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Phase 2- Endocrine > Week 1 > Flashcards

Week 1 Flashcards

1
Q

What can ATP be replenished by?

A

Creatine phosphate (muscle -short term)
Anaerobic metabolism CHO to lactate
Aerobic metabolism of CHO, fat and/or protein (in mitochondria)

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2
Q

What different CHOs can come from diet?

A

Polysaccharides (starch, cellulose) dissacharides (maltose, succose and lactose) and monosaccharides (glucose and fructose)

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3
Q

What is the difference between glucose and fructose?

A

Same chemical formula, but different structure

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4
Q

What links di and polysaccharides?

A

Glycosidic bonds (alpha, beta)

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5
Q

What does digestibility of starch vary with?

A

Properties of food: trapped in intact starch granules/ plant cell wall structure, resistant to amylase as 3D structure too tightly packed, associated with dietary fibre (slows absorption and digestion as gut contents become viscous)

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6
Q

Can humans digest cellulose?

A

No, we do not have enzymes to cleave beta-1,4 links of cellulose

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7
Q

Where is glycogen stored?

A

Liver, and skeletal muscle

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8
Q

What cells are dependent on blood glucose?

A

RBCs (no mitochondria), brain (lipids cannot cross the blood-brain barrier, neurotransmitters are made from glucose metabolites)

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9
Q

What hormones regulate plasma glucose concentration?

A

Insulin (storage) and glucagon (glucose synthesis)

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10
Q

How is glucose transported into cells?

A

Either transported down concentration gradient by facilitated diffusion (GLUT 1-5), or transported against concentration gradient using energy provided by co-transport of sodium (SGLUT 1 and 2). SGLUT is required in the intestine to absorb from gut lumen, and in the kidney to reabsorb from filtrate

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11
Q

Where is GLUT-1 found?

A

In all cells, it is ubiquitous. It transports glucose (high affinity) and galactose, not fructose

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12
Q

Which glucose transporter transports fructose?

A

GLUT-5, transports fructose but not glucose or galactose

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13
Q

Which glucose transporter is insulin responsive?

A

GLUT-4, in adipose and muscle, therefore more glucose is transported in when plasma glucose concentration after a meal.

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14
Q

Which glucose transporter is exercise responsive?

A

In muscle, GLUT-4 translocates in response to physical activity/exercise (independent of insulin) therefore, more glucose use for ATP production

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15
Q

What are pentoses essential for?

A

DNA/RNA synthesis

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16
Q

What is the fate of glucose within a cell?

A

Production of ATP, storage as glycogen, storage as lipid, synthesis of sugars for RNA/DNA, minor fraction to synthesis glycolipids and glycoproteins

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17
Q

What is the first step of cellular glucose metabolism?

A

All pathways require phosphorylation of glucose to glucose-6-phosphate as a first step. This traps glucose inside the cell, and is catalyst by hexokinases I-IV

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18
Q

What is glucokinase?

A

An enzyme, also known as hexokinase IV), which is expressed by beta cells of pancreas and liver. It has a low affinity for glucose

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19
Q

What are hexokinases I-III?

A

Enzymes expressed in all other cells, with a high affinity for glucose. They are inhibited by G6P (feedback inhibition)

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20
Q

What is phosphofructokinase?

A

An enzyme that determines whether G6P is used for glycolysis. It is inhibited by ATP, citrate (downstream products)

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21
Q

What enzyme is involved in the final step of glycolysis?

A

Pyruvate kinase

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22
Q

Describe glycolysis:

A

Uses 2ATP and degenerates 4ATP and 2NADH. Net gain of 2ATP and 2NADH. Phosphofructokinase is the committed step for glycolysis. NADH must be used so that NAD+ is replenished:

  • under anaerobic conditions get lactate formation (no further ATP)
  • under aerobic conditions NADH can be used to make more ATP in mitochondria
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23
Q

What are the fates of pyruvate?

A

Lactate (anaerobic conditions), or acetyl-CoA (occurs in mitochondria by pyruvate hydrogenase)

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24
Q

What are the diagnostic criteria for diabetes mellitus?

A

Fasting blood glucose: < 6 normal, 6.1 - 6.9 impaired, >7 diabetes
OGTT (?): <7.7 normal, 7.8-11 impaired, >11.1 diabetes
Need 2 abnormal tests or 1+ symptoms
HbA1c (average glucose over 6-7 weeks): 42-47 pre-diabetes, >48 diabetes (not yet rolled out in Glasgow)

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25
Q

What are the different types of diabetes?

