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Endocrine > Week 5 Review Q's > Flashcards

Week 5 Review Q's Flashcards

Anatomy of islets of L (1-36) obesity clinical overview (37-55) physiology obesity and diabetes (56-88) integration of fuel metabolism (89-112) Imunopathogenesis of T1DM (113-128) epidemiology of diabetes (129-159) KDA (160-179) clinical medicine (180-188) seminar haemoglobin A1c (189-220) lab investigation for obesity+diabetes (221-227) pancreatic hormones pharma (228-297)

1
Q

Describe the location of the pancreas

a. intraperitoneal
b. retroperitoneal

A

b. retroperitoneal

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2
Q

Which of the following parts of the pancreas is relates to the spleen? a. head b. tail

A

b. tail

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3
Q

What two ducts join to secrete enzymes into the duodenum?

A

pancreatic duct bile duct

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4
Q

Which part of the pancreas takes up more volume? a. exocrine b. endocrine

A

a. exocrine

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5
Q

Which of the following parts of the pancreas is relates to the duodenum loop? a. head b. tail

A

a. head

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6
Q

Where are the islets of Langerhans more numerous?

A

tail

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7
Q

Which appears darker in H&E? a. pancreatic islets b. pancreatic acini

A

b. pancreatic acini

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8
Q

Which forms the exocrine function of the pancreas? a. pancreatic islets b. pancreatic acini

A

b. pancreatic acini

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9
Q

Which of the following produces insulin? a. α cells b. β cells c. D cells

A

b. β cells

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10
Q

Which of the following produces somatostatin? a. α cells b. β cells c. D cells

A

c. D cells

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11
Q

Which of the following do you expect to become more active after a fatty meal? a. α cells b. β cells c. D cells

A

a. α cells because they secrete Cholecystokinin (CCK) and it secretes bile to help digest

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12
Q

What are three things somatostatin inhibits?

A

α cells β cells GH

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13
Q

Where are D cells mostly located?

A

at the periphery (of islets of langerhan)

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14
Q

Which cell secretes a hormone thats structurally equivalent to Growth hormone-releasing hormone (GHRH)? a. α cells b. β cells c. D cells

A

c. D cells (somatostatin is structurally the same as GHRH)

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15
Q

Which cell secretes ACTH? a. α cells b. β cells c. D cells

A

a. α cells

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16
Q

Which hormone do you expect to raise in levels if theres a cancer of the center of the pancreatic islets?

A

insulin

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17
Q

Which cells stimulate the gastric chief cells? a. D1 cell b. EC cell c. F cell d. Epsilon cell

A

c. F cell (AKA PP cells)

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18
Q

Which do you expect to inhibit glycogen phosphorylase? a. insulin b. glucagon

A

a. insulin (to stop using glycogen and start making it instead)

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19
Q

Which acts to stimulate appetite? What does it release? a. D1 cell b. EC cell c. F cell d. Epsilon cell

A

d. Epsilon cell (release ghrelin)

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20
Q

Which of the following acts to self-regulate pancreatic secretion activities? a. D1 cell b. EC cell c. F cell d. Epsilon cell

A

c. F cell (self regulate by inhibiting bile secretion and pancreatic enzymes)

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21
Q

Which secretes Substance P? (what does Substance P mean?) a. D1 cell b. EC cell c. F cell d. Epsilon cell

A

b. EC cell (has neurotransmitter properties)

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22
Q

What does the EC cell stand for?

A

Enterochromaffin cell

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23
Q

Which secretes vasoactive intestinal peptide (VIP)? a. D1 cell b. EC cell c. F cell d. Epsilon cell

A

a. D1 cell

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24
Q

Which cell acts to stimulate HCO3? Through which enzyme did achieve this? a. D1 cell b. EC cell c. F cell d. Epsilon cell

A

b. EC cell (by secreting secretin)

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25
Q

Which two are also available in exocrine acini and duct epithelium? a. D1 cell b. EC cell c. F cell d. Epsilon cell

A

a. D1 cell & b. EC cell

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26
Q

Which cell inhibits intestinal motility and which cell increases it? a. D1 cell b. EC cell c. F cell d. Epsilon cell

A

c. F cell (decreases) d. Epsilon cell (increases)

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27
Q

Which cell is also found in the stomach and parts of the intestine? a. D1 cell b. EC cell c. F cell d. Epsilon cell

A

d. Epsilon cell

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28
Q

Where are G cells present? What do they produce?

A

present in the intestine make gastrin (D cells in the islets of Langerhans may also produce gastrin)

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29
Q

A cancer affected the islets of Langerhans and caused ulcerations. Can you explain the mechanism?

A

hyperactivity of the islets causes high gastrin secretion-> chief cells stimulated-> they produce HCl, which causes the ulcerations

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30
Q

Describe the “abdominal romance” What can go wrong?

A

the head of the pancreas incircled by the duodenum, this is abdominal romance. But an annular pancreas (which is a congenital anomaly) may occur, and that causes the pancreas to grow and surround the duodenum causing problems.

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31
Q

Reduced insulin and IGF production in the brain causes… a. diabetes millitus b. type 1 diabetes c. type 2 diabetes d. none of the above

A

d. none of the above Reduced insulin and IGF production causes degeneration of brain cells, causing alzheimer’s

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32
Q

What (three things) regulate blood flow to the islets?

A
  1. blood glucose level
  2. autonomic nervous system
  3. gastrointestinal peptides
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33
Q

What happens to insulin and glucagon levels during cholinergic stimulation?

A

both increase

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34
Q

What happens to insulin and glucagon levels during adrenergic stimulation?

A

increase glucagon and inhibit insulin

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35
Q

Which system stimulates glucagon release? a. parasympathetic b. sympathetic c. both d. neither

A

c. both

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36
Q

Which system stimulates insulin release? a. parasympathetic b. sympathetic c. both d. neither

A

a. parasympathetic

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37
Q

higher incomes are associated with a decreased risk of obesity in which of the following? a. men b. women c. caucasians d. all of the above

A

b. women

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38
Q

A person has BMI=25. what does he classify as? a. underweight b. normal c. overweight d. obese class I e. obese class II f. obese class III

A

c. overweight

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39
Q

A person has BMI=45. what does he classify as? a. underweight b. normal c. overweight d. obese class I e. obese class II f. obese class III

A

f. obese class III

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40
Q

A person has BMI=19. what does he classify as? a. underweight b. normal c. overweight d. obese class I e. obese class II f. obese class III

A

b. normal

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41
Q

A person has BMI=35. what does he classify as? a. underweight b. normal c. overweight d. obese class I e. obese class II f. obese class III

A

e. obese class II

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42
Q

A person has BMI=18.5. what does he classify as? a. underweight b. normal c. overweight d. obese class I e. obese class II f. obese class III

A

b. normal (less than this is underweight)

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43
Q

Which gender is has more obese people?

