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Semester 4 > Case 6 > Flashcards

Case 6 Flashcards

1
Q

The islets of langerhans account for what proportion of cells in the pancreas?

A

1%

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2
Q

What are the four types of cells in pancreatic islets?

A

Alpha cells, Beta cells, Delta cells and F cells

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3
Q

What is the role of alpha cells in pancreatic islets?

A

Release of the hormone glucagon that raises blood glucose levels by increasing the rate of glycogen and glucose release by the liver

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4
Q

What is the role of the beta cells of the pancreatic islets?

A

Release of the hormone insulin that lowers blood sugar levels by increasing the rate of uptake of glucose by most body cells and increasing glycogen synthesis in skeletal muscle

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5
Q

What is the role of delta cells in the islets of langerhans?

A

Release of a peptide hormone identical to growth hormone inhibiting hormone (GH-IH/somatostatin) that suppresses the release of glucagonn and insulin by other islet cells and slows the rate of food absorption and enzyme secretion along the digestive tract

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6
Q

What is the role of the F cells of the islets of langerhans?

A

They produce pancreatic polypeptide which inhibits gall bladder contractions and regulates the production of some pancreatic enzymes thereby helping to control the rate of nutrient absorption by the digestive tract

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7
Q

Elevated levels of what stimulate the release of insulin?

A

glucose blood levels and raised levels of some amino acids such as arginine and leucine

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8
Q

What is the general structure of insulin?

A

It is a peptide hormone composed of two amino acid chains attached to each other by disulphide bridges

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9
Q

What is the clearance of insulin in the blood?

A

It has a half life of 6 minutes and so is mostly cleared from circulation in 10-15 minutes insulin that does not bind to a receptor generally is degraded by insulinase in the liver and to a lesser extent the kidneys and muscle

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10
Q

Whatis the structure of the insulin receptor?

A

It is composed of four subunits. two alpha subunits that lie entirely outside the membrane and two beta subunits that penetrate through the membrane protruding into the cytoplasm

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11
Q

What happens when insulin binds to the alpha subunits of the insulin receptor?

A

the portion of the beta subunits that protrude into the cell become autophosphorylated

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12
Q

Activation of an insulin receptor and subsequent autophosphorylation of its beta subunits caused the activation of what enzyme? what effect does this have?

A

a local tyrosine kinase is activated which causes phosphorylation of multiplee other intracellular enzymes most notably the insulin receptor substrates (IRS)

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13
Q

The formation of what is stimulated by insulin in adipose tissue?

A

triglycerides

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14
Q

What is GLUT4?

A

an insulin dependent glucose transporter

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15
Q

What happens to the majority of glucose that enters cells upon its insulin stimulated uptake?

A

It is phosphorylated and becomes a substrate for usual carbohydrate metabolic functions

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16
Q

What is insulin’s effect on amino acid potassium and phosphate metabolism?

A

Cells become more permeable to amino acids phosphate and potassium, amino acid absorption and protein synthesis is enhanced.

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17
Q

What is the slower effect of insulin that happens 10-15 minutes after stimulation?

A

Changed phosphorylation states of several enzymes occur acting to accelerate glucose utilization and enhance ATP production.

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18
Q

What are the slower effects of insulin stimulation that take effect several hours/days after initial stimulation?

A

rates of translocation and slower changes in rates of transcription of DNA can occur serving to further accelerate metabolism

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19
Q

What is the name of the glucose transporter that allows glucose into beta cells at a rate proportional to the blood concentration of glucose?

A

GLUT2

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20
Q

What is glucose converted to when it first enters a beta cell of the pancreas? What enzyme canalizes this reaction? Why is this reaction particularly important to the release of insulin?

A

It is converted to glucose-6-phosphate by glucokinse. This step is particularly important as it is the rate limiting step in the series of reactions that stimulate insulin secretion upon glucose entering a beta cell.

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21
Q

What happens to molecules of glucose-6-phosphate in beta cells of the pancreas? What does this cause?

A

glucose-6-phosphate molecules are oxidized to form ATP this interacts with ATP sensitive K+ channels cause their closure and a subsequent depolarization of the Beta cell membrane.

