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BioScience II > Diabetes PPt-josh > Flashcards

Diabetes PPt-josh Flashcards

1
Q

Diabetes:

DM is a disease process that is a resut of what 2 things?

A
  1. Inadequate supply of insulin
  2. inadequate tissue response to insulin
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2
Q

Diabetes:

what are the 2 types?

A
  • Type I
  • Type II

IDDM and NIDDM are no onger terms reccommended for use

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3
Q

Insulin:

is synthesized by what cells?

A

Beta cells

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4
Q

Insulin:

is regulated by what 3 ways

A
  1. Chemical
  2. Hormonal
  3. Neural
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5
Q

Insulin:

facilitates the uptake of what”?

A

Glucose

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6
Q

Insulin:

is metabolized by what organs

A

Liver and kidneys

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7
Q

Type I DM:

represents what % of cases?

A

5-10%

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8
Q

Type I DM:

___ cells mediated autoimmune destruction of beta cells within the pancreatic islets!

A

T-cells

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9
Q

Type I DM:

what is teh exact cause?

A

Unk

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10
Q

Type I DM:

what is up with the insulin?

A

there is minimal to complete absence of circulating Insulin

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11
Q

Type II DM:

makes up what % of cases

A

90%

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12
Q

Type II DM:

what is up with the insulin

A

Slow insensitivity and resistance to insulin

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13
Q

Type II DM:

there is a slow exhaustion of what cells?

A

Beta

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14
Q

Type I vs Type II:

onset sudden?

A

1

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15
Q

Type I vs Type II:

onset gradual

A

II

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16
Q

Type I vs Type II:

onset mostly adulthood

A

II

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17
Q

Type I vs Type II:

onset any age (mostly young)

A

I

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18
Q

Type I vs Type II:

THIN bodies

A

I

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19
Q

Type I vs Type II:

chuncky monkies

A

II

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20
Q

Type I vs Type II:

Ketoacidosis

A

I-often

II-rare

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21
Q

Type I vs Type II:

has autobodies

A

I

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22
Q

Type I vs Type II:

endogenous insulin low or absent

A

I

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23
Q

Type I vs Type II:

endogenous insulin normal, decreased, or increased

A

II

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24
Q

DM:

cllinical features!

A
  • Polydipsia
  • Polyuria
  • Polyphagia
  • Tired
  • Fungal infection
  • poor wound healing
  • Deterioration of vision
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25
Q

DM:

complications

A
  • DKA
  • HHS
  • Microvasular
  • Macrovascular
  • Autonomic neuopathy
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26
Q

DM:

what are the 3 main microvascular comlications

A
  1. Nephropathy
  2. Neuropathy
  3. Retinopathy
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27
Q

DKA:

most common in what DM

A

Type I

28
Q

DKA:

the glucose levels exceed what

A

Renal excretion

29
Q

DKA:

what happens to fluids in the body

A

Diuresis

Hypovolemia

30
Q

DKA:

give me quick patho

A
  • Glucose levels exceed renal tubular excretion
  • Diuresis and hypovolemia ensue
  • Increased ketoacidosis
  • Substantial deficits of water K+ Na+ and Phosphorus
31
Q

HHS:

more common in what type

A

II

32
Q

HHS:

onset is how long or fast

A

days weeks

33
Q

HHS:

the persistent glycosuric diuresis leads to what?

A
  • Polyuria
  • polydipsia
  • hypovolemia
  • hypotension
  • tachycardia
  • organ hypoperfusion
  • mental obdunation
34
Q

DKA:

treatment

A

rehydration with normal saline,

insulin drip

electrolyte supplementation

Important to note that you must correct sodium level as you correct hyperglycemia or devastating cerebral edema may result.

35
Q

HHS:

treatment

A
  • rehydration with normal saline
  • insulin drip
  • electrolyte supplementation
  • (electrolyte disturbances won’t be as severe)
36
Q

Nephropathy

occurs more with what type

A

type I

37
Q

Nephropathy:

causes what complication to kidneys

A

Glomerulosclerosis

-a scarring and hardening of the glomeruli, tiny blood vessels that are involved in filtering urine. Along with this, glomerular basement membrane thickening and arteriosclerosis and tubulointerstitial disease.

