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Year 2 > Endocrine Week 2 > Flashcards

Endocrine Week 2 Flashcards

1
Q

What are the different types of starch and their structures?

A

Amylase - unbranched, a-1,4-glycosidic bonds

Amylopectin - a-1,4-glycosidic bonds with a-1,6-glycosidic bond branches

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2
Q

How are carbohydrates digested?

A

Starch converted by salivary amylase into glucose, disaccharides like maltose and dextrins.
Pancreatic amylase then converts into disaccharides.
Maltose (maltase) into glucose x 2.
Sucrose (sucrase) into glucose and fructose.
Lactose (lactase) into glucose and galactose.

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3
Q

What is glycaemic index?

A

Indicates the proportion of a food that is glucose.

GI = area under curve for 50g carbohydrate/area under curve for 50g pure glucose X 100.

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4
Q

What are the two main modes of glucose transport and name the transporters?

A

1) Facilitated diffusion, down a concentration gradient by GLUT 1-5
2) Co-transported wth Na against a concentration gradient by SGLUT1/2

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5
Q

Where are SGLUT1/2 found and what do they transport?

A

Intestines and kidneys.

Co transport glucose/galactose with Na.

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6
Q

Where are GLUT1 found and what do they transport?

A

Everywhere.
Transport glucose and galactose.
High glucose affinity.

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7
Q

Where are GLUT2 found and what do they transport?

A

Liver, pancreatic B cells, intestines and kidneys.
Transports glucose, galactose and fructose.
Low glucose affinity.

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8
Q

Where are GLUT3 found and what do they transport?

A

Brain, placenta and testes.
Transport glucose and galactose.
High glucose affinity.

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9
Q

Where are GLUT4 found and what do they transport?

A

Muscle (skeletal and cardiac) and adipocytes.
Insulin responsive glucose transport.
High glucose affinity.

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10
Q

Where are GLUT5 found and what do they transport?

A

Small intestine and sperm.

Fructose transport.

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11
Q

What are the different hexokinase enzymes used by tissues and describe them?

A

All convert glucose -> G6P

Hexokinase 1-3:

  • expressed in all tissues (except pancreatic B-cells and liver)
  • inhibited by G-6-P
  • low Km therefore high ability to phosphorylate glucose

Hexokinase 4 (glucokinase):

  • expressed in pancreatic B cells and liver
  • regulated by insulin
  • has high Km therefore low ability to phosphorylate glucose
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12
Q

Outline glycolysis?

A

Glucose —(hexo/glucokinase)–> G6P —> F6P —(PFK1)—-> F-1,6-BP ——-> DHAP + G3P —-> PEP —(pyruvate kinase)—-> Pyruvate

—(lactate dehydrogenase)—>Lactate

OR

—> Co-enzyme A —(pyruvate dehydrogenase)—> acetyl CoA -> TCA cycle

Acetyl CoA (2C) combines with oxaloacetic acid (4C) forming citrate (6C) then becomes 5C and 4C intermediates. Overall 36 ATP made.

  • for every NADH = 3ATP
  • for every FADH2 = 2ATP
  • for every GTP = 1ATP
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13
Q

What is the pentose phosphate pathway?

A

Important for synthesis of cholesterol, FA’s and nucleotides

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14
Q

Outline glycogenesis (synthesis of glycogen)?

A

Glucose —-(hexokinase)—> G6P —-> G1P —-(G1P uridyltransferase)—-> UDP glucose —-(UDP given off and then glycogen synthase)—-> glycogen

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15
Q

Outline glycogenolysis (breakdown of glycogen to glucose)?

A

Glycogen + Pi ——(glycogen phosphorylase)—-> G1P —-> G6P —-(G6Pase)—-> glucose

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16
Q

What is gluconeogenesis and what 4 substrates can be used?

A

Formation of glucose from a non-carbohydrate source: - lactate (made into pyruvate)

  • pyruvate
  • amino acids (made into pyruvate)
  • glycerol (made into DHAP)
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17
Q

Outline gluconeogenesis?

A

4 enzymes needed as various stages of glycolysis use ATP and so cannot be reversed.

  • PCOX (pyruvate to oxaloacetate)
  • PEPCK (oxaloacetate to PEP)
  • F-1,6-BPase (F-1,6-BP to F6P)
  • G6Pase (G6P to glucose)
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18
Q

What hormones stimulate gluconeogenesis in the liver and how do they function?