A

women

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44
Q

Which gender is has more overweight people?

A

men

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45
Q

In which gender is age more strongly associated with higher BMI?

A

women

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46
Q

Which of the following men are more obese on average? a. post-graduate education b. primary education only

A

a. post-graduate

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47
Q

Which of the following are more overweight/obese on average? a. single individuals b. married individuals

A

b. married individuals

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48
Q

Which plays a bigger role in weight control? a. diet b. exercise

A

a. diet

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49
Q

The loss of function of which chromosome causes Prader–Willi syndrome (PWS)? a. chromosome 21 b. chromosome 4 c. chromosome 19 d. chromosome 15

A

d. chromosome 15 (monogenic cause of weight gain)

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50
Q

Which causes weight gain? a. melanocortin 1 receptor deficiency b. melanocortin 2 receptor deficiency c. melanocortin 3 receptor deficiency d. melanocortin 4 receptor deficiency

A

d. melanocortin 4 receptor deficiency

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51
Q

satiety vs satiation

A

satiety= fullness in between meals satiation= instant (while eating etc.)

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52
Q

When are pharmaceutical agents used for weight management?

A

when BMI is over 30 or when BMI is over 27 and the patient has a co-morbidity/ failed a previous intervention

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53
Q

When is bariatric surgery used for weight management?

A

when BMI is over 40 or when BMI is over 35 and the patient has a co-morbidity

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54
Q

Which type of bariatric surgery is most common?

A

vertical sleeve gastrectomy

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55
Q

What two things are both causes and symptoms of obesity?

A

overeating and low physical activity

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56
Q

Whats the likely hood a male above the age of 50 has type 2 diabetes mellitus?

A

50%

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57
Q

POMC/CART activate which of the following? a. hunger b. satiety

A

b. satiety

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58
Q

What two cytokines are released from adipose tissue?

A

IL-6 TNF-alpha

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59
Q

What’s the primary function of brown adipose?

A

thermoregulation

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60
Q

what’s the main difference between brown and beige adipose tissue?

A

the location

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61
Q

NPY/AgRP activate which of the following? a. hunger b. satiety

A

a. hunger

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62
Q

What produces cytokines to counter-regulate white adipose cytokines?

A

brown adipose

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63
Q

What type (or types) of adipose tissue is in visceral fat?

A

white and beige

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64
Q

Who has a high leptin concentration? What are the two ways of lowering it?

A

high in obese people. they can lower it by fasting or losing body fat mass

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65
Q

Whats is Resistin? What does it do?

A

it’s a protein hormone that highers serum glucose (by impairing adipose cells from uptaking glucose) and decreases insulin sensitivity (so increasing resistance)

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66
Q

What acts as the feeding center of the body?

A

lateral nuclei

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67
Q

What acts as the satiety center of the body?

A

ventromedial nuclei

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68
Q

What occurs when the stomach is stretched and the stretch inhibitory signals are activated?

A

stretch inhibitory signals are released from the stomach and duodenum by vagi to stop the feeding center

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69
Q

What are the four orexigenic hormones?

A

NPY AGRP cortisol ghrelin

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70
Q

Whats a Glucagon-like peptide-1 (GLP-1) agonists?

A

Saxenda Liraglutide (GLP-1 receptor agonist)

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71
Q

How does GLP-1 (and its analogs) act to decrease obesity?

A

its usually released subsequent to food intake and stimulates the secretion of insulin, inhibits the release of glucagon, delays gastric emptying, and decreases food intake through increased satiety.

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72
Q

A known diabetic patient has high insulin levels, what can you conclude about the type of diabetes he has?

A

type 2 (high insulin but insulin resistant) (type 1 has low insulin)

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73
Q

What secretes pancreatic polypeptide (PP)? a. α cells b. β cells d. δ cells e. ε cells f. F cells

A

f. F cells

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74
Q

What secretes ghrelin? a. α cells b. β cells d. δ cells e. ε cells f. F cells

A

e. ε cells

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75
Q

Which is found in the endoplasmic reticulum? a. proinsulin b. preproinsulin c. insulin d. C peptide

A

b. preproinsulin

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76
Q

Which is found in the golgi? a. proinsulin b. preproinsulin c. insulin d. C peptide

A

a. proinsulin

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77
Q

T/F: you can extract the insulin from animals and use it to treat humans

A

true

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78
Q

What’s the half-life of insulin?

A

5-8 minutes

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79
Q

along with insulin, what is available in the secretory vesicles of the beta cells?

A

C peptide (and insulin) are in the secretory granules

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80
Q

During exercise what happens to insulin levels? how about glucagon levels?

A

decrease insulin increased glucagon

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81
Q

How do alpha 2-adrenergic agonists affect insulin?

A

inhibit its release (sympathetic nervous system stimulation)

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82
Q

How does insulin increase glucose uptake in the liver? a. increase GLUT-1 availability b. increase GLUT-2 availability c. increase GLUT-3 availability d. increase GLUT-4 availability

A

b. increase GLUT-2 availability

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83
Q

What helps transport/carry glucagon in the serum?

A

nothing, it’s unbound (tricked you)

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84
Q

How does insulin increase glucose uptake in the muscle/adipose tissue? a. increase GLUT-1 availability b. increase GLUT-2 availability c. increase GLUT-3 availability d. increase GLUT-4 availability

A

d. increase GLUT-4 availability

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85
Q

How do beta 2-adrenergic agonists affect glucagon?

A

stimulate its release (sympathetic nervous system stimulation)

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86
Q

how do ketone bodies affect insulin and glucagon?

A

stimulate insulin inhibit glucagon

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87
Q

how many amino acids make up glucagon?

A

29

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88
Q

how does somatostatin affect insulin and glucagon?

A

inhibit insulin and glucagon

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89
Q

How does glucose-6-phosphate affect glycogen?

A

it increases its levels by activating glycogen synthase (a key enzyme in glycogen synthesis) via allosteric stimulation

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90
Q

What enzymes transforms 2 ADP’s to an ATP and AMP?

