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Flashcards in Pathophysiology of DM Deck (59):
1

the renal threshold (RT) for glucose in the blood is what?

10 mmol/L

2

If the glucose levels exceed 10 mmol/L, what occurs?

the excess glucose will appear in the urine

3

How will this excess glucose appear in the urine?

It increases the concentration in the filtrate, therefore fluid from blood into filtrate increases urine output (polyuria)

4

Define polyuria:

Excessive fluid loss / frequency of urination

5

The full proccess of Patho T1/T2 DM...

Insulin Deficiency --> impaired glucose utilization --> the body senses that the cells don't have energy, so the liver goes through glucogenesis (formation of glucose from glycogen in the liver) --> hyperglycemia (11-67 mmol/L) -->RT exceeded --> glucosuria / glycosuria --> increased osmotic pressure in the filtrate (pull pressure by the glucose) --> fluid enters filtrate --> polyuria (large volumes of urine / frequency) --> dehydration --> polydipsia (excessive thirst followed by excessive fluid intake)

6

A not yet diagnosed / treated patient with DM may present with large urine output. Why?

The increased concentration pulls fluid into the filtrate, causing the patient to urinate more.

7

DM causes impaired glucose function.. this leads to what else being metabolized in the body?

Lipids and Proteins

8

The breakdown of lipids and proteins results in what being prsesnt in the blood?

Increased metabolites of lipids and proteins

9

What would be a byproduct of the metabolization of lipids?

ketones

10

what are the 2 problems that ketone accumulation can lead to?

1. ketoacidosis (can lead to acidotic coma & death?)
2. Ketoneuria (enhances polyuria)

11

What are the MNFTS of DM?

1. Polyuria
2. Polyphasgia
3. Polydipsia
4. Weight loss
5. Other complications

12

Define polyuria:

Excessive volume of urination and frequency

13

Define polyphasgia:

Excessive hunger d/t loss of calories in the urine

14

Define polydipsia:

dehydration, therefore you drink more, cycle continues!

15

What are the 3 Acute Complications of DM?

1. Hypoglycemia
2. Diabetic Ketoacidosis (DKA)
3. Hyperosmolar Hyperglycemic state (HHS)

16

Hypoglycemia:
1. What type of DM usually?
2. D/t what?

1. Type 1 DM
2. D/t missed meal, insulin overdose, overexcertion

17

What is the treatment for Hypoglycemia?
1. Mild
2. Moderate
3. If patient in hypoglemic coma?

1. 15 mg of carbs PO
2. 20 mg of carbs PO
3. 1 mg of glucagon SC or IM

18

What is occuring to the brain in a hypoglycemia coma?

It is being deprived of glucose

19

Explain Diabetic Ketoacidosis

Gotta look at that figure in Porth

20

Define Hyperosmolar Hyperglycemic state
1. Usually occurs in what type of DM? or who else?
2. D/t what?

1. Type 2, or elderly
2. Increased carb intake OR increased insulin resistance

21

Explain the proccess of HHS?

sever hyperglycemia --> hyperosomlarity (concentration in the blood) --> cellular fluid efflux (fluid movies from cells to IS to blood because of the pull force) --> glycosuria --> water loss --> dehydration

22

Why is no ketoacidosis occuring in HHS?

Because ketoacidosis occurs when lipids are being metabolized... In this case, there are lots of carbs, no lipid breakdown.

23

When do the chronic complications of DM typically surface? What are they?

approximately 15 years post disease onset
1. Vascular damage --> atherosclerosis, MI, CVA
2. Retinopathy
3. Nephropathy
4. Neuropathy
5. Infections (particularly foot and UTI)

24

The Vascular Damage in DM is a chronic complication, occurs d/t...
1. What affect does the altered metabolism have?
2. Explain the glycolysated proteins
3. Explain the platelet aggregation and its implications
4. Why is healing impaired? How about the anaerobic metabolism?

1. Altered metabolism = accumulation of lipid (ketones) / protein metabolites which inflict damage
2. Glucose + protein = glycolysated protein, ex. HB glycolysated has a higher affinity for O2, therefore wont dissociate O2 at low levels
3. Platelets aggregating will impede the blood flow
4. Impaired healing d/t impeded perfusion (d/t the platelet aggregation). Anaerobic microbes will then grow because the lack of O2 here.

25

How do the abnormal metabolites inflict damage?

glucose + proteins = glycosylated proteins --> non -fx
ex. Hb, affinity for 02 increases, therefore at low levels 02 will not dissociate as easily

26

what are other proteins that can be affected and lead to vascular damage?

Abs, albumins, collagen

27

The glycosylated proteins deposit on where?

