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Endocrinology > TBL4 Pancreas > Flashcards

TBL4 Pancreas Flashcards

1
Q

Insulin has 2 categories of action

A
  1. Metabolic

2. Mitogenic (growth and development)

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2
Q

What general effects does insulin have on glucose, protein and lipid metabolism?

A
  1. Decrease glucose output
  2. Decrease proteolysis
  3. Decrease lipolysis

=> Overall, insulin has anabolic effects.

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3
Q

Glucose is stored in _______ and ________ as glycogen.

A

Liver and muscle cells

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4
Q

Insulin stimulates ________ to be recruited to the plasma membrane to allow extracellular glucose to be taken up by the cell via its hydrophilic pore.

A

GLUT-4 transporter

  • particularly muscles and adipose tissue
  • increases uptake of glucose into cells to decrease blood glucose levels
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5
Q

Muscle cells contain a large amount of _______.

A

proteins

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6
Q

Insulin effects on muscle cells:

A
  1. Inhibits proteolysis
  2. Inhibits oxidation of amino acids
  3. Stimulates protein synthesis (stimulate transport of AA into the muscles)
  4. Increase GLUT-4 to increase uptake of glucose into muscle cells
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7
Q

Insulin effects on hepatocytes:

A
  1. Inhibits gluconeogenesis
  2. Stimulates glycogenesis
  3. Increased protein synthesis
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8
Q

Insulin effects on adipocytes:

  1. Activates (enzyme) to breakdown triglycerides in the blood to glycerol and NEFA
A
  1. Activates endothelial lipoprotein lipase to breakdown triglycerides into NEFA and glycerol
  2. Increased glucose uptake by GLUT-4
  3. Inhibits lipolysis
  4. Stimulates combination of glycerol and NEFA back into triglycerides
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9
Q

_______ is a good measure of CV risk.

A

Waist circumference

  • adipocytes in the gut are more metabolically active as their products drain into the liver directly
  • omental circulation
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10
Q

The brain can only utilise ______ and ______ as energy substrates.

A

glucose and ketones

cannot use fatty acids!

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11
Q

Ketogenesis occurs in the ________. It is (stimulated/inhibited) by insulin.

A

Ketogenesis

  • occurs in liver cells
  • inhibited by insulin (in the fed state, no need for ketones as energy substrates)
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12
Q

Ketone bodies released from the liver cells include

A

FA –> acyl-CoA –> acetyl-CoA –> acetone and 3-hydroxybutyrate

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13
Q

Fasted state:

  1. (Low/High) insulin to glucagon ratio
  2. (Decreased/Increased) concentration of fatty acids
  3. (Decreased/increased) concentration of amino acids
  4. (Decreased/increased) proteolysis, lipolysis and hepatic glucose output from __________ and _________
  5. (increased/decreased) ketogenesis when fasting is prolonged
A

Fasted state:

  1. Low insulin to glucagon ratio
  2. Increased fatty acids due to lipolysis
  3. Decreased amino acid concentration when prolonged due to gluconeogenesis
  4. Increased proteolysis, lipolysis and hepatic glucose output from gluconeogenesis and glycogenolysis
  5. increased ketogenesis when prolonged fasting
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14
Q

________ DM is characterised by absolute insulin deficiency.

A

Type 1 DM
- autoimmune destruction of B cells
- leading to increased hepatic glucose output, proteolysis and lipolysis, ketone output
=> continued release of nutrients even in the fed state

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15
Q

In a hypoglycemic event due to insulin, hepatic glucose output is switched off, and patients may be treated with

A

oral glucose

or

intramuscular glucagon (to mobilise glycogen stores)

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16
Q

_______ DM is characterised by insulin resistance and a relative insulin deficiency.

A

Type 2

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17
Q

Biochemical pathways of insulin

  1. Mitogenic
  2. Metabolic
A
  1. Mitogenic: Ras-MAPK pathway (cellular proliferation and growth)
  2. Metabolic: PI3K-Akt pathway (insulin resistance)
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18
Q

In type 2 DM, the growth pathway becomes amplified due to ___________.

