Brainscape's Knowledge GenomeTM

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


See full index

Clinical Chemistry 3 > Lecture 4: Adrenal > Flashcards

Lecture 4: Adrenal Flashcards

You may prefer our related Brainscape-certified flashcards:
AP® Chemistry flashcards Periodic Table flashcards Chemistry 101 flashcards Organic Chemistry 101 flashcards
1
Q

Structure of the adrenal gland and what each one secretes

A
  1. Cortex
    - Glomerulosa
    -Fasciculata
    -Reticularis

Secerete …
Mineralocorticoids
Glucocorticoids
Adrenal Androgens

  1. Medulla
    - Chromaffin cells
    -Medullary veins

Secrete…
Ephinephrine
Norephinephrine

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

Where is the adrenal gland located and what does it consist of

A

The adrenal glands, located on the cephalad portion of each kidney consist of a
Cortex
Medulla

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

Structure of cortex vs medulla

A

Cortex:
Zona glomerulosa
Zona fasciculata
Zona reticularis

Medulla: Modified post-ganglionic neurons intimately connected to sympathetic neurons.

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

Adrenal regulation axis

A

Adrenal glands interact with the hypothalamus and pituitary gland in the brain.

  1. The hypothalamus makes corticotropin-releasing hormone (CRH).
  2. This stimulates the pituitary gland to make adrenocorticotropin hormone (ACTH).

3.The ACTH stimulates the adrenal glands to make and release hormonesinto the blood.

  1. Both the hypothalamus and the pituitary gland can sense whether the blood has the right amount of a hormone in it. If there is too much or too little cortisol, these glands change the amount of CRH and ACTH they release.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Adrenal function and regulation diagram (short and long term stress response)

A

Lecture Slide

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

What does the adrenal cortex make and their primary substance

A

Glucocorticoids (primarilycortisol)

Mineralocorticoids (primarilyaldosterone)

Androgens (primarily dehydroepiandrosterone and androstenedione)

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

Function of Glucocorticoids

A

Promote and inhibit gene transcription

anti-inflammatory actions

increased hepatic gluconeogenesis.

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

Function of Mineralocorticoids

A

Regulate electrolyte transport across epithelial surfaces, particularly renal conservation of sodium in exchange for potassium.

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

Glucocorticoid-Cortisol functions

A

Cortisol stimulates fat, protein and carb metabolism

Inhibits synthesis of protein in tissues.

Promotes the the use of fatty acids as energy source and decreases the use of glucose.

Stimulates gluconeogenesis

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

3 Effects on Inflammation and Immune Function (Glucocorticoid)

A
  1. Regulate adaptiveimmunityby inhibiting lymphocyte activation and promoting lymphocyte apoptosis.
  2. At high concentrations inhibit the production of B cells and T cells.

3.Glucocorticoids have potent anti-inflammatory and immunosuppressive properties.

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

Regulation Cortisol diagram

A

Lecture Slide

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

Mineralocorticoid-Aldosterone function

A

Affects the body’s ability to regulate blood pressure.

It sends the signal to organs, like the kidney and colon, that can increase the amount of sodium the body sends into the bloodstream or the amount of potassium released in the urine.

The hormone also causes the bloodstream to re-absorb water with the sodium to increase blood volume.

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

Aldosterone functions diagram

A

Lecture Slide

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

Androgen information

A

A group of chemically related sex steroid hormones.
eg The major sex hormone in men is testosterone, which is produced mainly in the testes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Adrenal insufficiency:
Primary vs secondary Where is the problem?

A

Adrenal gland lacks secretion of cortisol, aldosterone and adreanlline.

Primary (malfunction of the adrenal gland itself, as inAddison disease)

Secondary: due to lack of adrenal stimulation by issue in the pituitary or hypothalamus

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

ADDISON’S DISEASE (Primary Adrenal Insufficiency) KEY features and symptoms

A

Hypofunction of adrenal gland

In Addison’s disease,
There is increased excretion of Na and decreased excretion of K, chiefly in the urine

Low blood concentrations of Na and Cl and a high concentration of serum K result.

  1. changes in electrolyte balance,
    2.produces severe dehydration,
    3.plasma hypertonicity, 4.acidosis,
  2. decreased circulatory volume
  3. hypotension
    7.circulatory collapse.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What causes Addison disease

A

Both mineralocorticoids (aldosterone) and glucocorticoids (cortisol) are deficient.

