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PATH2220 > w7 > Flashcards

w7 Flashcards

1
Q

define metabolism

A

the chemical processes that occur in a living organism in order to maintain life

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2
Q

how much energy does the transfer of ATP–>ADP release

A

3.6 kcal/mol

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3
Q

how much energy does the brain use at rest

A

about 25% of the bodes energy, 600kcal

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4
Q

what molecules do the brain use

A

ketones and glucose

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5
Q

what do gluconeogenesis and ketogenesis ensure

A

ensure substrates are available for the brain during starvation

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6
Q

what does the body store energy as

A

triglyceride

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7
Q

what is triglyceride formed from

A

acetyl-coA

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8
Q

how can acetyl-coA be formed from

A

carbohydrate, protein or fat

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9
Q

what is a hormone

A

a chemical messenger that is released by one cell stat acts on other cells

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10
Q

what is the hormone that lowers glucose

A

insulin

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11
Q

how does insulin work

A

Glucose stimulates the synthesis, activation and release of insulin from pancreatic β cells
• Actions
– Suppresses hepatic gluconeogenesis
– Suppresses hepatic glycogenolysis
– Suppresses ketogenesis
– Promotes glucose utilisation
– Promotes glycogen production in the liver and skeletal muscles
– Promotes FFA synthesis and storage in adipocytes, inhibits lipolysis
– Inhibits glucagon production
– Promotes protein synthesis and
decreases proteolysis

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12
Q

what are the hormones that raise glucose

A

glucago, adrenalin and cortisol and growth hormone

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13
Q

how does glucagon work

A

• Released by the α cells in the pancreas as the inhibition by insulin is removed
• Acts on the liver
– Increases glycogenolysis – Increase gluconeogenesis

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14
Q

how does adrenalin (noradrenalin) work

A 
• Stimulated by hypoglycaemia
• Acts on the liver
–  Increases glycogenolysis
–  Increase gluconeogenesis
–  Inhibits insulin secretion (α receptors)
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15
Q

how does cortisol and growth hormone work

A

– Limits glucose utilisation

– Increase glucose synthesis

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16
Q

who discovered the use of insulin and how

A

Dr F. Banting and Mr C. Best, his medical student, discover insulin in dogs
• They ligated their pancreatic ducts and waited until the exocrine cells degenerate, then ground up the remaining pancreatic cells and injected this substance into dogs rendered diabetic via pancreatectomy
• This was a summer studentship - perhaps the best studenship ever!

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17
Q

what is Phaeochromocytoma are catecholamine

A 
secreting tumours of chromaffin cells of the adrenal medulla
Tyrosine
Fuels
Lipids
Stress hormones
Controls
Metabolism

•  Paragangliomas if they arise from the sympathetic Dopa ganglia
18
Q

what are the symptoms of Phaeochromocytoma are catecholamine

A

headache, palpitations, sweating, pallor, nausea, flushing, anxiety/panic and paroxysmal HT, sustained HT

19
Q

explain Catecholamine metabolism

A
  • Metabolism occurs mainly in the cytoplasm of the cell the catecholamine was produced.
  • The vast majority of metabolism is of passively leaked catecholamine
  • The metabolism of cats is proportional to the volume of the storage vesicles – thus the higher the metanephrines, the larger the volume of vesicles, and the more cells
20
Q

explain Metanephrine metabolism

A
  • The adrenal medulla produces both adrenaline and noradrenaline.
  • Sympathetic nerves only produce noradrenaline.
  • Mostnoradrenalineis neuronal in origin.
  • Neurones do not contain COMT, thus do NOT produce metanephrines.
  • Metanephrine production is relatively independent of catecholamine secretion.
21
Q

what is diabetes characterised by

A

• increase circulating blood glucose levels (hyperglycaemia) due to
• reduced or ineffective use of insulin
(which is a hormone produced by the pancreas)