A

compensatory hyperinsulinaemia
- pancreas responds to the high blood glucose by producing more insulin to allow to glucose to remain normal for many years

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19
Q

________ occurs in type 2 DM due to changes in the lipid metabolism that results from amplified mitogenic pathway.

A

Dyslipidaemia

  • low HDL, high LDL
  • risk factor for many macrovascular complications
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20
Q

What is the gastrointestinal incretin effect?

A
  • demonstrated by differences between response to oral and intravenous glucose
  • higher insulin response to oral glucose which passes through the gut due to GLP-1 secreted by the gut to stimulate insulin and suppress glucagon.
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21
Q

____________ (PPARy agonists) target the hormone response element within DNA and act as insulin sensitisers in peripheral tissues.

A

Thiazolidinediones

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22
Q

DPPG-4 inhibitors, also known as _______, can be used to treat DM by preventing the degradation of GLP-1 by DPPG-4.

A

Gliptins

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23
Q

_______ is the only hormone that decreases blood glucose.

A

Insulin

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24
Q

Hormones that increase blood glucose

A

Glucagon, somatotrophin (growth hormones), stress hormones (e.g. cortisol, adrenaline)

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25
Q

Most cells produce ________ secretions which travel via the pancreatic ducts to the small intestine.

A

exocrine secretions (pancreatic enzymes)

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26
Q

___________ of the pancreas secrete hormones (endocrine) directly into the bloodstream to control blood glucose.

A

islets of Langerhans

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27
Q

3 types of cells in the islets of Langerhans and its relative positions:

A
  1. a-cells secreting glucagon (at the peripheries)
  2. B-cells secreting insulin (at the middle)
  3. d-cells secreting somatostatin (scattered)
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28
Q

Cell junctions present between cells in the islets of Langerhans

A
  1. Gap junctions
    - small molecules to pass directly between cells
  2. Tight junctions
    - form small intercellular spaces which trap fluid to allow hormones to be accumulated in high concentrations
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29
Q

Insulin is synthesised as ________. In the (organelle), the linking C-peptide is cleaved, resulting in the insulin made of A and B chain linked by 2 _______.

A

Insulin:

  • synthesised as proinsulin
  • in the GA, C-peptide is cleaved and insulin is released as A chain and B chain linked by 2 disulphide bridges.
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30
Q

B-cells have ______ transporters present on the cell surface to allow glucose to move down its concentration gradient into the cell.

A

GLUT-2 transporter

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31
Q

Insulin production by B-cells:

  1. Glucose enters the B-cell via _____ transporters.
  2. (Enzyme) converts glucose to glucose-6-phosphate.
  3. Glucose-6-phosphate participates in metabolic pathways to produce ____.
  4. ____ deactivates the K+ channel, preventing K+ efflux from the cell, resulting in depolarisation of cell membrane.
  5. The depolarisation activates and opens voltage-gated ___ channels, which allows ___ ion influx to stimulate migration of insulin-containing vesicles to the membrane.
A

Insulin production:

  1. Glucose enters cell by GLUT-2.
  2. Glucose converted to glucose-6-phosphate by glucokinase.
  3. Glucokinase forms ATP.
  4. ATP deactivates K+ channels and prevents K+ efflux, causing depolarisation.
  5. Depolarisation activates voltage-gated Ca2+ channels that stimulate the migration of insulin-containing vesicles.
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32
Q

Insulin response to an increase in glucose concentration occurs in ___ phases.

A

2 phases (biphasic)

  1. Initial immediate release of pre-synthesised and stored insulin
  2. Newly-synthesised insulin
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33
Q

Somatostatin released by ___ cells act on

A

Somatostatin

  • released by delta cells
  • inhibit both a and B cells
  • inhibit secretion of both insulin and glucagon
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34
Q

Sympathetic activation via a receptors will (inhibit/promote) insulin secretion.

A

inhibit insulin secretion (to increase blood glucose levels during sympathetic activity)

a receptors - inhibit insulin

B receptors - promote insulin (B cells, B B)

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35
Q

Parasympathetic activation will result in (increased/decreased) insulin secretion.

