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Yr 2 EOYS > MET EOYS8 > Flashcards

MET EOYS8 Flashcards

1
Q

Which one of the following is aldosterone?

Mineralocorticoid
Catecholamine
Androgens
Glucocorticoid

A

Which one of the following is aldosterone?

Mineralocorticoid
Catecholamine
Androgens
Glucocorticoid

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2
Q

Which one of the following is cortisol?

Mineralocorticoid
Catecholamine
Androgens
Glucocorticoid

A

Which one of the following is cortisol?

Mineralocorticoid
Catecholamine
Androgens
Glucocorticoid

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3
Q

A 47-year-old man presents with episodes of a racing heartbeat that occur 4 to 6 times daily and are associated with sweating and facial flushing. In between episodes, he is asymptomatic. Assuming a tumor is the cause of these symptoms, how does the tumor affect blood glucose regulation?

A. Decrease serum glucose and increase insulin secretion
B. Increase serum glucose only
C. Decrease serum glucose only
D. Increase serum glucose and decrease insulin secretion

A

D. Increase serum glucose and decrease insulin secretion

Pheochromocytoma is a tumor of the adrenal medulla that causes excess catecholamine release.

Catecholamines increase glucagon secretion via beta-2 receptors and activate glycogenolysis. This results in increased serum glucose.

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4
Q

A 48-year-old man embarks on a road trip across the country and becomes stranded in Nevada when his car breaks down. He is without food or water for over 72 hours. A hormone is released from which part of the adrenal gland in response to his hydration status?
A. Zona fasciculata
B. Zona glomerulosa
C. Adrenal medulla
D. Zona reticularis

A

A 48-year-old man embarks on a road trip across the country and becomes stranded in Nevada when his car breaks down. He is without food or water for over 72 hours. A hormone is released from which part of the adrenal gland in response to his hydration status?
A. Zona fasciculata
B. Zona glomerulosa
C. Adrenal medulla
D. Zona reticularis

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5
Q

Which of the following is the underlying problem in neurogenic diabetes insipidus?

Lack of vasopressin (antidiuretic hormone)
Lack of prolactin
Lack of oxytocin
Overproduction of prolactin
Overproduction of vasopressin (antidiuretic hormone)
Overproduction of oxytocin

A

Which of the following is the underlying problem in neurogenic diabetes insipidus?

Lack of vasopressin (antidiuretic hormone)
Lack of prolactin
Lack of oxytocin
Overproduction of prolactin
Overproduction of vasopressin (antidiuretic hormone)
Overproduction of oxytocin

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6
Q

In males which hormone stimulates Sertoli cells to produce androgen binding globulin (ABG)?
Oxytocin
Follicle stimulating hormone (FSH)
Luteinizing hormone (LH)
Gonadotrophin releasing hormone (GnRH)

A

In males which hormone stimulates Sertoli cells to produce androgen binding globulin (ABG)?
Oxytocin
Follicle stimulating hormone (FSH)
Luteinizing hormone (LH)
Gonadotrophin releasing hormone (GnRH)

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7
Q

Which of the following causes of Cushing’s syndrome does the phrase “Cushing’s disease” specifically refer to?

Pituitary adenoma
Adrenal adenoma
Ectopic ACTH production
Iatrogenic

A

Which of the following causes of Cushing’s syndrome does the phrase “Cushing’s disease” specifically refer to?

Pituitary adenoma
Adrenal adenoma
Ectopic ACTH production
Iatrogenic

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8
Q

Which one of the following statements best describes an Addisonian crisis?

Severe adrenal insufficiency resulting in dangerously low serum cortisol levels
Dangerously high serum cortisol levels
Severe adrenal insufficiency resulting in dangerously low serum testosterone levels
Dangerously high levels of testosterone

A

Which one of the following statements best describes an Addisonian crisis?

Severe adrenal insufficiency resulting in dangerously low serum cortisol levels
Dangerously high serum cortisol levels
Severe adrenal insufficiency resulting in dangerously low serum testosterone levels
Dangerously high levels of testosterone

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9
Q

Oral glucose tolerance test + Growth hormone measurement

Serum IGF 1 measurement is useful to screen for acromegaly however is not ideal for diagnosis. Measuring growth hormone alone is not useful as it is secreted in a pulsatile matter therefore levels vary greatly throughout the day. The oral glucose tolerance test combined with growth hormone measurement is the ideal combination of investigations to make the diagnosis.