22
Q

what is glucose stored as in the liver and muscle

A

glycogen

23
Q

what is the storage process of glucose called

A

glycogenesis

24
Q

what is the breakdown of glycogen to glucose called

A

glycogenolysis

25
Q

describe type 1 diabetes

A
  • earlier onset
  • 80% under the age of 10 yrs
  • M=F
  • unknown trigger
  • associated with autoantibodies
  • assoc with other autoimmune disease
  • Symptomatic on presentation
26
Q

describe type 2 diabetes

A 
• usually later onset
(>30yrs)
• linked to obesity
• associated family hx
•  Progresses
• Insulin resistance pay a major role
• Usually asymptomatic / few classic symptoms
27
Q

what are the risk factors for developing type 2 diabetes

A
  • Family history
  • Age usually over 40 but children and young adults now developing type 2
  • History of Gestational Diabetes • Excess weight
  • Aboriginality
  • Other specific ethnic groups eg Chinese and those from Indian sub-continent
  • Insulin resistance syndrome (Metabolic Syndrome )
28
Q

what are the symptoms of diabetes

A

smell of acetone, nausea, vomiting, abdominal pain, polyuria, smell of acetone, blurred vision, stupor, weight loss,

29
Q

what are acute complications with diabetes

A
  • Diabetic Ketoacidosis (DKA) Usually occurs in Type 1 but may be seen in Type 2s
  • Hyperglycaemia Hyperosmolar state • Type 2 DM
  • Hypoglycaemia
  • Occurs as a result of therapy
30
Q

what are the long term microvascular complications of diabetes

A
  • DM retinopathy • Non proliferative • Proliferative
  • Macular edema
  • Nephropathy
  • Micoralbuminuria
  • Macroalbuminuria
  • End stage renal failure
  • Neuropathy
  • Autonomic neuropathy • Peripheral neuropathy • Erectile dysfunction
31
Q

what are some macro vascular complications of diabetes

A
  • Cerebrovascular • TIA
  • Stroke
  • Cardiovascular • Angina
  • IHD
  • Heart failure
  • Peripheral vascular disease
  • Gangrene
32
Q

what are the risk factors that impact on the risk of developing complications

A
  • Persistently high blood glucose levels & duration of diabetes
  • Smoking
  • High blood pressure
  • High cholesterol and triglycerides • Genetic predisposition • Excessive alcohol intake
33
Q

what are the two tools for diagnosis of glucose

A

glucose level and oral glucose tolerance test (given 75g of glucose and see how the body reacts to it)

34
Q

what is the biochemical markers of diabetes

A

• Auto Antibody levels
• Ab to islet cell components • IA2 antibody levels
• GAD 65 antibody levels
• Positive in > 90% , ~4% of 1st degree rela@ves- highly
predictive of DM in 5 yrs
• C-peptide
• Endogenous insulin production

35
Q

what do you do to treat diabetes (T1)

A
  • Achieve glycaemic control • Target BP and

* Target lipid profile

36
Q

what do you do to treat T2

A

• T2DM have a relative insulin deficiency
• Step 1 reduce insulin resistance with lifestyle modification…
weight loss and exercise
• Step 2 add Oral Hypoglycaemics..insulin sensitisers and/or secretagogues
• Step 3 Add insulin

37
Q

what is autocrine signalling and what is an example

A

secretes a hormone, or chemical messenger - that binds to autocrine receptors on the same cell, leading to changes in the cell. Interluekin 1 in monocytes – secreted by monocytes – stimluates the monocyte.

38
Q

what is paracrine signalling and what is an example

A
  • Paracrine signaling – local signaling • diffuse over a relatively short distance
  • Eg Clotting factors and Histamine
39
Q

what is endocrine signalling and what is an example

A

• Secreted by one cell
• Travels some distance and effects
different target cell
• Reach target tissue and act on receptor –
– On cell surface
– Inside cell – eg at DNA / Nuclear level.

40
Q

what are the gonadotrophins

A
  • Luteinizing hormone (LH)

* Follicle Stimulating hormone (FSH)

41
Q

what are the sex steroids

A
  • Androgens – Testosterone • Oestrogen

* Progesterone

PATH2220 (14 decks)

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