diabetes + DKA

Question 1

islet of langerhans in pancreas consist of

Answer 1

α cells: glucagon
ß cells: insulin
delta cells: somatostatin (D cell in gastric mucosa, CNS cells too)

Question 2

inadequate insulin:

hyperglycemia

Answer 2

diabetes mellitus

Question 3

symptoms of hyperglycemia in DM

Answer 3

↑ glucose →
polyuria (osmotically active -draws H20 into urine)
polydispia (losing H20)
polyphagia: skeletal muscle + adipose tissue: glucose not used as fuel
weight loss

Question 4

complication of type 1 DM

Answer 4

diabetic ketoacidosis (DKA)
may be first presentation of type 1 DM, esp children!
ketosis-prone type 2 DM (

Question 5

complication of type 2 DM

Answer 5

hyperosmolar hyperglycemic state (HHS)

may be first presentation!

Question 6

diagnostic testing for diabetes mellitus

Answer 6

1) glucose-based tests: ↑ glucose
fasting serum glucose or
2-hr glucose tolerance test
2) Hb A1C (average glucose over past 3 mo -good for surveillance once dx made): glucose binds to Hb in non-enzymatic rxn (glycosylation), measure % of surface covered by glucose

Question 7

complications of hyperglycemia in DM

Answer 7

1) nonenzymatic glycosylation:
Hb
leaky small vessels → retinopathy + nephropathy
osmotic damage
vascular disease in large vessels → atherosclerosis: CAD, cerebral vascular disease, PVD (dry gangrene)
2) osmotic damage: sorbitol

Question 8

retinopathy in DM

Answer 8

early: leaky vessels (non-proliferative retinopathy)
late: new blood vessels form in eye (proliferative retinopathy) → break → hemorrhage → can cause blindness

Question 9

“dot and blot” + larger flame hemorrhages + yellow blotches (hard exudate) in fundoscopic exam

Answer 9

retinopathy in DM

Question 10

eye findings in DM

Answer 10

retinopathy: small vessel proliferation “flame, dot hemorrhages”
macular edema
soft exudates: “cotton wool” spots
↑ risk cataracts, glaucoma

Question 11

cotton wool spots on fudus

Answer 11

DM
HTN
AIDS

Question 12

diabetic nepropathy

Answer 12

glycosylation of small vessels → leaky vessels → microscopic proteinuria → progressive proteinuria
afferent arterioles
glomerular capillaries
efferent arterioles
tx: ACEi/ARB: reduce progressive proteinuria

Question 13

kimmelstiel wilson nodules on renal bx

Answer 13

diabetic nephropathy

in glomeruli: pink nodules

Question 14

osmotic damage in DM

Answer 14

↑ sorbitol in cells
schwann cells: motor neuropathy, sensory neuropathy, autonomic neuropathy (may be asymptomatic neuropathy, numbness in tips of toes → progresses proximally, may lose vibration/proprioception)
neuropathic pain: gabapentin, duloxetine, pregabalin, amitriptyline

Question 15

treatment of type 1 DM

Answer 15

insulin: still have insulin sensitivity

Question 16

profound insulin deficiency: no glucose to cells → hyperglycemia
cells think starving →
↑↑↑ glucagon (catabolic):
↑ glucose → polyuria, dehydration
↑ lypolysis: FFA → ↑ ketones (acetoacetic acid, ß hydroxybutyric acid) → acidosis (get sick quickly)

Answer 16

DKA

Question 17

causes of DKA: put stress on body →

↑ endogenous catecholamines, glucagon, or glucacorticoids →↑ blood sugar

Answer 17

infection: pneumonia, gastroenteritis, URI, UTI
missed insulin doses
severe illness: MI, CVA, trauma
undiagnosed diabetes
dehydration
alcohol/drug abuse (stimulants)

Question 18

sx before acute illness:
polyuria/dehydration, polydipsia, weight loss (hyperglycemia sx)
ab pain, N/V
confusion, delerium
signs of ANION GAP metabolic acidosis:
sweet, fruity odor to breath (ketone in breath)
Kussmaul breathing: regular, deep/labored breathing (compensation for acidosis by hyperventilating)
hyperglycemia > 300 (can occur at any glucose level since problem is absence of insulin)
serum + urine ketones
hyperkalemia: compensation for acidosis (H/K countertransporter: keep H+ in cells, remove K+), DEADLY
↑ K+ in urine (→↓ intracellular K+ = low total body K): kidneys remove K+ from blood

Answer 18

DKA

Question 19

causes of high ANION GAP metabolic acidosis

Answer 19

MUD PILES
Methanol
Uremia
DKA
Propylene glycol
Iron tables/INH
Lactic acidosis
Etheylene glycol
Salicylates

Question 20

treatment of DKA

Answer 20

1) IV fluids -dehydrated
2) IV insulin: inhibit lypolysis from glucagon = stop ketones!
3) monitor anion gap (not glucose levels!): continue insulin (stops ketones) until gap closes
4) switch to injected insulin
3) RESTORE K+ +/- Mg AGGRESSIVELY: may have normal or hyperkalemia BUT low total body K+ (excreting excess K+ in urine) → give K+ to replete intracelluar stores

Question 21

complications of DKA

Answer 21

arrhythmias: due to hyperkalemia, low total body K+ (if low K+, Mg+ may also be low → vtach, Torsades de pointes)
invasive fungal infections (rhizopus infection) due to hyperglycemia (mucormycosis: invade sinuses → brain abscess)

Question 22

insulin prevents lipolysis - ß oxidation)→ no ketone bodies → NO ketoacidosis → NO Kussmaul breathing
EXTREME hyperglycemia: >800 →↑ serum hyperosmolarity >340 (vs DKA-none)

Answer 22

hyperosmolar hyperglycemic state (HHS)

Question 23

initial sx: mental confusion, delerium, coma, dehydration, ab pain, N/V (like DKA but more neuro sx initially)
ABG:
no ketones
hyperosmolar
glucose >800

Answer 23

hyperosmolar hyperglycemic state (HHS)

Question 24

treatment of HHS: hyperosmolar hyperglycemic state

Answer 24

1) IV fluids
2) insulin: ↓ serum glucose + correct hyperosmolarity (not to close anion gap)
3) K+

Question 25

treatment of type 2 DM

Answer 25

#1) dietary modification + exercise (can avoid meds): ↓ sugar intake → ↓ ß cell activity
meds:
biguanides
sulfonylureas
thiazolidinediones
DPP-4 inhibitors
GLP-1 agonists
SGLT-2 inhibitors
insulin
others: pramilintide, α-glucosidase inhibitors