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22
Q

What is the effect of the depolarization of the membrane of beta cells?

A

Voltage gated Ca calcium channels are stimulated causing an influx of calcium and stimulating the release of insulin via the fusion of docked insulin containing vessicles with the outer plasma membrane

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23
Q

What amino acids can cause insulin release? How do they do this?

A

arginine and lysine can be metabolized by beta cells forming ATP causing depolarization leading to insulin release

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24
Q

How do hormones like gastric inhibitory peptide, secretin, gastrin, cholecystokinin and acetylcholine effect insulin release?

A

They can cause the release of calcium via other signalling pathways, this is so there is an anticipitory release of insulin before meals

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25
Q

How do sulfonyurea drugs stimulate insulin secretion?

A

They bind to ATP sensitive K+ channels in beta cells causing depolarization

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26
Q

What causes muscle cells to take up more glucose during heavy and moderate exerise?

A

The contraction process of muscles causes their membranes to become more permeable to glucose

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27
Q

How do muscle cells react if they are made to take up a surplus of glucose by insulin or other means?

A

They convert it to glycogen for storage

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28
Q

What enzyme in inactivated in order to enhance glucose uptake in the liver? What does this enzyme usually do?

A

liver phosphatase as it usually breaks down glycogen forming glucose

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29
Q

What liver enzymes are enhanced when spikes in blood glucose occur? What is the effect of this?

A

glucose kinase as it makes glucose that has diffused into hepatocytes temporarily trapped in liver cells and enzymes that promote glycogen synthesis such as glyocogen synthase

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30
Q

What enzyme in the liver allows glucose recently detached from glycogen to exit liver cells more easily? Why is this?

A

glucose phophatase allows the easy exit as it removes a phosphate group from the glucose making it more permeable in regards to the hepatocyte membrane

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31
Q

What effect does insulin have on the conversion of excess glucose into fatty acids?

A

it promotes it

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32
Q

What effect does insulin have on gluconeogenesis?

A

it inhibits it

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33
Q

Insulin promotes the conversion of glucose into fatty acids what usually happens to these?

A

They are packaged as triglycerides and transported via very low density lipoproteins to adipose tissue

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34
Q

What is unique about brain cells in regards to response to insulin why does this make maintenance of blood glucose so important?

A

They have very little response to insulin as their cell membrane are permeable to glucose and only use glucose for energy this means blood glucose must be above a critical level in order for brain cells to have energy

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35
Q

In what pathway is glucose split to pyruvate?

A

glycolytic

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36
Q

What is the substrace derive from pyruvate from which all fatty acids are synthesised?

A

Acetyl CoA

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37
Q

When excessive amounts of glucose are being used to make energy in the citrate cycle what ions are released? How do they effect cell metabolism and what is the secondary effect of this?

A

An excess of citrate and iso ctrate collects within cells this causes the activation of acetyl CoA carboxylase that catalises the reaction that forms malonyl CoA from acetyl CoA which is the first step of fatty acid synthesis

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38
Q

How does insulin promote the uptake of fatty acids in the form of triglycerides into adipose tissue?

A

insulin activates lipoprotein lipase the the capillary walls of adipose tissue which splits triglycerides into fatty acids so they can enter the adipose cells and then be converted back into triglycerides

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39
Q

What is insulin’s effect on hormone sensitive lipase in adipose cells? What function does this serve?

A

it inhibits it so triglycerides in adipose cells are not hydrolysed to form fatty acids so fatty acid release from adipose tissue is inhibited

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40
Q

Insulin promotes the uptake of glucose into adipose cells in the same way as it does with muscle cells, what is this glucose used to form that helps fatty acid storage?

A

It forms alpha-glycerol phosphate, the substance three fatty acids fuse with to form triglcerides

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41
Q

How can insulin deficiency promote atherosclerosis?

A

In the absence of insulin, hormone sensitive lipase is activated this causes hydrolysis of stored triglycerides releasing these into the blood, the high levels of circulating triglycerides promote the conversion of fatty acids into phospholipids and cholesterol. The release of these promote the growth and atherosclerotic plaques

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42
Q

What causes ketosis in diabetes?