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

Addison disease: Mineralocorticoid deficiency (aldosterone) effects…

A

Mineralocorticoids stimulate sodium reabsorption and potassium excretion:

Deficiency results in increased excretion of sodium and decreased excretion of potassium, chiefly in urine but also in sweat, saliva, and the gastrointestinal tract.

A low serum concentration of sodium (hyponatremia) and a high concentration of potassium (hyperkalemia) result.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Addison disease: Glucocorticoid deficiency (Cortisol) effects…

A

Contributes to hypotension and causes severeinsulinsensitivity and disturbances in carbohydrate, fat, and protein metabolism.

In the absence ofcortisol, insufficient carbohydrate is formed from protein; hypoglycaemia and decreased liver glycogen result.

Weakness follows, due in part to deficient neuromuscular function.

Myocardial weakness and dehydration reduce cardiac output, and circulatory failure can occur.

20
Q

Addison disease: Glucocorticoid deficiency (Cortisol) hyperpigmentation

A

Decreased cortisol blood levels result in increased pituitary ACTH production and increased blood levels of lipotropin, which has melanocyte-stimulating activity and produces the hyperpigmentation of skin and mucous membranes characteristic of Addison’s disease.

21
Q

Laboratory Findings for Addison disease

A

Abnormal serum electrolyte levels
including
1. low Na (< 130 mmol/L),
2. high K (> 5 mmol/L),
3. low HCO3 (15 to 20 mmol/L)
4. high BUN (A patient who is severely dehydrated may also have a high BUN due to thelack of fluid volume to excrete waste products)

Diagnosed by demonstrating failure to increase plasma cortisol levels, or urinary free-cortisol excretion, upon administration of ACTH (cosyntropin 5 to 250 µg IV).

Patients with Addison’s disease have low or normal values that do not rise.

22
Q

Draw the addison crisis pathway

A

Lecture slide

23
Q

SECONDARY ADRENAL INSUFFICIENCY and symptoms/effects

A

Adrenal hypofunction due to a lack of ACTH (issue at pituitary level)

No hyperpigmentation
relatively normal electrolyte levels.
NO Hyperkalaemia and elevated BUN generally are not present because of the near-normal secretion of aldosterone in these patients.

24
Q

ACTH and CRH stimulation tests for primary and secondary adrenal insufficency

A

ACTH Stimulation Test
The normal response after an injection of ACTH is a rise in blood and urine cortisol levels. Patients with either form of adrenal insufficiency respond poorly or do not respond at all.

CRH Stimulation Test
CRH stimulation test is required to determine the cause of adrenal insufficiency

Patients with primary adrenal insufficiency have high ACTHs but do not produce cortisol.

Patients with secondary adrenal insufficiency have deficient cortisol responses but absent or delayed ACTH responses. Absent ACTH response points to the pituitary as the cause; a delayed ACTH response points to the hypothalamus as the cause.

25
Q

Examples of adrenal hyperfunction

A

Hypersecretion of aldosterone results inhyperaldosteronism.

Hypersecretion of glucocorticoids results inCushing syndrome.

Hypersecretion of androgens results inadrenal virilism.

Hypersecretion ofepinephrineandnorepinephrineresults in symptoms ofpheochromocytoma.

26
Q

HYPERALDOSTERONISM or Primary Aldosteronism


What is it?
Na and K levels
Primary vs secondary

A

is a disease in which the adrenal gland(s) make too much aldosterone which leads to hypertension (high blood pressure) and low blood potassium levels.

Increases the renal distal tubular exchange of sodium for potassium and hydrogen

Progressive depletion of potassium and hydrogen leads to hypokalemia and acidosis

Excess sodium reabsorption leads to hypertension

Classification
Primary – excess secretion by the adrenal glands

Secondary – renin-mediated secretion
Seen in congestive heart failure, nephritic syndrome, cirrhosis, renal artery hypertension

27
Q

Causes of HYPERALDOSTERONISM

A

1) an adrenal tumour that autonomously secretes aldosterone;

2) unilateral or bilateral hyperplasia of the zona glomerulosa that oversecretes aldosterone;

3) or germline or somatic mutations that induce aldosterone hypersecretion

28
Q

Diagnosis of PRIMARY HYPERALDOSTERONISM

A

Initial laboratory testing consists of plasma aldosterone levels and plasma renin activity (PRA).

