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Endocrine > LT Review Q's > Flashcards

LT Review Q's Flashcards

1
Q

Where does ADH act?

A

at the target site of the cortical collecting duct of the kidney

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2
Q

What does the protein aquaporin 2 (AQP2) do?

A

forms a channel that carries water molecules across cell membranes

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3
Q

diabetes incipidus is more likely to be aquired by which sex?

A

males (60%)

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4
Q

Which of the following is due to a defect in the thirst control mechanism?

a. nephrogenic diabetes insipidus
b. neurogenic diabetes insipidus
c. dipsogenic diabetes insipidus
d. gestational diabetes insipidus

A

c. dipsogenic diabetes insipidus

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5
Q

Which of the following usually resolves?

a. nephrogenic diabetes insipidus
b. neurogenic diabetes insipidus
c. dipsogenic diabetes insipidus
d. gestational diabetes insipidus

A

d. gestational diabetes insipidus

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6
Q

Which of the following is due to ADH resistance?

a. nephrogenic diabetes insipidus
b. neurogenic diabetes insipidus
c. dipsogenic diabetes insipidus
d. gestational diabetes insipidus

A

a. nephrogenic diabetes insipidus

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7
Q

Which of the following can occur due to head trauma?

a. nephrogenic diabetes insipidus
b. neurogenic diabetes insipidus
c. dipsogenic diabetes insipidus
d. gestational diabetes insipidus

A

b. neurogenic diabetes insipidus

trauma affecting the pituitary gland

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8
Q

Which of the following occurs due to interference with protein aquaporin 2 (AQP2)?

a. nephrogenic diabetes insipidus
b. neurogenic diabetes insipidus
c. dipsogenic diabetes insipidus
d. gestational diabetes insipidus

A

a. nephrogenic diabetes insipidus

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9
Q

A patient presents with polyuria and polydipsia. Which one of the following diagnostic tests would NOT suggest a diagnosis of central or pituitary diabetes insipidus?
A. Low urine osmolality and high plasma osmolality
B. High plasma sodium
C. increased urine osmolality after administration of ADH in a water deprivation test
D. low urine osmolality after administration of ADH in a water deprivation test
E. High plasma osmolality and low ADH

A

D. low urine osmolality after administration of ADH in a water deprivation test

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10
Q

Which of the following features are relevant to Addison’s disease?
A. Immunological destruction of adrenal medullar cells
B. Increased production of cortisol
C. Increased production of aldosterone
D. Immunological destruction of steroid cells in the adrenal cortex
E. Increased growth of adrenal cortex cells

A

D. Immunological destruction of steroid cells in the adrenal cortex

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11
Q

What percent of Addison’s disease are autoimmune in origin?

A

75-80% of the cases are autoimmune in origin

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12
Q

What two hormones are low in Addison’s disease?

A

cortisol and aldosterone

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13
Q

The majority of Addison’s disease is due to which autoimmune condition?

A

autoimmune adrenalitis

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14
Q

What two body antigens are targeted in Addison’s disease?

A 
21-alpha-hydroxylase
corticotrophin receptors (autoantibodies against them)
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15
Q

infiltrating lymphocytes are available when adrenal damage is mediated by

a. autoantibodies
b. cell-mediated immunity
b. both

A

b. both

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16
Q

Which is located extra-adrenally?

a. Pheochromocytoma
b. Paragangliomas

A

b. Paragangliomas

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17
Q

Which enzyme is indicative of Pheochromocytoma?

A

Phenylethanolamine N-methyltransferase (PNMT)

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18
Q

Which is the most common symptom of Pheochromocytoma?

a. pulmonary edema
b. cardiomyopathy
c. hypertension

A

c. hypertension

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19
Q

T/F: the hypertension of Pheochromocytoma is only dependant upon the amount of catecholamines in circulation

A

false, it depends on many other factors (their diffusion rate, rate of inactivation, smooth muscle reactivity, receptor sensitivity/number, renin, etc.)