A

adenylate kinase (aka myokinase)

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91
Q

AMPK promotes a. anabolism b. catabolism

A

b. catabolism (inhibits anabolic processes that consume ATP, while promoting catabolic processes that generate ATP)

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92
Q

Explain how insulin and muscle contractions both enhance glucose uptake.

A

INSULIN- binds to receptors which cause increased expression of GLUT 4 in sarcolemma MUSCLE CONTRACTION- causes an increase in AMP and decrease in creatinine phosphate, this activates AMPK, which will increase GLUT 4 expression on T-tubules (Both insulin and muscle contraction trigger translocation of GLUT-4)

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93
Q

Which (one or multiple) of the following does the brain use for energy? a. fatty acids b. glucose c. ketone bodies d. amino acids

A

b. glucose & c. ketone bodies

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94
Q

Which (one or multiple) of the following do RBC’s use for energy? a. fatty acids b. glucose c. ketone bodies d. amino acids

A

b. glucose

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95
Q

Energy metabolism is controlled by three things. What are they?

A

insulin, glucagon, catecholamines

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96
Q

Describe how regulatory hormones (ex/insulin) effect: energy storage blood glucose gluconeogenesis

A

increase energy storage lower blood glucose decrease gluconeogenesis

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97
Q

Which (one or multiple) of the following do muscle cells use for energy? a. fatty acids b. glucose c. ketone bodies d. amino acids

A

a. fatty acids b. glucose d. amino acids

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98
Q

What cell makes the major counter-regulatory hormone?

A

alpha cells (make glucagon)

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99
Q

Which (one or multiple) of the following does the liver use for energy? a. fatty acids b. glucose c. ketone bodies d. amino acids

A

a. fatty acid (oxidization)

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100
Q

What is the major regulatory hormone?

A

insulin

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101
Q

Whats the most important glucose-sensing cell in the body?

A

beta cells

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102
Q

After a meat-filled meal, describe insulin and glucagon levels. Why does this occur?

A

both increase (amino acids stimulate both). insulin increases immediately after high amino acid levels, and glucagon increases to stop hypoglycemia due to the insulin release.

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103
Q

Explain how beta cells trap glucose inside cells via phosphorylation?

A

they’re glucose-sensing cells that have GLUT-2 transporters and glucokinase activity. So they phosphorylate glucose based on the amounts they sense

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104
Q

What are incretins? What do they do?

A

they’re a group of metabolic hormones that stimulate a decrease in blood glucose levels by increasing insulin

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105
Q

How does insulin affect the following liver gluconeogenesis glycolysis

A

Suppresses liver gluconeogenesis Stimulates glycolysis

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106
Q

How does high glucose decrease beta oxidization?

A

high glucose produces more Acetyl-CoA which becomes Malonyl-CoA. Malonyl-CoA inhibits carnitine palmitoyltransferase-1, which is needed to transport the free fatty acids to the mitochondria to start beta oxidization.

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107
Q

What does perilipin phosphorylation do?

A

help mobilize the triglycerol (free the fat and let HSL do its thing- which is hydrolyze the fat esters)

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108
Q

What occurs if the keto diet is applied? a. high insulin/glucagon ration b. low insulin/glucagon ration

A

b. low insulin/glucagon ration

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109
Q

What happens to glycogen and fat stores during an acute stress response?

A

epinephrine released causing glycogen breakdown and lipolysis

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110
Q

Which of the following has a thermogenic effects on brown adipose tissue? a. Glucocorticoids b. Growth hormone c. Thyroid hormones d. Cortisol e. Epinephrine

A

c. Thyroid hormones

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111
Q

Thyroid hormones Sensitize which two organs to the effects of epinephrine.

A

liver and adipose tissue

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112
Q

Which of the following has anti-insulin activity while also stimulating insulin secretion? a. Glucocorticoids b. Growth hormone c. Thyroid hormones d. Cortisol e. Epinephrine

A

b. Growth hormone

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113
Q

Which two mechanisms cause type 1 diabetes?

A

Delayed-type hypersensitivity cytotoxic T cell

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114
Q

What initially causes autoimmune destruction in type 1 diabetes?

A

abnormal expression of HLA molecules (class 2 MHC) in beta cells

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115
Q

You biopsy the islets of Langerhans of a patient with type 1 diabetes, what do you see?

A

lymphocytic infiltration

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116
Q

A cell of an animal with type 1 diabetes was given to a healthy counterpart. The counterpart also got diabetes. What cell is capable of doing this and how?

A

Th1 cells, they activate other cell types leading to the formation of inflammation, damage, then disease

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117
Q

What causes the damage to beta cells in type 1 diabetes?

A

cytokines (IFN-gamma and TNF-alpha), enzymes, and cytotoxic T cells (mainly kills via apoptosis)

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118
Q

Whats the difference between necrosis and apoptosis?

A

apoptosis is mediated from the inside of the cell while necrosis is death from the outside

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119
Q

T/F: Necroptosis is like both necrosis and apoptosis, using caspases to occur

A

false, it’s caspase independent

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120
Q

Autoantigens against which of the following is a marker for type 1 diabetes? a. GAD b. Insulin c. IA-2 d. all of them e. none of them

A

e. none of them (a diagnostic marker needs to be available in close to 100% of the cases)

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121
Q

Autoantigens against which of the following is the first to appear in T1DM (type 1 diabetes mellitus)? a. GAD b. Insulin c. IA-2 d. all of them e. none of them

A

b. Insulin

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122
Q

Autoantigens against which of the following is found in 70% of T1DM cases? a. GAD b. Insulin c. IA-2 d. all of them e. none of them

A

a. GAD

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123
Q

can you conclude that a patient has T1DM if autoantigens against GAD, Insulin, and IA-2 are present?

A

yes

124
Q

What genetic component can most accurately predict T1DM?

