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Acute Comp. DM
Clinical Medicine II
| Question | Answer |
|---|---|
| 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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