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Quiz 3 Fundamentals > diabetes > Flashcards

diabetes Flashcards

1
Q

hot and dry

A

sugar high

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2
Q

cold and clammy

A

need some candy

sugar low

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3
Q

hyperglycemia

A

high sugar

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4
Q

hyperglycemia symptoms

A 
headache
sweaty
blurry vision
ringing in the ears
increase heart rate
hunger
trembling
feeling anxious
weakness tired
imitability
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5
Q

DKA

A

diabetic ketoacidosis

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6
Q

what is DKA

A

without insulin - glucose cannot get into cells (remain in blood steam)

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7
Q

DKA: as _____ rises, the liver produces ____

why?

A

blood glucose rise the liver produces more glucose becuase it senses that the cells are starving

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8
Q

DKA: what happens when blood glucose rises

A

lead to dehydration

lowering of the bloods pH (acidodic)

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9
Q

DKA: kidneys kick in when? what do they try to do?

A

kidneys kick in as blood glucose rises

  • kidneys attempt to get rid of the excess glucose
  • glucose is spilled into the urine, water follows it - resulting in polyuria and the ensuing thirst polydipsia
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10
Q

acidodic: DKA

A

blood pH lowers

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11
Q

number one treatment for DKA

A

fluid treatment for dehydration - although putting out lots of urine very dehydrated

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12
Q

DKA: where do cells get energy from?

A

can’t get it from glucose. get energy from fat but in doing so produce ketones

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13
Q

DKA: what happens when you use ketones?

A

ketones are acidic and as they build up they lower the pH of blood. oH needs to stay normal - breaths become faster to raise pH level in blood

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14
Q

precipitating factors of DKA

A 
illness
infection
inadequate insulin dosage
undiagnosed type 1 diabetes
poor self management
neglect
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15
Q

DKA - clinical manifestations

A
  • abdominal pain, anorexia, nausea
  • dehydration
  • sweet fruity breath from ketones
  • polyuria
  • polydipsia
  • Kuusmaul respirations
  • blood glucose level higher than 250
  • blood pH lower than 7.3
  • serum bicarbonte level lower than 16
  • moderate to high ketones in urine or serum
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16
Q

polyuria

polydipsia

A

excess urine output

excess hunger

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17
Q

Kuusmaul respirations (DKA)

A

trying to blow off CO2

to increase blood PH

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18
Q

DKA - blood glucose level

A

250 mg/dL or more

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19
Q

DKA - blood pH

A

lower than 7.30

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20
Q

DKA - serum bicarbonate level

A

lower than 16 mEQ/L

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21
Q

Signs of DKA

A
  • onset over 4-10 hours
  • breath smeels fruity
  • Kussmaul Respirations
  • thirsty/dehydrated
  • acidosis (overproduction of acid in blood)
  • tachycardia
  • hypotension
  • high blood sugar
  • hyperkalemia (high potassium levels)
  • polyuria
  • low potasium and electrolytes
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22
Q

Early signs of DKA

A
  • dry craked lips
  • lethargy weakness
  • dry skin
  • ski tenting
  • polyuria
  • fever
  • sunken eyes and loose skin
  • decreased BP
  • ketones in urine
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23
Q

First thing you do to a DKA patient

A

rehydrate

-normal saline - 2 to 8 liters over 24 hours

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24
Q

how much saline do you give first to a DKA patient

A

1 liter in first hour

2-8 liters over 24 hours

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25
Q

Treatment of DKA - Insulin

A

-“bolus” of regular insulin
-continuous IV insulin
NEVER GIVE SQ INSULIN TO A DKA PATIENT

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26
Q

Electrolyte Replacement - DKA

A

Restore potassium balance - hypokalemia

  • potassoim needed with insulin to move glucose in cells
  • correct pH
27
Q

Treatment of DKA in hospital

A
  • Rehydrate
  • Insulin
  • Electrolytes
28
Q

HHNS

A

hyperosmolar hyperglycemic nonketoic syndrome

29
Q

HHNS - what is it

A
  • most common type 2 DM
  • High BS without ketones
  • extreme dehydration
  • decreased consiousness
  • usually seen in people with poor control of Type II
  • gradual onset
30
Q

DKA & HHNS - onset

A

DKA - sudden

HHNS - gradual

31
Q

Sugar Levels - HHNS

A

extremely high

600-2000

32
Q

Osmolality of HHNS

A

extreme lack of water - 6 to 8 L lost

-serum now has high osmolality to it greater than 350 because so much water was taken out of bloo

33
Q

normal level of osmolality

A

275 - 295 Osm/kg

34
Q

HHS may be brought on by what?

A
  • infection
  • other illness (heart attack, stroke)
  • medicines that decrease effect of insulin in body
  • medicines that increase fluid loss
  • diaharrea, nausea, vommiting
  • decreased potassium level
35
Q

What is HHS

A

Hyperosmolar Hyerglycemic Syndrome

36
Q

HHS - what does dehydration cause?

A

increased blood concentration or hyperosmolarity - a condition which the blood has a high concentration of sodium, glucose and other substances that normally cause water to move into the blood stream
-this draws the water out of ht ebody’s other organs, including the brain

37
Q

HHS treatment

A
  • rehydrate (improves BP, urine output, circulation)
  • fluids and K+
  • insulin drip
38
Q

Hypoglycemia

A

too much insulin in proportion to glucose in the blood

39
Q

Hypoglycemia blood glucose level

A

50mg/dL

40
Q

normal glucose level

A

70-110

41
Q

symptoms of hypoglycemia

A
  • depend on the patient
  • shaking
  • sweating
  • anxious
  • dizziness
  • hunger
  • tachycardia (increased hear rate)
  • blurry vision
  • weakness fatigue
  • headache
  • irritable
42
Q

hypoglycemia risk factors

A
  • too much insulin (insulin reaction or insulin shock)
  • too little food
  • excessive exercise
  • sleeping in late
  • nutritional/fluid imbalances (nausea vomitting)
  • alcohol intake/drugs
43
Q

Hypoglycemia Treatment - pt awake

Rule of 15

A

consume 15g of a simple carb (juice)

  • recheck glucose level 15 minutes
  • repeat if less than 70
44
Q

Hyoglycemia - what to avoid

A
  • foods with fat (decrease absorption of sugar)

- avoid overtreatment (stay within 15g)

45
Q

Hypoglycemia - patient not alert enough to swallow

A

D50 (dextrose 50%)

IV push

46
Q

Hypoglycemia - what to do when no IV

A

glucagon 1 mg, IM or SQ

-helps release glucose from the liver

47
Q

hyperglycemia causes non-enzymatic glycosylation - what is it?

A

reversible attachment of glucose to proteins, lipids, nucleic acids without the activation of enzymes

48
Q

Chronic hyperglycemia - what happens to glucose

-what does this form

A

becomes irreversibly bound to collagen and other proteins in the blood vessel wals and interstitial tissue
-advanced glycosylation end-products (AGE)

49
Q

AGE - what does it damage

A

blood vessels and tissue

50
Q

3 macrovascular chronic diabetes complications

A

medium to large BV

  • cardiovascular
  • cerebrovascular (stroke)
  • peripheral vascular (ulcerations on ankle)
51
Q

3 microvascular chronic diabetes complications

A
  • nephropathy
  • neuropathy
  • retinopathy
52
Q

proliferative retinopathy - what is it

A
  • growth of abnormal blood vessels
  • retinal neovascularization (create more BV lead to vitreous hemmorrhage) stimulated by retinal isschemia (lack of oxygen)
53
Q

proliferative retinopathy - untreated what does it cause

A
  • vitreous hemmorrhage

- retinal detachment

54
Q

proliferative retinopathy - treatment

A

laser therapy

55
Q

nephropathy - what is it

A

*single most common cause of end stage renal disease (ESRD)

  • sclerosis (hardening) or thickening of the capilarry basement membrane
  • due to chronic filtering of high serum glucose levels
56
Q

what causes nephropathy

A

chronic filtering of high serum glucose

57
Q

early sign of nephropathy

A

micro-proteinuria

-protein in urine

58
Q

what causes nephropathy

A
  • smoking
  • hypertension
  • genetic predisposition
59
Q

Treatment of nephropathy

A
  • dialysis

- kidney transplant

60
Q

what causes neuropathy

A
  • common complication in diabetes
  • vascular insufficiency
  • chronic glucose elevation
  • hypertension
  • cigarete smoking
61
Q

mono-neuropathy

A

sharp stabbing pains

  • damage to single nerve
  • ciadica or carpal tunnel
62
Q

polyneuropathy

A

tingling,numbness, burning

  • total sensory loss
  • damage to multiple nerves
  • worse at night
  • hyperestisia (hypersensitive)
63
Q

treatment of mono neuropathy

A

surgical decompression for compression lesions

64
Q

treatment of polyneuropathy

A

foot care

-education to prevent trauma/ulcers

Quiz 3 Fundamentals (5 decks)

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