Brainscape's Knowledge GenomeTM

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


See full index

Block 1: Pathophysiology + Pharmacology > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Define diabetes

A

Metabolic disorder characterised by elevated blood glucose concentration either due to insulin resistance, insufficient insulin secretion, or both

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

What is the difference between Type 1 and Type 2 diabetes?

A

Type 1 = Insufficient secretion due to autoimmune destruction of Beta cells
Type 2 = Insulin resistance (loss of first phase insulin response and beta cell exhaustion)

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

What is the main metabolic fuel for the brain?

A

Glucose

Requires continuous supply due to inability to store or synthesise glucose in the brain

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

Where do we get our glucose supplies from?

A

Diet
Glycogenolysis (breakdown of glycogen)
Gluconeogenesis (formation of glucose)

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

Where does gluconeogenesis occur?

A

Liver and kidneys

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

What substrates form glucose in gluconeogenesis?

A

Glycerol (from fats)
Lactate (produced from non-oxidative metabolism of glucose - process reversed in liver in gluconeogenesis)
Glutamine and Alanine (from proteins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is glycogen?

A

Multi-branched polysaccharide
Energy storage molecule
Stored in liver and muscle cells

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

What are the main hormones that maintain glucose homeostasis?

A

Insulin

Glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where is insulin produced?

A

Beta cells (Islets of Langerhans within Pancreas)

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

What cells are found in Islets of Langerhans and what does each produce?

A 
Alpha cells (produce glucagon) 
Beta cells (produce insulin) 
Delta cells (produce somatostatin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the role of Somatostatin?

A

Inhibits action of insulin and glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the phases of insulin secretion?

A

First phase = rapid onset, lasting approx. 10 minutes

Second phase = prolonged plateau lasting as long as necessary (e.g. whilst body is in hyperglycaemic state)

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

What occurs during the first phase of insulin secretion?

A

Release of pre-docked and primed vesicles

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

What occurs during the second phase of insulin secretion?

A

Release of insulin from granules - a complex process involving a process of transport, docking, priming and fusion

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

How do actions of insulin come about?

A

Activation of insulin receptors on target cell membrane which activates secondary pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the actions of insulin?

A
  1. Glucose transport
  2. Glycogen synthesis
  3. Protein synthesis and inhibition of protein breakdown
  4. Lipogenesis and inhibition of lipolysis
  5. Promotes mitogenesis (induces cell division)
17
Q

How does insulin facilitate glucose transport?

A

Promotes fusion of vesicles containing GLUT-4 and insertion into cell walls to facilitate glucose transport into cells (by facilitated diffusion)

18
Q

How does insulin facilitate glycogen synthesis?

A

Promotes activation of Glycogen Synthase

19
Q

What regulates Glucagon secretion?

A
  1. Blood glucose levels - low blood glucose increases secretion and high blood glucose inhibits secretion
  2. Insulin secretion
20
Q

What are the actions of Glucagon?

A

Stimulates gluconeogenesis and glycogenolysis
Increases hepatic fatty acid (beta) oxidation and therefore ketone formation
Stimulates lipolysis in adipose cells, increasing circulating free fatty acids and reduces adipocyte glucose uptake

21
Q

What hormone is primarily responsible for responding to drop in blood glucose levels?

A

Glucagon

22
Q

At what state is insulin favoured?

A

Post-pandrial (fed) state - insulin responding to increased glucose levels

23
Q

How does the sympathetic nervous system alter insulin and glucagon levels?

A

Activation of sympathetic nervous system increases Adrenaline (and noradrenaline) release which inhibits insulin and promotes glucagon secretion

24
Q

How does cortisol and growth hormones impact insulin and glucagon levels?

A

Promote gluconeogenesis
Inhibits glucose transport
Inhibits insullin secretion

25
Q

What symptoms characterise Type 1 diabetes?

A

Hyperglycaemia
Polyuria (increased urination)
Polydipsia (increased thirst)
Weight loss

26
Q

What causes hyperglycaemia in Type 1 diabetics?

A

Loss of insulin secretion (due to destruction of beta cells) leads to an inability to take up glucose into cells and an inability to store glucose as glycogen and unopposed glucagon action (e.g. glycogenolysis and gluconeogenesis)

27
Q

What causes polyuria in Type 1 diabetes?

A

Glycosuria due to glucose levels exceeding the kidneys capacity to reabsorb glucose
Glucose in urine inhibits the concentrating ability of the kidneys

28
Q

What causes polydipsia in Type 1 diabetes?

A

Physiological response to dehydration to maintain fluid balance
High blood glucose stimulates thirst response

29
Q

What causes weight loss in Type 1 diabetes?

A

Unopposed lipolysis and proteolysis for gluconeogenesis precursors

30
Q

What causes ketoacidosis?

A

Ketones produced as alternative energy source (as a product of fatty acid metabolism)
Seen in T1D and is a medical emergency

31
Q

What are the symptoms of DKA?

A

Shock (due to severe dehydration)
High respiratory rate
Abdominal pain

32
Q

What are the modifiable risk factors for T2 DM?

A 
Overweight/ obesity (esp. central obesity) 
Lack of physical activity
Smoking 
Poor diet (e.g. high fat, low fibre) 
Low SES
33
Q

What are the non-modifiable risk factors for T2 DM?

A 
Age (40+) 
Family history 
Ethnicity (Black African, South Asian)
Impaired glucose regulation ("prediabetes") 
Mental health conditions (or antipsychotic medications) 
History of hypertension, CVD or stroke 
Low birth weight 
PCOS
34
Q

How is Type 2 DM treated?

A

Diet, exercise, lifestyle measures
Oral hypoglycaemic agents (e.g. Metformin which decreases hepatic gluconeogenesis)
Injectable agents (e.g. Insulin)

35
Q

What are the potential complications of Diabetes?

A

Hypoglycaemia (of treatment)
Microvascular (e.g. retinopathy, neuropathy, nephropathy)
Macrovascular (e.g. Ischaemic Heart Disease, Cerebrovascular Disease, Peripheral Vascular Disease)

36
Q

What is Diabetes Insipidus?

A

Inability to reabsorb water from distal nephron due to either inadequate production (cranial DI) of ADH or insensitivity (nephrogenic DI) to ADH

37
Q

What are the physiological consequences of Diabetes Insipidus?

A

Polyuria (10-15 litres/day)
Thirst & polydipsia (need access to fluids to keep pace with losses)
Low urine osmolality (dilute)
High / high normal plasma osmolality & serum [Na]

38
Q

What test can aid diagnosis of Diabetes Insipidus?

A

Water/fluid deprivation test

Block 1: Pathophysiology + Pharmacology (7 decks)

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