A

Glucagon and adrenaline, affect gene expression causing enhanced/reduced activity.

  • decrease glucokinase activity
  • increase G6Pase activity
  • increase PEPCK activity
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19
Q

What enzymes does insulin affect the activity of?

A
  • increases glucokinase
  • decreases G6Pase activity
  • decreases PEPCK activity
  • stops an increase in cAMP so TAG’s cannot be broken down
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20
Q

Draw the pathways of glucose metabolism in muscle, liver and adipose and the enzymes involved, also showing how insulin/adrenaline/glucagon affect these hormones:

A

Week 10 Lecture notes p6

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21
Q

What happens to glucose in adipose tissue in the fed state?

A

Week 10 Lecture notes p6

Glucose —> DHAP

DHAP has 2 branches

1) —-> G3P
2) —> acetyl CoA —> malonyl CoA —(FAS) —> FA’s
- G3P is acted upon by (DGAT - diacylglycerol acyl transferase) and combines with FA forming TAG
- FA’s can also be obtained in periphery by VLDL –(LPL)–> FA’s

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22
Q

What happens to glucose in adipose tissue in the fasted state? How is adrenaline involved?

A

TAG’s are broken down.
TAG —(HSL)—> glycerol and FA’s
- glycerol can then be used by the liver for gluconeogenesis
- Adrenaline causes production of cAMP which activates PKA which activates HSL

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23
Q

How does an electronic device calculate blood glucose levels?

A

ExacTech machine
Blood sample on the paper card
The enzyme glucose oxidase is in the machine and converts any glucose in the blood into glucoronic acid
Current generated in this reaction, the larger the current the greater the glucose content.

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24
Q

How is glucose detected on urinalysis stick?