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20
Q

What’s the function of Phenylethanolamine N-methyltransferase (PNMT) enzyme?

A

converts norepinephrine to epinephrine

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21
Q

How can you differentiate if the hypertension of Pheochromocytoma is due to excess renin? (what drug do you use?)

A

By seeing the effect of Captopril on hypertension. Captopril is an angiotensin-converting enzyme inhibitor (ACE inhibitor)
(if it helped then renin was the issue)

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22
Q

How could you differentiate between a patient with pheochromocytoma or one with essential hypertension?

A

plasma atrial natriuretic peptide and adrenomedullin levels increase in pheochromocytoma patients only

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23
Q

What is true in patients who got pheochromocytoma due to a hereditary familial disorder?

a. no hypertension symptoms
b. bilateral tumors
c. affects men four times as much

A

b. bilateral tumors

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24
Q

Whats the only reliable clue to suggest pheochromocytoma malignancy?

A

metastases

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25
Q

What four syndromes are associated with pheochromocytoma?

A

Multiple Endocrine Neoplasia, type 2A (MEN2A)
Multiple Endocrine Neoplasia, Type 2B (MEN2B)
Von Hippel-Lindau disease (VHL)
Neurofibromatosis type 1 (NF1)

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26
Q

Describe the headache of patients with essential hypertension

A

occipital, not temporal

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27
Q

Where are pheochromocytoma found?

a. biochemical phase
b. prebiochemical phase

A

a. biochemical phase

diagnosis is established by the biochemical confirmation of catecholamine hypersecretion

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28
Q

After pheochromocytoma presence is confirmed, what tests do you run?

A

tomography scan (CT scan) & magnetic resonance imaging (MRI)

(after catecholamine hypersecretion is confirmed, do imaging studies)

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29
Q

Which is most commonly used for preoperative control of blood pressure?

a. α- adrenoceptor blocker
b. β-adrenoceptor blocker

A

a. α- adrenoceptor blocker

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30
Q

pheochromocytoma presence is confirmed but MRI is negative, which test do you do next?

a. tomography scan (CT scan)
b. MIBG scintigraphy

A

b. MIBG scintigraphy

MIBG (metaiodobenzylguanidine) scans help locate and diagnose certain types of tumors in the body because it gathers in some tumors. When combined with radioactive iodine (tracer), it provides a way to identify primary and metastatic disease.

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31
Q

Where are incidentaloma found?

a. biochemical phase
b. prebiochemical phase

A

b. prebiochemical phase

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32
Q

Which is most commonly used for preoperative control of arrhythmias, tachycardia or angina?

a. α- adrenoceptor blocker
b. β-adrenoceptor blocker

A

b. β-adrenoceptor blocker

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33
Q

Pheochromocytoma are:

a. Neuroendocrine tumours of the adrenal cortex
b. More common in women compared with men
c. The cause of hypertension in about 0.2% of hypertensive subjects
d. Always malignant
e. Never inherited

A

c. The cause of hypertension in about 0.2% of hypertensive subjects

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34
Q

β-adrenoceptor blockers should never be employed without… (explain why?)

A

blocking α-adrenoceptor mediated vasoconstriction

(β-adrenoceptor cause vasodilation to balance out the vasoconstriction of α-adrenoceptor. If you block β-adrenoceptors alone, the vasoconstriction will be unbalanced and cause high BP)

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35
Q

How do you treat pheochromocytomas?

A

surgical excision (laparoscopy is the first choice)

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36
Q

What is the most common cause of hypothyroidism in developed countries?

a. Autoimmune thyroiditis
b. Hypothalamic and pituitary disorders
c. Iodine deficiency
d. Congenital disorders
e. Postpartum thyroiditis

A

a. Autoimmune thyroiditis

hashimotos

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37
Q

What percent of women acquire postpartum thyroiditis?
versus
What percent of women who have anti-thyroid antibodies acquire postpartum thyroiditis?