A

HLA genes (DR3-DQ2 OR DR4-DQ8)

125
Q

T/F: gut microbiota plays a role in development of T1DM

A

true

126
Q

Which of the following can reduce recurrence of disease? a. Stem cell transplant b. Azathioprine c. Pancreatic transplantation d. Islet cell transplantation e. Anti-T cell antibodies f. Cyclosporin

A

f. Cyclosporin

127
Q

Which of the following is relatively non-invasive? a. Stem cell transplant b. Pancreatic transplantation c. Islet cell transplantation

A

c. Islet cell transplantation

128
Q

Which of the following can lower HbA1c? a. Stem cell transplant b. Azathioprine c. Pancreatic transplantation d. Islet cell transplantation e. Anti-T cell antibodies f. Cyclosporin

A

e. Anti-T cell antibodies

129
Q

A study was done to see the prevalence of T2DM among Chinese people living in different countries. Whats FALSE about this study? a. suggests that life style plays an important role in T2DM b. it does not limit genetic makeup as a confounder

A

b. it does not limit genetic makeup as a confounder (it does limit gentics as a confounder. That just means that it made sure the genetics are the same so the study finds the effect of environment on T2DM)

130
Q

What are two risk factors of T2DM?

A

high fat diet obesity

131
Q

What can we assume from a cohort study relating higher HgbA1 to heart conditions? a. the higher the HgbA1 the greater likelihood of heart conditions b. they are correlated c. one aspect causes the other

A

b. they are correlated (its a correlation study, it doesn’t indicate causation)

132
Q

What can we assume from a randomized control study relating higher HgbA1 to heart conditions? a. the higher the HgbA1 the greater likelihood of heart conditions b. they are correlated

A

a. the higher the HgbA1 the greater likelihood of heart conditions (randomized control studies determine causation)

133
Q

Whats the prevalence of T2DM in kuwaitis above the age of 60? a. 19% b. 7% c. 36% d. 63%

A

d. 63% (he brings questions with precentages)

134
Q

How can we reduce macro/microvascular outcomes of diabetes mellitus?

A

intensive glucose control

135
Q

Does a tighter control of hypertension reduce risk of complications in T2DM? If yes, by how much?

A

yes, in total it reduces risk by 25%

136
Q

Which THREE of the following has a statistically significant reduction after tighter control of hypertension? a. myocardial infections b. stroke c. peripheral vascular disease d. microvascular diseases e. total mortality f. diabetes death

A

b. stroke & d. microvascular diseases & f. diabetes death

137
Q

Which of the following does adding ace-inhibitors to the hypertension regimen decrease? a. microvascular diseases b. macrovascular diseases

A

b. macrovascular diseases

138
Q

Which drug was shown to reduce cholesterol by 24% in DM patients?

A

simvastatin

139
Q

T/F: diabetes is growing 5 times faster than the population growth

A

10 times faster

140
Q

What percent of T2DM cases are undiagnosed?

A

40%

141
Q

Whats the ratio of DM in boys vs girls?

A

3.0 boys : 1.7 girls

142
Q

Which HLA type does the majority of people with DM have?

A

DR3 or DR4

143
Q

Why are there seasonal variations in new cases of DM?

A

due to viral infections (more common in winter, so more cases) (why? infections and stressors cause an increase in counter-regulatory hormones, like cortisol and glucagon, and they counter regulate the insulin and so insulin demand is higher)

144
Q

Explain the thrifty gene hypothesis?

A

a theory that says that people who have rapid food storage would survive more because they would have extra storage to get through famine or starvation.

145
Q

Which age group has the highest susceptibility to diabetes?

A

65-74

146
Q

Whats the metabolic syndrome?

A

a group of conditions that hangout together (obesity, T2DM, hyperlipidemia, high BP)

147
Q

T/F: women who get gestational diabetes have a higher risk of getting diabetes later

A

true

148
Q

How does DM increase the risk of death?

A

X2 risk of death

149
Q

Which two of the following studies find macrovascular event reduction? a. The UKPDS-33 Study b. The DCCT Trial c. The MICRO-HOPE Trial d. UKPDS-38 e. Heart Protection Study

A

c. The MICRO-HOPE Trial & e. Heart Protection Study

150
Q

Which of the following does the UKPDS-38 study find a reduction in? a. microvascular diseases b. macrovascular diseases

A

a. microvascular diseases

151
Q

Which of the following test patients with T2DM? a. The UKPDS-33 Study b. The DCCT Trial c. both d. neither

A

a. The UKPDS-33 Study

152
Q

Which of the following test the affects of intensive insulin treatment? a. The UKPDS-33 Study b. The DCCT Trial c. both d. neither

A

c. both

153
Q

Does fetal life have an effect on chronic diseases?

A

yes, fetal life, childhood, and adolescence all determine the trajectory that results in higher or lower risk

154
Q

When are chronic disease risk factors established?

A

before adulthood, they establish the risk factors and the trajectory is somewhat set. If they start at a higher risk in adulthood, they’re then likely to get the bad outcomes.

155
Q

Which uses ramipril? (what is ramipril and what does it do?) a. The UKPDS-33 Study b. The DCCT Trial c. The MICRO-HOPE Trial d. UKPDS-38 e. Heart Protection Study

A

c. The MICRO-HOPE Trial ramipril is the ace inhibitor. if you add it to the regimen you decrease macrovascular events

156
Q

Which uses simvastatin? (what is simvastatin and what does it do?) a. The UKPDS-33 Study b. The DCCT Trial c. The MICRO-HOPE Trial d. UKPDS-38 e. Heart Protection Study

A

e. Heart Protection Study simvastatin is a lipid-lowering medication. using it reduces macrovascular events by 24%

157
Q

Which of the following found a decrease in macrovascular complications? a. The UKPDS-33 Study b. The DCCT Trial c. both d. neither

A

d. neither they both found decreased microvascular complications

158
Q

Which of the following test patients with T1DM? a. The UKPDS-33 Study b. The DCCT Trial c. both d. neither

A

b. The DCCT Trial

159
Q

Which tests tight vs less tight BP control? a. The UKPDS-33 Study b. The DCCT Trial c. The MICRO-HOPE Trial d. UKPDS-38 e. Heart Protection Study

A

d. UKPDS-38

160
Q

Patients with which are more likely to get diabetic ketoacidosis (DKA)? a. T1DM b. T2DM

A

a. T1DM

161
Q

What true about insulin action when having low insulin levels?

A

the insulin is not as effective when there are low levels of it (why? because when insulin is low, glucagon is activated and it activates downstream pathways that go against insulin)

162
Q

Which of the following is a symptom of DKA? a. dehydration b. abdominal pain c. kussmal’s respirations d. hypothermia

A

b. abdominal pain (the rest were signs, not symptoms)

163
Q

What happens to the pH and bicarbonate levels as DKA becomes more severe?

A

pH is lowered (more acidic) bicarbonate levels decrease (less of the basic bicarb.)