A

in the absense of insulin excessive amounts of acetoacetic acid are formed in the liver cellsthis can be oxidise forming acetyl CoA or released into the blood where it enters cells and is converted into Acetyl CoA there. If too much is produced however some acetoacetic acid is converted to beta-hydroxybutyric acid and acetone, these are ketone bodies and their presence in high quantities is ketosis

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43
Q

How does insulin promote the synthesis of protein and its storage?

A

It stimulate the uptake of amino acids into cells, increases the rate of translation of mRNA and over a longer period of time increases the rate of transcription of DNA. It also inhibits catabolism of existing proteins and depresses the rate of gluconeogenesis conserving amino acids that would be used up in this process.

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44
Q

How can insulin lack lead to enhanced urea secretion in urine?

A

insulin lack causes widespread protein catabolism meaning more amino acids are released into the blood and are used as an energy source. As amino acids being used as a source of energy/ degrading releases urea more use of amino acids leads to high urine urea

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45
Q

What cells type in the islets of langerhans releases glucagon?

A

alpha cells

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46
Q

What is the main mechanism by which glucagon increase blood glucose?

A

glucagon actives adenylyl cyclase in the hepatic cell membrane leading to increased levels of cyclic AMP. The cAMP activates protein kinase regulator protein activting protein kinase that in turn activates phosphorylase b kinase. This converts phosphhorylase b to phosphorylase a there by promoting the release of glucose-1-phosphate from glycogen

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47
Q

What are the three main factors that stimulate glucagon release?

A

raised blood amino acids, low blood glucose and exercise

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48
Q

As well as glucokinase what other enzyme promote the formation of glucose-6-kinase from glucose upon entering a hepatocyte?

A

hexokinase

49
Q

What is the monomer glycogen is made from?

A

uridine diphosphate glucose

50
Q

What are the two main messengers that initiate glycogenolysis?

A

glucagon and epinephrine

51
Q

how is glycerol used in active tissues to create energy

A

it is phosphorylated forming glycerol-3-phosphate then enters the glycolytic pathway for glucose

52
Q

What transports fatty acids into mitochondria for their use for production of ATP/

A

Carnitine

53
Q

How many molecules of Acetyl CoA form each molecule of acetoacetic acid?

A

2

54
Q

What two ketone bodies can acetoacetic acid be converted into?

A

beta-hydroxybutyric acid and acetone

55
Q

What is epinephrine and norepinephrine’s effect on hormone sensitive lipase?

A

it directly activates it

56
Q

What is thyroid hormone’s effect on fat?

A

it causes its rapid mobilization

57
Q

What is the main difference between amino acids and carbohydrates & fats that is why the body typically uses amino acids as an energy source less?

A

amino acids have no storage form

58
Q

How are excess amino acids removed from the body?

A

They are degraded and the excess nitrogen is excreted in urea

59
Q

The catabolism of amino acids typically begins with what? what is produced?

A

it typically begins with the removal of the alpha amino group from the amino acid and its transfer to alpha ketoglutarate forming glutamate

60
Q

Alanine transaminase catalyses what reaction what direction does it favour?

A

It catalyses the trans amination of Alanine with alpha ketoglutarate forming pyruvate and glutamate and favors neither direction

61
Q

What is unique about the reaction catalysed by Aspatate transaminase compared to other transaminase enzymes?

A

It catalyses the transfer of the alpha amino group forming oxaloacetate in the process

62
Q

What two enzymes allow the conversion of glutamine into ammonia and in what order? How much ammonia is formed?

A

First glutaminase then glutamate dehydrogenase it forms two ammonia per glutamate molecule

63
Q

What is the second route by which ammonia can be transported to the liver?

A

The alanine glucose shuttle whereby alanine deliveres ammonia via ALT, the resultant pyruvate undergoes gluconeogenesis and the original glucose is returned to the muscle

64
Q

How is ammonia excreted?

A

It is combined with one other ammonia molecule and one bicarbonate ion forming urea which is then excreted in the urine

65
Q

What secondary diseases and interventions of diabetes are primarily caused by diabetes

A

end stage renal disease, adult onset blindness and lower extremity amputations

66
Q

What are the normal boundaries blood glucose is kept within?