A

Peroxidase enzyme, oxidises glucoronic acid from colourless to blue form

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25
How would the results of a FGTT differ in a diabetic patient compared to a normal patient?
In diabetic patient, results would be that the ingestion of glucose would cause an abnormally high blood glucose concentration, which would be maintained for a greater time period.
26
What hormonal changes occur in a FGTT?
Adrenaline, cortisol and other inflammatory mediators released. Adrenaline will cause HSL to be activated and glycogen to be broken down and will stimulate gluconeogenesis.
27
What are the two main metabolic complications of diabetes?
Diabetic ketoacidosis | Hyperosmolar hyperglycaemic state
28
What happens in DKA?
Usually in T1DM Without insulin body cannot use glucose for energy so fatty acids released from adipose Fatty acids undergo B-oxidation producing ketone bodies e.g. acetoacetate The ketone bodies are acidic causing metabolic acidosis Glucose levels increase as proteolysis occurs and amino acids are used for gluconeogenesis The reabsorption threshold of glucose at the kidneys is exceeded so osmotic diuresis occurs Aldosterone is released to try to reabsorb Na in exchange for K, so hyperaldosteronism occurs and there are huge K losses 3 counter regulatory hormones are also released: - adrenaline: glycogenolysis, gluconeogenesis and lipolysis - cortisol: gluconeogenesis, lipolysis and inhibition of glucose uptake - GH: same as cortisol
29
What are the 4 biochemical abnormalities seen in DKA?
- Low HCO3 (being used to neutralise acidic ketones) - High blood H+ - Low pH - low CO2 (as breathing rate increases to try to move eq. to LHS) H2O + CO2 H2CO3 H+ + HCO3-
30
How can HSS/HONK occur?
HHS = hyperosmolar hyperglycaemic state HONK = hyperosmolar non-ketotic Occurs mainly in type 2 patients with very high glucose levels. There is STILL SOME INSULIN PRODUCTION and so no beta-oxidation or ketoacidosis occurs Kidneys glucose reabsorption threshold is still exceeded so glucose and solutes are lost in the urine and water follows causing osmotic diuresis Clotting of blood and comas are common risks
31
How are DKA and HSS treated?
1. IV fluids 2. IV insulin 3. IV potassium 4. Supportive treatment (NG tube, antiemetics)
32
What are symptoms of hypoglycaemia, who can get it and why is it dangerous?
Sweating, tremor, palpitations, anxiety, confusion and possibly impaired consciousness. Can affect anyone taking glucose lowering medication Danger is hypoglycaemia unawareness - CNS fails to produce symptoms to warn the patient that their blood glucose is low = sudden unconsciousness If you experience 1+ episodes of severe hypoglycemia in a year the DVLA must be informed
33
How is hypoglycaemia treated?
Mild (when blood glucose <4mmol/l) treated with 15-20g glucose More severe may require IV glucose or dextrose
34
Describe fasting blood glucose levels in a healthy/impaired/diabetic patient:
<6/6.1-6.9/>7 mmol/l
35
Describe the OGTT results in a healthy/impaired/diabetic patient:
<7.7/7.8-11/>11.1 mmol/l
36
Describe HbA1C levels in a prediabetic and diabetes patient
Pre: 42-47 mM Dia: >48 mM
37
Is Type 1 diabetes insulin resistant or insulin deficient
Deficient
38
Is Type 2 diabetes insulin resistant or insulin deficient
Resistant
39
Is MODY diabetes insulin resistant or insulin deficient
Deficient
40
Is Secondary diabetes insulin resistant or insulin deficient
Deficient
41
Is Steroid induced diabetes insulin resistant or insulin deficient
Resistant
42
Is gestational diabetes insulin resistant or insulin deficient
Resistant
43
Which autoantibodies are tested for in T1DM?
ICA - islet cell autoantibody IA2 - islet antigen 2 GAD65 - glutamic acid decarboxylase 65
44
What does MODY stand for and what are causes of monogenic diabetes forms?
Maturity onset diabetes of the young Mutation in a gene that causes impaired insulin production Very rare
45
What are the 5 most common MODY mutations and how do they impair insulin production?
HNF 1 alpha - an important transcription factor to regulate the start of the insulin pathway, normally no treatment needed Glucokinase gene - dysfunctional allowing resting glucose levels to be higher than normal, usually no treatment required HNF 4 alpha - at birth low blood sugar and heavy, treat with sulphonylurea and possibly insulin HNF 1 beta Neonatal diabetes mellitus - mutation at sulphonylurea receptor, treatment with sulphonylurea tablets usually treats
46
What are main dietary lipids?
Triglycerides, cholesterol and phospholipids
47
What is triglyceride structure?
Glycerol backbone, joined to three fatty acid molecules by ester bonds
48
How are lipids digested?
- Lipase in small intestine breaks triglycerides into monoG and FA's - Bile salts emulsify lipids into micelles with large SA for enzymes to act on - Micelles are packages of MAG and FA
49
How are lipids absorbed?
- Micelles absorbed into intestinal cells and TAG's formed again - TAG's packaged with cholesterol and lipoproteins forming chylomicrons - Chylomicrons released by exocytosis into lymphatic system and eventually into bloodstream - In bloodstream LPL removed FA from chylomicrons leaving chylomicron remnants - Liver takes up these remnants via APOE protein/receptor and breaks them up into FA's and cholesterol
50
How are fatty acids synthesised?
F (FAS)atty A(ACC)cids are synthesised by FAS (fatty acid synthase) and ACC (acetly CoA carboxylase) enzymes. Acetyl CoA converted into malonyl CoA by ACC FAS then produces fatty acids from malonyl CoA in 7 steps
51
How are fatty acids oxidised to make energy after they have been synthesised??
