Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endocrinology > Adrenal disorders > Flashcards

Adrenal disorders Flashcards

1
Q

What is a Adrenocorticoids?

What are the three kinds?
3

A

Steroid hormones secreted by the adrenal cortex and classified by biological activity

Glucocorticoids
Mineralocorticoids
Androgens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

WHat is a Glucocorticoid?

A

primarily active in protecting against stress and in affecting protein and carbohydrate metabolism
–THINK CORTISOL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is a Mineralocorticoid?

A

Steroid hormone regulating the retention and excretion of fluids and electrolytes (especially Na and K) by the kidneys
–THINK ALDOSTERONE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is a Corticosteroid?

2

A

This term can refer to any of the steroid hormones secreted by the adrenal cortex

OR…

Steroid hormones manufactured synthetically for use as a drug (This is the way this term is used most often)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Adrenal sex hormones exert what kind of effect on sexual function?

What is an example?

A

Adrenal Sex Hormones
Exert little effect on sexual function

DHEA (dehydroepiandrosterone)
Pubertal growth of body hair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Adrenal medulla creates what?

2

A

Epinephrine

Norepinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the three layrers of the adrenal cortex and what do they make?

A

Zona Glomerulosa
-Mineralocorticoid: Aldosterone
Zona Fasciculata
-Glucocorticoids: Cortisol, Corticosterone
Zona Reticularis
-Androgens: Dehydroepiandrosterone (DHEA), Androstendione

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What cells are in the adrenal medulla and what do they make?

How do they recieve the signal to make these hormones and who do they recieve it from?

Cortisol produced in the adrenal cortex reaches the medulla in high levels causing what?

A

main source of catecholamines, epinepherine (adrenaline) and norepinepherine (noradrenaline) – hormones underlying the fight-or-flight response

Receives input from the SNS through preganglionic fibers originating in the thoracic spinal cord segments 5-11

up regulation increasing production of epinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Hypothalamus releases what which works on what?

A

Hypothalamus releases CRH which works on ant pit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Anterior pit secretes what which works on what?

A

ACTH and that works on the adrenal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does ACTH working on the adrenal do?

A

make cortisol and androgens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

When are cortisol levels the highest?

A

right away in the morning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why cant we stop steriods abruptly?

Surgery?

Epi works more where?

A

They could get adrenal insuffiency and the adrenals atrophy.

Have to have these steroids (way more) to get through the stress of the surgery. IV steriods

On the beta receptors of the heart to increase rate. (AFIB = beta blocker)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Review of Sympathetic System:
Main Functions?
5

A

think “fight or flight”

  1. Increase heart rate and blood pressure
  2. Mobilize energy stores of the body
  3. Increase blood flow to skeletal muscles and heart while diverting flow from the skin and internal organs
  4. Dilation of bronchioles
  5. Dilation of pupils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Epinephrine and Norepinephrine
interact with what kind of receptors?

Cardiovascular affects? 4

Respiratory affects?
1 but its important!!

Hyperglycemia affects? 1

Hepatocytes will do what when these are released?

A

Alpha and Beta receptors

  1. Strengthens the contractility of the myocardium (Beta1 action, inotropic action)
  2. Increases rate of contraction (Beta1 action, chronotropic action)
  3. Constricts arterioles in the skin (Alpha1 action)
  4. Dilates vessels to liver and skeletal muscle (Beta2 action)
  5. Powerful bronchodilation by acting directly on bronchial smooth muscle (Beta2 action)(This is critical to understand because it relieves all known allergic- or histamine-induced bronchoconstriction and can be life saving in the case of anaphylactic shock!!)

Lypolysis (mobilize fatty acids)

release Glucose to for the body to use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

A tumor derived from neural crest cells of the sympathetic nervous system that is responsible for about 0.1-2% of all cases of hypertension?

The tumor releases catecholamines which causes what? 8

What is the key to diagnosis? 2

How do we treat it?

A

Pheochromocytoma

episodic or sustained signs and symptoms, such as

  1. palpitations,
  2. sweating,
  3. headaches,
  4. fainting spells,
  5. tachy,
  6. flushing,
  7. cold hands and feet, and
  8. hypertensive emergencies.
  9. Its episodic/paroxismal.
  10. Will have bad headaches

A surgically correctable form of HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What medications can be used to help lower the blood pressure in the patient with Pheochromocytoma?

2

A

Can never give beta blockers alone because alpha receptors will be unopposed and will cause malignant hypertention

GIve Benoxybenzomene with an alpha blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Pheochromocytoma:
Symptoms can be described by the effects that epinephrine and norepinephrine have on the various organ systems:
Heart? (2, what are they mediated by?)

Blood vessels?
(2- what are they mediated by?)

A

Heart: Catecholamines have two major effects, each mediated by a Beta1 receptor

  1. Increased heart rate
  2. Increased contractility (or force of contraction)

Blood vessels:

  1. Vasoconstriction of cutaneous blood vessels via Alpha1 receptor
  2. Vasodilation of skeletal muscle blood vessels via Beta2 receptor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Pheochromocytoma:
90% tumor rule?
4

A
  1. 90% of the time they arise from the adrenal medulla (with the other 10% they can arise anywhere but the majority occur in the mediastinum or abdomen)
  2. 90% of the time adrenal pheochromocytoma will be unilateral (otherwise it is bilateral and is likely a genetic syndrome)
  3. 90% of the time it is not malignant
  4. 90% of the time it occurs in adults
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Lab for Pheochromocytoma?3

A

Demonstrating elevated urinary excretion of

  1. catecholamines or their metabolites (
  2. metanephrines and
  3. vanillylmandelic acid) DURING a period of hypertension
    - -24 hour urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Once diagnosis is made:
Hunt for the source
how?
2

A
  1. CT of abdomen with focus on adrenal glands or

2. MRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

If a patient had bad asthma, what would you expect would happen with her asthma symptoms during an attack from her pheochromocytoma?

A

self resolve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Aldosterone
increases what?
3

What does this regulate?
2

A

INCREASES

  1. sodium (Na) and
  2. water reabsorption by the kidneys AND
  3. increases the secretion of potassium (K),

thereby indirectly regulating 1. blood volume and
2. blood pressure
(regulates salt and water balance)

The most important Sodium retaining hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Secretion of aldosterone dictated to a much greater degree in what?

Secretion dictated minimally by what?

Decreased? 2

Increased?
3

A

in association with changes in blood pressure

adrenocorticotropic hormone from pituitary

  1. Adrenal failure,
  2. when volume is fine
  3. dehyrdation,
  4. shock,
  5. trauma
    - anytime they sense low pressure they are going to depend on sodieum to bring it back in
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What will be on the BMP if adrenal insufficieny is low?

HIgh?

A

hyperkalemia

hypokalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Blood pressure is lowereed and this is sensed by what?

When this is sensed what happens?

A

The kidneys

Release of Aldosterone via Renin- Angiotensin-Aldosterone
System

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the steps in the angiotensin-Aldosterone system?
3

Higher aldosterone equals what?

What can we block Aldosterone with?

Why do we use these?

A
  1. angiotensinogen to angiotensin 1.
  2. ACE converts Angiotensin 1 to 2.
  3. Angio 2 increased sodium absorption and kicks out potassium

aldosterone = sodium absorption.

can block ald by diuretics

use these for hypertension- get rid of volume and blood pressure will go down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What system regulates blood volume in the kidneys?

A

The kidneys provide a hormonal mechanism - regulation of blood pressure by managing blood volume - renin-angiotensin-aldosterone system of the kidneys regulates blood volume.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

When blood pressure lowers what cells scerete renin?

A

juxtaglomerular cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What does renin convert?

What does the lungs convert?

A

angiotensinogen to angiotensin I, which,

in turn, is converted to angiotensin II by the lungs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Angiotensin II activates two mechanisms that raise blood pressure. What are they?

A
  1. Angiotensin II constricts blood vessels throughout the body –> raising blood pressure. Constricted blood vessels reduce the amount of blood delivered to the kidneys, decreasing excretion of water (raising blood pressure by increasing blood volume). Hold Na and increase K
  2. Angiotensin II stimulates the adrenal cortex to secrete aldosterone, reducing urine output by increasing retention of H2O by the kidneys (increasing blood pressure by increasing blood volume).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Aldosterone works on the kidney to cause reabsorption of what?

A

Na

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q 
What happens in the presence of increased aldosterone:
Blood Volume?
Blood Pressure?
Potassium levels?
Potassium secretion in urine?

Meaning what?

A

INCREASED blood volume and blood pressure

becoming hypokalemic
INCREASED potassium excretion in the urine

hypernatremia
hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q 
What happens in the presence of decreased aldosterone:
Blood Volume?
Blood Pressure?
Potassium levels?
Potassium secretion in urine?
A

DECREASED blood volume and blood pressure

DECREASED potassium excretion in the urine

Meaning what?
hyperkalemic
hyponatremic
hypotensive

35
Q

What are some causes of decreased aldosterone?