A

70 to 120mg

67
Q

At what concentration might a fasting glucose concentration test indicate diabetes?

A

126mg/dL on more than one occasion

68
Q

At what concentration might a random glucose concentration indicate diabetes?

A

over 200mg/dL

69
Q

What does euglycemic mean?

A

a normal level of glucose is present in the blood

70
Q

What response to an oral glucose tolerance test (OGTT) might indicate diabetes?

A

blood glucose exceeding 200mg/dLafter 2 hours

71
Q

Fasting glucose of what level would be classed as prediabetic?

A

above 100mg but below 126mg

72
Q

What response to an OGTT is prediabetic?

A

above 140mg/dl and below 200mg/dl

73
Q

What is HbA1C?

A

glycated haemoglobin

74
Q

What proportion of people with diabetes have the type 1 subtype?

A

5-10%

75
Q

What causes type 1 diabetes to present in adults?

A

latent autoimune diabetes in adults (LADA)

76
Q

What immune cells are most responsable for the destruction of pancreatic islets in type 1 diabetes?

A

CD4+ and CD8+ T cells as well as macrophages that invade the islets

77
Q

What is thought to be the role of glutamic acid decarboxylase (GAD) protein tyrosine phosphate (IA-2) and the cation transport ZnT8 in diabetes?

A

They are thought to be antigens that elicit an autoimmune response in type 1 diabetes

78
Q

What is the most common susceptibility loci for type 1 diabetes?

A

human leukocyte antigen (HLA) on chromosome 6p21

79
Q

What are the two main ways viruses can increase the likelyhood of diabetes

A

They can induce inflammation and cell damage of the pancreas releasing isolated beta cell antigens that activate sensitized lymphocytes or virus can produce proteins that mimic beta cell antigens causing the immune system to cross react with beta cells.

80
Q

what racial backgrounds have a higher prevalence of type 2 diabetes?

A

South asian, african caribbean, polynesian, middle eastern and american indian

81
Q

What are the main two metabolic defects in the pathogensis of type 2 diabetes?

A

decreased response to insulin and beta cell dysfunction that manifests as inadequate insulin secretion

82
Q

How do non-esterified fatty acids (NEFA’s) observed in much greater levels in obese individuals contribute to the pathgenesis of type 2 diabetes?

A

excess NEFA’s overwhelm the fatty acid oxidation pathway cause the build up of intermediates like DAG and ceramide which activate serine/threonine kinases that cause damaging sering phosphorylation of insulin receptors

83
Q

What is the name for the group of hormones released by adipose tissue that help co-ordinate changes in metabolism?

A

adipokines

84
Q

What are the main two pro-hyperglycemic adipokines?

A

resistin and retinol binding protein 4

85
Q

What are the main two anti-hyperglycemic adipokines?

A

leptin and adiponectin

86
Q

What is leptin’s and adiponectin effect on insulin sensitivity? How does it achieve this?

A

it increases it by enhance the activity of AMP activated protein kinase that promotes fatty acid oxidation

87
Q

AMPK is the target for whawt insulin sensitivity increasing drug?

A

metformin

88
Q

lispo and aspart are what?

A

rapid acting insulins

89
Q

How do rapid acting insulins (lispo and aspart) effect blood glucose over time?

A

They start to reduce it after 15 minutes and their effect lasts usually lest than 4 hours

90
Q

What is the use for rapic acting insulins?

A

to control spikes in glucose such as after meals

91
Q

What is the only form of insulin that can be delivered intravenously, how does it effect blood glucose over time?

A

it only starts having an effect 30-60 minutes after being administered but lasts 6-8 hours

92
Q

What is Neutral protamine Hagedorn (NPH) how does it effect blood glucose?

A

an intermediate acting insulin. It reduces blood glucose 2 hours after being administered, has its peak effect 4-12 hours after injection and lasts 18-24 hours

93
Q

what are glargine and insulin determire? How do they effect blood glucose?

A

They are long acting insulins and provide a steady decrease of insulin that lasts over 24h

94
Q

When might a patient with type 2 diabetes be given insulin as part of their therapy?