A

Which of the following investigations is the gold standard for diagnosing acromegaly?

Growth hormone measurement

Oral glucose tolerance test + Growth hormone measurement

Growth hormone releasing hormone measurement

Serum IGF1 measurement

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10
Q

What is the most common cause for the overproduction of growth hormone in acromegaly?

Hypothalamic lesion
Pituitary adenoma
Pituitary lesion
Hyperplasia of the pituitary stalk

A

What is the most common cause for the overproduction of growth hormone in acromegaly?

Hypothalamic lesion
Pituitary adenoma
Pituitary lesion
Hyperplasia of the pituitary stalk

In around 99% of cases, acromegaly is caused by a pituitary adenoma, specifically overgrowth of the somatotrope cells which are responsible for growth hormone production. In very rare cases acromegaly can be caused by ectopic production of growth hormone by carcinoid tumours.

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11
Q

What is Addison’s disease?

Addison’s disease is a long-term endocrine disorder in which the adrenal glands do not produce enough steroid hormones.
Addison’s disease involves the overproduction of androgens by the adrenal medulla.
Addison’s disease involves the underproduction of androgens by the adrenal medulla.
Addison’s disease involves the overproduction of cortisol and aldosterone by the adrenal cortex.

A

What is Addison’s disease?

Addison’s disease is a long-term endocrine disorder in which the adrenal glands do not produce enough steroid hormones.
Addison’s disease involves the overproduction of androgens by the adrenal medulla.
Addison’s disease involves the underproduction of androgens by the adrenal medulla.
Addison’s disease involves the overproduction of cortisol and aldosterone by the adrenal cortex.

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12
Q

What is the most common cause of Cushing’s syndrome?
Ectopic ACTH production
Glucocorticoid treatment (iatrogenic)
Adrenal adenoma
Pituitary adenoma

A

What is the most common cause of Cushing’s syndrome?
Ectopic ACTH production
Glucocorticoid treatment (iatrogenic)
Adrenal adenoma
Pituitary adenoma

The most common cause of Cushing’s syndrome is the long term use of glucocorticoid treatments (steroids). These treatments are commonly used to suppress inflammation in many diseases. If these treatments are used long term they can result in the development of Cushing’s syndrome. As a result, most steroid treatments are only given for short durations with the smallest dose possible.

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13
Q

Which enzyme is most commonly deficient in congenital adrenal hyperplasia? [1]

Which hormones does this mean are increased? [2]

A

21-hydroxylase

21-hydroxylase needed to produce cortisol and aldosterone; causes more androgens to be made

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14
Q

Which enzyme is the final step in cortisol production?

21-hydroxylase
11B-hydroxylase
5a-reductase
17B-HSD

A

Which enzyme is the final step in cortisol production?

21-hydroxylase
11B-hydroxylase
5a-reductase
17B-HSD

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15
Q

Which enzyme is the final step in testosterone production?

21-hydroxylase
11B-hydroxylase
5a-reductase
17B-HSD

A

Which enzyme is the final step in testosterone production?

21-hydroxylase
11B-hydroxylase
5a-reductase
17B-HSD

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16
Q

Which one of the following is most characteristically caused by thiazides?

Hypocalcemia
Hypercalcemia
Hyperkalaemia
Hypernatraemia

A

Which one of the following is most characteristically caused by thiazides?

Hypocalcemia
Hypercalcemia
Hyperkalaemia
Hypernatraemia

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17
Q

Side-effects include gastrointestinal upset and lactic acidosis:

Metformin
SGLT-2 Inhibitors
GLP-1 agonists
Thiazolidinediones

A

Side-effects include gastrointestinal upset and lactic acidosis (common in exams)

Metformin
SGLT-2 Inhibitors
GLP-1 agonists
Thiazolidinediones

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18
Q

What is the effect of GH on gluconeogenesis? [1]

A

Increases

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19
Q

Which type of Ig caused activation of TSH receptor in Graves Disease?

IgA
IgG
IgM
IgD
IgE

A

Which type of Ig caused activation of TSH receptor in Graves Disease?

