s syndrome) - the pathophysiology is poorly understood.
  • Impaired glucose tolerance or frank diabetes are common, especially in the ectopic ACTH syndrome.
  • Hypokalaemia due to the mineralocorticoid activity of cortisol is common with ectopic ACTH secretion
73
Q

what are the two phases of the investigation into cushing’s syndrome?

A
  1. Confirmation of the presence or absence of Cushing’s syndrome
  2. Differential diagnosis of its cause (e.g.pituitary, adrenal or ectopic)
74
Q

how do you confirm diagnosis of cushings syndrome?

A

48-hour low-dose dexamethasone test.
•24-hour urinary free cortisol measurements.
•Circadian rhythm.
•Other tests.
•insulin stress test, desmopressin stimulation test and CRH tests.

75
Q

what results would you look for in a lab to confirm the presence of cushings syndrome?

A 
inc cortsol
inc insulin
inc na+
inc glucose
inc RBC
76
Q

how do differentially diagnose cushings syndrome?

A
  • Classical ectopic ACTH syndrome is distinguished by a short history, pigmentation and weight loss, unprovoked hypokalaemia, clinical or chemical diabetes and plasma ACTH levels above 200 ng/L
  • Many ectopic tumours are benign and mimic pituitarydisease closely both clinically and biochemically.
  • Severe hirsutism/virilization suggests an adrenal tumour.
77
Q

how do you biochemically and radiological diagnose cushing’s syndrome?

A 
Adrenal CT or MRI scan..
Pituitary MRI.
Plasma potassium levels. Hypokalaemia is common with ectopic ACTH secretion. (All diuretics must bestopped.)
High-dose dexamethasone test
Plasma ACTH levels.
CRH test..
Chest X-ray
78
Q

what happens if you leave cuhsings syndrome untreated?

A

with death from hypertension, myocardial infarction, infection and heart failure.

79
Q

what should be controlled in cushings syndrome prior to surgery or radiotherapy?

A

cortisol hypersecretion

80
Q

how do you treat cushings syndrome?

A

Usual drug ismetyrapone, an 11β-hydroxylase blocker – inhibits the cortisone and corticosterone;no effect on hypothalamus and pituitary- markedincrease in ACTH in blood .
doses of 750 mg to 4 g daily in 3 to 4 divided doses.
Ketoconazole, antifungal agent (200 mg three times daily) is also used and is synergistic with metyrapone.
•Mitotane supresses glucocorticoids synthesis by direct (and unknown) mechanism on adrenal gland.
Used in treatment of adrenocortical carcinomas.
•Trilostane (which reversibly inhibits 3β-dehydrogenase) used in Cushing syndrome and primary hyperaldosteronism - occasionally used
•Aminoglutethimide inhibits the initial step in thebiosynthetic pathway and has same overall effect asmetyrapone

81
Q

what should be monitored when treating cushings syndrome?

A

Plasma cortisol should be monitored, aiming to reduce the mean level during the day to 150-300nmol/L, equivalent to normal production rates

82
Q

what are examples of diseases where glucocorticoid therapy is useful?

A

acute inflam disease
chronic inflam diseases: renal ,hepatic,bowel eye and connective tissue disorders
neoplastic diseases
miscellaneous-bell’s palsy

83
Q

what are some of the s/e of glucorticoids?

A 
Physiological
•Adrenal and/or pituitary suppression
Pathological
Cardiovascular
•Increased blood pressure
Gastrointestinal
•Peptic ulceration exacerbation
•Pancreatitis
Renal
•Polyuria
•Nocturia
Central nervous
•Depression
•Euphoria
•Psychosis
•Insomnia
endocrine
bone and muscle
skin
eyes 
inc susceptibility to infection

PHA 332 (42 decks)

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