High plasma aldosterone>15 ng/dL

Low levels of PRA, with a ratio of plasma aldosterone to plasma renin activity>20.
Low K+ and high Na+

29
Q

Secondary Hyperaldosteronism information and examples of causes

A

Caused by something outside the adrenal glands.

Occurs in states of low effective arterial blood volume, which activates the renin-angiostensin concentration and stimulates the distal reabsorption of sodium by the kidney to restore blood volume.

Examples:
a blockage or narrowing of the renal artery
chronic liver disease
heart failure
diureticmedications

30
Q

Differential Diagnosis for primary (adenoma, hyperplasia) and secondary HYPERALDOSTERONISM

A

Lecture slide

31
Q

What is Adrenal Virilism

A

Is a syndrome in which excessive adrenal androgens cause virilisation.

32
Q

What are two ways which cause Adrenal Virilism

A
  1. Androgen-secreting adrenal tumours secrete excess androgens,cortisol, or mineralocorticoids (or all three).

2.Adrenal hyperplasia
usually congenital; delayed virilising adrenal hyperplasia is a variant ofcongenital adrenal hyperplasia.
Both are caused by a defect in production of androgens.

33
Q

Enzymes missing that cause Congenital Adrenal Hyperplasia and effects of this

A

Autosomal recessive (mutation of chromosome 6 = 21-hydroxylase enzyme impairment)
and 11 Beta hydroxylase

In these forms, precursors proximal to the enzyme block accumulate and are shunted into adrenal androgens.

The consequent excess androgen secretion causes varying degrees of virilization in external genitals of affected females; no defects are discernible in external genitals of males.

34
Q

In Congenital Adrenal Hyperplasia a decrease in cortisol secretion leads to increased ACTH production, which in turn stimulates …

A

(1) excessive synthesis of adrenal products in those pathways unimpaired by the enzyme deficiency and

(2) a build-up of precursor molecules in pathways blocked by the enzyme deficiency.

35
Q

Biochemistry enzyme pathway, what precusors are built up?

A

Lecture Slide for diagram

21-hydroxylase
= build up of progesterone
NO aldosterone

11 Beta hydroxylase
= build up of 170H progesterone and 11-deoxycortisol
SO no cortisol

36
Q

Adrenal Virilism clinical manifestation

A

Cortisol deficiency – hypoglycemia, inability to withstand stress, vasomotor collapse, hyperpigmentation, apneic spells, muscle weakness & fatigue.

Aldosterone deficiency – hyponatremia, hyperkalemia, vomiting, urinary sodium wasting, salt craving, acidosis, volume depletion, hypotension, dehydration, shock, diarrhea.

Androgen excess – ambiguous genitalia, virilization of external genitalia , hirsutism, early appearance of pubic hair, penile enlargement , excessive height gain and skeletal advance.

37
Q

Adrenal Virilism diagnosis

A

Karyotyping (determine sex chromosome)

Abdominal Ultrasound – to detect presence of uterus, cervix and vagina.

Elevated 17-hydroxyprogesterone.
The most characteristic biochemical abnormality in 21-hydroxylase deficiency is elevation of 17-hydroxyprogesterone (17-OHP), the main substrate for the enzyme.

38
Q

Adrenal Virilism complications for men and women

A

Females – suboptimal breast enlargement, late menarche, amenorrhea, irregular menses, *reduced insulin sensitivity, PCOS

Males – oligospermia, testicular tumor

39
Q

Hypercortisolism
: CUSHING’S SYNDROME caused by

A

A constellation of clinical abnormalities due to chronic exposure to excesses of cortisol or related corticosteroids.

Hyperfunction of the adrenal cortex may be:

ACTH- independent
eg, production of cortisol by an adrenocortical adenoma or carcinoma.

ACTH-dependent hyperfunction of the adrenal cortex may be due to

  1. hypersecretion of ACTH by the pituitary gland
  2. secretion of ACTH by a nonpituitary tumor, such as small cell carcinoma of the lung (the ectopic ACTH syndrome)

3.administration of exogenous ACTH.

