Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A

Intestines and kidneys.

Co transport glucose/galactose with Na.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where are GLUT1 found and what do they transport?

A

Everywhere.
Transport glucose and galactose.
High glucose affinity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where are GLUT3 found and what do they transport?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Where are GLUT5 found and what do they transport?

A

Small intestine and sperm.

Fructose transport.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the pentose phosphate pathway?

A

Important for synthesis of cholesterol, FA’s and nucleotides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Outline glycogenesis (synthesis of glycogen)?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Outline glycogenolysis (breakdown of glycogen to glucose)?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How is glucose detected on urinalysis stick?

A

Peroxidase enzyme, oxidises glucoronic acid from colourless to blue form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How would the results of a FGTT differ in a diabetic patient compared to a normal patient?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What hormonal changes occur in a FGTT?

A

Adrenaline, cortisol and other inflammatory mediators released.
Adrenaline will cause HSL to be activated and glycogen to be broken down and will stimulate gluconeogenesis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the two main metabolic complications of diabetes?

A

Diabetic ketoacidosis

Hyperosmolar hyperglycaemic state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What happens in DKA?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the 4 biochemical abnormalities seen in DKA?

A
  • 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-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How can HSS/HONK occur?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How are DKA and HSS treated?

A
  1. IV fluids
  2. IV insulin
  3. IV potassium
  4. Supportive treatment (NG tube, antiemetics)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are symptoms of hypoglycaemia, who can get it and why is it dangerous?

A

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
Q

How is hypoglycaemia treated?

A

Mild (when blood glucose <4mmol/l) treated with 15-20g glucose
More severe may require IV glucose or dextrose

34
Q

Describe fasting blood glucose levels in a healthy/impaired/diabetic patient:

A

<6/6.1-6.9/>7 mmol/l

35
Q

Describe the OGTT results in a healthy/impaired/diabetic patient:

A

<7.7/7.8-11/>11.1 mmol/l

36
Q

Describe HbA1C levels in a prediabetic and diabetes patient

A

Pre: 42-47 mM
Dia: >48 mM

37
Q

Is Type 1 diabetes insulin resistant or insulin deficient

A

Deficient

38
Q

Is Type 2 diabetes insulin resistant or insulin deficient

A

Resistant

39
Q

Is MODY diabetes insulin resistant or insulin deficient

A

Deficient

40
Q

Is Secondary diabetes insulin resistant or insulin deficient

A

Deficient

41
Q

Is Steroid induced diabetes insulin resistant or insulin deficient

A

Resistant

42
Q

Is gestational diabetes insulin resistant or insulin deficient

A

Resistant

43
Q

Which autoantibodies are tested for in T1DM?

A

ICA - islet cell autoantibody
IA2 - islet antigen 2
GAD65 - glutamic acid decarboxylase 65

44
Q

What does MODY stand for and what are causes of monogenic diabetes forms?

A

Maturity onset diabetes of the young
Mutation in a gene that causes impaired insulin production
Very rare

45
Q

What are the 5 most common MODY mutations and how do they impair insulin production?

A

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
Q

What are main dietary lipids?

A

Triglycerides, cholesterol and phospholipids

47
Q

What is triglyceride structure?

A

Glycerol backbone, joined to three fatty acid molecules by ester bonds

48
Q

How are lipids digested?

A
  • 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
Q

How are lipids absorbed?

A
  • 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
Q

How are fatty acids synthesised?

A

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
Q

How are fatty acids oxidised to make energy after they have been synthesised??

A

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
Q

When are ketones formed?

A

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
Q

How are triglycerides synthesised?

A

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
Q

How are phospholipids formed?

A

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
Q

How does lipolysis occur?

A

HSL (hormone sensitive lipase) breaks down TAG into glycerol + 3FA’s

56
Q

In triglyceride formation and metabolism, what enzymes does insulin stimulate or inhibit?

A

Stimulates enzymes in FA synthesis: ACC, FAS and LPL

Inhibits enzymes in lipolysis: HSL

57
Q

In triglyceride formation and metabolism, what enzymes does noradrenaline stimulate or inhibit?

A

Stimulates enzymes in lipolysis: HSL

58
Q

In what state is LPL active in adipocytes?

A

In the fed state

59
Q

In what state is LPL active in skeletal muscle?

A

In the fasted state

60
Q

Why are essential fatty acids needed and give examples?

A

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
Q

What are normal fasting/fed blood glucose levels?

A

Fasting: 4-5mM
Fed: 8-12mM

62
Q

How is insulin release triggered and what is the process?

A

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
Q

How does insulin secretion in a diabetic patient differ to normal?

A

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
Q

How is insulin synthesised?

A

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
Q

Why are the C chains that are cut off from proinsulin relevant?

A

They can be counted in the body to look at how much natural insulin is being made

66
Q

What is the half-life of insulin

A

4-6 minutes

67
Q

How does insulin signal to tissues?

A 
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
Q

What effects does insulin have on liver?

A

Increases glycogen and FA synthesis

Decreases gluconeogenesis

69
Q

What effects does insulin have on muscle and adipose?

A

Increases FA synthesis and GLUT4 translocation

Decreases lipolysis

70
Q

What effects does insulin have on protein in the body?

A

Increases amino acid transport and protein synthesis

71
Q

How is glucagon produced and how does it signal to other cells?

A

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
Q

What are risk factors and presenting features of T1DM?

A

RF: genetics, environmental trigger (Coxsackie), dietary factors, geographical variation

Features: Polyuria, polydipsia, tired, thin, young age onset, blurred vision, slow wound healing

73
Q

How is T1DM diagnosed?

A
  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
Q

What is the cause of T1DM?

A

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
Q

What is the pathophysiology of T1DM?

A

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
Q

How is T1DM treated?

A 
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
Q

What is the main complication of T1DM?

A

Hypoglycaemia

78
Q

What types of insulin exist and give examples?

A

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions