Brainscape's Knowledge GenomeTM

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


See full index

Post Midterm Patho > Pathophysiology of DM > Flashcards

Pathophysiology of DM Flashcards

1
Q

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

A

10 mmol/L

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

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

A

the excess glucose will appear in the urine

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

How will this excess glucose appear in the urine?

A

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

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

Define polyuria:

A

Excessive fluid loss / frequency of urination

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

The full proccess of Patho T1/T2 DM…

A

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)

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

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

A

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

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

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

A

Lipids and Proteins

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

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

A

Increased metabolites of lipids and proteins

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

What would be a byproduct of the metabolization of lipids?

A

ketones

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

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

A
  1. ketoacidosis (can lead to acidotic coma & death?)

2. Ketoneuria (enhances polyuria)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the MNFTS of DM?

A
  1. Polyuria
  2. Polyphasgia
  3. Polydipsia
  4. Weight loss
  5. Other complications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Define polyuria:

A

Excessive volume of urination and frequency

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

Define polyphasgia:

A

Excessive hunger d/t loss of calories in the urine

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

Define polydipsia:

A

dehydration, therefore you drink more, cycle continues!

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

What are the 3 Acute Complications of DM?

A
  1. Hypoglycemia
  2. Diabetic Ketoacidosis (DKA)
  3. Hyperosmolar Hyperglycemic state (HHS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Hypoglycemia:

  1. What type of DM usually?
  2. D/t what?
A
  1. Type 1 DM

2. D/t missed meal, insulin overdose, overexcertion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the treatment for Hypoglycemia?

  1. Mild
  2. Moderate
  3. If patient in hypoglemic coma?
A
  1. 15 mg of carbs PO
  2. 20 mg of carbs PO
  3. 1 mg of glucagon SC or IM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is occuring to the brain in a hypoglycemia coma?

A

It is being deprived of glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Explain Diabetic Ketoacidosis

A

Gotta look at that figure in Porth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Define Hyperosmolar Hyperglycemic state

  1. Usually occurs in what type of DM? or who else?

2. D/t what?

A
  1. Type 2, or elderly

2. Increased carb intake OR increased insulin resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Explain the proccess of HHS?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Why is no ketoacidosis occuring in HHS?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A

approximately 15 years post disease onset

  1. Vascular damage –> atherosclerosis, MI, CVA
  2. Retinopathy
  3. Nephropathy
  4. Neuropathy
  5. Infections (particularly foot and UTI)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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?
A
  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
Q

How do the abnormal metabolites inflict damage?

A

glucose + proteins = glycosylated proteins –> non -fx

ex. Hb, affinity for 02 increases, therefore at low levels 02 will not dissociate as easily

26
Q

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

A

Abs, albumins, collagen

27
Q

The glycosylated proteins deposit on where?

A

Endothelium

28
Q

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

A

It thickens

29
Q

What does this thickenning of the endothelium cause to occur?

A

movement across the membrane is affected, therefore impaired capillary exchange

30
Q

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

A

platelet aggregateion

31
Q

The vascular damage leads to impaired healing: why?

Why would growth of anarobic bacteria increase?

A
  1. impeded perfusion

2. thrive in low 02

32
Q

What are the Chronic Complications of DM?

A
  1. Vascular Damage
  2. Neuropathy
  3. Nephropathy
  4. Retinopathy
  5. Infections
33
Q

Explain how retinopathy occurs in DM?

A

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

34
Q

Explain how nephropathy occurs in DM?

A

glomerular damage –> decreased renal fx –> renal failure

35
Q

Explain how neuropathy occurs in DM?

A 
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
Q

Neurodeficit would cause a diabetic patient what?

A

Unable to feel pain in the foot

37
Q

Why is HTN common in DM?

A

d/t damaged vessel walls and impeded perfusion

38
Q

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

A

MI, CVA, nephropathy

39
Q

Why is CAD a common chronic complcation in diabetic patients?

A

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

40
Q

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

A

hyperlipidemia –> atheroscerlosis –> CVA

41
Q

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

A

Patients without DM

42
Q

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

A
  1. foot

2. UTI

43
Q

What are the 5 Tests for Diagnosing DM?

A
  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
Q

What would the Hx include in diagnosing DM?

A

3 P’s

  1. Polyphagia
  2. Polydipsia
  3. Polyuria
  4. unexplained weight loss
45
Q

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

A

11 mmol/L on ongoing basis

46
Q

Dx of DM: Numbers should be above what?

  1. IFG
  2. IGT
  3. HBa1c
A
  1. above or = 7 mmol/L
  2. above or = 11 mmol/L
  3. above or = 6.5%
47
Q

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

A

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
Q

Treatment for DM includes what 2 things?

A
  1. Lifestyle modifications

2. Glycemic control

49
Q

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

A
  1. Oral hypoglycemics

2. Insulin

50
Q

Oral hypoglycemic medications are aiming to bring about what response?

A

Hypoglycemic response (decrease the blood glucose levels)

51
Q

What are 3 things that oral hypoglycemics cause to occur?

A
  1. increase tissue response to insulin
  2. stimulate Beta cells to secrete insulin
  3. Decrease hepatic glucogensis
52
Q

What is a common oral hypoglycemic drug that is given?

A

Metformin

53
Q

When would Metformin be prescribed?

A

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

54
Q

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

A

insulin

55
Q

Could oral hypoglycemic be given to a type 1 diabetic?

A

No. They do not cause the production of insulin

56
Q

Type 1 DM patients require what medication?

A

Insulin

57
Q

Why is insulin injected SC?

A

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

58
Q

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?
A
  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
Q

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

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

Post Midterm Patho (16 decks)

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