38
Q

Nephropathy:

Symptoms

A
  • hypertension
  • albuminuria
  • peripheral edema
  • progressive decrease in GFR.
39
Q

Nephropathy:

When the GFR decreases below \_\_-\_\_ ml/min the body cannot excrete potassium and acids leading to hyperkalemia and metabolic acidosis.
 Hypertension, hyperglycemic episodes, high cholesterol, and microalbuminuria decrease the GFR as well
A

15-20ml/min

40
Q

Nephropathy:

treatment

A

tx HTN

ACEi’s

41
Q

Nephropathy:

what part of the nephron is affected first and most severly?

A

distal

42
Q

Neuropathy:

which fibers are affected

A
  • Small- unmyelinated C fibers
  • Large myelinated A fibers
43
Q

Neuropathy:

Complications

A
  • recurrent infection
  • foot fractures
  • amputations
44
Q

Neuropathy:

treatments

A
  • tight glucose control
  • NSAIDs
  • Antidepressants
  • Anticonvulsants
45
Q

Neuropathy:

what is a dangerous end product from hyperglycemia

A

AGE- advanced glycosylation end product!

46
Q

AGE:

what does it do? why is it bad?

A
  • forms on collogen cause loss f elasticity, predisposes them to sheering and endothelial injury
  • decreasing cell adhesion and allowing leakage
  • Increases rate of athrogenesis
47
Q

Retinopathy:

is a result of what?

A

result of vessel occlusion, dilation, increased permeability, and microaneurysm.

48
Q

Retinopathy:

occurs in what 3 stages?

A
  1. Stage 1: Nonproliferative retinopathy. Increase in capillary permiability, venous dilation and tortuosity, microaneurysm formation, flame and blot hemmorhages, cotton wool spots and macular edema.
  2. Stage 2: Preproliferative retinopathy. Progression of retinal ischemia, poor perfusion, culminates in infarcts.
  3. Stage 3: Proliferative diabetic retinopathy. Neovascularization and fibrous tissue formation in retina and optic disc, can lead to retinal detachment and/ or hemorrhage.

Causes visual impairments from minor color changes to total blindness.

49
Q

Retinopathy:

S/S

A
  • visual impairment
50
Q

Retinopathy:

treatment

A

No specific treatment

51
Q

DM and CV:

20-30% of the pt’s who present to the Hospital w/ a ___ have DM

A

MI

52
Q

DM and CV:

the incidence of ____ is higher in DM pt’s and may be r/t increased amouts of collagen in teh ventricular wall, whch reduces the mechanical compliance of teh heart during filling, inflammatiom and changes in the Ca++ handleing

A
53
Q

DM and CV:

most DM pt’s have what presenting sign w/ an MI

A

NONE usually a silent MI- may have back pain or indigestion pain

54
Q

Insulin and preop:

insulin pumps should be decreased by ___% the night before sx, then the basal rate the morning of sx

A

30%

55
Q

Insulin and preop:

what about long acting insulin

A
  • usual dose at usual time ( continue to monitor BS throughout the day)
56
Q

Insulin and preop:

short acting insulin

A
  • should be omitted day of sx
  • or 1/2’d
57
Q

Insulin and preop:

70/30 mixed

A

should be 1/2’d AM of sx

58
Q

Insulin and preop:

oral hypoglycemic

A
  • stopped 24-48 hrs prior to sx
59
Q

Why should you avoid LR w/ DM pt’s

A
  • Large volumes will raise BS 12-24 hrs post op BC liver converts Lactate to Glucose
60
Q

1 ml of D50 will raise a 70kg pt’s BS by how much?

A
  • 2 mg/dl
61
Q

1 unit of regular insulin will lower BS by how much?

A

25-30 mg

62
Q

be aware of possible allergic reaction (death) in pt’s who use ____ and are reversed w/ protamine. you should give a small test dose (1-5mg) over 5-10 min prior to full dose

A

NPH

63
Q

what is optimal BGL postop

A

none

ADA states 140-180

insulin for anyone over 180

64
Q

It is important to note that __-___ min after the insulin drip is stopped, the patient will be insulin depleted unless they have endogenous insulin, or long acting insulin was delivered. It is recommended not to stop the insulin infusion until subcutaneous insulin has been delivered and is absorbed and taking effect.

A

10-15 min

65
Q

Thats is awesome job Diana

A

your greeeaaaaat

BioScience II (39 decks)

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