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BDS2 - endocrinology > Steroids > Flashcards

Steroids Flashcards

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1
Q

what are the main adrenal issues

A

• Destruction of adrenal tissue
○ Addison’s Disease

• Excess adrenal action
○ Cushing’s Disease

• Therapeutic corticosteroids
○ Suppression of adrenal action
○ Steroid adverse effects

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2
Q

what are the different areas of the adrenal gland and what do they produce

A

• Zona glomerulosa
○ Aldosterone
§ (renin / angiotensin)

• Zona fasicularis 
○ Cortisol 
	§ Hypothalamus / pituitary 
	§ Controlled by negative feedback loop system
	§ Released by pituitary production …

• Zona reticularis
○ Adrenal androgens

the zonas are found in the cortex of the adrenal gland histologically
the zona reticularis is the closest to the medulla

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3
Q

what are the 2 main parts to the adrenal gland

A

outer cortex

inner medulla

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4
Q

explain adrenal regulation

A

hypothalamus causes CRH to have positive affect on the pituitary gland (i think - picture isn’t clear lol) and this produces ACTH which has a positive effect on the adrenal cortex which then produces DHEA, aldosterone and cortisol which then triggers the negative feedback loop which acts on the hypothalamus and the pituitary gland

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5
Q

explain adrenal hormones

A

• Largely the same compound but tweaked differently - a small change can alter the shape
○ Synthetically very similar but quite different
○ They all tend to come broadly from cholesterol (same precursors)

• Some people are lacking certain metabolic enzymes
○ Eg no progesterone then cannot make cortisol but can make more of another

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6
Q

what is the function of aldosterone

A

Salt and water regulation
○ Enhances sodium (Na+) reabsorption and potassium (K+) loss
○ Renin-angiotensin system
○ Indirect effect on blood pressure
§ Part of blood pressure control system as Angiotensin 2 increases blood pressure
○ Released from adrenal gland
End product of renin-angiotensin system

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7
Q

how is the action of aldosterone inhibited

A

inhibited / reduced in effect by:

○ ACE inhibitors 
§ Angiotensin converting enzyme inhibitors
§ Side effects
	□ Cough
	□ Angio-oedema 
	□ Oral lichenoid drug reactions

○ AT2 blockers
§ Angiotensin 2 reduced availability to work
§ Block angiotensin receptor
□ Sits on receptor and then nothing can get in to make the blood vessel constrict
□ Tends to be very effective against blood pressure

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8
Q

what is angio-oedema

A
  • Sudden onset tissue fluid
  • Complement system firing off gives the features you expect with inflammation
    ○ This system can fire off for no reason
    ○ Caused by the complement cascade instead of being caused by bacteria or tissue damage
  • There is nothing harmful in the tissues but they react as if they are (inflammation)
  • Causes fluid and blood changes
  • Lasts an hour or so
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9
Q

what is a lichenoid reaction

A
  • ACE inhibitor has caused a tissue reaction
  • Yellow bits are lost epithelium
  • Common for dentist to ask the patient’s GP to change the patient’s medication from a ACE inhibitor to AT2 blocker - This allows you to control blood pressure without this side effect
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10
Q

name a drug acting on angiotensin

A

Losart 50

= Losartan Potassium INN 50mg

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11
Q

what is cortisol

A

• natural Glucocorticoid
• “physiological” steroid effects
• Doesn’t work through the surface receptor
○ The receptor will take the steroid into the nucleus where it changes the protein transcription
○ Steroids work within the cell
• Works inside the cell nucleus

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12
Q

how is cortisol released in the body

A

• Circadian release - nocturnal peak
○ Release more at night time than during the day
§ This is why you grow more when you are asleep than when you are awake

○ If you want to measure a hormone that naturally has a variation then:
§ Know level at time of day
Or
§ Take samples all at the same time of day to have a way of measuring
□ Difficult

Cortisol is present in your blood at normal levels

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13
Q

what are the physiological steroid effects of cortisol

A

○ Antagonist to insulin
§ Glucogenesis, fat and protein breakdown
§ Makes it harder for insulin to do what insulin does □ Cortisol makes it difficult for glucose to move into cells

