Physio: Adrenal Gland Flashcards

(70 cards)

1
Q

Which statement accurately describes the anatomical shape of the adrenal glands?
a) Both adrenal glands are semilunar in shape.
b) The right adrenal gland is semilunar, and the left is pyramidal.
c) The right adrenal gland is pyramidal, and the left is semilunar.
d) Both adrenal glands are pyramidal in shape.

A

c) The right adrenal gland is pyramidal, and the left is semilunar.

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2
Q

Which hormone is primarily secreted by the zona glomerulosa?
a) Cortisol
b) Dehydroepiandrosterone
c) Aldosterone
d) Adrenaline

A

c) Aldosterone

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3
Q

Glucocorticoids are primarily secreted by which zone of the adrenal cortex?
a) Zona glomerulosa
b) Zona fasciculata
c) Zona reticularis
d) Adrenal medulla

A

b) Zona fasciculata - Cortisol

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4
Q

Which of the following hormones is the main representative of glucocorticoids?
a) Aldosterone
b) Cortisol
c) Dehydroepiandrosterone
d) Noradrenaline

A

b) Cortisol

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5
Q

Androgens are primarily secreted by which zone of the adrenal cortex?
a) Zona glomerulosa
b) Zona fasciculata
c) Zona reticularis
d) Adrenal medulla

A

c) Zona reticularis

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6
Q

What is the main representative androgen produced in the adrenal cortex?
a) Testosterone
b) Estradiol
c) Aldosterone
d) Dehydroepiandrosterone

A

d) Dehydroepiandrosterone

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7
Q

Which hormone stimulates the synthesis of corticosteroids from cholesterol in the adrenal cortex?
a) CRH
b) ACTH
c) Aldosterone
d) Adrenaline

A

b) ACTH

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8
Q

Corticosteroids exert their physiological effects by binding to which type of receptor?
a) Plasma membrane receptors
b) Cytosolic receptors
c) Nuclear receptors only
d) Cell surface tyrosine kinase receptors

A

b) Cytosolic receptors

Also intracellular receptors

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9
Q

Following binding to its receptor, the hormone-receptor complex for corticosteroids translocates to which cellular compartment to influence gene expression?
a) Endoplasmic reticulum
b) Golgi apparatus
c) Mitochondria
d) Cell nucleus

A

d) Cell nucleus.. and attaches to the DNA to stimulate synthesis of proteins

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10
Q

Lipid-soluble hormones like corticosteroids are primarily transported in the blood in what form?
a) Free (dissolved) form
b) Bound to carrier proteins
c) Encapsulated within vesicles
d) Bound to red blood cells

A

b) Bound to carrier proteins

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11
Q

Why must lipid-soluble hormones like corticosteroids dissociate from carrier proteins at the target tissue?
a) Carrier proteins are rapidly degraded by enzymes.
b) Only the free hormone fraction can penetrate the vascular endothelium.
c) The receptor only binds to the protein-bound form.
d) Dissociation activates the hormone.

A

d) Dissociation activates the hormone.

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12
Q

Aldosterone controls the homeostasis of which two electrolytes?
a) Calcium and Phosphate
b) Sodium and Potassium
c) Chloride and Bicarbonate
d) Magnesium and Sulfate

A

b) Sodium and Potassium

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13
Q

In the kidney, aldosterone primarily acts on cells located in which structure?
a) Proximal convoluted tubule
b) Loop of Henle
c) Distal convoluted tubule
d) Cortical collecting ducts

A

c) Distal convoluted tubule — Transcellular pathway

Proximal tubule and loop of henle — Paracellular pathway

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14
Q

Aldosterone affects Na+ reabsorption and K+ secretion by changing the activity of which cells in the cortical collecting ducts?
a) Principal cells
b) Intercalated cells
c) Podocytes
d) Mesangial cells