40
Q

Clinical Symptoms of Cushing

A

Thinning hair
Thin skin
Amenorrhea
Diabetes
Moon face
central obesity
Hypertension
Adrenal hyperplasia
Muscle weakness
Osteoporosis

41
Q

Cushing Pathophysiology and effects on feedback loop

A

Caused by a benign monoclonal pituitary corticotroph adenoma that secretes excessive ACTH which causes supraphysiological secretion of glucocorticoids from the adrenal glands.

The excess circulating cortisol disrupts the normal physiological diurnal variation in cortisol levels and exerts negative feedback inhibition on CRH secretion from the hypothalamus.

42
Q

Diagnostic tests for Cushing and what general result for someone with Cushing

A
  1. Measurement of midnight plasma cortisol or late-night salivary cortisol
    Elevated cortisol between 11:00 p.m. and midnight appears to be the earliest detectable abnormality in many patients with this disorder. Cortisol secretion is usually very low at this time of the day
  2. 24-hour urinary free cortisoltest
    Reflect the cortisol secretion throughout an entire day. Although most patients with Cushing’s have elevated levels of urine free cortisol, mild Cushing’s syndrome will have normal levels of urine free cortisol.

3.Dexamethasone suppression screeningtest.
Dexamethasone is a synthetic steroid that should suppress the cortisol production in normal subjects to a very low level.
Measures whether ACTH secretion by the pituitary can be suppressed.
Dexamethasone is given and levels of cortisol are measured.
Cortisol levels should decrease in response to the administration of dexamethasone (either low dose (1mg) followed by high dose (8mg)

43
Q

Causes of ACTH-dependent disease and ACTH-independent disease

A

ACTH-dependent disease:
1. Pituitary Adenoma
a small tumour causes increased ACTH production.

2.Ectopic ACTH-producing Tumour
tumour outside of the pituitary is making too much ACTH (eg small cell lung carcinoma)

ACTH-independent Disease
adrenal glands are hyperactive or there is an adrenal tumour that is making too much cortisol.

44
Q

The two flowcharts to diagnose Cushing based on tests

A

Lecture Slide

45
Q

Why is high dexamethasone performed after low dose? In relation to ACTH independent and dependent causes of cushing

A

If there is suppression of ACTH and cortisol after low dose, this means that there is no abnormality in pit gland causing excess ACTH production as a low dose can reduce secretion, suggestion its ACTH independent (adrenal source) (no hyperscretion of ACTH). However, if ACTH is not decreased then there is too much ACTH secretion to be suppressed by the low dose, suggesting its from pit gland/ectopic (issue of hypersecretion of ACTH). So if high dose suppresses ACTH/cortisol then it was enough to suppress the ACTH thus Pit gland issue. If it cant be suppressed, then there is an extra source of ACTH secretion compensating for the high secretion at pit gland suppressed by high dose. But the high dose doesnt target other ACTH sites thus can cause high cortisol (ectrophic).

46
Q

why does BUN increase in Addison’s disease

A

The most consistent finding is elevated blood urea nitrogen (BUN) and creatinine due to the hypovolemia, a decreased glomerular filtration rate, and a decreased renal plasma flow.

47
Q

Why does Cushing’s cause
Central obesity/moon face/fat around base of neck
Diabetes
osteoporosis
Thin skin
Striae

A

Cortisol affects carb, protein and fat metabolism, increase use of fatty acids for energy and increase gluconeogenesis to increase blood sugar levels. Cushing’s causes excess cortisol levels and therefore ENHANCED metabolism of fat, carb and protein causing a greater stimulation of appetite causing the weight gain (central obesity, moon face and fat around the neck) and the effect of glucocorticoids to promote deposition of visceral fat.

This also causes diabetes where the high level of cortisol causes MORE gluconeogenesis and therefore more blood glucose leading to diabetes. Further, with the use use of fatty acids as energy source and decreases the use of glucose causes glucose to remain in the blood.

Excess glucocorticoids increase bone resorption and decrease bone formation and acts to depress intestinal calcium absorption and increase urinary calcium excretion

Cortisol causes the breakdown of some dermal proteins along with the weakening of small blood vessels. This causes the skin to become very sheer
Striae due to the weight gain stretching the thin skin which is prone to bruising

Clinical Chemistry 3 (11 decks)

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