A

Parasympathetic - increases insulin secretion ( to decrease blood glucose)

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36
Q

Main effects of insulin work to

A

increase energy storage (anabolism)

decrease energy formation (catabolism)

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37
Q

Insulin receptor is a _______ receptor.

A

RTK
- upon binding of insulin to RTK receptor, they dimerise and activate the intracellular tyrosine kinase domains
- autophosphorylation and cross-phosphorylation of receptors
=> phosphorylation of cell protein substrates

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38
Q

Why are the effects of insulin on hepatocyte glucose metabolism direct?

A

The movement of glucose into the cells is insulin-independent because it is GLUT-2 mediated, not GLUT-4.

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39
Q

Glucagon is released in the (Fasted/fed) state to (increase/decrease) blood glucose.

A

Glucagon

  • released during the fasted state
  • to increase blood glucose
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40
Q

Glucagon receptor

A

GPCR

  • Gs protein
  • adenylyl cyclase activation
  • cAMP
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41
Q

Glucagon (stimulates/inhibits) insulin production, whereas insulin (stimulates/inhibits) glucagon production.

A

Glucagon stimulates insulin production; insulin inhibits glucagon production

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42
Q

Pathophysiology of Type 1 DM

A
  • viral infection
  • coupled with genetic predisposition
    => abnormal antigen presentation and recognition by the immune system
  • islet B-cell destruction
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43
Q

Type 1 DM is known to be _____ and _____ associated. (genetic)

A

HLA-DR3 and DR4 associated

  • Th cells with surface HLA-DR4 can recognise the viral antigen to activate the immune system
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44
Q

HLA-____ is known to be protective against diabetes.

A

HLA-DR2

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45
Q

Viral trigger for type 1 DM

A
  • direct infection of B cells
  • molecular mimicry
  • viral proteins incorporated into B cell membrane => B-cell altered expression
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46
Q

Immune mechanisms for type I DM against islet B cells

A
  • Cytotoxic T cells
  • Th cells
  • Antibodies
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47
Q

Why does weight loss occur in type 1 DM?

A

Proteolysis and lipolysis

  • due to the absence of insulin to prevent these from happening
  • wastage of proteins and fats (not stored)
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48
Q

Typical symptoms of T1DM

A

Osmotic symptoms

  • polyuria
  • polydipsia
  • nocturia
  • blurring of vision
  • thrush
  • weight loss
  • fatigue
  • glycosuria
  • ketonuria
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49
Q

Why does hyperventilation occur in type 1 DM?

A

type 1 DM

  • insulin deficiency
  • ketogenesis => ketones
  • ketoacidosis
    => compensatory hyperventilation to remove excess CO2
50
Q

Diet changes in diabetes

A
  • increase complex carbohydrates and soluble fibers
  • reduce fat and refined carbs
  • regular meals and snacks
51
Q

Soluble insulin is (short-/intermediate) acting.

NPH is (short/intermediate-) acting.

A

soluble insulin: short-acting

NPH - intermediate

52
Q

Background regime of insulin treatment for DM

A

Insulin taken twice daily via mixed soluble and NPH insulin

- not very physiological => not effective

53
Q

Basal bolus regime of insulin treatment for DM

A

NPH insulin at bedtime and soluble insulin with meals

54
Q

Actrapid is a (short/long)-acting insulin.

A

short-acting

55
Q

Lispro/novorapid are examples of ___________.

A

insulin analogues

- shorter peaks to prevent hypoglycemic events

56
Q

What is HbA1c?

A
  • shows amount of glucose bound to Hb over the lifespan of a RBC
  • ideal measure of long-term glycemic control
  • related to the risk of complications (particularly microvascular)
  • alternatively, fructoasmine can be used for pregnant/patients with haemoglobinopathy instead.
57
Q

Hyperglycemia can be caused by insulin deficiency or _________.

A

stress hormones (cortisol, catecholamines)

58
Q

How does metabolic acidosis occur in DM?

