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Acute Comp. DM

Clinical Medicine II

Characteristics of DKA marked hyperglycemia, dehydration and ketosis MC in type 1 DM
What causes ketoacidosis ↓ glucose uptake, so ↑lipolysis a Free FA release from adipose→acetyl-CoA, ↑ free FA release and b-oxidation w/ deficit of glucose overrides acetyle-CoA uptake and therefore oxidation via the Kreb cycle, results in hepatic ketogenesis, ↑ keto-acids and ac
What do we measure for serum ketones Beta-hydroxybuteric acid
What are we managing in a pt w/ DKA plasma acidosis
Two components from ketogensis beta-hydroxybuteric acid and acetoacetic acid
What increases w/ ketogenesis VLDL and TG
In what pts do we see DKA in type 1 diabetics, type 2 ONLY if SEVERELY stressed or sepsis but very rare
What is MC causes of DKA poor compliance and pump complications, alcohol and drug addiction
RF’s for DKA type 1 DM, undiagnosed DM, interruption of insulin therapy, insulin pump (failure), stress of acute or chronic illness, fxn problems w/ compliance of medicaitons
Precipitating factors of DKA ↓ insulin intake, infx (uti, pneumonia, GE), illness, stroke, MI, mesenteric infarction, emotional stress, renal failure
Signs of DKA hyperventilation, dehydration, warm, dry, flushed skin, hypotension, postural dizziness tachy, shock, hypothermia, cerebral edema (kids), fruity breath
Symptoms of DKA vomiting, abd pain, thrist, polyuria, wt loss, weakness, lethargy, SOB
If a diabetic has a fever, what can be causing this dehydration, more importantly check for an underlying infx
Key dx DKA findings serum glucose>250 (<80), + betahydroxybuterate and + ketones, Arterial pH <7.3, bicarb <15, anion gap >12
Nl ABGs pH: 7.35-7.45, PaCO2 35-45, PaO2: 80-100, HCO3 21-27, O2: 95-98%
Why can BUN and Creat be high ↓ RF d/t dehydration
Why are TGs higher d/t ↑ FA metabolism
What are electrolytes usually like serum Na+ usually low but may read high d/t dehydration
Nl serum bicarb 22-29
Nl anion gap 7-16
What electrolyte can be dangerously high w/ DKA hyperkalemia shows EKG abnormalities life threatening
Problems w/ hypokalemia ↓ ventilator drive and cardiopulmonary arrest
What must we monitor w/ DM and hypovolemia K+UO, and EKG
DKA tx hydration, insulin, acid-base balance, note electrolytes
DKA hydration tx rapid replacement of first 2 liters then slow down
Complication of too rapid of replacement for hyperkalemia cerebral edema
Problem with giving insulin as tx will drive K+ into cells, if K+<3.3mEq/L must replace prior to insulin infusion
When do we replace K+ if low initially prior to insulin, and if initially nl, but given NS and insulin, should replace later
Who should we NOT give K+ to no or ↓ UO, renal insufficiency, K+> 6.0 mEq/L, EKG c/w hyperkalemia
Effects of phosphate depletion rhabdo, respiratory failreu, cardiac dysfxn, hemolysis
Why would phosphorus get depleted insulin + glucose will drive it into the cell
Monitoring of DKA BG, electrolytes, ABGs or Venous pH, serum osmolality, Ketones, UO
Goals of tx Supress lipolysis, stop ketosis, suppress HGP
DO we need to suppress BG as fast as we can no, and watch insulin drips, can dangerously overshoot
When do we add dextrose to replacement fluids, when GB <200mg/dL
How do we d/c tx once homeostasis is achieved, start SQ insulin, Taper insulin drip, oral diet: once nl start Long or intermediate insulin
When do we start to taper insulin infusion when glucose <200
DKA complications hyperglycemia, CNS depression or coma, cerebral edema (children)
Less common complications of DKA venous thrombosis, ARDS, UGI bleed, and pancreatitis secondary to severe hypertriglyceridemia
Prevention of DKA Early DMT1 dx, SBGM, ketones should be checked if BG usually >300, pt education!
What do we educate pt’s on to prevent DKA precipitating factors, distinguish early sxs of hyper,hypoglycemia, compliance, control of BG
When do we add sodium bicarb to tx of DKA when pH <7.0, lactic acidosis present? Severe hyperkalemia, (nl not required)
What electrolytes need to be supplemented as well K+, phosphate, and mg
When do we not add K+ to DKA tx no ↓ UO, renal insufficiency, K+ >6.0, EKG c/w hyperkalemia
What must we do with insulin TAPER it to prevent rebound hypoglycemia
HHS hyperosmolar hyperglycemic state
Main diff b/w HHS and DKA both d/t uncontrolled hyperglycemia which induces a hyperosmolar state in the absence of significant ketosis (HHS)
What are the BG’s like the HHS >600,>1000!