A

5%

50%

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38
Q

Which of the following methods of preventing thyroid diseases is not justified?

a. providing adequate iodine intake
b. Screening for congenital hypothyroidism
c. Screening for subclinical hypothyroidism and hyperthyroidism in adults

A

c. Screening for subclinical hypothyroidism and hyperthyroidism in adults

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39
Q

How much did the incidence of thyroid cancer increase from 1975 to 1996?

A

50%

40
Q

In which regions did the incidence of thyroid cancer increase?

A

industrialized countries

41
Q

What are dietary goitrogens? What are some examples of them? How do they work?

A

They’re substances that disrupt the production of thyroid hormones by interfering with iodine uptake. This triggers the pituitary to release thyroid-stimulating hormone (TSH), which then promotes the growth of thyroid tissue, eventually leading to goiter. (Cassava root, broccoli, cauliflower, and brussel sprouts)

42
Q

What is the most common cause of hypothyroidism in the world?

a. Autoimmune thyroiditis
b. Hypothalamic and pituitary disorders
c. Iodine deficiency
d. Congenital disorders
e. Postpartum thyroiditis

A

c. Iodine deficiency

43
Q

Graves’s disease is classified as which of the following?

a. primary hypothyroidism
b. secondary hypothyroidism
c. tertiary hypothyroidism

A

a. primary hypothyroidism

44
Q

T/F: Nodules in a multi-nodular goiter are less likely to be malignant than a solitary thyroid nodule

A

true

45
Q

What are three ways Testosterone improves bone health

A

has anti-resorptive effects
provides the substrate for aromatization to estradiol
increasing bone size (in men)

46
Q

T/F: low levels of testosterone in elderly men have been found to correlate with low bone density

A

false, estrogens play an important role in maintaining bone mass in men.

47
Q

Osteoporosis occurs in men:
A. Due to loss of parathyroid hormone
B. Who consume protein supplements for muscle building
C. Aged 30 years is more common than aged 50 years
D. is associated with high SHBG levels and low estrogen
E. is highly prevalent in black men compared to white men

A

D. is associated with high SHBG levels and low estrogen

Sex hormone binding globulin (SHBG) bind to sex steroids and restricts their access to target tissues

48
Q

What happens to the concentration of sex hormone-binding globulin (SHBG) as age increases? What effect does it have?

A

it increases which sex steroids and restricts their access to target tissues

49
Q

How does tobacco use lead to bone loss (what does it have a direct on?)

A

decreased bodyweight
decreased calcium absorption
decreased estradiol levels
direct toxic effect on bone metabolism

50
Q

How is alcohol related to osteoporosis?

A

it has a direct toxic effect on osteoblastic function

51
Q

How can you treat patients who acquired osteoporosis due to anticonvulsant or glucocorticoid therapy?

A

treat with bisphosphonate supplementation
(Patients on anticonvulsants should take calcium and vitamin D supplements and may be considered for bisphosphonate therapy if their bone density is low.)

52
Q

Explain how anticonvulsant therapy may lead to osteoporosis

A

they cause an increased hepatic metabolism of vitamin D and 25-hydroxyvitamin D, (lowers vit D) resulting in decreased intestinal calcium absorption

53
Q

Long term excess intake of how much energy (%) leads to weight gain and obesity?

A

excess of over 0.5% (irrespective of whether it is from carbohydrate, protein or lipid)

54
Q

Blood glucose level is an important indicator of energy balance in the body. How do glucose levels lead to changes in eating behavior?

A

the central nervous system (satiety center) responds directly to hypoglycemia (hunger)

55
Q

Long term energy storage is controlled by which two enzymes?

A

insulin and leptin

56
Q

hormonal and paracrine signals are generated in response to food ingestion. What secretes these hormones?

A

the gastrointestinal tract

57
Q

Why do oral glucose gave a larger plasma insulin response than intravenous infusion of the same glucose load?

A

due to Incretins which are a group of metabolic hormones that stimulate a decrease in blood glucose levels. They’re released after eating and aid insulin secretion.