A
  1. Production of acidic ketone bodies
  2. Polyuria results in low circulating volume in the kidneys => reduced hydrogen ion excretion in the distal convoluted tubule => acidosis of blood

In DKA, the main cause is the drop in bicarbonate concentration.

59
Q

Dealing with _________ can improve DKA.

A

dehydration

  • patient needs fluid to allow their circulating volume to return to normal
  • kidneys can be perfused and have filtrate to excrete H+ ions
60
Q

Why are recurrent hypoglycemias especially dangerous?

A

recurrent hypoglycemias result in the loss of warning signs before onset

61
Q

Alcohol can lead to (hypo/hyper)glycemia.

A

Alcohol

  • hypoglycemia
  • use up glycogen stores
62
Q

How to treat hypoglycemia?

A

oral glucose or IM glucagon (to liberate glucose from glycogen stores)

63
Q

LADA

A

Type 1-like

  • insulin-deficient
  • ketosis-prone
  • but presents older and not as acutely
64
Q

MODY (Maturity onset diabetes of the young)

A

Type 2 diabetes

  • but occurs younger
  • patients less likely to be obese
65
Q

Diagnosis for diabetes

  1. Fasting glucose
  2. 2h 75g Oral glucose tolerance test
  3. Random glucose test
A
  1. Fasting glucose > 7.0mM
  2. OGTT > 11.1mM
  3. Random glucose > 11.1 (least ideal)
66
Q

T2DM is a combination of ___________, intrauterine environment and adult envrionment.

A
  • genetic predisposition
  • intrauterine environment
  • adult environment
67
Q

Insulin resistance is affected by genes and _________.

A

omental fat

- abnormalities in the fatty acid mechanism which contribute to insulin resistance

68
Q

Why does gradual islet B cell failure occur over time in type 2 DM?

A

Insulin resistance => B cells try to secrete more insulin => eventually worn out and destroyed => absolute B cell failure (requires insulin)

69
Q

There is a greater genetic basis for (Type 1/Type 2) DM.

A

Type 2 DM

70
Q

Unfortunately, weight gain is a common side effect of most diabetic treatments. ________ is the only treatment which does not cause weight gain.

A

Metformin

71
Q

Orlistat

A
  • gastrointestinal lipase inhibitor
  • reduce fat absorption to help with obesity
  • associated with an improvement in glycemic control
72
Q

Metformin

A
  • insulin sensitiser
73
Q

Sulfonylureas

e.g. Glibenclamide

A
  • insulin secretagogue

prevents insulin secretion by closing the Katp channel

74
Q

Acarbose

A
  • a-glucosidase inhibitor

- prolongs absorption of oligosacchrides

75
Q

Thiazolidinediones

A
  • PPARy agonists

- peripheral insulin sensitisers

76
Q

GLP-1

A
  • gut hormone

- stimulates insulin and suppress glucagon

77
Q

DDP4-inhibitors

A
  • gliptins

- inhibit DDP4 to prolong the action of GLP-1

78
Q

Microvascular complications of diabetes are related to _______, hypertension.

A

severity of hyperglycemia

79
Q

Glucose can cause tissue damage via various pathways, which are all related to ___________.

A

mitochondrial superoxide over-production

80
Q

__________ is a chronic complication of diabetes, and it is primarily a disorder of retinal circulation, caused by compromising delivery of oxygen and nutrients to the retina.

A

Diabetic retinopathy

81
Q

Diabetic retinopathy: The inner layer of endothelial cells in retinal blood vessels are connected with ___________, and _________ lie outside to control vessel calibre and blood flow.

A

Endothelial cells in retinal blood vessels connected with tight junctions; contractile pericytes lie outside to control blood flow.

82
Q

Diabetic retinopathy: Hyperglycemia is associated with damage to _________ and _________ of retinal blood vessels.

A

Hyperglycemia is associated with damage to endothelial and pericyte damage of retinal blood vessels.

83
Q

Diabetic retinopathy: Intracellular glucose activates ________, causing the release of _________ upon endothelial damage and causes the release of _____ which induces new vessel formation.