IgA
IgG
IgM
IgD
IgE

20
Q

Relative deficiency of insulin due to an excess of adipose tissue and insulin resistance:

MODY
DMT1
DMT2
Gestational Diabetes
LADA

A

Relative deficiency of insulin due to an excess of adipose tissue and insulin resistance:

MODY
DMT1
DMT2
Gestational Diabetes
LADA

21
Q

Which one of the following actions is directly caused by cortisol?

Increases gastric motility
Decreases osteoclastic activity
Decreases renal reabsorption of phosphate
Upregulates alpha1 receptors on arterioles

A

Which one of the following actions is directly caused by cortisol?

Increases gastric motility
Decreases osteoclastic activity
Decreases renal reabsorption of phosphate
Upregulates alpha1 receptors on arterioles

22
Q

Thyrotoxicosis is most likely to present with the following blood tests:

High TSH; Low T4
Low TSH; Low T4
High TSH; High T4
Low TSH; High T4

A

Thyrotoxicosis is most likely to present with the following blood tests:

High TSH; Low T4
Low TSH; Low T4
High TSH; High T4
Low TSH; High T4

23
Q

Explain the difference in primary and secondary hyperaldosteronism

A

Primary hyperaldosteronism:
* excess production of the adrenal gland (zona glomerulosa)
* can present more commonly as a primary tumor in the gland known as Conn syndrome or bilateral adrenal hyperplasia

Secondary hyperaldosteronism:
* Excessive activation of RAAS
* renin-producing tumor, renal artery stenosis, or edematous disorders like left ventricular heart failure, pregnancy, cor pulmonale, or cirrhosis with ascites.

24
Q

Explain the difference in primary and secondary hyperthyroidism?

A

Primary hyperthyroidism:
* due to thyroid pathology

Secondary hyperthyroidism:
* the condition where the thyroid is producing excessive thyroid hormone as a result of overstimulation by thyroid stimulating hormone.
* The pathology is in the hypothalamus or pituitary.

25
Q

Describe the difference in primary, secondary & tertiary hyperparathyroidsm [3]

For each of the above, state what would be the causes [3] and what Ca2+ and PTH levels would be like [3]

A

PTH raises Ca2+ levels

Primary hyperparathyroidism:
* Parathyroid adenoma
* Paraythyroid hyperplasia
* Over-secreting PTH; high calcium

Secondary hyperparathyroidism:
* Due to low serum calcium levels as a result of another condition: commonly CKD or Vit D deficiency
* High PTH, low Ca2+

Tertiary hyperparathyroidism:
* Prolonged period of secondary hyperparathyroidism: secrete PTH autonomously
* High PTH, High Ca2+

26
Q

Smooth muscle in the gall bladder wall contracts under influence of which hormone? [1]

Where is it secreted from? [1]

A

Smooth muscle in the gall bladder wall contracts under influence of hormone cholecystokinin: from duodenum

27
Q

Which pro-inflam makers are produced when cirrhosis occurs? [3]

A

Chronic inflammation (TNF alpha, TGF beta, IL1 from Kupffer cells, endothelial cells, bile duct cells and hepatocytes)

28
Q

Explain how alcoholism can induce steatosis?

A

Alcoholism can also induce steatosis because the metabolism of ethanol produces NADH which shifts the metabolism of hepatocytes toward lipid synthesis

  • Hepatocyte swelling and necrosis
  • If chronic then fibrosis
29
Q

Name other signals that can potentiate the insulin other than last slide [6]

A
  1. Intracellular catobolsim of amino acids increases cellular ATP / ADP ratio (leucine, arginine)
  2. Fatty acids
  3. Glucagon like peptide 1 (GLP-1)
  4. Glucose-dependent insulinotropic
    peptide (GIP)
  5. PNS release of Ach
  6. CCK

(most require glucose for activation)

30
Q

What is glucagon secretion stimulated by? [3]

What is glucagon secretion inhibited by? [5]

A

Stimulated:
* Low blood glucose conc
* Increased blood A.A (especially alanine and arginine)
* Exercise

Inhibited:
* Hyperglycaemia
* GLP-1
* Somatostatin
* Insulin
* Zinc

31
Q

Explain MoA of glucagon working
- Which type of receptor does it bind to?