164
Q

What do SGLT2 inhibitors do?

A

they inhibit resorption of glucose

165
Q

When should you give dextrose to a patient with DKA? Why would they need more sugar?

A

you give it if blood glucose is less than 14. They have low sugar because you gave them a whole liter of normal saline and that diluted the sugar concentration in the blood.

166
Q

Why do we give insulin to a patient with DKA? a. to reduce sugar b. to reduce ketones

A

b. to reduce ketones

167
Q

How much normal saline do you give a patient with KDA?

A

one liter

168
Q

Which must you do if a DKA patient has normal K? a. don’t give K b. add 40mmol/L to each normal saline liter c. don’t give insulin until K is corrected

A

b. add 40mmol/L to each normal saline liter Always give K because they have a TOTAL K deficiency

169
Q

Which must you do if a DKA patient 1.5 mmol/L of K? a. don’t give K b. add 40mmol/L to each normal saline liter c. don’t give insulin until K is corrected

A

c. don’t give insulin until K is corrected (this concentration is too low, if you start insulin therapy the K will go inside the cell and thus K is further decreased leading to serious damage)

170
Q

What three things can you adjust the insulin rate according to?

A

ketones glucose bicarbonate

171
Q

Which must you do if a DKA patient 4.6 mmol/L of K? a. don’t give K b. add 40mmol/L to each normal saline liter c. don’t give insulin until K is corrected

A

b. add 40mmol/L to each normal saline liter

172
Q

In what case of KDA do you give bicarbonate replacement?

A

when pH less than 6.9

173
Q

In what case of KDA do you give IV phosphate replacement? Why?

A

when phosphate is less than 0.32mmol/L, less than this amount is associated with cardiac and muscle dysfunction.

174
Q

Which is taken once a day? a. basal insulin b. bolus insulin

A

a. basal insulin

175
Q

A patient with diabetes weighs 88Kg. What is the subcutaneous starting total dose per day? What are the basal/bolus units?

A

44 total dose units taken as 22 basal and 22 bolus (subcutaneous starting dose is 0.5 units per Kg BUT when a patient has DKA and you start giving them insulin via IV its 0.5 units/Kg/hour)

176
Q

You see your diabetic friend inject insulin after eating pasta, what type of insulin do you think it is? a. basal insulin b. bolus insulin

A

b. bolus insulin (correct temporary glucose elevation)

177
Q

What glucose level must the patient reach to be able to resolve DKA? What other tests must they pass to be considered resolved of DKA?

A

less than 11mmol/L (they must also pass two of the following three: bicarb more than or equal to 15, Ph more than 7.3, anion gap less than or equal to 12)

178
Q

Should you give IV phosphate replacement to DKA patients? Why?

A

no, it can precipitate hypocalcemia and it doesn’t benefit (only given if phosphate is less than 0.32mmol/L though)

179
Q

How do you switch from IV insulin to subcutaneous insulin?

A

As you switch, continue giving IV insulin 2 hours after the subcutaneous injection (this gives it time to absorb)

180
Q

What three components cause diabetic foot disease?

A

neuropathy ischemia infection

181
Q

What usually starts the ulcer formation of diabetic foot disease?

A

most common cause are plaques of callus skin (which becomes necrotic and breaks through the skin surface)

182
Q

What can you assume about a diabetic foot that has a white residue?

A

fungal infection (usually starts between the toes) (look at the picture in the clinical skills lab)

183
Q

The diabetic patient has a non-healing foot ulcer and he doesn’t consent to amputation. What can you do?

A

surgically remove the necrotic tissue from the ulcer (until you get to clean, wet-looking tissue) then the ulcer is more likely to heal

184
Q

Why do diabetic patients have decreased vision?

A

optic nerve involvement

185
Q

The pupil of the eye of a diabetic patient appears white. What is this?

A

cataract (occurs in young age)

186
Q

What is the macula?

A

is the functional center of the retina. It gives us the ability to see “20/20” and provides the best color vision.

187
Q

Why do diabetic patients get hemorrhage in the retina?

A

retinal blood vessels become more permeable (patients usually also have high BP and inflammatory cells that both also contribute)

188
Q

How can scatter laser treatment aka panretinal photocoagulation help prevent diabetic retinopathy?

A

they use the laser to burn off the abnormal blood vessels and prevent hemorrhage

189
Q

What is the normal result of fasting blood sugar level test?

A

normal= less than 100 mg/dL (5.6 mmol/L) prediabetic= 100 to 125 mg/dL (5.6 to 6.9 mmol/L) diabetes= 126 mg/dL (7 mmol/L) or higher on two separate tests

190
Q

What is the normal range for the hemoglobin A1c level?

A

normal= 4% - 5.6% prediabetic= 5.7% - 6.4% diabetic= 6.5% or higher (the precentage is basically the number of Hb bound to sugar divided by total Hb)

191
Q

What two tests can be used to measure blood glucose levels?

A

High Performance Liquid Chromatography (HPLC) (tests HbA1c) Immunoassay

192
Q

What gene mutation can interfere with High-Performance Liquid Chromatography (HPLC) results?

A

hemoglobin Wayne

193
Q

What produces HbA1c? a. glycation b. glycosylation

A

a. glycation

194
Q

glycation VERSUS glycosylation

A

glycation= non-enzymatic glycosylation, it occurs spontaneously so it may disrupt protein conformation and cause the loss of the biological function of the proteins glycosylation= a controlled process, so it actually helps the proteins do their thing (their function)

195
Q

After discovering that a patient has a high glucose level, the doctor prescribed a higher dose of insulin. Then, a month later he had them take a HbA1c test, what do you expect the findings to be and why?

A

the HbA1c would be high because they reflect the last three months of glucose levels. A month of low glucose does help the HbA1c levels decrease, but they would still be high.

196
Q

Formation of which of the following is a reversible reaction? a. ketoamine b. aldimine

A

b. aldimine

197
Q

Making Schiff base is a(n) a. reversible reaction b. irreversible reaction

A

a. reversible reaction

198
Q

You cook a steak to a well-done state, and it has a crispy brown exterior. What is this an example of?

A

Maillard reaction (Advanced glycation of free amino groups on proteins and amino acids)

199
Q

Formation of which of the following is formed via the Amadori rearrangement? a. ketoamine b. aldimine

A

a. ketoamine

200
Q

Making an Amadori produce a(n) a. reversible reaction b. irreversible reaction

A

b. irreversible reaction

201
Q

How can we reverse the Schiff base?