A

Intracellular glucose activates protein kinase C, causing release of endothelin-1 upon endothelial damage and causes the release of VEGF which induces new vessel formation.

84
Q

Background diabetic retinopathy (reversible early changes)

A
  • Hard exudates
  • Microaneurysms
  • Blot haemorrhages
  • no cause to visual field
85
Q

Proliferative diabetic retinopathy

A
  • new vessels as a compensatory mechanism to correct retinal ischemia
  • vessels are growing into the vitreous humor => minimal injury can cause blood vessel to shear off and bleed into the humour => vision loss
86
Q

Diabetic retinopathy: Maculopathy

A
  • hard exudates present near the macula
  • similar to background retinopathy but in the macula
  • threaten vision
87
Q

In diabetic nephropathy, __________ is a particularly important contributing factor.

A

hypertension (resulting in increased GFR)

88
Q

_______ is a hallmark of diabetic nephropathy.

A

Proteinuria

89
Q

Early nephropathy effects on:

  • glomerular capillary pressure
  • fenestrae size
  • charge on membrane
A
  • increased glomerular capillary pressure
  • slightly larger fenestrae
  • less negative charge on membrane
    => increased microalbumin loss
90
Q

Late nephropathy effects on:

  • fenestrae size
  • charge on membrane
  • glomerular capillary pressure
A
  • bigger fenestrae
  • less negative charge on membrane
  • glomerular capillary pressure remains elevated
    => macroalbuminuria
91
Q

________ can be used to control blood pressure and reduce progression of proteinuria in diabetic nephropathy.

A

ACE inhibitors

92
Q

____________ occurs when small vessels supplying nerves (_________) become blocked, causing nerve dysfunction.

A

Diabetic neuropathy

- small vessels supplying nerves (vasa nervorum) become blocked

93
Q

The most common diabetic neuropathy is ________, where the longest sensory nerves that supply the feet cause numbness.

A

diabetic peripheral neuropathy

- affects longest nerves e.g. sensory nerves to feet

94
Q

Macrovascular complications with diabetes is associated with the metabolic syndrome.

A

Insulin resistance

  • causing hyperinsulinemia (compensatory)
  • leading to smooth muscle hypertrophy (mitogenic effect of insulin)
  • worsening of atheroma (necrotic lipid core)
95
Q

Dyslipidemia (due to alterations of lipids and lipoproteins as a result of diabetes) is also associated with lipid accumulation in early atheroma.

A

-

96
Q

What are the main differences between microvascular and macrovascular complications of diabetes?

A

Microvascular

  • related to glycemic control mainly
  • hardly seen outside DM

Macrovascular

  • related to lipids, BP, weight, etc. beyond glycemic control
  • seen outside DM
97
Q

2 most common ways of measuring body mass - indication of nutritional status

A
  1. BMI

2. waist circumference

98
Q

In growing children, BMI may not be a reliable indicator of nutrition. What indicator should we use?

A

Growth chart

  • normal if they grow along certain percentile lines in a growth chart
  • abnormal (faltering growth) if their growth cuts across percentile lines
99
Q

Using body weight measurements in assessment of undernutrition is often not reliable, so _________ is used instead.

A

arm circumference

  • midpoint of the upper arm
  • measured after raising skin folds and subcutaneous fat
100
Q

Dietary reference values reflect the nutritional needs of a (individual/population) and is a way of assessing nutritional adequacy.

A

Dietary reference values

- nutritional needs of a population

101
Q

____________ refers to the amount of each nutrient needed, which are different across nutrients and varies between individuals and life stages.

A

nutritional requirement

102
Q

_____________ refers to the mean requirement of a nutrient. It is the daily intake value that is estimated to meet the nutrient requirement of half the healthy individuals in a population.

A

Estimate Average requirement (EAR)

103
Q

Calculation of nutrient requirement takes into account 2 aspects.