A
  • Glucagon receptor is a GPCR
  • Upon ligand bonding, GTP displaces GDP on the a subunit. A subunit binds to the adenyly cyclase protein to activate
  • Causes activation of Adenyly Cyclase pathway
    (pathway is a key signalling cascade activated by glucagon).
  • Causes synthesis of cAMP as a second messenger (v important!) which actiavtes protein kinase A causes phosphorylation of enzymes used for reactions to make glucose
32
Q

How does insulin switch off glucagon dependent signaliing?

A

Phosphodiesterase

33
Q

Effect of glucagon on [4]

glycogenlysis
glycogensis

At the liver: gluconeogenesis
glycolysis

A

Glucagon increases glycogenolysis
Glucagon inhibits glycogenesis

AND

At the liver: Inhibits glycolysis and increases GNG

34
Q

What is the effect of glucagon on precursors for GNG?

COME BACK

A

Glucagon increases amino acids, lactate, and glycerol intake by hepatic cells

35
Q

Catecholamines monoamines (Dopamine, norepinephrine, and epinephrine) are synthesised from which two molecules? [2]

Where? [1]

A

Adrenaline synthesised from Phenylalanine and Tyrosine

At: chromaffin cells of the adrenal medulla

36
Q

Effect of cortisol in:
a) the liver [2]
b) the muscle [2]
c) adipocytes [2]

A

(opposite of insulin; similar to glucagon)

In the liver:
* enhances gluconeogenesis
* inhibits glycogen synthesis

In muscle:
* inhibits glucose uptake/utilisation
* stimulates protein degradation

In adipocytes:
* it stimulates lipolysis
* Rapid mobilisation of glucogenic amino acids and glycerol/fatty acids from cellular stores

37
Q

Growth hormone is stimulated by the release of which hormone? [1]

Growth hormone is inhibited by the release of which hormone? [1]

A

Growth hormone:

  • stimulated by growth hormone-releasing hormone (GHRH)
  • inhibited by somatostatin (SSTN)
38
Q

What are the metabolic effects of growth hormone at:

a) liver [2]
b) sk. muscle
c) adipose tissue

A

What are the metabolic effects of growth hormone at:

a) adipose tissue:
* reduces lipogenesis
* Increases lipolysis
* Overall effect: reduces body fat mass

b) sk. muscle
* Reduces glucose uptake
* Increases b oxidation

c) liver:
* increases production and uptake of IDL, LDL and HDL

39
Q

What is the effect of growth hormone on IGF-1?

What is the effect of IGF-1 activated on renal GNG [1] and glucose transport? [1]

A

IGF1 = Insulin-like growth factor 1

GH is a regulator of IGF1, specifically it decreases renal GNG and increases glucose transport

40
Q

Thyroid hormone release causes increased basal metabolic rate. Explain how [3]

A

Increase in the number and
activity of mitochondria
* Increases the rate of ATP synthesis

Stimulation of carbohydrate metabolism
* Rapid glucose uptake
* Enhanced glycolysis and gluconeogenesis
* Increased insulin secretion

Stimulation of fat metabolism
* Lipids mobilised rapidly from fat tissue
* Increased fatty acids concentration in the plasma

41
Q

Why do follicular epithelial cells change in shape and how does this occur? [2]

A

Follicular cells - are almost columnar in appearance in some regions, whilst elsewhere they have a low cuboidal appearance.

This is because in active glands, the follicles are smaller, and have reduced colloid - the cuboidal lining cells are relatively tall because they are actively making and secreting hormones - so packed full of ER and golgi.

Hypothyroidism = squamous or cuboidal Hyperthyroidism = columnar

42
Q

What is this adrenal histopathology depicted? [1]

A

Pheochromocytoma

43
Q

Name this liver disease [1]

A

steatosis

44
Q

What is this liver pathology? [1]

A

cirrhosis

45
Q

What is this liver pathology?

A

Chronic cholecystitis characterized by gallbladder wall thickening secondary to muscularis hypertrophy, with a dilated Rokitansky-Aschoff sinus and adjacent transmural lymphoid aggregate.

Yr 2 EOYS (58 decks)

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