58
Q

T/F: Incretins acts on the brain

A

true, it acts to modulate appetite/satiety

59
Q

T/F: incretin release only depends on dietary carbohydrate intake

A

false, dietary fats and proteins in the intestinal lumen also stimulate the release of incretins

60
Q

Using what three methods does GLP-1 regulate energy metabolism?

A

1- stimulating glucose-dependent insulin synthesis in β-cells
2- inhibiting glucagon secretion from α-cells
3- decreasing food intake through neuromodulation within the hypothalamus

61
Q

Where is GLP-1 (glucagon-like peptide 1) generated? How? explain the mechanism.

A

in the small intestine, by proteolysis of proglucagon in response to food ingestion.

62
Q

What degrades GLP-1? Where does this take place?

A

rapidly degraded in the plasma by dipeptidyl-peptidase IV (DPP-IV) to inactive product

63
Q

Where is each of the following produced?
PYY (peptide tyrosine- tyrosine)
CCK (cholecystokinin)

A

PYY produced from the distal small intestine

CCK produced by the duodenum and upper jejunum

64
Q

How does CCK (cholecystokinin) affect appetite?

A

effects on appetite via vagus nerve

increases the sensation of fullness in the short-term during a meal rather than between meals.

65
Q

What can override satiety signals & lead to excessive energy intake?

A

CNS input

66
Q

In a normal individual which action would be most likely to increase blood levels of GLP-1 about 30-40 minutes later?

a) Injection of low dose insulin
b) Injection of low dose glucagon
c) Vigorous aerobic exercise for ten minutes
d) Consumption of a meat sandwich
e) Consumption of two cups of unsweetened tea

A

d) Consumption of a meat sandwich

67
Q

Why do some surgical interventions (EX/gastric bypass surgery) have therapeutic benefits for T2DM treatment?

a. due to the decreased obesity
b. it decreases the amount of sugar the patient can consume
c. A&B
d. none

A

d. none

Rapid improvements in glucose homeostasis independent of decrease in obesity supports an important (but still poorly understood) role for GI hormones in control of glucose homeostasis in humans.

68
Q

What is the most efficacious primary prevention modality for Type 2 diabetes?

A

Weight loss

69
Q

Small amounts of weight loss reduce T2DM risk by how much (%)?

A

60%

70
Q

Which screening method should be applied to Kuwait?

a. “population-based” prevention strategy
b. “high-risk” prevention strategy

A

a. “population-based” prevention strategy

( since the prevalence of diabetes is so high in Kuwait, it may be cost-effective to screen all adults, not just those with risk factors.)

71
Q

Explain what tertiary prevention is in diabetes.

A

refers to interventions in the clinical phases of the disease that are meant to reduce the frequency of complications and their effects (EX/ control of blood pressure and lipids to prevent heart disease in diabetics without heart disease)

72
Q

Which is broader? why?

a. health promotion
b. health education

A

a. health promotion

because it helps and motivates people to change their diets, not just educates them on why they should

73
Q

In most population-based cross-sectional studies, approximately what proportion of diabetics are undiagnosed?

a. <5%
b. 5-14%
c. 15-24%
d. 25-39%
e. >40%

A

e. >40%

74
Q

Where do Islet cells originate from?

A

neural crest cells, aka, APUD cells

75
Q

What percent of Pancreatic endocrine tumors are non-functional?

A

20%

76
Q

Pancreatic tumors are associated with what three conditions?

A

MEN-1
VHL
NF

77
Q

Which is used to can detect small tumors?

a. Angiography
b. CT
c. Intraoperative ultrasound
d. Endoscopic ultrasound
e. MRI

A

d. Endoscopic ultrasound

78
Q

Which procedure is done when there’s a malignancy of the pancreatic head?

A

Whipple procedure (pancreaticoduodenectomy)

79
Q

What is the Whipple procedure?

A

pancreaticoduodenectomy; an operation to remove the head of the pancreas, the first part of the small intestine (duodenum), the gallbladder and the bile duct.