A

Type 1, Type 2, Maturity Onset Diabetes of the Young (MODY), Gestational (pregnant women), Secondary (pancreatitis, cystic fibrosis, haemochromatosis (causes toxicity to beta cells), steroid-induced (cause insulin resistance in tissues), acromegaly)

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26
Q

Which types of diabetes are insulin deficient, and which are insulin resistant?

A 
Insulin deficient:
- Type 1
- MODY
- Pancreatitis
- Cystic fibrosis
- Haemochromatosis 
Insulin Resistant:
- Type 2
- Gestational
- Steroid-induced
- Acromegaly
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27
Q

What are the auto-antibody marker involved in type 1 diabetes?

A

ICA (islet cell antibody), I-A2 (insulinoma-associated antigen-2), IAA (insulin auto-antibody), GAD65 (glutamic acid decarboxylase 65), ZnT8 (zinc transporter)

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28
Q

What are the precipitating events for type 1 DM?

A

Enteroviruses (especially coxsackie), rotavirus, bacteria (Mycobacteria Avium paraTB), environmental (cow’s milk, what proteins), vitamin D deficiency, insulin resistance (e.g. puberty), maybe psychological stress

29
Q

What are exocrine cells?

A

Cells secreting substances via ducts which are then released onto epithelial surfaces

30
Q

What are endocrine cells?

A

Cells producing hormones which are released into the bloodstream and act at distant sites

31
Q

What are paracrine cells?

A

Cells secreting chemical messengers which act nearby

32
Q

What are autocrine cells?

A

Cells secreting substances into the extracellular space which then act upon the same cells which produced them

33
Q

What is primary hypothyroidism?

A

Underproduction of T3/T4 due to abnormal thyroid gland. Low T3/T4, high TSH

34
Q

What is secondary hypothyroidism?

A

Underproduction of T3/T4 due to abnormal anterior pituitary. Low T3/T4, low TSH

35
Q

What is tertiary hypothyroidism?

A

Underproduction of T3/T4 due to abnormal hypothalamus. Low T3/T4, variable TSH, low TRH

36
Q

How does the pancreas form?

A

Two buds extend from primitive duodenum at junction of foregut and midgut. The buds fuse together to form pancreas and bile system.

37
Q

What is the histology of the pancreas?

A

Lobulated gland, divided by fibrous septa. Main bulk of tissue is exocrine. Secretory acini are densely packed cells with granular cytoplasm, which produce enzymes and watery alkaline fluid. Tiny central lumen in each, draining to the duct system. The duct system is a highly branched system, covering to form the pancreatic duct which joins with the common bile duct to enter the duodenum at ampulla of Vater. It has a cuboidal to columnar lining.

38
Q

What is the histology of the endocrine pancreas?

A

Islets of Langerhans are small, roundish collections of endocrine cells. They are highly vascular (for secretion of hormones into blood), and they produce peptide hormones insulin, glucagon and some others. Different cell types produce different hormones: beta cells produce insulin, alpha cells produce glucagon and gamma cells produce somatostatin

39
Q

How does malignant tumour of the head of pancreas present?

A

Presents with obstructive jaundice by blocking common bile duct. May invade into adjacent structure such as stomach, duodenum, transverse colon and major vessels. Can spread to lymph nodes, liver and peritoneal cavity

40
Q

What is the embryology of the adrenal glands?

A

Cortex; is mesodermal, from urogenital ridge. Before birth, foetal zone with large eosinophilic cells. Postnatally, this involutes and cuter layer forms the definitive cortex with three zones. Medulla; derived from neural crest cells (ectodermal), part of the sympathetic nervous system

41
Q

What are the parts of the adrenal glands?

A

Outer cortex and inner medulla (anatomical and functional divisions)

42
Q

What are the three layers of the cortex of the adrenal gland?

A 
Zona glomerulosa (outer; produces aldosterone)
Zona fasciculata (80% of cortex, lipid-rich, produces glucocorticoids and androgens)
Zona reticularis (like fasciculata but less lipid)
43
Q

What is the histology of the medulla of the adrenal gland?

A

Central area, part of the sympathetic nervous system. Produces adrenaline and noradrenaline, released in response to physiological stress

44
Q

What is an adrenal adenoma?