A

a) Principal cells

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15
Q

Aldosterone increases Na+ reabsorption in principal cells by increasing the synthesis of which proteins?
a) Aquaporins
b) Na+-K+ ATPase, ENaC, and ROMK
c) H+-ATPase and HCO3-/Cl- antiporter
d) Sodium-glucose cotransporters

A

b) Na+-K+ ATPase, ENaC, and ROMK

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16
Q

Aldosterone increases H+ secretion by changing the activity of which cells in the cortical collecting ducts?
a) Principal cells
b) Intercalated cells
c) Juxtaglomerular cells
d) Macula densa cells

A

b) Intercalated cells

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17
Q

Aldosterone increases H+ secretion in intercalated cells by increasing the synthesis of which protein?
a) Na+-K+ ATPase
b) ENaC channel
c) H+-ATPase
d) ROMK channel

A

c) H+-ATPase

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18
Q

Which of the following factors is considered less important in controlling aldosterone secretion by the adrenal cortex compared to others listed in the source?
a) Plasma Na+ and K+ levels
b) Renin-angiotensin-aldosterone system
c) Adrenocorticotropic hormone (ACTH)
d) Plasma glucose levels

A

d) Plasma glucose levels

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19
Q

Reduced plasma Na+ levels stimulate aldosterone secretion via what mechanism?
a) Positive feedback
b) Negative feedback
c) Feed-forward loop
d) Paracrine signaling

A

b) Negative feedback

Reduced plasma Na+ levels stimulate aldosterone secretion, which in turn leads to increased Na+ reabsorption leading to increase in Na+ levels in the blood

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20
Q

Increased plasma K+ levels stimulate aldosterone secretion, which in turn leads to increased K+ excretion. This is an example of what type of regulation?
a) Positive feedback
b) Negative feedback
c) Autocrine signaling
d) Allosteric modulation

A

b) Negative feedback

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21
Q

Explain the Renin- angiotensin- aldosterone system.

A

Angiotensin —> Renin —> Angiotensin I —> ACE —> Angiotensin II.

Angiotensin II stimulates the Adrenal cortex —> Aldosterone > decreases Na+ H2O excretion > increase blood plasma levels.

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22
Q

Hypoaldosteronism is associated with which of the following electrolyte imbalances?
a) Hypernatremia and hypokalemia
b) Hyponatremia and hyperkalemia
c) Hyponatremia and hypokalemia
d) Hypernatremia and hyperkalemia

A

b) Hyponatremia and hyperkalemia

Decrease Na+ reabsorption > leads to increase Na+ in urine > hypoatremia

Decrease K+ secretion > decrease k+ excretion > increase K+ in blood

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23
Q

A consequence of reduced aldosterone secretion is increased diuresis. This is primarily due to:
a) Decreased ADH secretion.
b) Na+ loss creating an osmotic gradient for water.
c) Increased glomerular filtration rate.
d) Reduced responsiveness of collecting ducts to ADH.

A

b) Na+ loss creating an osmotic gradient for water.
Thus, decreasing CO, blood volume and BP.

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24
Q

Metabolic acidosis is a clinical manifestation of hypoaldosteronism due to which effect on kidney tubules?
a) Decreased HCO3- reabsorption
b) Increased H+ secretion
c) Decreased H+ secretion
d) Increased NH4+ excretion

A

b) Increased H+ secretion .. decrease in H+ excretion leading to H+ accumulating in the body.