80
Q

Which procedure is done when there’s a malignancy of the pancreatic tail?

A

Spleen preserving (Distal pancreatectomy)

81
Q

satellite nodules is a sign of

A

malignancy (a feature of it)

82
Q

Which has “Salt and pepper” nuclei?

a. Differentiated neuroendocrine tumors
b. Poorly differentiated neuroendocrine carcinomas

A

a. Differentiated neuroendocrine tumors

83
Q

Which has mitotic figures and necrosis?

a. Differentiated neuroendocrine tumors
b. Poorly differentiated neuroendocrine carcinomas

A

b. Poorly differentiated neuroendocrine carcinomas

84
Q

Which is the most common functioning pancreatic neuroendocrine tumor?

a. VIPoma
b. Somatostatinoma
c. Insulinomas
d. Glucagonoma
e. Gastrinoma
e. PPomas

A

c. Insulinomas

85
Q

What percent of PPomas are malignant?

A

66% (2/3 of them)

86
Q

Which affects the Duodenum more than the pancreas?

a. VIPoma
b. Somatostatinoma
c. Insulinomas
d. Glucagonoma
e. Gastrinoma
e. PPomas

A

e. Gastrinoma

87
Q

Which TWO effect the tail more than the head of the pancreas?

a. VIPoma
b. Somatostatinoma
c. Insulinomas
d. Glucagonoma
e. Gastrinoma
e. PPomas

A

a. VIPoma
&
d. Glucagonoma

88
Q

Which has a 5-yr survival rate of 50%?

a. VIPoma
b. Somatostatinoma
c. Insulinomas
d. Glucagonoma
e. Gastrinoma
e. PPomas

A

e. PPomas

89
Q

Which is the SECOND most common functioning pancreatic neuroendocrine tumor?

a. VIPoma
b. Somatostatinoma
c. Insulinomas
d. Glucagonoma
e. Gastrinoma
e. PPomas

A

e. Gastrinoma

90
Q

Which is mostly benign?

a. VIPoma
b. Somatostatinoma
c. Insulinomas
d. Glucagonoma
e. Gastrinoma
e. PPomas

A

c. Insulinomas

91
Q

Which causes necrolytic migratory erythema?

a. VIPoma
b. Somatostatinoma
c. Insulinomas
d. Glucagonoma
e. Gastrinoma
e. PPomas

A

d. Glucagonoma

92
Q

Which causes an excess of stomach acid? explain.

a. VIPoma
b. Somatostatinoma
c. Insulinomas
d. Glucagonoma
e. Gastrinoma
e. PPomas

A

e. Gastrinoma

causes gastrin secretion, which stimulates the secretion of gastric acid (HCl) by the parietal cells

93
Q

Which is malignant in 80% of cases?

a. VIPoma
b. Somatostatinoma
c. Insulinomas
d. Glucagonoma
e. Gastrinoma
e. PPomas

A

e. Gastrinoma

94
Q

Which causes Verner-Morrison syndrome? What is it?

a. VIPoma
b. Somatostatinoma
c. Insulinomas
d. Glucagonoma
e. Gastrinoma
e. PPomas

A

a. VIPoma

Verner-Morrison syndrome, AKA the WDHA syndrome, causes watery diarrhea, hypokalemia, and achlorhydria

95
Q

Which causes Zollinger-Ellison syndrome? What is it?

a. VIPoma
b. Somatostatinoma
c. Insulinomas
d. Glucagonoma
e. Gastrinoma
e. PPomas

A

e. Gastrinoma

secrete large amounts of the hormone gastrin, which causes your stomach to produce too much acid.

96
Q

MEN1 is characterized by

A
  • Parathyroid hyperplasia
  • Pituitary tumors
  • Pancreatic endocrine tumors (PET)
97
Q

T/F: Pancreatic endocrine tumors (PET) occur at a young age

A

true

Endocrine (8 decks)

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