3

A

diabetes, kidney disease, certain drugs

36
Q

What is primary aldosteronism from?

A

Occasionally, a small tumor of the zona glomerulosa cells occurs and secretes large amounts of aldosterone

37
Q
  1. What does an increase in aldosterone cause from primary aldosteronism?
  2. Sodium levels? (leads to?)
  3. Potassium levels? (leads to)
  4. Treatment for primary aldosteronism?
  5. This is pretty rare but in what kind of pt might you want to include it in the diff?
  6. What two things makes the diagnosis for primary aldosteronism (adrenal tumor?) 2
  7. What will our renin levels be?
A
  1. Therefore with primary aldosteronism we have sodium conservation and potassium excretion
  2. Hypernatremia ➔ increased volume ➔ Hypertension
  3. Hypokalemia ➔ if severe enough can cause muscle paralysis
  4. Usually surgical removal of the adrenal tumor
  5. A pretty young pt with hypertension
  6. Pretty high blood pressure and hypokalemic
  7. low or very low
38
Q

If our plasma renin activity is low in the lab what should we do?

A

A CT of the adrenals

39
Q

Zona Fasciculata secretes what?

2

A

Glucocorticoids

  1. Cortisol
  2. Corticosterone
40
Q

Cascade for the release of cortisol initiated at the level of the hypothalamus in response to the following:
7

When cortisol goes up, what does ATCH do?

A
  1. Infection,
  2. pain,
  3. hypoglycemia,
  4. trauma,
  5. hemorrhage,
  6. sleep (all of these associated with stress except for sleep)!!!

***In response to stress, perform necessary functions and are essential for survival

Aid in
7. regulating metabolic functions, essential for normal glomerular filtration

ACTH goes down. Its a negative feedback loop (when ACTH goes down, cortisol willl eventually)

41
Q

Cortisol stimulates the liver to do what?

What else does it do? 3

A

stimulates the liver to make glucose (gluconeogenesis)
this raises blood sugars

  1. Promotes protein breakdown
  2. Mobilization of fatty acids
  3. Immunologic and Antiinflammatory effects
42
Q

How does cortisol suppress the immune response? 2

How do pharmalogical doses differ than physiologic doses for cortisol?
2

It also blocks the release of what which is the precursor to prostaglandins and leukotrienes?

What will pts look like if they have a cortisol problem?

A

Suppresses immune response by reducing

  1. humoral and
  2. cell-mediated immunity

blocks inflammation by

  1. decreasing capillary permeability and
  2. stabilizing lysosomal membranes so inflammatory mediators are not released

arachidonic acid

skinny arms and great big middle

CORTISOL IS ESSENTIAL FOR SURVIVAL

43
Q

Some major adverse effects of excess glucocorticoid (cortisol) are?
6

You ABSOLUTELY have to understand these major side effects!!!!!!!!!

A
  1. Elevated glucose levels (hyperglycemia)
  2. Suppresses the immune system
  3. Decreased bone density
  4. Central nervous system and mental status effects
  5. Elevation of blood pressure
  6. Stimulate gastric acid and pepsin production
44
Q

Describe the steps in the release and regulation of cortisol.

  1. Stress excites _____?
  2. This causes the release of what?
  3. The release of the above answer stimulates what?
  4. What does this release?
  5. The release of the above stimulates what?
  6. And this releases what?
A
  1. Hypothalamus
  2. Corticotropin-releasing Hormone (CRH)
  3. Anterior pituitary
  4. Adrenocorticotropin Hormone (ACTH)
  5. Adrenal cortex
  6. Cortisol
45
Q

What does cortisol do once it is released?
6

Which ones relieve stress so that no more cortisol is released?
4

Which ones are part of the negative feedback system?
2

A
  1. Gluconeogenesis
  2. Protein metabolism
  3. Fat mobilization
  4. Stabilizes lysosomes
  5. Inhibits the anterior pituitray from releasing ACTH
  6. Inhibits the hypothalamus from releasing CRH
46
Q

Zona Reticularis
secretes what?
2

A

Androgens:

  1. Dehydroepiandrosterone (DHEA)
  2. Androstendione
47
Q

Sweeter towards the center for the adrenal cortex. Explain?