What patients do we see DKA and HHS in DKA: DMT1 and HHS: DMT2
HHS patho ↓ glucose transport and utilization, ↑ gluconeogenesis, glycogenolysis, ↑↑ BG, ↑ osmotic diuresis, dehydration, brain ↓ fluis: cerebral hyperosmolar state→lethargy, stupor, coma, death
Whatcoorelates w/degree of hyperosmolality severaty of neurological changes
What kind of azotemia is this prerenal
s/s of HHS dehydration, hypotension, ↑BG: >600, ↑ BUN, lactic acidosis
note table b/w DKA and HHS yup
Dx of DKA serum glucose >250, art. pH 7.3, serum bicarb <18, moderate ketonuria or ketonemia
HHS dx serum glucose >600mg/dl, arterial pH 7.3 Serum bicarb >15
HHS tx NS 0.9%, colloids if profound, Insulin (hospital protocols), K+ if deficits are large: monitor w/ EKG (PO3 and Mg)
Why must we be careful of rate of rehydration risks of cerebral edema d/t hyperosmolar states
Rate of replacement 1000ml first 1-2 hrs, then 500ml/2-4 hrs
Common risks for HHS elderly, ↓ thirst, non-compliant w/ oral agent or insulin, inappropriate therapy, underlying infx ( sepsis, pneumonia), Acute illness: MI, Stroke, burns, ↓ RF
Initial tx for DKA and HHS NS
What MUST we monitor during tx of HHS potassium
Monitoring for DKA and HHS EKG, K+, glucose, electrolytes, venous pH, RF,
What impacts 90% of T1DM Hypoglycemia (<70mg/dL)
What results in a release of counter-regulatory hormones BG <40-50mg/dL
What are counter-regulatory hormones epi, glucagon, GH, and cortisol
When are we more likely to be symptomatic with hypoglycemia a rapid depletion in BG
Signs for sympathetic discharge homrones release diaphoresis, tremors, nausea, irritability, tachy, hnger, pallor
Signs for neuroglycopenia (lack of glucose to the brain) HA, lethargy, confusion, poor judgment, blurred vision, dizzinesss, paralysis, Coma Seizures, Permanent brain damage, death
What is associated w/ demential in the elderly severe hypoglycemia
Causes of hypoglycemia intentional or accidental OD insulin, ↓ food, ↑ exercise ↓ insulin requirement, potentiating meds, rapid fluctuating BG (brittle) alcohol
Tx for hypoglycemia glucose 15-20g
Forms glucose can come from tabs, instant glucose (SL), juice, reg pop, hard candy
Length of tx effectiveness w/I 15mins recheck bg 15 mins
Tx for severe hypoglycemia glucagon shots, given when cant be controlled w/ oral CHO, (usually administered by other people is serious situations)
Tx severe hypoglycemia 25% dextrose in water IV (10% children)
Tx for pt’s who can’t detect hypoglycemia raise their glycemic targets
Leading limitating factor in tx of DM hypoglycemia
When sxs are non-specific and labs aren’t available tx? Give glucose/glucagon (don’t wanna ↓ glucose anymore!)
If pt is unresponsive, what must we do? protect their airway
Problem w/ DM and employment issues DM and driving, possible discriminant
Tx for Sick days continue w/ oral meds and insulin, consult Dr, BG q4hrs, test for ketones, rest, drink liquids
When do we test for ketones BG>240, vominting, sxs of hyperglycemia or ketoacidosis
Somogyi effect hypoglycemia followed by rebound hyperglycemia d/t counter regulatory homrones
What do counter-regulatory hormones induce gluconeogenesis, glycogenolysis, mobilization of AAs and fAs from stores, inhibition of peripheral glucose uptake→hyperglycemia
When do we commonly see somogyi effect at night time
Associated sxs w/ somogyi effect morning Has, fluctuating BG levels,
Why somogyi effect so important pts can’t dectect the hypoglycemia during sleep, need to adjust insulin dose at night
Tx somogyi effect ↓ insulin dose at night time (snack?)
Dawn phenomenon early morning hyperglycemia in the absence of nocturnal hypoglycemia
Cause os dawn phenomenon diurnal ↑ in GH, ↓ peripheral glucose uptake, ↓ clearance of insulin
Tx of dawn phenomenon increase insulin dose, adjust timing, may precipitate the somogyi effect
Sxs of hyperglycemia polydipsia, phagia, uria, (sticky urine?)
Sxs hypoglycemia nausea, diaphoresis, tremors, irritability (behavior changes)
Characteristics of reactive, postprandial hypoglycemia a dz not for DM occurs w/I 4 hrs of a meal, recovery sxs as BG rises,
When do hypoglycemia usually happen in response to a high CHO high simple sugar meal
Pathology of reactive hypoglycemia ↑ glucose utilization, and glucose sensitivity: leads to high CHO/osmotic load →diarrhea, insulin response to rapid glucose load, rapid droop in glucose
Tx of MNT low simple sugars, use complex CHO and ↑ fiber, high protein, moderate higher fat, smaller/more frequent meals, avoiding excess fluids w/ meals, avoiding caffeine
Characteristics of Fasting HOglycemia 12-hr post prandial
Sxs of Fasting hypoglycemia dipolopia, HA, confusion, Abnl behavior, unconsciousness, amnesia, tonic-clonic szs
Causes of above excess insulin/oral agents, alcohol, D/o of counter-regulatory hormones, glycogen storage dz, organ failure, enocrine abnl, non-beta cell tumors, sepsis, liver failure
4 MC causes of FHB DM>alcohol>sepsis>liver failure
Tx of FHB tx underlying cause, requires glucose, and frequent feedings
Created by: becker15
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