Nov. 13, 2019 Flashcards

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1
Q

Mnfts of DM

A
  • The 3 P’s
    • Polyuria + frequency
    • Polydipsia
    • Polyphagia
  • Weight loss (type 1)
  • Obesity (type 2)
  • Complications
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2
Q

Why does polyuria occur?

A

Because inc OSMOTIC PRESSURE pulls more fluid into vessels

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3
Q

Why is there weight loss in type 1 diabetes?

A

Because most calories in a person are from carbohydrates, but in type 1 diabetes carbos are excreted in urine

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4
Q

3 examples of ACUTE COMPLICATIONS from DM

A
  • Hypoglycemia
  • DKA
  • HHS
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5
Q

Why is HYPOGLYCEMIA acutely life threatening?

A

Because the brain is unable to metabolize anaerobically, and is dependent on glucose for metabolism, therefore if glucose is absent the brain may die w/in min

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6
Q

T or F:

HYPOGLY is usually more of a problem in Type 1 DM

A

T

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7
Q

What 4 causes of HYPOGLY

A
  • Caused by mismanagement
  • Taking too much INSULIN6
  • Overexertion
  • Missed meal
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8
Q

Altered brain Fx cause what to kick in?

A

The AUTONOMOUS NERVOUS SYSTEM

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9
Q

What is the Tx for HYPOGLY?

A

Admin of carbos PO

  • Mild = 15g
  • Severe ( <2.8) = 20g
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10
Q

When does someone enter a HYPOGLY coma?

A

When the brain is deprived of glucose

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11
Q

Signs of HYPOGLY coma?

A

LOC

…duh

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12
Q

What happens to GLUCAGON and EPINEPHRINE after about 5 yr w diabetes

A

Their responses become dampened

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13
Q

Tx of HYPOGLY coma:

A
  • 1mg GLUCAGON subq or IM

- 50% sol’n of GLUCOSE IV

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14
Q

What does GLUCAGON do?

A

It breaks down GLYCOGEN in the liver

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15
Q

What is DIABETIC KETOACIDOSIS?

A

A form of acidosis triggered by KETONE bodies

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16
Q

Does DKA usually occur in type 1 or 2 DM?

A

Type 1

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17
Q

What are the 3 major problems that result in DKA?

A

1) HYPERGLY
2) KETOSIS
3) METB ACIDOSIS

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18
Q

What is KETOSIS?

A

The formation of KETONES

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19
Q

What is broken down to create KETONES?

A

LIPIDS

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20
Q

Why is DKA METB as opposed to RESP ACIDOSIS?

A

It involves a fixed acid, making it METB

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21
Q

What is GLUCOGENESIS?

A

Formation of GLUCOSE from breaking down CARBOS

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22
Q

What is GLUCONEOGENESIS?

A

Formation of GLUCOSE from non-CARBOS, such as LIPIDS/PROTEINS

23
Q

Who is most commonly affected by HYPEROSMOLAR HYPERGLYCEMIC STATE (HHS)?

A

Usually people w type 2 DM or the elderly

24
Q

Severe infct can lead to what?

A

HHS

25
Q

T or F:

HHS leads to acute pancreatitis

A

F, the other way around

26
Q

3 causes of HHS

A

1) Elevated GLUCOSE in fluid
2) Inc CARBO intake
3) Inc INSULIN resistance

27
Q

Severe HYPERGLY leads to _________

A

HYPEROSMOLARITY

28
Q

Why does HYPERGLY lead to HYPEROSMOLARITY?

A

Because the inc in GLUCOSE in the BVs causes an imbalance in the cell and the V pulls fluid from the interstitial space

29
Q

What is the link between dehydration and HYPEROSMOL?

A

The osmotic pressure pulls fluid out of cells and is excreted in the urine

30
Q

If you have no LIPOLYSIS, you have _______.

A

INSULIN

31
Q

If you don’t have LIPOLYSIS, are you at risk for KETOACIDOSIS?

A

No, KETONES are from lipids being broken down

32
Q

When do the chronic complications of DIABETES generally mnft?

A

10-15 years post onset, might be longer if condition is managed well

33
Q

Altered METB results in an excess of what?