A

Glomerulosa-Salt (Mineralocorticoid)
Fasciculata -Sugar (Glucocorticoid)
Reticularis -Sex (Androgens)

Moving towards the center

48
Q

When a medical provider uses the term corticosteroid, they are most often referring to what?

Name the major adverse effects associated with excess cortisol (or of course excess exogenous steroid analogue)
6

What might happen with my potassium level if there was an excessive amount of aldosterone in my system? How about my blood pressure? And why?

Besides pts with Cushings, who else will exhibit a buffalo hump?

A

Steroid hormones manufactured synthetically for use as a drug

  1. Elevated glucose levels (hyperglycemia)
  2. Suppresses the immune system
  3. Decreased bone density
  4. Central nervous system and mental status effects
  5. Elevation of blood pressure
  6. Stimulate gastric acid and pepsin production

low K, hypertensive, Because of volume retention

pts that are on steriods will have this a lot. and puffy face

49
Q

What are cortisol levels like in cushings syndrome?

  1. What is Type 1 Cushings syndrome caused by?
  2. What is Type 2 Cushings caused by?
  3. What is Type 3 Cushings syndrome caused by?
  4. What is Type 4 Cushings caused by?

What could be another reason that causes Cushings but not very often?

Cushings syndrome is a general term for what?

A

high

  1. Excessive ACTH coming from a tumor of the pituitary. This is cushings disease (most common)
  2. bengign or malignant adrenal tumor (2nd most common type)
  3. Ectopic nonpituitary ACTH secreteing tumor. Small cell lung cancer secretes ADH and ACTH which will cause increase in cortisol
  4. iatrogenic from high dose steriod use

Excess secretion of CRH

Anytime you have hypercortisol

50
Q 
In Cushings syndrome what will the labs look like?
Serum Na?
Serum K?
Fasting Glucose?
***24h urinary free cortisol?
Serum ACTH?
A 
Na- normal
K- low
FG- high
24 hr urine- increased
ACTH- elevated
51
Q

What are the endogenous etiologies of cushings?

2 categories with 2 possibilities each

What are the Exogenous etiologies of cushings? (what pts do we see this in? 3)

A

ACTH dependent
excessive production of adrenocorticotropic hormone (ACTH)
1. (pituitary tumor)
2. Ectopic sources of ACTH (usually from small cell lung cancer)

ACTH independent

  1. Adrenal adenomas,
  2. adrenal carcinomas

Excessive steroid administration (such as with treating

  1. severe rheumatoid arthritis or
  2. systemic lupus,
  3. COPD)
52
Q

Symtpoms of Cushings disease?
8

What confirms the diagnosis of cushings?

A
  1. hypertension,
  2. moon face,
  3. buffalo hump,
  4. limb muscle wasting,
  5. abdominal obesity (body telling her to break down fat and muscle from the limbs)
  6. purple straie. ,
  7. acne,
  8. hair growth

24h urinary free cortisol was elevated which along with the clinical signs confirms the syndrome

53
Q
  1. IN Cushing’s syndrome – Cushing’s disease (ACTH dependent) where is the disease located and how do we know?
  2. In Cushing’s syndrome – Ectopic source (ACTH dependent) where is the disease and how do we know it?

How can we tell the difference?

A
  1. Anterior pituitary
    ACTH is increased
  2. Lung cancer (which produces increased ACTH and directly affects the adrenal cortex without touching the pituitary

The anterior pituitary wont shut down on normal cortisol levels. But at a gigantic dose of dexamethasone the pituitary will stop even with a tumor.
The small cell lung cancer will not though stop producing cortisol even with the large dose of dexamethazone

54
Q

In Cushing’s syndrome – Adrenal adenoma (ACTH independent) where is the disease and how do we know it?

A

Disease is at the adrenal cortex and ACTH becomes undetectable

There is so much cortisol that there wont be any ACTH at all

  • Excess cortisol from the adrenal cortex
  • GREATLY inhibits the anterior pituitary
  • GREATLY inhibits the Hypothalamus
55
Q

Cushing’s syndrome – Exogenous
is caused by what?

What happens if you take away steriods abruptly?

A

Administered glucocorticoids are in excess and GREATLY inhibit the anterior pituitary and GREATLY inhibit the hypothalamus.

anterior pituitary will completely stop working because someone is doing his job

take it away abruptly = bad. no cortisol (you need it for survival! usually only in long term steriod pts)

56
Q

What is cushings syndrome most often seen?

A

Cushing’s syndrome is most often seen from exogenous administration of glucocorticoids

57
Q

What provides the most direct and reliable practical index of cortisol secretion (sensitivity and specificity exceeds 95 and 98% respectively)?