A

when life style changes and an excess of 2 different oral drugs have not successfully caused a decrease in blood glucose

95
Q

What do do sulfonylureas drugs do that helps treat type 2 diabetes?

A

They bind to the ATP sensitive K channels in beta cells causing thei closure subsequenly causing beta cell membrane depolarization and thereby enhance insulin release

96
Q

How do alpha glucosidase inhibitors help those with diabetes?

A

It inhibits intestinal enzymes that digest carbohydrates meaning that there is less sugar for the body to process

97
Q

How do Sodium glucose co-transporter 2 inhibitors help diabetics?

A

They stop re-absorption of glucose from urine by SGLT2’s thereby decreasing blood glucose

98
Q

What are the leading causes of death among people being treated for diabetes and in what proportions?

A

70% cardiovascular problems, 10% renal failure and 6% infections

99
Q

Is lower extremity gangrene the effect of macro or microvascular disease?

A

macrovascular disease

100
Q

What does AGE stand for in the context of diabetes?

A

advances glycation end products

101
Q

What are RAGE’s what tissues are they found in and what are the three effects of their activation?

A

They are receptors for Advanced glycation end products and they are found in inflammatory cells, endothelial cells and vascular smooth muscle. Their activation leads to the release of inflammatory mediators and growth factors from macrophages, the generation of reactive oxygen special in the endothelium and cause enhanced proliferation of vascular smooth muscle and production of smooth muscle ECM

102
Q

Why is the cross linking of proteins caused by AGE’s so damaging to blood vessels?

A

when type 1 collagen is cross-linked their elasticity is decreased making it more succeptable to shear stress. This encourages the formation of new ECM but makes existing protein harder to remove

103
Q

Nuclei from where serve as the feeding center of the brain?

A

the lateral hypothalamus

104
Q

Stimulation of the lateral nuclei of the hypothalamus that make up the feeding center causes what?

A

hyperphagia (excessive hunger and increased appetite)

105
Q

Nuclei from where make up the satiety center of the brain?

A

the vetromedial medulla

106
Q

Stimulation of the satiety center causes what?

A

An inhibition of the action of the feeding center

107
Q

What is ghrelin’s nickname? What cells release it?

A

it is also known as the hunger hormone and is produced by ghrelin cells in the GI tract

108
Q

What does ghrelin act on? what is its effect?

A

hypothalamic cells in the arcuate nucleus. It increases hunger and increases gastric secretion and gut motility in preparation for a meal

109
Q

What is the nickname for leptin? What produces it? Where does it act on and what is the effect of this?

A

It is know as the satiety hormone, it is produced by adipose cells and it acts on the arcuate nucleus in the hypothalamus regulating hunger to help achieve homeostasis

110
Q

What are the three regions of the cortex of the adrenal glands?

A

the zona glomerulosa, zona fasciculata and the zona reticularis.

111
Q

What do all the hormones produce by the adrenal cortex have in common

A

They are all steroid hormones?

112
Q

What is the difference between the embryological origins of the adrenal cortex and the medulla?

A

The cortex is derived from similar parts to te gonad and the medulla has its origins in the same tissue as the sympathetic nervous system

113
Q

What is the outermost section of the adrenal medulla? What does it secrete?

A

The zona glomerulosa, it secretes mineralcorticoids

114
Q

What is the role of the glucocorticoids released by the zona glomerulosa of the adrenal cortex?

A

They help maintain fluid homeostasis

115
Q

Why does the zona glomerulosa stain weaker than the adjacent layers of cortex?

A

it contains fewer lipid droplets

116
Q

What does the zona fasciculata of the adrenal cortex secrete? What is the role of this?

A

glucocorticoids that help regulate carbohydrate lipid and protein metabolism

117
Q

What give the zona fasciculata its foamy appearnce on histalogical slides?

A

The abundance of ER and lipid droplets

118
Q

What is produced by the zona reticularis?

A

predominantly sex hormones but also small amounts of gluccorticoids

119
Q

What is produced by the medulla of the cortex?

A

epinephrine and norepinephrine

Semester 4 (10 decks)

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