A

BENIGN METABOLITES

34
Q

What problem arises d/t altered metb and vasc damage?

A

Perfusion problems

35
Q

What is MICROVASCULAR damage affecting?

A

The CAPILLARIES

36
Q

3 examples of MICROVASC damage?

A

1) NEPHROPATHY
2) NEUROPATHY
3) RETINOPATHY

37
Q

What is MACROVASCULAR damage affecting?

A

The ARTERIES

38
Q

MACROVASC contributes to which major conditions?

A
  • ATHERO
  • CAD
  • MI
  • CVA
  • PVD
39
Q

4 complications of VASC damage

this ones fucking loooooooong

A

1) Def METB
- Abn METABOLITE accum which inflicts injury
2) Impaired perf
- GLUCOSE + PROTEINS = GLYCOSULATED
PROTEINS
- These proteins become dysfxal
- Cause oxidative damage and FREE RADICALS
- They deposit on the endothelium, causing impaired
TRANSCAP EXCHANGE
- Foreign deposits cause PLATELET AGGREGATION
which impairs perf
3) Prolif of ANAEROBIC bacteria
- In deficiency of air
- In DIABETES there is an abundance of HYPOXIC
areas eg the foot
4) Poor healing
- Dec perf
- Can’t bring nutrients to the damaged area

40
Q

Explain the process of ANEURYSM formation in RETINOPATHY

A
  • Vs in eye are damaged (MICROVASC damage)
  • ANEURYSMS form
  • If ANEURYSM ruptures, this causes visual impairment
41
Q

Explain the process of CATARACT formation in RETINOPATHY

A
  • Sorbitol (a sugar alcohol) accumulates in the lens fibrils
  • Swelling of lens fibrils occurs when water moves in to maintain osmotic balance
  • The excess water causes disruption of fibrils and cataract formation
  • Lens becomes opaque, light cannot properly pass through and refract
42
Q

Explain the process of GLAUCOMA formation in RETINOPATHY

A
  • Glaucoma is caused by damage to the optic nerve d/t increased intraoccular pressure
43
Q

Is the increased intraoccular pressure in GLAUCOMA caused by VASC?

A

No, its caused by the pressure from the AQUEOUS HUMOR and VITEOUS HUMOR

44
Q

What causes NEPHROPATHY?

A

MICROVASC damage = impaired perf = GLOMERULAR injury = impaired renal Fx = RF?

45
Q

3 causes of NEUROPATHY?

A

1) DEMYLINATION
2) NEURAL ISCHEMIC INJURY
3) POOR CONDUCTION

46
Q

How do CAD, CVA, and PVD relate to DM?

A

They mobilize LIPIDS = inc LIPIDS = HYPERLIPIDEMIA = ATHERO = major risk factor for MI, CVA, PVD

47
Q

Is HTN more or less prevalent in DIABETICS?

A

More prevalent

48
Q

Are INFCTs more or less prevalent in DIABETICS?

A

Much more prevalent

49
Q

What 2 INFCTS are most commonly seen in DIABETICS?

A

Foot INFCTS and UTIs

50
Q

Why are INFCTS difficult to manage in DIABETICS?

A
  • Impaired perf (VASC insufficiency)
  • Impaired WBC Fx
  • Neuropathy (Dec sensation)
51
Q

What are the Dx tests for DM?

A
  • A detailed Hx (fam, 3 P’s, extreme wt loss or gain)
  • Random GLUC test (>11 mmol/L)
  • IFG (> or equal to 7)
  • IGT (>11 mmol/L)
  • HgbA1C (> or equal to 6.5%, 5% is normal)
52
Q

What are the main Dx for DM?

A
  • Random GLUC test (>11 mmol/L)
  • IFG (> or equal to 7)
  • IGT (>11 mmol/L)
53
Q

Tx for DM?

A
  • Lifestyle mod
  • GLYCEMIC control
    • PO HYPOGLYCEMICS (type 2)
      • Inc cell response to I
      • Dec hepatic GLUCOGENESIS
      • Stim B cells
    • Metformin if HgbA1C still >7% after 2-3 months of
      lifestyle mods
    • Metformin +1 if HgbA1C > or equal to 9%
    • I for type 1