DM pales

Question 1

DKA definition

Answer 1

hyperglycemia >250
pH <15
serum ketones

Question 2

DKA and DMI

Answer 2

usually initial presentation in kids
insulin non-compliance
increase in anti-insulin hormones d/t stress

Question 3

DKA and DMII

Answer 3

late stages of beta cell failure

during stress or in extremely high BG

Question 4

signs and symptoms of DKA

Answer 4

onset 1-2 days
weakness
anorexia, nausea, abdominal pain
mental status changes (confusion, lethargy, coma, seizures)

Question 5

signs of acidosis

Answer 5

confusion
lethargy
kussmal respiration (hyperventilating)
fruity breath odor

Question 6

signs of dehydration

Answer 6

oral membranes dry
turgor of skin
hypotensive/tachy

Question 7

finger stick glucose

Answer 7

not accurate if 500

Question 8

labs of DKA

Answer 8

high glucose
low CO2/bicarb/pH
high ketones, acetone, ketoacids
high BUN and Cr
low Na
high K

Question 9

DKA Tx

Answer 9

INSULIN- do not stop insulin until anion gap is corrected, give glucose once glucose is under 200
IV FLUIDS
electrolytes
ventilatory support

Question 10

hyperosmolar, hyperglycemic, non-ketotic state

Answer 10

aka hyperosmolar coma
hyperglycemia >600
serum osmolality >310 (thick blood)
no acidosis
bicarb >15
normal anion gap

Question 11

pathology of hyperosmolar hyperglycemic non-ketotic state

Answer 11

hyperglycemia -> osmotic diuresis -> dehydration -> increased osmolality -> decrease in free fluid -> hyperglycemia
ONLY IN DMII, type I would get DKA

Question 12

causes of hyperosmolar hyperglycemic non-ketotic state

Answer 12

non-compliance with meds
acute infection/stress
dehydration
usually older patients with poor care and/or dementia
insidious onset

Question 13

Tx of hyperosmolar hyperglycemic non-ketotic state

Answer 13

IV FLUIDS!!!
A little IV insulin
electrolyte replacement
ventilatory support

Question 14

hypoglycemic coma

Answer 14

symptoms at 80 (unless long standing hyperglycemia can become symptomatic at 200 or 150)
coma/passing at 50 (usually only DM or insulinoma)

Question 15

non-proliferative retinopathy

Answer 15

most common cuase of visual impairment in DMII
earlier stage
microaneurisms
dot hemorrhages
retinal edema

Question 16

proliferative retinopathy

Answer 16

growth of new capillaries and fibrous tissue w/in retina d/t ischemic infarcts (cotton wool spots)
more common in DMI
vitreous hemorrhage and retinal detachment

Question 17

other eye issues

Answer 17

lens swelling- reversible with correction of BG

diabetic cataracts

Question 18

Diabetic nephropathy

Answer 18

focal segmental glomerulosclerosis (FSGS)
screen for albuminurea early, later proteinuria
can lead to nephrotic syndrome or end-stage renal disease and dialysis

Question 19

what CN are often involoved in DM neuropathy

Answer 19

III
IV
VI
diploplia

Question 20

femoral n neuropathy

Answer 20

diabetic amyotrophy
severe pain on front of thigh and quads
may last for months or even years

Question 21

charcot foot

Answer 21

deformity dt neuropathy -> collapse of arch 
loss of sensation
initial trauma
repetitive traumas (mircrofractures)
not a vascular issue

Question 22

autonomic neuropathy

Answer 22

NO Tx, most frustrating symptoms

• postural hypotension
• diabetic gastroparesis (Dx with GES)
• diarrhea/constipation
• neurogenic bladder (urinary retention, incontinence)
• impotence
• profuse sweating/temp dysregulation

Question 23

acclerated atherosclerosis in DM dt

Answer 23

hyperglycemia
hyperlidemia
abnormalities of platelet adhesion
HTN
oxidative stress
inflammation

Question 24

CV complications

Answer 24

heart disease (2-4x more likely )
Stroke
PVD

Question 25

derm in DM

Answer 25

pyogenic infections- boils yeast necrobiosis lipoidica diabetorum

Question 26

factors which affect glycoemoglobin

Answer 26

- conditions that shorten erythrocyte life span will falsely decrease hA1C - diseases with lack of new reticulocytes with falsely raised hA1C (aplastic anemia)

Question 27

goal for HA1C

Answer 27

7

Question 28

oral meds

Answer 28

``` secretagogues (SUs, and nonSUs) incretins metformin TZDs alpha-glycosidase inhibiotors ```

Question 29

injectable meds

Answer 29

insulins pramlintide incretins

Question 30

down fall of SUs

Answer 30

tolerance | 50% failure in 5 yrs

Question 31

CIs of SUs

Answer 31

prego/breast feeding liver or renal insufficiency sulfa allergies

Question 32

side effects of SU

Answer 32

``` GI upset urticaria jaundice SIADH (low Na, high BP) weight gain hypoglycemia ```

Question 33

which SU can be used in renal failure

Answer 33

glipizide glimeperide only metabolized by liver

Question 34

meglitinides

Answer 34

-glinide | very short acting so can be taken right before meal

Question 35

biguandies

Answer 35

metformin | DOC

Question 36

metformin side effects

Answer 36

GI lactic acidosis decrease B12 and folate absorption

Question 37

CI of metformin

Answer 37

renal and liver insufficiency chronic hypoxia past Hx of lactic acidosis alcoholism

Question 38

TZDs

Answer 38

``` -glitazone not great significant weight gain water retention cannot be used with CHF pt liver damage ```

Question 39

alpha-glycosidase inhibiots

Answer 39

``` acarbose miglitol decrease absoroption of CHO GI issues not really used dt side effects ```

Question 40

incretins

Answer 40

``` oral- DPP4 inhibitors (-agliptine) injectible- GLP1 (-tide) significant weight loss early satiety glucose dependent insulin production ```

Question 41

pramlintide

Answer 41

analoge of amyloid supresses glucagon secretion rarely used

Question 42

beginning insulin Tx

Answer 42

long acting first to increase baseline | fixed combos should not be used right away

Question 43

dawn phenomenon

Answer 43

diurnal increase of anti-insulin hormones secretion in am 3 am BG normal or high no night sweats insulin dose not high enough

Question 44

samojyi effect

Answer 44

rebound hyperglycemia after night time lows 3am BG very low night sweats present dose of insulin too high if you think its dawn effect and increase insulin can kill them