Endothelium

28

The deposition of gycoslyated proteins leads to what to happen to the endothelium?

It thickens

29

What does this thickenning of the endothelium cause to occur?

movement across the membrane is affected, therefore impaired capillary exchange

30

What would cause the blood flow to be impeded in regards to Vascular Damage, a chronic complication of DM?

platelet aggregateion

31

The vascular damage leads to impaired healing: why?
Why would growth of anarobic bacteria increase?

1. impeded perfusion
2. thrive in low 02

32

What are the Chronic Complications of DM?

1. Vascular Damage
2. Neuropathy
3. Nephropathy
4. Retinopathy
5. Infections

33

Explain how retinopathy occurs in DM?

Capillaries are damage --> aneurysms --> rupture --> visual impairment
causes cataracts and glaucoma

34

Explain how nephropathy occurs in DM?

glomerular damage --> decreased renal fx --> renal failure

35

Explain how neuropathy occurs in DM?

Neural ischemia (lock of 02 to the neurons) causes inadequate perfusion to neurons in the brain and others, which can lead to demylination of nerons
-Leads to poor conductions (leads to neurodeficit)

36

Neurodeficit would cause a diabetic patient what?

Unable to feel pain in the foot

37

Why is HTN common in DM?

d/t damaged vessel walls and impeded perfusion

38

The HTN in a diabetic patient increases their risk for what?

MI, CVA, nephropathy

39

Why is CAD a common chronic complcation in diabetic patients?

hyperlipidemia (d/t altered metabolosim) --> atherosclerosis --> MI

40

Why is CVA a common chronic complication in a diabetic patient?

hyperlipidemia --> atheroscerlosis --> CVA

41

Patients with DM have an increased prevalance of infections as compared to who else?

Patients without DM

42

What are the two most common infections in a patient with DM? Name 2.

1. foot
2. UTI

43

What are the 5 Tests for Diagnosing DM?

1. Hx
2. Random glucose above 11 mmol/L on ongoing basis
3. IFG (above or = 7 mmol/L)
4. IGT (above 11 mmol/L)
5. HBa1c (above or = 6.5%)

44

What would the Hx include in diagnosing DM?

3 P's
1. Polyphagia
2. Polydipsia
3. Polyuria
4. unexplained weight loss

45

When Dx DM, random glucose levels would be above what?

11 mmol/L on ongoing basis

46

Dx of DM: Numbers should be above what?
1. IFG
2. IGT
3. HBa1c

1. above or = 7 mmol/L
2. above or = 11 mmol/L
3. above or = 6.5%

47

What is considered to be a histologic marker for DM? Why?

Hba1c: looking for glucose bound to Hb in RBC, lasts the red blood cell life cycle (120 days) therefore you can look at over a long period of time how many of these have been bound to

48

Treatment for DM includes what 2 things?

1. Lifestyle modifications
2. Glycemic control

49

Glycemic control of DM involves 2 main forms of medications. What are they?

1. Oral hypoglycemics
2. Insulin

50

Oral hypoglycemic medications are aiming to bring about what response?

Hypoglycemic response (decrease the blood glucose levels)

51

What are 3 things that oral hypoglycemics cause to occur?

1. increase tissue response to insulin
2. stimulate Beta cells to secrete insulin
3. Decrease hepatic glucogensis

52

What is a common oral hypoglycemic drug that is given?

Metformin

53

When would Metformin be prescribed?

Hba1c still above 7% after 2-3 months of lifestyle modifcations

54

If HBa1c still above 9% while on metformin, what else would be prescribed?

insulin

55

Could oral hypoglycemic be given to a type 1 diabetic?

No. They do not cause the production of insulin

56

Type 1 DM patients require what medication?

Insulin

57

Why is insulin injected SC?

avoid intestine, so that insulin can't be broken down (insulin is a protein!)

58

The Vascular Damage in DM is a chronic complication, occurs d/t...
1. What affect does the altered metabolism have?
2. Explain the glycolysated proteins
3. Explain the platelet aggregation and its implications
4. Why is healing impaired? How about the anaerobic metabolism?

1. Altered metabolism = accumulation of lipid (ketones) / protein metabolites which inflict damage
2. Glucose + protein = glycolysated protein, ex. HB glycolysated has a higher affinity for O2, therefore wont dissociate O2 at low levels
3. Platelets aggregating will impede the blood flow
4. Impaired healing d/t impeded perfusion (d/t the platelet aggregation). Anaerobic microbes will then grow because the lack of O2 here.

59

Why are infections difficult to manage for a patient with DM? (3)

1. Vascular insufieciency (02, ab, nutrients)
2. impaired leukocyte function in severe hyperglycemia
3. neuropathies (unable to feel)