Quiz 4

Question 1

What is the difference between diabetes inspidus and diabetes mellitus (Type 1 + 2)

Answer 1

Diabetes inspidus: inability to concentrate the urine, so produce large quantities of dilute urine.
Cause- from deficiency in ADH, or nephrogenic (unresponsive renal tubules)

Diabetes Mellitus
-chronic hyperglycaemia
-can affect every system in the body
Type 1- insulin deficiency
type 2- insulin resistance and deficiency
-inability to sequester (hide away) glucose from blood so levels are highly elevated.
-increased glucose prevents reabsorption of water this increased levels of sweet urine.

Question 2

The cause of Diabetes Mellitus

General differences between type 1 and 2 Diabetes

Answer 2

-disease of impropper glucose utilization and metabolism
-chronic hyperglycemia- affects every system in bidy.
Type 1- sever or abolute insulin deficiency (autoimmune etc, hereditary)
Types 2- insulin deficiency, insulin resistance (diet, obesity)

Type 1:

• insulin dependant
• ketosis prone
• juvenile onset
• growth onset
• disease is deficiency of autoimmune att on insulin producing cells of pancreas

Type 2:

• insulin independant
• ketosis resistance
• adult onset
• maturity onset

Question 3

What are the symptoms of Type 1 Diabetes?

Answer 3

Polyuria, polydipsia, polyphagia, weight loss, fatigue, lethargy, blurred vision, tingling numbness in feet, erectile dysfunction, arterial disease, nausea and vomiting, abdominal pain, tachypnoea, skin infections, mood changes.

Question 4

describe the progression of Type 1 diabetes:

Answer 4

1. exposure to a virus or toxin may start process of B cell destruction in individuals with genetic predisposition
2. Slow B cell destruction- over period of years, B cells are destroyed, resulting in decreased production of insulin
3. When insulin secretory capacity falls below a threshold the symptoms of type 1 diabetes suddenly appear.

Question 5

What are the metabolic changes assosiated with type 1 diabetes?

The consequences of Insulin deficiency in DM

Answer 5

Resulting from a deficiency in insulin and a high glucagon levels in 3 tissues- liver, muscle and adipose tisse. Abnormalities result in:
1. Hyperglycaemia- elevated glucose levels caused by an increase in gluconeogenesis in liver coupled by a dimished use in tissues that are unable to take up glucose (muscle adipose tissue)

2. Ketoacidosis- increased mobilisation of fatty acids from adipose tissue, combined with an increase in ketone body synthesis by the liver
3. Hypertriacylglycerolaemia- not all fatty acids are disposed of by oxidation or ketone body production in liver. Excess fatty acids are converted to TAG then packaged into VLDL and there is also an accumulation of chylomicrons from dietary sources.

Consequences of insulin deficiency:

• hyperglycaemia- elevated glucose levels caused by increased gluconeogenesis in liver coupled by a diminished use in tissues that are unable to take up glucose (muscle adipose tissue)
• Lipolysis–> inc. free fatty acids –> ketonaemia –> Ketonuria –> acidosis –> coma and death
• long term complications: cataracts, retinopathy, neuropathy, nephropathy, premature atheroma.

Question 6

Treatment for type 1 diabetes

Symptoms of hypoglycaemia

Answer 6

-insulin treatment only option. must continue through pt life
-change fo diet neccessaey: low-fat, high-fibre, low simple sugar, high complex sugar is recommended.
Adverse reactions- overdose, long term diabeteic often dont produce adequate amounts of counter hormones (glucagon, adrenaine, cortisol, GH) which normaly provide adequate defence against hypoglycaemia

Symtoms of hypoglycaemia:

• tachycardia
• confusion
• vertigo
• excess sweating
• hypersensitivity

Question 7

Inter-tissue relationship in Type 1 diabetes

Answer 7

refer to notes
basically hyperglycemia results from increased hepatic gluconeogenesis and decreased glucose uptake bin the peripheral tissue

-ketosis results from massive mobilization of fatty acids from adipose followed by hepatic gluconeogensis.

Question 8

The role of insulin resistance in type 2 diabetes

Answer 8

• combination of insulin resistance and dysfunctional B cells
• decreased abilityof target tissues like liver, adipose tissue and muscles to respond to normal circulating levels of inuslin.
• resistance increases with weight gain and diminished with weight loss. As fat tissue secretes hormones which may contribute to insulin resistance eg leptin

Question 9

The role of dysfunctional B cells in type 2 diabetes

Answer 9

-pancreas is originally able to secrete elevated levels of insulin to deal with hyperglycaemia, the B cells eventually deteriorate and levels of insulin decline. Hyperglycaemia and elevated levels of free fatty acids can accelerate disease progression.

Question 10

The progression of type 2 diabetes

Answer 10

The metabolic abnormalities of type 2 diabetes occur as a result of insulin resistance primarily in the liver, muscle and adipose tissue.

1. Hyperglycaemia- cause by increased hepatic glucose production and decreased peripheral usage. Ketosis is minimal coz the presence of insulin, even with insulin resistance, diminished hepatic ketogenesis.
2. Hypertriacylglycerolaemia- excess fatty acids are converted to TAG then packaged into VLDL and there is also an accumulation of chylomicrons from dietary sources

Question 11

Treatment of type 2 diabtes

Answer 11

goal is to maintain glucose levesl within normal limits and prevent long-term complications
-weight reduction, exercise, diet modification often correct hyperglycaemia

1. Oral Hypoglycaemi drugs

Question 12

Tell me about the oral hypoglycaemic drugs

Answer 12

pg 49
1. First generation sulfonylureas (tolbutamide)- stimulates insulin secretion, risk of hypo-glcemia, has well estabilished effectiveness, weight gain can occur.

2nd generation sulfonylureas (glipizide)-stimulates insulin secretion, risk of hypoglyecmia, etc

3. Meglitinide analogs