What could cause a false negative or a false positive test result?

What else should be collected to confirm?

A

24-hour urinary cortisol excretion

Stressful setting

Urine creatinine
 Male
20-25mg/kg
Female
15-20mg/kg
58
Q

Why are we doing a 24 hour urine and not just ordering a spot cortisol?

A

Fluctuation of cortisol

59
Q

An elevated urinary cortisol just tells you the patient has steroid excess. Following this, the following may be useful:

3

A
  1. Plasma ACTH (recommended measurement between midnight and 2AM)
  2. Abdominal CT scan (looking for adrenal mass)
  3. MRI of the sella for pituitary tumor
60
Q

When is ACTH the highest?

When is cortisol the highest?

A

12-2 am

8 to 9 am

61
Q

What is the Dexamethasone Suppression Test?

A

1mg dexamethasone (a steroid) given orally in the evening… then,

Serum cortisol determination at about 8am the next AM

What should happen?
HPA axis should be suppressed with normal physiology
If cortisol is still elevated, then there is a problem.
(can differentiate b/w ectopic and pit ATCH dependant cushings)

62
Q

Adrenal insufficiency, of which there are two forms. What are they?

A

Primary adrenal insufficiency Secondary adrenal insufficiency

63
Q

What does primary adrenal insuffiency result from?

What does secondary adrenal insufficiency result from?

Tertiarty?

A

(Addison’s disease)
Results from destruction or dysfunction of the adrenal cortex

Results from inadequate stimulation of adrenal cortex by ACTH (pit)

Lack of CRH from the hypothalamus

64
Q
  1. Pathophysiology of primary adrenal insufficiency results from what most commonly?

What secretions are diminished in this condition?

How serious is this disease?

Function of what is usually spared?

  1. Secondary adrenal insufficiency
    usually occurs from what?
A
  1. autoimmune destruction of the adrenal glands (otherwise known as Addison’s disease)

BOTH glucocorticoid AND mineralocorticoid secretion diminished in this condition

May be fatal if untreated

Adrenal medulla function usually spared

  1. Usually occurs after discontinuation of exogenous steroids after prolonged suppression of the HPA (Hypothalamic-pituitary-adrenal) axis
65
Q

Adrenal Insufficiency clinical presentation?

10

A
  1. Hypotension
  2. Weight loss
  3. Increasing fatigue
  4. Vomiting
  5. Diarrhea
  6. Anorexia
  7. Muscle and joint pain
  8. Abdominal pain
  9. Postural dizziness
  10. Hyperpigmentation
66
Q

What two interetsing findings are only seen with addison’s disease?

Why do we see this?
2

A

hyperpigmentation and salt craving are only seen with Addison’s disease

increased levels of proopiomelanocortin (POMC) synthesis which is a precursor for ACTH. This POMC molecule contains melanocyte-stimulating hormone (MSH) fragments. Therefore, when POMC levels are increased, so are levels of MSH, which leads to pigmentation of the skin

With Addison’s disease (because the disease is in the adrenal gland) we have low secretion of aldosterone which leads to hyponatremia and salt craving

67
Q

FOr Primary Adrenal Insufficiency where is the disease located?

How does this affect cortisol levels?
Aldosterone levels?

So how does this affect the stimulation or inhibition of the anterior pituitary and hypothalamus?

What will our ACTH levels look like and why?

A

adrenal cortex

Low cortisol levels
Low aldosterone levels

The hypothalamus and Anterior pituitary are stimulated less

Increased levels of ACTH because of less inhibition!!

68
Q 
In Primary Adrenal Insufficiency what will our:
Renin levels be?
Pigmentation?
K levels?
Na levels?
BP?
A 
high renin
Hyperpigmentation
hyperkalemic
hyponatremia
hypotension
69
Q

Water house pendricksons syndrome is what?

A

adrenal insufficiency

70
Q

In Secondary Adrenal Insufficiency where is the disease located?

What will our ATCH levels be and what symptoms will be different than primary?

How does this affect cortisol levels?