○ Lowers the immune reactivity
§ Makes system less excitable than it would otherwise be (duller than it should be)

○ Raises blood pressure

○ Inhibits bone synthesis
§ Makes bone less enthusiastically - Cortisol makes bone production gradually reduce

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14
Q

explain cortisol control

A

stressors act on the hypothalamus to release CRH
this has a positive impact on the pituitary gland and this releases ACTH
ACTH has a positive effect on the adrenal gland
which then produces cortisol which then inhibits CRH

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15
Q

name therapeutic steroids

A
  • Hydrocortisone (cortisol equivalent = 1)
  • Prednisolone (4)
  • Triamcinolone (5)
  • Dexamethasone (25)
  • Betamethasone (30)
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16
Q

explain prednisolone in terms of hydrocortisone and the problems that arises with therapeutic steroids

A
  • 5mg prednisolone = 20 mg hydrocortisone
    ○ 4 times more potent than cortisol
    ○ Switch off negative feedback to make any more

○ Problems:
§ Swap natural cortisol and its effect on hypothalamus
§ Switches off release of ACTH □ Appropriate if you have enough and you don’t want anymore
§ However, when you stop taking the tablets then the adrenal system needs to switch back on again

So if you take tablets for a while then the adrenal gland isn’t used to it for a while so it shrivels up a little and when you stop it takes a bit longer to get the system back into action again

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17
Q

explain adrenal suppression

A

dexamethasone suppression of ACTH release

DXM mimics effect of cortisol so reduce the CRH release which acts on the anterior pituitary gland
this means ACTH release is reduced acting on the adrenal cortex
as a result cortisol release is reduced as well

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18
Q

what are the positive effects of therapeutic steroids

A

• Enhanced glucocorticoid effect
○ Not just doing what cortisol will do but doing much more than you would expect

• Enhanced mineralocorticoid effect
○ Salt and water retention
○ Hypertension
○ Mimics aldosterone but is not the same shape

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19
Q

what are the adverse effects of therapeutic steroids

A

○ Hypertension

○ Type 2 diabetes
§ Antagonist effect of insulin □ Raise insulin secretion to keep blood glucose normal
§ More insulin needed for blood sugar to be constant the the quicker you get type 2

○ Osteoporosis

○ Increased infection risk

○ Peptic ulceration
§ Stop prostaglandin secretions and this changes mucous secretion layer in the stomach
§ Steroid tablet - risk for months / years, some changes in weeks but will go back to normal □ Amount given is important

○ Thinning of the skin

○ Easy bruising

○ Cataracts and glaucoma

○ Hyperlipidaemia (atherosclerosis)

○ Increased cancer risk

○ Psychiatric disturbance

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20
Q

explain adrenal dysfunction in terms of hyperfunction

A

Hyperfunction - too much

○ Glucocorticoids - Cushing’s Syndrome = High level of cortisol in blood
§ Adrenal tumour - primary
§ Pituitary tumour - secondary
□ Producing ACTH = makes lots of cortisol

○ Aldosterone - Conn’s Syndrome
§ Adrenal tumour - Lots of aldosterone

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21
Q

explain adrenal dysfunction in terms of hypofunction

A

Hypofunction - too little

○ Addison’s disease - primary
§ Not enough function
§ Gland itself is damage or destroyed and cannot produce cortisol

○ Pituitary failure - secondary
§ Cannot ask pituitary to make it

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22
Q

what is cushings syndrome

A

Cushings Syndrome [F 4:1 M]

○ Cushing’s disease
§ Pituitary tumour (ACTH)
□ Secondary to this is high levels of cortisol
§ 70% spontaneous Cushing’s patients

○ Adrenal adenoma or hyperplasia

○ Ectopic ACTH production
§ Some lung tumours
□ Produce as a by product of a hormone similar to ACTH
□ Causes a lot of cortisol to be produced