A
  1. Metabolic demand

2. Efficiency of utilisation

104
Q

3 types of energy expenditure

A
  1. Obligatory energy expenditure
    - basal metabolic rate
  2. Physical activity
  3. Adaptive thermogenesis
    - thermic effect of food
    - keep warm/digest food
105
Q

2 methods to measure energy expenditure

  1. Measures rate of O2 consumption and CO2 production to calculate RQ
  2. 2H2 eliminated as water; O eliminated as water and CO2
A
  1. Indirect calorimetry
    - measures respiratory quotient which represents the ratio between oxidation of sugars and lipids
  2. Doubly labelled water (DLW)
106
Q

Taking in nutrients is feeding 3 biochemical pathways which converge at _________.

A

acetyl-CoA molecule

  1. glucose => acetyl-CoA (glycolysis, link)
  2. Fatty acids => acetyl-CoA (B-oxidation)
  3. Amino acids => acetyl-CoA (deamination, oxidation)
107
Q

_______ cannot be stored in the body, hence it must be used/oxidised as a priority for fuel.

A

Alcohol

=> perfect auto-regulation

108
Q

Obese people have (lower/higher) percentage of water in their bodies.

A

lower

109
Q

Different signals are integrated in the __________ of the brain to regulate feeding in humans, in order to maintain body weight.

A

hypothalamus

110
Q

_________ is a collection of neural cell bodies in the hypothalamus which constitutes an external environment. It is the key brain area involved in the regulation of food intake.

A

Arcuate nucleus - possess an incomplete blood-brain barrier to integrate hormonal and central feeding signals

111
Q

2 neuronal populations exist in the arcuate nucleus of the hypothalamus

A
  1. Stimulatory: NPY/AgRP

2. Inhibitory: POMC/CART neurones

112
Q

POMC deficiency and MC4-R mutations have been found to cause ________.

A

morbid obesity

POMC neurons are present in the arcuate nucleus as inhibitory

113
Q

Satiety centre in hypothalamus:

Feeding centre in hypothalamus:

A

Satiety centre: ventromedial hypothalamus (VMH)

Feeding centre: lateral hypothalamus (LH)

114
Q

Neurotransmitters: AgRP, GABA, GHRH, MCH, NPY

A

Orexigenic action (feeding, stimulatory)

115
Q

Neurotransmitters: POMC, a-MSH, GLP-1/2, Leptin, Insulin

A

Anorexigenic action (satiation, inhibitory)

116
Q

Adipostat mechanism

A

circulating hormone produced by fat cells which is sensed by hypothalamus to cause hypothalamus to alter neuropeptides in order to increase/decrease food intake

117
Q

PYY is released from the ____ into circulation and acts as a (satiety/feeding) factor.

A

PYY

  • released from the gut
  • satiety factor
  • inhibits NPY release and stimulates POMC neurons to decrease appetite
118
Q

_______ is a gastric hormone which directly modulates neurons in the arcuate nucleus by stimulating _______ neurones and inhibiting _____ neurones to increase appetite.

A

ghrelin

  • gastric hormone
  • stimulates NPY/AGRP and inhibits POMC
  • increases appetite (feeding factor)
119
Q

Leptin is made by _________ in white adipose tissue, which signals to hypothalamus about the fat status of the body.
It triggers thermogenesis, reduced food take and nutrient levels and is therefore (orexigenic/anorexigenic).

A

Leptin

- orexigenic

120
Q

Leptin regulatory loop can potentially lead to obesity in 3 ways:

Which one is the main pathophysiological mechanism?

A
  1. Leptin deficiency
  2. Regulatory defects => low stimulation of hypothalamus
  3. Leptin resistance develops in the hypothalamus
    * MAIN mechanism*
121
Q

Developmental defect:
___________ occurs when the right and left sides of the ventral pancreatic bud migrate in opposite directions, resulting in a ring of pancreatic tissue around the duodenum.

A

Annular pancreas

- may cause stenosis and even complete obstruction (atresia), blocking the passage of food

122
Q

___________ is an endocrine marker used to stain islet cells in immunohistochemical staining methods.

A

Synaptophysin

- Positive (islet) cells appear brown

Endocrinology (7 decks)

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