A

lowered glucose concentration will unhook the sugars from the amino groups to which they are attached

202
Q

“Maillard reaction”, is influenced by what factors?

A

intracellular glucose concentrations, pH, and time. (she also said temperature)

203
Q

Which are more efficient initiators of intracellular advanced glycation? WHY? a. glucose b. glucose metabolites

A

b. glucose metabolites (glucose exists as glucopyranose, which is cyclic. So it can hide its -CHO ring from the reactions. However, glucose metabolites ex/short-chain intermediates cannot hide their reactive bits. so, BOOM, glycation occurs)

204
Q

WHat two things increase AGEs?

A

hyperglycemia and oxidative stress (ROS)

205
Q

Describe the relationship between AGE and ROS.

A

ROS causes AGE formation. and AGE formation causes ROS release. its a cycle!

206
Q

Where are AGEs more rapidly generated?

A

within cells

207
Q

How do alterations in the krebs cycle or the pentose phosphate pathway increase AGEs?

A

cause more glucose intermediate release ex/short-chain intermediates (leftover from the bad pathways)

intermediates stimulate AGEs and are much more easily glycosylated

208
Q

What occurs in the liver and kidney when AGE binds with the receptor (RAGE)?

A

liver phagocytosis activates kidney clearance (receptors) activate

209
Q

Where is RAGE highly expressed? What is its function?

A

in mucous membranes; its function is activating immune and inflammatory reactions

210
Q

give two sources of extracellular AGEs

A

burned/crispy/brown meat smoking

211
Q

give me five AGE associated conditions

A

Atherosclerosis Stroke Diabetic Retinopathy Alzheimer’s Disease skin aging

212
Q

What tests are used to measure renal function?

A

urea (released by kidneys) creatinine (waste product produced by muscles and is released by kidneys) albumin (if found in urine then problem)

213
Q

What can prevent chronic diabetes complications?

A

maintaining a normal level of sugar in blood

214
Q

What are HbA1c levels better indicators of? a. pre-diabetic patients b. risk of diabetic complications

A

b. risk of diabetic complications HbA1c= realted to risk of retinopathy Also it’s less specific indicator of pre-diabetes (than a normal impaired fasting glycemia test)

215
Q

What can we use to reduce HbA1c levels?

A

IV iron and erythropoietin stimulating agents (they do this without altering glycemic control)

216
Q

T/F: anemia is more frequent in diabetic patients with kidney disease than nondiabetic patients with kidney disease

A

true

217
Q

Which patients present false HbA1c values?

A

patients with anemia or renal disease (and ones with hemoglobin variants)

218
Q

Why do some conditions present false HbA1c values?

A

Any condition that affects the blood may alter the levels. If they have anemia, for example, it may lower the life span of RBC’s and decrease HbA1c. If the disease increases the RBC life span (EX/ prenicous anemia) then the HbA1c levels will increase. Chronic Renal Failure also lowers the HbA1c readings (shorter RBC life) and may sometimes even higher the readings (no erythropoietin).

219
Q

Describe the relationship between RBC lifespan and HbA1c levels?

A

shorter life span -> low HbA1c levels higher life span -> high HbA1c levels

220
Q

Which of the following do you expect to have low HbA1c levels? Explain. a. liver disease b. jaundice

A

a. liver disease (it’s associated with anemia and decreased RBC life, thus low HbA1c) however jaundice increases bilirubin and that increases HbA1c

221
Q

Which tests are used to diagnose diabetes?

A

fasting sugar blood test HbA1c blood test Oral glucose tolerance test (OGTT)

222
Q

How does insulin and bicarbonate affect potassium levels?

A

decrease them by forcing K inside cells

223
Q

microalbuminuria is a marker for which two diseases?

A

renal damage and cardiovascular disease

224
Q

Which affects T2DM patients more? a. Diabetic ketoacidosis b. Nonketotic hyperglycinemia

A

b. Nonketotic hyperglycinemia (also called Hyperosmolar Hyperglycemic Nonketotic Syndrome) (DKA more in T1DM)

225
Q

Describe the glucose levels in Diabetic ketoacidosis versus Nonketotic hyperglycinemia

A

Diabetic ketoacidosis (high but still) less than 35mmol/L Nonketotic hyperglycinemia more than 35mmol/L (very, very high)

226
Q

What are two reasons a diabetic patient may collapse and die?

A

MI or Stroke

227
Q

What three things are required to diagnose Hyperglycaemic Hyperosmolar Nonketotic Coma (HONK)?

A

Plasma osmolarity > 320 mOsm/l serum glucose > 35 mmol/L Negative/low level ketone

228
Q

generally speaking, the structure of insulin is a. acidic b. based

A

a. acidic

229
Q

Describe the structure of insulin

A

two peptide chains referred to as the A chain and B chain. A and B chains are linked together by two disulfide bonds, and an additional disulfide is formed within the A chain

230
Q

What is more common in the body, insulin or proinsulin?

A

insulin

231
Q

Which is found in the rough ER? a. preinsulin b. proinsulin

A

a. preinsulin

232
Q

What two things are found in beta granules?

A

C peptide and insulin (low C peptide means you have diabetes)

233
Q

What aids beta granule fusion to the plasma membrane?

A

myosin filaments

234
Q

Which is found in the Golgi? a. preinsulin b. proinsulin

A

b. proinsulin

235
Q

What the main stimulus for insulin secretion?

A

glucose

236
Q

What traps glucose in the cell? Which enzyme used?

A

adding a phosphate traps it in, and hexokinase does that

237
Q

What is needed for calcium to activate protein kinase in beta cells?

A

Ca needs to bind to calmodulin (two Ca can bind to it) to phosphorylate protein kinase

238
Q

Which of the following releases Ca from the SR? a. Inositol 1,4,5 Triphosphate b. Diacylglycerol

A

a. Inositol 1,4,5 Triphosphate

239
Q

Which is activated when epinephrine mediates insulin secretion? a. phospholipase C b. protein kinase c. adenyl cyclase

A

c. adenyl cyclase

240
Q

Which adrenoreceptor activates insulin secretion when stimulated? a. alpha 2 b. beta 2

A

b. beta 2 (alpha 2 inhibit insulin secretion)

241
Q

Which is activated when acetylcholine mediates insulin secretion? a. phospholipase C b. protein kinase c. adenyl cyclase

A

a. phospholipase C

242
Q

Which of the following phosphorylates (activates) protein kinase? a. Inositol 1,4,5 Triphosphate b. Diacylglycerol

A

b. Diacylglycerol

243
Q

Which hormone activates both insulin and somatostatin?