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23
Q

what is conn’s syndrome

A
  • Adrenal tumour

* Adrenal hyperplasia

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24
Q

what are the signs of cushing’s syndrome

A 
○ Centripetal obesity
	§ Moon face
	§ Buffalo hump
○ Hypertension
○ Thin skin and purpura 
○ Muscle weakness
○ Osteoporotic changes and fractures
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25
what are the symptoms of cushing's syndrome
○ 'diabetes mellitus' features § Thirsty § Peeing a lot § Tired ○ Poor resistance to infections § Fungus infection □ Candida more likely (cannot fight as well) ○ Osteoporotic changes § Back pain § Bone fractures § Get this early in life ``` ○ Psychiatric disorders § Depression § Emotional lability § Psychosis § Affects how the brain works □ Get agitated □ Can't sleep ``` ○ Hirsutism ○ Skin and mucosal pigmentation § Happens due to ACTH ○ Amenorrhoea, impotence & infertility § Related to the fact that adrenal antigens are similar chemically to the glucocorticoids § Starts interfering with adrenal antigens
26
what is abdominal striae
thinning of the skin skin stretches, leaves stretch marks bruising and bleeding under the surface
27
what does a buffalo hump change (cushing's disease)
how fat is distributed / stored
28
in the protein sequence containing ACTH, what other segment is found within the ACTH segment and what effect does it have on the body
melanocyte protein segment is found within the ACTH segment | so if the patient has high levels of ACTH then they will start to develop pigmentation of the skin and mucosa
29
what are causes of adrenal hypofunction
``` Gland failure ○ Autoimmune gland destruction § Eg type 1 diabetes § Affects western world more - part of specific organ diseases ○ Infection § Affects the world as a whole more § Tuberculosis - gets into adrenal gland and causes problems ○ Infarction ``` ``` Pituitary failure ○ Compression from adenoma ○ Sheehan's syndrome § Very sudden drop in blood pressure § Patient's pituitary gland doesn’t work as well ```
30
describe the onset of addison's disease
usually slow onset | takes months to develop
31
dont know what this means but it sounds important to know about addison's disease
• Autoimmune adrenalitis (90%) ○ Organ-specific autoimmune disease ○ Thyroid, diabetes mellitus, pernicious anaemia
32
what are the signs of addison's disease
○ Postural hypotension - standing up / lying down makes you feel faint § Salt and water depletion □ Absence of aldosterone and aldosterone effects of glucocorticoids § Weight loss and lethargy □ Not retaining enough fluid so losing fat □ Fluid makes up Kg per L § Hyperpigmentation (not in secondary hypofunction) □ Scars, mouth, skin crease ® Pigmentation effect of increased ACTH secretion ® Pituitary over producing ACTH - kick cortisol out of gland ® Melanocytes stimulate hormone - pigmentation □ Vitiligo
33
what are the symptoms of addison's disease
Weakness Anorexia Loss of body hair (females)
34
how do you investigate cushing's syndrome
○ High 24 hour urinary cortisol excretion ○ Abnormal dexamethasone suppression tests § Feedback suppression of cortisol via ACTH ○ CRH tests § Cushing's disease show rise in ACTH with CRH
35
how do you investigate addison's disease
○ High ACTH level ○ Negative synACTHen test § No plasma cortisol rise in response to ACTH injection
36
what is in the diagnosis of hyperfunction in adrenal disease
``` ○ Pituitary adenoma ○ Ectopic ACTH production § High ACTH § High cortisol ○ Gland adenoma § Low ACTH § High cortisol ```
37
what is in the diagnosis of hypofunction in adrenal disease
``` ○ Pituitary failure - if pituitary gland is the problem then the gland can be okay, give injection and the cortisol levels will go up § Low ACTH § Low cortisol § Synacthen □ Positive ``` ``` ○ Gland destruction - gland is the problem and is unable to produce the cortisol (no gland to respond) § High ACTH § Low cortisol § Synacthen □ Negative ```
38
what is the treatment for adrenal hyperfunction
``` • Detect cause (adenoma) ○ Pituitary ○ Adrenal ○ Ectopic (lung) • Surgery ○ Pituitary ○ Adrenal - partial / complete adrenalectomy ```
39
what is in an addison's disease crisis
• Crisis ○ Hypotension ○ Vomiting ○ Eventual coma ○ This wont be recognised until a patient presents with a collapse (low blood pressure and low salt) § Treat with salty water § Need to replace cortisol and aldosterone that the body is not producing • Absence of mineralocorticoid and mineralocorticoid effects of glucocorticoids ○ Crisis takes time to develop ○ Hypovolaemic shock ○ Hyponatraemia