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25
Primary hyperaldosteronism (Conn's disease) is usually a consequence of: a) An aldosterone-secreting adenoma of the adrenal gland. b) A pituitary tumor secreting ACTH. c) Over-activation of the RAAS due to renal artery stenosis. d) Hypoproteinemia related to liver cirrhosis.
a) An aldosterone-secreting adenoma of the adrenal gland. B- Secondary hyperaldo C- Tertiary hyperaldp
26
The secretion of cortisol is stimulated by ACTH, which is released from the anterior pituitary. The release of ACTH is controlled by: a) Aldosterone b) Dehydroepiandrosterone c) Corticotropin-releasing hormone (CRH) in the hypothalamus. d) Adrenaline from the adrenal medulla.
c) Corticotropin-releasing hormone (CRH) in the hypothalamus.
27
Cortisol inhibits the secretion of ACTH and CRH. This is an example of what type of regulation? a) Positive feedback b) Negative feedback c) Autocrine signaling d) Paracrine signaling
b) Negative feedback
28
Cortisol secretion exhibits a strong diurnal rhythm, normally peaking at what time? a) Late evening b) During sleep c) Early morning d) Midday
c) Early morning
29
Cortisol secretion is markedly increased in response to which condition? a) Rest and relaxation b) Low blood glucose c) Stressful conditions d) High plasma sodium
c) Stressful conditions
30
The majority of cortisol in blood plasma is transported bound to: a) Albumin only b) Red blood cells c) Corticosteroid-binding globulin (transcortin) d) Beta-globulins
c) Corticosteroid-binding globulin (transcortin)
31
Cortisol increases blood glucose levels primarily by stimulating which process in the liver? a) Glycogenesis b) Glycogenolysis c) Gluconeogenesis d) Glycolysis
c) Gluconeogenesis
32
Cortisol stimulates protein catabolism in skeletal muscle, releasing amino acids into the blood. These amino acids are then used by the liver for: a) Protein synthesis b) Urea cycle c) Gluconeogenesis d) Ketogenesis
a) Protein synthesis
33
Cortisol stimulates lipolysis in adipose tissue, releasing free fatty acids. These fatty acids are used as metabolic fuel, thereby sparing glucose. This contributes to: a) Hypoglycemia b) Hypolipidemia c) Hyperglycemia d) Hypoproteinemia
c) Hyperglycemia
34
Cortisol has anti-inflammatory effects. It does this by inhibiting which enzyme responsible for forming arachidonic acid? a) Cyclooxygenase (COX) b) Lipoxygenase (LOX) c) Phospholipase A2 (PLA2) d) Nitric oxide synthase (NOS)
c) Phospholipase A2 (PLA2) Also, inhibits the formation of leukocytes and stimulates the formation of lysomal membrane.
35
Cortisol reduces the number of circulating T cells, inhibits antibody production, and inhibits cytokine release. These effects contribute to its use in treating: a) Bacterial infections b) Hypertension c) Autoimmune diseases d) Hypoglycemia
c) Autoimmune diseases
36
Cortisol increases blood pressure by increasing the expression of which receptors in the heart and vessels? a) Cholinergic receptors b) Serotonergic receptors c) Adrenergic receptors d) Dopaminergic receptors
c) Adrenergic receptors Vasoconstriction > increases BP, CO
37
Which condition is associated with hypercortisolism resulting from a pituitary tumor secreting large amounts of ACTH? a) Addison's disease b) Conn's disease c) Cushing's disease d) Adrenogenital syndrome
c) Cushing's disease
38
State the causes of the following: A) primary hypercortsolism B) secondary hypercort C) tertiary hypercort
Primary — tumor in adrenal cortex — increase cortisol Secondary — tumor in pituitary gland — increase ACTH Tertiary — tumor in hypothalamus — increase CRH, ATCH and cortisol
39
Clinical manifestations of Cushing's syndrome related to fat redistribution include: a) Generalized obesity with thin extremities. b) Muscle hypertrophy in the extremities. c) Centripetal obesity, moon face, and buffalo hump. d) Loss of fat from the face and neck.
c) Centripetal obesity, moon face, and buffalo hump.
40