A

glucagon

244
Q

What percent of insulin released from the body doesn’t make it to circulation? Why? How does it get inactivated?

A

40-50% doesn’t make it through the first-pass metabolism. The disulfide bonds get hydrolyzed

245
Q

Whats the half-life of insulin?

A

5-7 minutes (very short)

246
Q

Which part of the insulin receptor does insulin bond to?

A

alpha subunit

247
Q

What happens to the insulin receptor once insulin binds?

A

binding activates autophosphorylation of beta subunit, that activates tyrosine kinase which then activates PI3 kinase

248
Q

The beta subunit of the insulin receptor is bound to which enzyme?

A

tyrosine kinase

249
Q

Besides the amount of insulin, what three factors affect insulin action?

A

number of receptors affinity of insulin to receptors amount of intracellular mediators made after receptor activation

250
Q

What two insulin types are used for patients in a diabetic coma? Why?

A

Lisopro Insulin Crystalline Zinc Insulin (regular insulin) we use them because they’re admitted via IV and they’re fast acting

251
Q

How is Lisopro Insulin prepared?

A

proline B28→proline B29 lysine B29 → lysine B28 (basically proline of B28 is switched with lysine of 29)

252
Q

Intermediately acting insulin has an onset of

A

1-2 hours

253
Q

What two insulin types can be admitted via IV and can be mixed with other insulin types?

A

Lisopro Insulin Crystalline Zinc Insulin (regular insulin)

254
Q

long-acting insulin has an onset of

A

4-8 hours

255
Q

Which is made by this process: basic insulin reacts with protamin and zinc, then dissolve with phosphate buffer. a. Lente b. Isophane (NPH) c. Ultralente d. Glargine

A

b. Isophane (NPH)

256
Q

Which of the following has a duration of 36 hours? a. Lente b. Isophane (NPH) c. Ultralente d. Glargine

A

c. Ultralente

257
Q

How is the Glargine (long-lasting insulin) made?

A

Asparagine→ Glycine (substitute in alpha chain) then in beta chain the added two more Asparagines

258
Q

How can we make insulin last longer without changing its formula?

A

delay the rate of absorption

259
Q

Which of the following decreases insulin requirements? a. pregnancy b. surgery c. thiazide diuretics d. chronic exercise

A

d. chronic exercise

260
Q

What should you give a hypoglycemia patient that is conscious?

A

sugar

261
Q

Which of the following has no peak? What does this mean about the drug? a. Lente b. Isophane (NPH) c. Ultralente d. Glargine

A

d. Glargine (its not likely to produce hypoglycemia because its so stable)

262
Q

What should you give a hypoglycemia patient that is unconscious?

A

glucagon

263
Q

Which increases insulin sensitivity? a. Metformin b. Tolbutamide c. Rosiglitazone d. Sitagliptin e. Exenatide

A

c. Rosiglitazone

264
Q

How does Acarbose work?

A

Reduce blood glucose by making the GI stop glucose uptake

265
Q

Generally speaking, how do Sulfonylureas drugs work?

A

antidiabetic drugs that increase insulin release from the beta cells in the pancreas. (primarily works by increasing **glucose-mediated** insulin secretion)

266
Q

Which Sulfonylurea has the highest duration of action?

A

Chlorpropamide (the first generation, works for 60 hours)

267
Q

What occurs when Sulfonylureas drugs bind to sulfonylurea receptors?

A

they block ATP sensitive K channels, causing depolarization of cell and then release of insulin

268
Q

Which K channel subunit do most Sulfonylureas drugs bind to? a. 65Kd b. 140Kd

A

b. 140Kd

269
Q

Which sulfonylureas drug should be used for people with heart conditions? why?

A

glimepiride should be used because it binds to the 65Kd subunit of the K channels. The 65Kd subunit is found in beta cells and NOT in the cardiovascular system. So the heart would be unaffected by the medications.

270
Q

Which of the following sulfonylureas drugs causes an adverse reaction to alcohol leading to nausea, vomiting, flushing, dizziness, & throbbing headache (disulfiram-like effect)? a. Glipizide b. Chlorpropamide c. Glimepiride d. Glyburide

A

b. Chlorpropamide (causes a disulfiram effect AKA disulfiram syndrome)

271
Q

Which K channel subunit does glimepiride bind to?

A

65Kd subunit

272
Q

Which of the following is 50% excreted in the feces? a. Glipizide b. Chlorpropamide c. Glimepiride d. Glyburide

A

d. Glyburide

273
Q

Which of the following has the highest potency? a. Glipizide b. Chlorpropamide c. Glimepiride d. Glyburide

A

c. Glimepiride

274
Q

Which of the following has the lowest potency? a. Glipizide b. Chlorpropamide c. Glimepiride d. Glyburide

A

b. Chlorpropamide (its first generation, duh)

275
Q

Which of the following can be given to pregnant women? a. Glipizide b. Chlorpropamide c. Glimepiride d. Glyburide

A

d. Glyburide (least likely to cross the placenta)

276
Q

Which of the following most commonly causes dilutional hyponatremia? Why? a. Glipizide b. Chlorpropamide c. Glimepiride d. Glyburide

A

b. Chlorpropamide (due to the ADH-like effect)

277
Q

Explain disulfiram syndrome. What is it? What causes it? What’s the mechanism behind it? (symptoms, etc.)

A

it occurs when you take sulfonylureas drugs (especially Chlorpropamide) with alcohol. The drug inhibits the enzyme Aldehyde Dehydrogenase, which acts to metabolize the alcohol. The somewhat toxic acetaldehyde (which the substrate for the enzyme) builds up. Due to this, the patient experiences tachycardia and hyperventilation.