A

Benign tumour of the adrenal cortex; may produce excessive hormones (cortisol (Cushing’s syndrome), aldosterone (Conn’s syndrome) and adrenal androgens)

Rarely present with local symptoms- often too small

45
Q

What is adrenal cortical carcinoma?

A

Malignant proliferation of cells of adrenal cortex. Less common to produce excess hormones (malignant cells often less like cells of cortex, less differentiated). May invade into surrounding structures and metastasise to distant sites

46
Q

What adrenal cortical atrophy ?

A

Decrease in functional mass of the cortex. Often iatrogenic: administration of corticosteroids, usually long term. Negative feedback blocks ACTH production- no stimulus for activity of cortical cells. Sometimes due to autoimmune destruction (e.g. Addison’s disease)

47
Q

What is phaeochromocytoma?

A

Uncommon tumour of adrenal medulla. Important cause of secondary hypertension??

48
Q

What are pentoses important for?

A

Synthesis of fatty acids (generation of NADPH for reductive biosynthesis) and nucleotides (formation of ribose 5-phosphate)

49
Q

What cells use about 10% of their glucose on the pentose pathway?

A

Erythrocytes???

50
Q

Why is glycogen stored in the liver?

A

For blood glucose maintenance

51
Q

Why is glycogen stored in the muscle?

A

For local energy production (only used by muscle itself)

52
Q

What enzyme is important in the regulation of glycogenesis?

A

Glycogen synthase (very highly regulated)

53
Q

What enzyme is important in the regulation of glycogenolysis?

A

Glycogen phosphorylase- breaks down glycogen to glucose-1phosphate

54
Q

What is gluconeogenesis?

A

The syntheses of glucose from a nonhexose source (lactate, pyruvate, glycerol, certain AAs)

55
Q

Where does gluconeogenesis occur?

A

Mainly in the liver (kidneys can contribute with prolonged starvation)

56
Q

What enzymes in glycolysis are not reversible, and why are they not reversible?

A

Hexokinase/glucokinase, phosphofructokinase and pyruvate kinase. All involve use of ATP

57
Q

How is hexokinase bypassed in gluconeogenesis?

A

By glucose 6-phosphatase (principally expressed in liver- only organ that can convert G6P back to glucose)

58
Q

How is PFK bypassed in gluconeogenesis?

A

By fructose 1,6-bisphosphatase

59
Q

Where is G6Pase found?

A

Enzyme is in the lumen of the ER- needs transporters for substrates and products to get in/out. Expression stimulated by adrenaline, glucocorticoids, suppressed by insulin

60
Q

How is pyruvate kinase bypassed in gluconeogenesis?

A

Liver makes pyruvate carboxylase, and phosphoenolpyruvate carboxykinase (PEPCK) (see lecture)

61
Q

How are substrates used in gluconeogenesis?

A

Lactate to pyruvate, glycerol to dihydroxyacetone phosphate. Amino acids in various locations in TCA cycle and pyruvate

62
Q

What stimulates gluconeogenesis in the liver?

A

Glucagon and adrenaline (decreases glucokinase, increases G6Pase and PEPCK activity (increases gluconeogenesis)). Effect is at the level of gene expression

63
Q

How is insulin secretion regulated in beta cells?

A

Glucose transport into cell causes build up of ATP/ADP, which inhibits K-ATP channel. This causes influx of Ca2+ from L-Ca2+ channels, which stimulates secretion of insulin from beta cells

64
Q

What does insulin bind to?

A

Insulin receptor: tyrosine kinase receptor (found primarily in liver, striated muscle and adipocytes)

65
Q

What happens intracellularly when insulin binds to insulin receptor?

A

Insulin receptor self-phosphorylates, which activates insulin receptor substrate (IRS) which causes a downstream amplification of signals, eventually activating protein kinase B/Akt.

66
Q

What does PKB activate?

A

In muscle and adipocytes glucose transport, in muscle and liver glycogen synthesis and in liver and adipocytes fatty acid synthesis

67
Q

What does PKB inhibit?

A

In adipocytes lipolysis, and in liver gluconeogenesis

68
Q

What happens in glucagon signalling?

A

Glucagon binds to the glucagon receptor

  • G-protein coupled receptor
  • Only found in hepatocytes
  • Increases cyclic AMP
  • cAMP stimulates cAMP-dependent protein kinase (PKA)

Phase 2- Endocrine (4 decks)

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