Thinning of the skin and easy bruising observed in Cushing's syndrome are caused by: a) Increased fat deposition. b) Protein breakdown. c) Increased water retention. d) Suppressed immune response.
b) Protein breakdown.
41
Increased susceptibility to infections in Cushing's syndrome is due to: a) Hyperglycemia. b) Hypertension. c) Immunosuppressive effects of cortisol. d) Osteoporosis.
c) Immunosuppressive effects of cortisol.
42
Primary hypocortisolism resulting from structural changes (atrophy) in the adrenal cortex is observed in: a) Cushing's disease b) Conn's disease c) Addison's disease d) Adrenogenital syndrome
c) Addison's disease
43
Give some clinical presentations of Cushing’s syndrome.
Hyperglycemia Thinning of skin Muscle wasting C. Obesity Fat redistribution Hypertension Stratiea Osteoporosis Poor wound healing Emotional instability Susceptibility to infections
44
Deficiency in the production of glucocorticoids, mineralocorticoids, and androgens by the adrenal cortex is characteristic of: a) Primary hyperaldosteronism b) Secondary hypocortisolism c) Addison's disease d) Adrenogenital syndrome
c) Addison's disease
45
Explain the pathophysiology of Addison’s disease.
A disease brought on by antibodies that destroy the adrenal cortex or avoids/ blocks ACTH from binding to this receptors to initial its response.
46
The hyperpigmentation ("bronze appearance") often seen in Addison's disease is due to: a) Increased cortisol stimulating melanocytes. b) Reduced ACTH secretion. c) Increased ACTH secretion having melanocyte-stimulating hormone activity. d) Mineralocorticoid deficiency affecting skin pigmentation.
c) Increased ACTH secretion having melanocyte-stimulating hormone activity.
47
In females, adrenal androgens promote libido and are converted to: a) Progesterone b) Testosterone c) Estrogens d) Aldosterone
c) Estrogens
48
During menopause, when ovarian estrogen secretion ceases, the source of female estrogens is primarily the conversion of: a) Cortisol b) Aldosterone c) Adrenal androgens d) Pituitary gonadotropins
c) Adrenal androgens
49
In both sexes, adrenal androgens stimulate the early growth of axillary and pubic hair and contribute to the growth spurt during adolescence. Their synthesis is stimulated by: a) Gonadotropins b) Growth hormone c) ACTH d) Insulin
c) ACTH
50
Overproduction of androgens in the adrenal cortex is seen in which condition? a) Cushing's syndrome b) Addison's disease c) Conn's disease d) Adrenogenital syndrome
d) Adrenogenital syndrome
51
In adult males, overproduction of adrenal androgens typically does not induce clinical effects because: a) Adrenal androgens are only physiologically important in females. b) They are rapidly metabolized. c) Testosterone from the testes exerts much more powerful masculinizing effects. d) Negative feedback prevents their effects.
c) Testosterone from the testes exerts much more powerful masculinizing effects. What about adolescents?
52
In adult females, overproduction of adrenal androgens can lead to masculinization, including excessive growth of facial and body hair, a condition known as: a) Hyperpigmentation b) Gynecomastia c) Hirsutism d) Alopecia
c) Hirsutism
53
If overproduction of adrenal androgens develops during fetal life in females, what can be a significant consequence? a) Delayed puberty b) Development of male-pattern genitalia (e.g., enlarged clitoris). c) Development of female secondary sexual characteristics at an early age. d) Increased risk of breast cancer.
b) Development of male-pattern genitalia (e.g., enlarged clitoris).
54
Adrenogenital syndrome is often caused by a deficiency of enzymes involved in the synthesis of: a) Aldosterone b) Cortisol c) Adrenal androgens directly d) Catecholamines
b) Cortisol
55
In adrenogenital syndrome caused by cortisol synthesis deficiency, ACTH secretion is markedly increased because: a) ACTH stimulates androgen production. b) Only cortisol can inhibit ACTH secretion via negative feedback. c) Increased androgens stimulate ACTH release. d) Enzyme deficiency directly stimulates the pituitary.
d) Enzyme deficiency directly stimulates the pituitary. Only cortisol can inhibit ACTH secretion therefore because cortisol (hormone) is not secretion, secretion of ACTH will continue > increase androgens
56
Patients with adrenogenital syndrome may be sterile because increased adrenal androgens inhibit the secretion of: a) ACTH b) Cortisol c) Pituitary gonadotropins d) Aldosterone
c) Pituitary gonadotropins
57
The adrenal medulla secretes which hormones? a) Aldosterone and Cortisol b) Adrenaline and Noradrenaline c) Androgens and Estrogens d) CRH and ACTH
b) Adrenaline and Noradrenaline
58
Catecholamines from the adrenal medulla are released into the blood upon stimulation of what? a) Parasympathetic fibers b) Preganglionic sympathetic fibers c) Postganglionic sympathetic fibers d) Somatic motor neurons
b) Preganglionic sympathetic fibers
59
Catecholamines, adrenaline and noradrenaline, are synthesized from which amino acid? a) Tryptophan b) Glycine c) Tyrosine d) Alanine
c) Tyrosine
60
Catecholamines, being water-soluble hormones, act through stimulation of what? a) Intracellular receptors b) Cytosolic receptors c) Plasma membrane receptors d) Nuclear receptors
c) Plasma membrane receptors
61
According to the source, what is the approximate percentage of adrenaline released compared to noradrenaline from the adrenal medulla? a) 20% adrenaline, 80% noradrenaline b) 50% adrenaline, 50% noradrenaline c) 80% adrenaline, 20% noradrenaline d) 95% adrenaline, 5% noradrenaline
c) 80% adrenaline, 20% noradrenaline
62
Which subtype of beta-adrenergic receptor exhibits a greater affinity for adrenaline than for noradrenaline? a) Beta1-AR b) Beta2-AR c) Beta3-AR d) Alpha1-AR
b) Beta2-AR Beta1– same affinity for both Beta 3 — greater affinity for noradrenaline
63
Stimulation of Beta2-adrenergic receptors in the liver contributes to metabolic changes that increase blood glucose levels, specifically through: a) Stimulation of glucose uptake b) Inhibition of glycogenolysis c) Stimulation of gluconeogenesis d) Decreased plasma free fatty acids
c) Stimulation of gluconeogenesis Increase conversion of glycogen
64
In the pancreas, catecholamines exert a net inhibitory effect on insulin release. This effect prevails over Beta2-AR-mediated increase and is mediated by stimulation of which receptor subtype in pancreatic beta-cells? a) Alpha1-AR b) Alpha2-AR c) Beta1-AR d) Beta3-AR
b) Alpha2-AR
65
Which adrenergic receptor subtype, found in adipose tissue, is primarily responsible for mediating lipolysis induced by catecholamines? a) Alpha1-AR b) Alpha2-AR c) Beta1-AR d) Beta3-AR
d) Beta3-AR Results in increase plasma concentration of free fatty acids, which are used as alternative fuel. Fat catabolism results in thermogenesis, playing a important role in adapting to cold environments
66
According to the source, which of the following is listed as an adrenergic response that contributes to the fight-or-flight response? a) Decreased heart rate b) Vasoconstriction in skeletal muscle c) Bronchodilation d) Reduced blood pressure
c) Bronchodilation Other responses — Increase CO, BP, HR Vasodilation of skeletal muscles Dilation of pupil Increase blood glucose levels
67
Alpha1-adrenoreceptor stimulation in the radial muscle of the iris in the eye results in: a) Miosis (pupil constriction) b) Mydriasis (pupil dilation) c) Accommodation d) Decreased intraocular pressure
b) Mydriasis (pupil dilation)
68
Stimulation of Beta2-adrenergic receptors in the skeletal muscle contributes to metabolic changes that increase blood glucose levels, specifically through: a) Stimulation of glucose uptake b) Inhibition of glucose uptake c) Stimulation of gluconeogenesis d) Decreased plasma free fatty acids
b) Inhibition of glucose uptake
69
Alpha1-adrenoreceptor stimulation in the Vascular smooth muscle cells results in?
Vasoconstriction > increase BP
70
Alpha2-adrenoreceptor present in Presynaptic sympathetic terminals is involved in what response?
Negative feedback regulation of noradrenline release.