A

Disease up in the axis (anterior pituitary), NOT at the adrenal cortex

Low ACTH, No hyperpigmentation
Relatively normal aldosterone means no salt craving

Low cortisol levels

71
Q

Laboratory considerations for adrenal insufficiency:

  1. What is the best test and what do high and low levels suggest?
  2. What about in between in a patient with characteristic signs and symptoms?
    (Whats the test and explain the results)
A
  1. AM Cortisol level

Low plasma cortisol (20ug/dL) → strong evidence against diagnosis of adrenal insufficiency

2. ACTH (cosyntropin) 
stimulation test
ACTH (cosyntropin) test
Plasma cortisol measured
IV administration of 250 ug of ACTH
In 30-60 minutes…
Plasma cortisol measured again
(If they are still low then a positive test)
72
Q

Now we know the patient has adrenal insufficiency, how do we know if it’s Addison’s or from a secondary cause?
(whats the test and what do the results mean?)

A

Plasma ACTH
Increased?
-Primary Adrenal lnsufficiency

Decreased?
-Secondary Adrenal Insufficiency (thinking mostly pituitary)

73
Q

Treatment of addisons disease?
2

What should treatment mimic?

A

Lifelong replacement of glucocorticoids AND mineralocorticoids

Treatment with glucocorticoids should mimic physiology
Doses should mimic diurnal surges with larger dose administered first thing in the AM and then a smaller dose given around 4pm

74
Q

Main problem with treatment of addisons disease is what?

When do we have to dose higher?

What might we also want to dose women with?

How do we treat an addison’s crisis?

How many days can you libe without an adrenal gland?

How can treatment with mineralocorticoids be monitored (should aim for what value?)

A

overtreating with glucocorticoids and undertreatment with mineralocorticoids

periods of stress, surgery for example

might want to give DHEA in women

Addison crisis- high dose IV steriods

How may days without an adrenal gland 4 -14

can be monitored by measuring plasma renin (should aim for value of 1 to 3)

75
Q

ACUTE Adrenal Insufficiency

(Addisonian Crisis) treatment?

A

Prompt recognition and administration of IV hydrocortisone is lifesaving
Medical Emergency and will be discussed in ER course

76
Q

What is the test of choice to screen for Cushing’s?

What might you see on a basic metabolic panel in the patient with adrenal insufficiency?

What are the two fundamentals of treatment for Addison’s disease?

A

cortisol levels, ACTH levels, dethamexasone suppression test

Hyperkalemia
Hyponatremia

Lifelong replacement of glucocorticoids AND mineralocorticoids (aldosterone)

77
Q

Prescription Corticosteroids?

2

A

Glucocorticoids

Mineralocorticoids

78
Q

Glucocorticoid drugs? 4

Whats the DOC for renal insufficiency?

Mineralcorticoid drug?
(potent ____ ____ effects?

A
  1. Hydrocortisone DOC for renal insufficiency
  2. Prednisone
  3. Methylprednisolone
  4. Dexamethasone

Fludrocortisone (aldosterone)
potent sodium retaining effect

79
Q

Prescription Corticosteroids:
Synthetic glucocorticoids differ from endogenous ones how?
Why?

A

antiinflammatory effects primarily come from pharmacologic doses (as opposed to physiologic doses)

high dose for antiinflammtory affeccts

80
Q

Therapeutic uses for corticosteriods/glucocorticoids?

4

A
  1. Relief of inflammatory symptoms
  2. Replacement for adrenal insufficiency
  3. Acceleration of lung maturation
  4. Premature babies for prophylaxis for RSV and stimulates lung growth
81
Q

Therapeutic uses for corticosteriods/glucocorticoids use for relief of inflammatory symptoms like what?
4

A

Such as with

  1. rheumatoid arthritis,
  2. asthma,
  3. allergic rhinitis,
  4. allergic reactions
82
Q 
Rx Corticosteroids Pharmacokinetics
Generally, the following apply:
Absorbed where?
Metabolized where?
Excreted where?
Doasage forms? 5
A

Oral products readily absorbed in GI tract

Metabolized by the liver and products excreted by the kidneys

Several available

  1. IV,
  2. IM, and can be used
  3. intra-articularly (joint injection)
  4. Used in inhalation form all the time
  5. PO
83
Q

Prescription Corticosteroids
Adverse affects?
7

A
  1. Osteoporosis (most common effect)
  2. Cushingoid appearance (redistribution of body fat, puffy face, etc.)
  3. Hyperglycemia
  4. Suppresses the immune system
  5. Central nervous system and mental status effects
  6. Elevation of blood pressure
  7. Stimulate gastric acid and pepsin production
84
Q

What would you recommend a patient take who is on daily oral steroids?
2

A
  1. Calcium supplements

2. Bisphosphonates (Boniva, Fosomax)

Endocrinology (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions