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Pathophysiology > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Where is insulin made?

A

Insulin is made by the beta cells in the pancreatic islets.

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2
Q

Where is glucagon made?

A

Glucagon is made by the alpha cells in the pancreatic islets.

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3
Q

What does insulin do?

A

Insulin allows glucose to be transported into cells.

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4
Q

What does glucagon do?

A

Glucagon stimulates the break down of glycogen.

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5
Q

What are the features of pre-diabetes?

A

1) impaired fasting glucose (IFG) 6.1-6.9 mmol/L
2) HbA1C of 6-6.4% (normal is under 6)
3) impaired glucose tolerance test (IGT) 7.8-11 mmol/L (normally BG will return to ~5.5 mmol/L after 2 hrs of ingesting glucose)

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6
Q

Which type of diabetes has an absolute insulin deficiency?

A

Type 1 diabetes mellitus.

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7
Q

Why is metabolic syndrome important?

A

It may or may not precede diabetes. It predisposes you to type 2 diabetes and cardiovascular disease.

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8
Q

What are some features of metabolic syndrome?

A
  • IFG
  • IGT
  • insulin resistance (insulin is unable to bring about a hypoglycemic response in a hyperglycemic state)
  • hypertension
  • abdominal obesity/diabesity (in women, waist circumference of over 88 cm, in men over 102 cm)
  • hyperlipidemia
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9
Q

What are three acute complications of diabetes mellitus?

A

1) hypoglycemia
2) diabetic ketoacidosis
3) hyperosmolar hyperglycemic state (HHS)

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10
Q

What can cause hypoglycemia?

A
  • missed meal
  • insulin overdose
  • overexertion
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11
Q

What do we worry about with hypoglycemia?

A

If glucose is too low, the brain is deprived of glucose. As a result the patient will usually lose consciousness, enter hypoglycemic coma.

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12
Q

How is hypoglycemia treated?

A
  • if mild - give 15 g of carbs PO
  • if severe (under 2.8 mmol/L) - give 20 g of carbs PO
  • if pt unconscious - give 1 mg glucagon subcut or IM (this will break down glycogen stores)
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13
Q

Diabetic ketoacidosis develops when these two circumstances are in place.

A

1) very low insulin levels

2) high levels of glucagon

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14
Q

What 3 derangements are seen when diabetic ketoacidosis develops?

A

1) hyperglycemia
2) ketosis (formation of ketones from lipid breakdown)
3) ketoacidosis (depresses the CNS and can lead to coma)

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15
Q

Why does hyperosmolar hyperglycemic state normally occur in type 2 diabetes?

A

Because the cells are not completely deprived of glucose (insulin deficiency is not absolute) and there is no breakdown of lipids.

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16
Q

What two problems are caused by hyperosmolar hyperglycemic state?

A

1) hyperglycemia

2) hyperosmolarity

17
Q

What causes hyperosmolar hyperglycemic state?

A
  • excessive carb intake

- increased insulin resistance

18
Q

Explain what happens in hyperosmolar hyperglycemic state.

A
  • severe hyperglycemia leads to hyperosmolarity (an increase in the glucose concentration in blood)
  • this leads to cellular fluid efflux
  • the kidneys try to correct and excrete glucose = glycosuria
  • water follows
  • result is dehydration
19
Q

What are 5 chronic complications of diabetes mellitus?

A

1) vascular damage (that can lead to atherosclerosis, MI, CVA)
2) retinopathy
3) nephropathy
4) neuropathy
5) infections

20
Q

What are the different types of diabetes mellitus?

A
  • type 1 (type 1a is more prevalent, is immune-based, type 1b is rare and idiopathic)
  • type 2
  • gestational
21
Q

What is the etiology of both type 1 and type 2 diabetes?

A

complex trait (polygenic AND an environmental factor)

22
Q

What genes have been found to be affected in people with type 1 diabetes?

A
  • 10% have a defect of the insulin gene on chromosome 11 (this gene codes for a protein that regulates division and function of beta cells)
  • 40% have a problem with the MHC genes on chromosome 6, they code for self markers on beta cells (this problem causes autoimmunity)
23
Q

What gene is often affected in young people who develop type 2 diabetes?

A
  • 50% from a problem with glucokinase gene on chromosome 7 (codes for an enzyme that helps lock glucose in the cell by adding a phosphate group)
24
Q

If a member of your family has type 1 diabetes, does your risk for developing it increase? By how much?

A

yes, your risk inreases x10

25
Q

What happens at the cellular level to cause type 1 diabetes? What is the result?

A

In most cases beta cells in the pancreas are destroyed due to autoimmunity. The cells are destroyed by insulin and islet cell auto-antibodies, as well as T cells. This causes an absolute insulin deficiency.

26
Q

What is insulitis?

A

inflammation within the islets of Langherhans, can be caused by autoimmune destruction of beta cells preceding type 1 diabetes

27
Q

What happens in type 2 diabetes?

A

The beta cells in the pancreas are mostly intact but there is a relative insulin deficiency. There can be hyalinization occurring in the islets though, from the deposition of amyloid protein.

This can be from:

  • a delay in insulin secretion
  • defective target cell response
  • insulin resistance (can’t bring about hypoglycemic response to hyperglycemic state)
28
Q

Describe the pathology of diabetes.

A
  • insulin deficiency
  • impaired utilization of glucose causes cells to signal that there is no glucose
  • causes increased glucogenesis in liver, making more glucose
  • this adds to hyperglycemia (11 to 67 mmol/L)
  • renal threshold for glucose (10 mmol/L) is exceeded, glucose above this threshold is excreted in urine = glycosuria
  • all the glucose in the filtrate in Bowman’s capsule increases the osmotic pressure and causes fluid to follow
  • results in polyuria
  • eventually leads to dehydration
  • causes polydypsia (excessive thirst & excessive intake)

also at the cellular level:

  • impaired glucose utilization by cells
  • increased mobilization and use of proteins and lipids for energy
  • causes increase in protein and lipid metabolizes (ketone) in blood
  • when renal threshold exceeded ketones also excreted in urine = ketoneuria (also enhances polyuria)
  • ketone accumulation = metabolic acidosis = ketoacidosis
  • can lead to coma and death
29
Q

What are the major manifestations of diabetes?

A
  • polyuria (increased volume and frequency)
  • polydypsia (excessive thirst and excessive fluid intake)
  • polyphagia (increased food intake)
  • weight loss (calories lost in urine and energy stores used)
30
Q

Why is vascular damage a chronic complication of diabetes? What other problems can this cause?

A
  • increase/accumulation of metabolites in blood damages blood vessels
  • glucose attaches to proteins = glycosylated proteins and causes them to function abnormally (ex. Hb, albumin, collagen)
  • glycosylated proteins deposit on endothelium and impair transcapillary exchange, cause platelet aggregation and impede blood flow
  • this can cause atherosclerosis, MI, CVA
  • inadequate blood flow can impair healing and can allow anaerobic bacteria to grow
31
Q

Why is retinopathy a chronic complication of diabetes? What problems can this cause?

A
  • capillaries in the retina are damaged

- can cause visual impairment, ex. cataracts and glaucoma

32
Q

Why is nephropathy a chronic complication of diabetes? What major problem can this cause?

A
  • glomerulus can be damaged, this decreases renal function and can lead to renal failure
33
Q

Why is neuropathy a chronic complication of diabetes? What problem can this cause?

A
  • decreased blood flow to neurons = neural ischemia
  • causes some demyelination, which causes poor conduction
  • results in neural deficit
  • this can cause problems ex. foot ulcers d/t lack of sensation
34
Q

Why are infections a chronic complication in diabetes?

A
  • decreased blood flow impairs healing, can allow anaerobic bacteria to grow
  • neuropathies can mean infections not caught early
  • UTIs - glucose in urine facilitates bacterial growth
35
Q

How is diabetes diagnosed?

A 
- history (3 Ps, unexplained weight loss)
and
- random glucose over 11 mmol/L on ongoing basis
or
- IFG equal or over 7 mmol/L
or 
- IGT over 11 mmol/L
or
HbA1C equal or over 6.5 %
36
Q

How is diabetes treated?

A
  • lifestyle modification
  • glycemic control through:
  • — oral hypoglycemics for type 2 (give metformin if HbA1C is still over 7% after 2-3 months of lifestyle mod; give metformin and insulin if HbA1C is over or equal to 9%)
  • — insulin for type 1
37
Q

What are the different types of oral hypoglycemics?

A
  • thiazolidinediones: increases tissue response to insulin
  • insulin secretogogues: stimulate beta cells
  • biguanides: decrease hepatic glucogenesis

Pathophysiology (38 decks)

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