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Patho 2 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

BG in DKA vs HHS

A

DKA 300-500
HHS over 1000

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2
Q

Normal glucose metabolism

A

Glucose inc with diet, insulin is released from the pancreas, dec gluconeogenesis and glycogenolysis and inc glucose uptake by skeletal muscle and adipose tissue

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3
Q

DKA

A

insulin is less effective because there isn’t it any
- ketoacidosis and hyperglycemia

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4
Q

HHS

A

Ineffective insulin; have enough to not get ketoacidosis but not enough to control blood glucose

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5
Q

Counterregulatory hormones

A

Released under bodily stress
- catecholamines, cortisol, glucagon, GH
- causes inc glucose prod and impaired glucose use in peripheral tissues

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6
Q

Why does dehydration occur with HHS?

A

osmotic diuresis from glycosuria

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7
Q

Ketoacidosis sx

A

SOB, ab pain, N/V from inc gluconeogenesis, lipolysis, ketogenesis, dec glycolysis

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8
Q

Is DKA or HHS treated sooner?

A

DKA because get symptoms earlier from ketoacidosis

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9
Q

pH with ketoacidosis and DKA

A

Under 7.3

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10
Q

How does GFR affect DKA?

A

Can excrete glucose better, often while younger

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11
Q

s/s HHS

A

hypotension, hypoperfusion, weakness, n/v, ab pain, hypothermia, inc BUN and crt, neuro sx, FVD, polyuria, polydipsia, wt loss

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12
Q

Potassium with HHS

A
  • early or normal hyperK
  • later possible hypoK
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13
Q

Patho of HHS

A
  • relative ins deficiency
  • osmotic diuresis
  • hyperosmolality
  • serum K high or normal and dilutional hypoN
  • neuro sx bc dehydration
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14
Q

Tx for HHS

A
  • 0.9% NS
  • potassium (if sx or at least 4)
  • IV insulin—drive K back into cells
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15
Q

rf for HHS

A
  • mostly type 2, >65 (inadequate ins or infx w/o ins adjustment)
  • predisposed to PNA, UTI, MI, sepsis, inflam
  • meds that affect carb met like steroids, thiazide diuretics, SGLT2i, cocaine and subs
  • nonDM w/ predispose fx like pancreatitis
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16
Q

When is HHS resolved?

A
  • can eat
  • can transition back to SQ insulin
  • serum osmolality <315
  • mentally alert
17
Q

DKA s/s

A
  • BG 250-450 or over 600
  • rapid onset over 24h (dx sooner)
  • polyuria, polydipsia
  • n/v, abd pain—delayed emptying or ileus from met acid
  • AMS, obtunded w/ severe acidosis
  • FVD
  • fruity breath from exhaled acetone
  • compensatory hypervent
  • pH<7.3
  • coma and death
18
Q

patho of DKA

A
  • lack ins
  • release counterreg hor
  • b/d fat into FFAs and glycerol, proteolysis
  • ketone bodies accum
  • met acidosis
  • anion gap
  • hyperosmolality
  • osmotic diuresis
  • electrolyte imbalance
  • neuro sx from dehydration
19
Q

How does met acidosis occur with DKA?

A
  • lipolysis occurs as glucose can’t get into cells
  • FFAs form and become acetyl CoA then ketone bodies
  • ketone bodies accumulate in blood
  • ketones are acidic
  • exacerbates K imbalance bc H+ pushes K+ out of cell to balance
20
Q

What activates FFAs?

A

hepatocytes of the liver

21
Q

Anion gap

A

Difference between negative (Cl- and bicarb) and Na+ ions

22
Q

How is anion gap measured

A

with beta hydroxybutyrate—main met product of ketoacidosis

23
Q

Fx that affect severity of acidosis

A
  • rate and duration of ketone production
  • rat of ketone metabolism
  • rate of ketones in urine (depend on fluid vol and GFR_
24
Q

What speeds up the rate of ketoacids lost in urine?

A

isotonic fluids

25
Q

Electrolyte imbalance from DKA

A

K is high or normal and Na is dilutionally low
- osmotic diuresis causes loss of Na, K, and H2O

26
Q

DKA tx

A

0.9% NS
- With dextrose if gluc <200 and pt still has anion gap
Potassium (if symptomatic or at least 4)
IV insulin
- Watch for hypoglycemia and frequently monitor VS
Sodium bicarb if pH <7.2 or difficulty breathing
- Careful of overshoot as insulin is given

27
Q

rf for DKA

A
  • ppl<65 and type 1 mostly (inadequate ins, infx w/o ins adjust)
  • t2 extreme conditions
  • predisp to PNA, UTI, MI, sepsis, stroke, inflam, infx
  • emotional stress
  • steroids, thiazide diuretics, SGLT2i, cocaine sub abuse)
28
Q

How do you know when DKA is resolved?

A
  • anion gap closed
  • ketoacidosis fixed
  • can eat
  • can take SQ ins again
29
Q

Patho for microvascular comps

A
  • hypoxia and ischemia
  • microangiopathy—thick, weak cap membranes
  • freq and sever of damage depends on disease duration
30
Q

Neuropathy

A
  • most common
  • ischemia and demyelination of nerves
  • lose pain, temp, vibratic sens
  • ulcer, infx, amputation
31
Q

retinopathy

A
  • lead blindness
  • hypoxemia, damage to retinal BVs, RBC agg and HTN
  • small vessel infarc and death
32
Q

Nephropathy

A
  • leads to CKD and ESRD
  • GBM thick and hard
33
Q

Macrovascular comps

A
  • athero lead to CAD, PVD, stroke, infx
  • inc inflam
  • oxidative stress, endothelial dysfxn, alter mineral metab, inc cytokine prod
34
Q

Patho of infx in diabetics

A
  • tissue hypoxia and impaired skin integ from neuropathy—healthy cells can’t get there
  • pathogens feed on excess gluc and fewer WBCs circ

Patho 2 (17 decks)

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