278
Q

Which of the following acts to increase beta cell proliferation? a. Acarbose b. Repaglinide c. Rosiglitazone d. Metformin e. Exenatide f. Sitagliptin

A

e. Exenatide

279
Q

Which of the following has a side effect of Stevens-Johnson syndrome? a. Acarbose b. Repaglinide c. Rosiglitazone d. Metformin e. Exenatide f. Sitagliptin

A

f. Sitagliptin

280
Q

Which of the following mainly acts to inhibit hepatic glucose output? a. Acarbose b. Repaglinide c. Rosiglitazone d. Metformin e. Exenatide f. Sitagliptin

A

d. Metformin

281
Q

Which of the following is minorly excreted in the urine? a. Acarbose b. Repaglinide c. Rosiglitazone d. Metformin e. Exenatide f. Sitagliptin

A

b. Repaglinide

282
Q

Which of the following interferes with B12 absorption? a. Acarbose b. Repaglinide c. Rosiglitazone d. Metformin e. Exenatide f. Sitagliptin

A

d. Metformin

283
Q

Which of the following has a similar structure to GLP (Glucagon-like peptide) and thus can activate its receptors? a. Acarbose b. Repaglinide c. Rosiglitazone d. Metformin e. Exenatide f. Sitagliptin

A

e. Exenatide

284
Q

What is Stevens-Johnson syndrome?

A

rare, serious disorder of your skin and mucous membranes. It’s usually a reaction to a medication or an infection. Often, it begins with flu-like symptoms, followed by a painful red or purplish rash that spreads and blisters. (side effect of Sitagliptin)

285
Q

T/F: Exenatide is taken orally

A

false, its subcutaneous

286
Q

Which of the following inhibits GLP (Glucagon-like peptide) degradation? a. Acarbose b. Repaglinide c. Rosiglitazone d. Metformin e. Exenatide f. Sitagliptin

A

f. Sitagliptin

287
Q

What does GLP (Glucagon-like peptide) do? How can we use it for diabetes control?

A

promote insulin secretion so in diabetes, we want to increase it, activate its receptors, or limit its degradation

288
Q

T/F: Repaglinide has a short duration

A

true

289
Q

How does Metformin inhibit hepatic glucose output?

A

by decreasing gluconeogenesis

290
Q

Which is a pancreatic alpha-amylase inhibitor? a. Acarbose b. Repaglinide c. Rosiglitazone d. Metformin e. Exenatide f. Sitagliptin

A

a. Acarbose

291
Q

What are the side effects of Acarbose? explain them.

A

abdominal discomfort and diarrhea. this is due to the fact that the drug stays and act from within the GI system.

292
Q

Which has nausea and vomiting as a side effect? a. Acarbose b. Repaglinide c. Rosiglitazone d. Metformin e. Exenatide f. Sitagliptin

A

d. Metformin

293
Q

Which cannot be given to any patient susceptible to metabolic acidosis? why? a. Acarbose b. Repaglinide c. Rosiglitazone d. Metformin e. Exenatide f. Sitagliptin

A

d. Metformin (a side effect of it is lactic acidosis- because it blocks acetate flow through gluconeogenesis- so we don’t want to add on to the acidic environment)

294
Q

Acarbose is contraindicated in

A

Inflammatory bowel disease (IBD) and intestinal obstruction (remember, the drug works in the GI)

295
Q

Explain how Rosiglitazone increases insulin sensitivity?

A

by activating the “Peroxisome proliferator-activated receptor-gamma” (PPARγ). That receptor increases the promoter genes for glucose utilization, so we need less glucose to do the same effect -> insulin sensitivity

296
Q

Which causes fluid retention (and mild anemia)?

a. Acarbose
b. Repaglinide
c. Rosiglitazone
d. Metformin
e. Exenatide
f. Sitagliptin

A

c. Rosiglitazone

297
Q

What determines the duration of action of exogenous insulin?
A. Rate of absorption
B. Rate of elimination
C. Plasma protein binding
D. Receptor affinity
E. Hepatic metabolism

A

A. Rate of absorption

298
Q

Which of the following is a unique feature of Glargine?
A. Does not have a peak activity during its 24 hour duration
B. Can be mixed with other insulin
C. More likely to cause hypoglycemia
D. Given for postprandial hyperglycemia

A

A. Does not have a peak activity during its 24 hour duration

299
Q

Patient with diabetic ketoacidosis is taken to the hospital and immediately given
fluids, including normal saline. Which of the following electrolytes is also
important to monitor in this patient?
A. Sodium
B. Potassium
C. Calcium
D. Magnesium
E. Phosphorus

A

B. Potassium

300
Q

Which of the following characterized Type 2 Diabetes?
A. Complete insulin deficiency
B. Insulin sensitivity
C. Autoimmune destruction of pancreatic β cells
D. Concordance in monozygotic twins

A

D. Concordance in monozygotic twins

301
Q

Which of the following statements is true regarding the incidence of Type 1 and
Type 2 Diabetes Mellitus?
A. T1D is more common and occurs in young individuals.
B. T2D is more common and occurs in young individuals.
C. Both T1D and T2D are equally common, but T1D occurs in young
individuals whereas T2D occurs in older individuals.
D. T1D is more common and occurs in older individuals.
E. T2D is more common and occurs in older individuals.

A

E. T2D is more common and occurs in older individuals.

302
Q

If an obese individual is under diet restriction but feels hungry all of the time,
what is the underlying cause?
A. Leptin
B. Adipocytokines
C. Ghrelin

A

A. Leptin

303
Q

What is a primary mediator of immunological damage to pancreatic β cells in
Type 1 Diabetes Mellitus?
A. Anti-insulin autoantibodies
B. Autoantibody to glutamic acid decarboxylase
C. Autoreactive cytotoxic T cells
D. Natural killer cells

A

C. Autoreactive cytotoxic T cells

304
Q

What is a main mechanism of tissue damage in Type 1 Diabetes Mellitus?
A. Autoantibody to glutaminc acid decarboxylase
B. Autoantibody to islet antigen 2
C. Apoptosis
D. Complement-mediated

A

C. Apoptosis

305
Q

What type of adipose tissue protects against cardiovascular diseases?
A. White
B. Brown

C. Beige
D. Yellow

A

B. Brown

306
Q

Which of the following cells stimulates gastrin secretion and may lead to peptic
ulcers?
A. A cells
B. B cells
C. D cells
D. F cells

A

C. D cells

307
Q

33-year-old female presented with fatigue, episodes of fainting for the past 6
months, and a high insulin: glucagon ratio. Upon imaging, a single nodule
secreting high levels of insulin was detected. Upon microscopic studies, there
was monotonous cells with salt and pepper chromatin. What is the most likely
diagnosis?
A. Islet cell tumor
B. Adenocarcinoma
C. Acute pancreatitis
D. Fat necrosis

A

A. Islet cell tumor

Endocrine (8 decks)

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