40
how do you manage addison's disease
○ Hormone replacement § Cortisol § Fludrocortisone - Mimics aldosterone takes patient from a sub normal level to a normal physiological level just replacing what the patient should have - not giving them any extra
41
how can you manage cushing's disease
too much / high levels of cortisol | remove tumour and hormone should return to normal
42
when does cortisol levels vary in the body
varies during the day, higher at night time increased by physical / psychological stress and increased by infection (body naturally produces higher cortisol if you are unwell to allow what cortisol does to be enhanced) patients need to allow for these changes
43
what is the problem if an addison's disease patient has a vomiting infection
it means they are unable to keep the tablet / steroid down to have its effect Persisting more than a few hours needs IV steroids and hospital admission give normal dose and extra to the patient (needed for infection)
44
how do you treat an addison's patient who is suffering a significant infection
double oral cortisol dose during illness | not just for a mild cold or a stressful day at work
45
what is recommended for perioperative management for patient's with addison's disease
§ For general anaesthetic need 100mg hydrocortisone on induction (BNF) □ Need more steroids to cope with physiological stress □ Anaesthetist needs to be aware of the condition § Repeat every 8 hours § Halve every 24 hours until day 5 then return to normal dose □ Managed on a fixed level of tablets eg Patients with a fractured mandible or patients needing extractions need extra steroids
46
what is important in steroid prophylaxis
• Increase the steroid dose when increased physiological requirement anticipated ○ Infection ○ Surgery ○ Physiological stress - Not psychological stress
47
how is addison's dealt with in terms of pregnancy
○ No routine increase in hydrocortisone dose ○ Labour § Double oral dose for 24 hour, Increase dose for a 'few days'
48
is steroid cover in addison's disease needed for routine restorative treatment or simple dental extractions
usually no cover needed
49
is steroid cover is addison's disease needed for minor oral surgery
give steroid prophylaxis
50
is steroid cover in addison's disease needed for spreading dental or facial infection
give steroid prophylaxis
51
why do patient's with addison's disease have a tendency to hypotension
§ Don’t have enough aldosterone so not absorbing enough water or sodium § Circulating volume drops leading to a collapse and the lack of sodium causes the patient to fit
52
why is hydrocortisone given to addison's disease patients
as physiological replacement
53
what is the reason for taking steroids therapeutically
to achieve supra-physiological levels
54
what does 10mg prednisolone equal
40mg hydrocortisone
55
why might a patient take therapeutic steroids
treatment for organ transplant, rheumatoid arthritis, cancer treatments ie taking steroids beyond the level of what the body naturally makes
56
will a short course of steroids cause problems?
no | it will not suppress cortisol production in the body
57
what is the problem with taking a large dose of steroids for a long period of time
patient's normal physiological process of negative feedback will be switched off to a certain extent the body stops making its own cortisol but you still have enough in your body due to taking the steroids the body loses the ability to make the cortisol and there is no ACTH to give the adrenal gland a kick to work so the adrenal gland withers away
58
what problems arise when someone suddenly stops taking steroids after taking a big dose for a long period of time
the physiological processes try to kick in again ACTH looks for the adrenal cortex to get it to make cortisol but the gland has withered away can take weeks or months for the adrenal cortex to respond and be active enough to make the cortisol you body normally makes / needs cortisol production suppressed - can lead to an addisonian crisis
59
what role do steroids play in dentistry
- always discuss with the patient's GP if you are unsure - no evidence that routine dental care is a risk for patients on oral therapeutic steroids ie fillings and dentures are not an issue but anything more complicated ask for advice - no evidence of harm from small short duration increase in dose