FA + acetyl CoA -> fatty acyl CoA Fatty acyl CoA and carnitine join and pass through CPT1 Are split into CoA and fatty acyl carnitine These combine and pass through CPTII breaking up into carnitine and fatty acyl CoA again (CPT1 and CPTII are the transporters on the mitochondrial membranes) Fatty acyl CoA then undergoes B-oxidation and is reduced by 2C at a time, producing many acetyl CoA molecules which can enter the Krebs cycle to make energy.
52
When are ketones formed?
When there is XS acetyl CoA and it can't all enter the krebs cycle, some goes on to produce ketones. Ketones can be stored in tissues and later broken down to produce acetyl CoA
53
How are triglycerides synthesised?
Uses enzymes LPL (lipoprotein lipase) and DGAT (diacylglycerol acyl transferase) - glycerol obtained from glycolysis used DGAT - LPL releases fatty acids from chylomicrons in the blood - glycerol and fatty acids then combine
54
How are phospholipids formed?
Initial steps are the same as TAG formation and glycerol + 2FA's formed, which an alcohol is then added to producing a phospholipid (phosphatidylethanolamine)
55
How does lipolysis occur?
HSL (hormone sensitive lipase) breaks down TAG into glycerol + 3FA's
56
In triglyceride formation and metabolism, what enzymes does insulin stimulate or inhibit?
Stimulates enzymes in FA synthesis: ACC, FAS and LPL | Inhibits enzymes in lipolysis: HSL
57
In triglyceride formation and metabolism, what enzymes does noradrenaline stimulate or inhibit?
Stimulates enzymes in lipolysis: HSL
58
In what state is LPL active in adipocytes?
In the fed state
59
In what state is LPL active in skeletal muscle?
In the fasted state
60
Why are essential fatty acids needed and give examples?
Cannot be synthesised in body and must be obtained from diet Uses: cell membrane formation, growth and development, brain and nerve function, eicosanoid precursors (leukotrienes) Omega 3 and 6
61
What are normal fasting/fed blood glucose levels?
Fasting: 4-5mM Fed: 8-12mM
62
How is insulin release triggered and what is the process?
High glucose levels are the trigger High glucose causes ATP to ADP ratio in the cell to increase This closes K-ATP channels Cell then depolarises and voltage gated Ca channel open There is a sudden Ca influx and insulin is released by exocytosis Insulin secretion always biphasic
63
How does insulin secretion in a diabetic patient differ to normal?
There is a rapid rise in insulin which is given as medication (the insulin is exogenous) and this does not correlate with glucose levels. The insulin secretion is also not divided into two phases.
64
How is insulin synthesised?
As a pro-hormone Pre-proinsulin (signal sequence - B chain - C chain - A chain) Becomes proinsulin (signal sequence lost and disulphide bonds form between A and B chains) Becomes insulin when C chain is lost
65
Why are the C chains that are cut off from proinsulin relevant?
They can be counted in the body to look at how much natural insulin is being made
66
What is the half-life of insulin
4-6 minutes
67
How does insulin signal to tissues?
``` Binds to TKR causing autophosphorylation Receptor has docking sites which other proteins can bind to to be phosphorylated Proteins of IRS family are phosphorylated (including PIP3) which act as internal messengers Eventually PKB (Akt) is activated and this causes GLUT4 translocation ```
68
What effects does insulin have on liver?
Increases glycogen and FA synthesis | Decreases gluconeogenesis
69
What effects does insulin have on muscle and adipose?
Increases FA synthesis and GLUT4 translocation | Decreases lipolysis
70
What effects does insulin have on protein in the body?
Increases amino acid transport and protein synthesis
71
How is glucagon produced and how does it signal to other cells?
Produced by alpha cells as single polypeptide chain Released in response to low blood glucose Binds to G-protein coupled receptor and the alpha subunit of the receptor is released stimulating adenyl cyclase to activate cAMP and eventually PKA is activated PKA decreases glycolysis
72
What are risk factors and presenting features of T1DM?
RF: genetics, environmental trigger (Coxsackie), dietary factors, geographical variation Features: Polyuria, polydipsia, tired, thin, young age onset, blurred vision, slow wound healing
73
How is T1DM diagnosed?
1. History 2. Random plasma glucose test 3. Fasting plasma glucose test 4. Plasma/urinary ketones 5. HbA1C test 6. Fasting C peptide measurement 7. Autoimmune markers
74
What is the cause of T1DM?
Autoimmune destruction of pancreatic islet cells (B) Genetic predisposition and environmental trigger Dietary factors protective (Vit D) Diet can make worse (unhealthy) Certain genotype = HLA DQ2
75
What is the pathophysiology of T1DM?
B cells destroyed by autoantibodies Symptoms of hyperglycaemia only develop once 80-90% cell population is destroyed Body cannot produce enough insulin Glucose cannot get into cells therefore counter-regulatory hormones released - adrenaline, cortisol and GH promote gluconeogenesis in the liver Long term hyperglycaemia causes vascular complications - MICROVASCULAR COMPLICATIONS ARE THE BIGGEST CONCERN
76
How is T1DM treated?
``` Education (DAFNE) Glucose management Insulin therapies - fixed dose regime - basal bolus regime Low carb diet Diabetic nurse involved Attend diabetic clinics New treatments: B-cell transplants, combined monitors and pumps ```
77
What is the main complication of T1DM?
Hypoglycaemia
78
What types of insulin exist and give examples?
1) short acting - injected before meal and lasts 8hrs e.g. Novorapid 2) intermediate/long acting - last up to 20-24hrs e.g. Lantus 3) Biphasic insulin - mix of short and intermediate/long acting types e.g. Novomix 30

Year 2 (22 decks)

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