60
what are the guidelines regarding patients taking 15mg of prednisolone or more at treatment
○ No case for increased dose / cover § Cannot do a study on this - it is unethical to do a study if it puts a patient at a disadvantage to not give them steroids There is no indication to give extra as this amount is double what their physiological cortisol would be so it is fine
61
what are the guidelines regarding patients taking between 1-15mg of prednisolone at treatment
○ Cover with double oral dose if cover required § 'perioperative' period - surgery day & 2 days □ No evidence base § Low risk - have exogenous & endogenous steroids ○ Patient's adrenal gland might be suppressed so they might not be able to produce more if they have to § Takes months for the adrenal gland to stop working □ If only taking Prednisolone for 2-3 weeks then the adrenal gland should still kick in □ If taking Prednisolone for 6months the adrenal gland might take a while to work again ○ Take a cut off - so say patient is taking above physiological levels of Prednisolone (over 10mg) for 3 months assume the adrenal gland has been suppressed ○ If you suspect adrenal gland and the patient is having treatment that needs extra then double the dose but depends on the patient's level Lower down (closer to 1mg) is a higher risk as you are relying on the patient's body to kick back in
62
how do you treat patients who have just stopped taking prolonged systemic steroids in the last 3 months
○ Cover with 100mg intramuscular dose if cover required § If doing high risk procedure / patient has infection then you cannot double the dose as there is no dose so this is the treatment option then ○ If patient just stopped last week then the effect of the steroid will still be there for a while • Perioperative period - surgery day and 2 days • ALWAYS ask about STEROID use in the previous 6 months Need to know presently as well as history
63
what does an addisonian crisis evolve
due to Hypovolaemia | and Hyponatraemia
64
what is Hyponatraemia
defined as a serum sodium concentration below 135 mmol/l
65
what is Hypovolaemia
a decreased volume of circulating blood in the body
66
how quickly does addisonian crisis occur
not a quick thing | will affect down the line
67
how do you treat addisonian crisis
• Treat the problem ○ Hypovolaemia, hyponatraemia, hyperkalaemia ○ Treat by replacing fluid and sodium ``` • Fluid resuscitation ○ Saline infusions § Volume expansion with colloid if shock present ○ Corticosteroids IV § 100mg hydrocortisone every 6 hours ○ Correct hypoglycaemia § Present in crisis only ○ Treat precipitating event § Infection ``` ○ Nothing you can do about it in the dental practise § Not included in medical emergencies kit § Only thing dentist can do is recognise the patient is unwell and call an ambulance The treatment they need to get needs to be done in A&E
68
what is hyperkalaemia
hyperkalaemia is the medical term that describes a potassium level in your blood that's higher than normal
69
what steroid precautions are should be remembered when treating patients on therapeutic steroids
- Less than 3 months should be no problem with adrenal gland - More than 6 months might have adrenal suppression - More than 15mg the patient is fine - Less than 15mg might need to give more but it is hard to know as they might have adrenal suppression
70
what do you suspect in a patient with wide spread oral candida?
- Are they immunosuppressed? - Are they on steroid tablets? - Have they undiagnosed Cushing's?
71
why do you often see oral pigmentation in addison's / cushing's
○ Increasing brown pigmentation ○ ACTH levels high - Addison's - if there is no response with the gland they are still producing ACTH - Cushing's - tumour, producing lots of ACTH Often get referrals from dentists of patients with pigmentation but usually there is nothing going on
72
what are causes of oral pigementation other than addison's or cushing's
``` • Racial • Smoking • Melanotic macule ○ Freckle - isolated spot • Drugs / medicines ○ Oral contraceptive ○ Minocycline ○ Antimalarials ○ AZT • Pigmented Naevus ○ Not the same as a freckle, Thicker lesion, Not seen as often • Pregnancy • Chronic trauma • Melanoma - Sometimes a melanoma doesn’t produce any pigment at all ```

BDS2 - endocrinology (3 decks)

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