Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
50 Cards in this Set
- Front
- Back
|
what will b ein P with alcoholic ketoacidosis
|
impaired mental function, ketonuria and mildly elevate s glucose in blood
plasma glucose can be normal. low a or high |
|
|
why plasma glucose can be elevated inP with alcoholic ketoacidosis
|
impaired insulin secretion + increased insulin resistance
|
|
|
what is biochem in inP with alcoholic ketoacidosis
|
increased anion gap and osmolar gap
|
|
|
in diabetic ketoacidosis level of glucose should be
|
in diabetic ketoacidosis level of glucose should be above 250 mg/ dl
|
|
|
what is management in P with alcoholic ketoacidosis
|
1 no need to give insulin
2. dont forget tiamin 3 fluids ) dextose) 4 dexrose will lead to increase of insulin secretion thjs will lead to metobolization of ketones to bicarb administration of glucose may increase the utilazation of thiamine and could lead to Wernike (НЕ ДАВАЙ) |
|
|
what is going on with electrolytes in P with severe alcoholism
what level of phosphate is in urine |
chronic depletion of Phosphate (hypophosphatemia). why?- 1) secondary to decrease of Vit D and phosphate intake and 2) decrease of intestinal uptake in those with chronic diarrhea.
urinary excretion of Ph is increased( hyperphosphaturia).. why? 1)secondary hyperparathyroidism from decreased Vit D intake. 2)proximal tubular reabsorbtion defect from alcohol itself. Despite the depletion of Ph , serum level is maintained( extracell shift) until the P is admitted and fluid is initiated |
|
|
what is going on with P after initiation of fluid in hospital( P with severe alcoholism)
|
despite the depletion of Ph , serum level is maintained( extracell shift) until the P is admitted and fluid is initiated
once the P is fed or receives Iv fluid with glucose, insulin secretion is increased and shift of Ph in to the cell and unmask the previously compensated phsphate depletion respiratory alcalosis occurs in mane of those P wich can also shift Ph into the cell, out os serum |
|
|
what is going on with P after initiation of fluid in hospital( P with severe alcoholism) what clinical picture could be
|
may be developing muscle weakness--- > rhabdomyolysis from hypophosphatemia
1) check the serum CPK |
|
|
why in P with alcoholism is risk of rhabdomyolysis
|
patient with severe alcoholism frequently have underlying myopathy and addition of hypophosphatemia on the top of myopathy will lead to rhabdomyolysis
|
|
|
Refeeding syndrome and hypophosphatemia.
|
Hypophosphatemia is a potentially life-threatening complication of reinstating nutrition in a malnourished patient. Refeeding syndrome is a term that refers to various metabolic abnormalities that may complicate carbohydrate administration in subnourished patient populations. Hypophosphatemia is the most well-known, and perhaps most significant, element of the refeeding syndrome and may result in sudden death, rhabdomyolysis, red cell dysfunction, and respiratory insufficiency
|
|
|
paralytic ileum and hypokalemia and hyponatremia( check if he is taking loop diuretics!)
|
no pain. not tender abdomen, but distended, bowels sound decreased,
look to K- if depleed- 1 line- give K look for medication is taking_ maybe loop diuretics in P with CHF also check ecg abdminal x ray may confirm the paralytiuc ileum, with dilatation of gastric chamber and small bowel and colon |
|
|
hepatic encephalopathy- etiology
what to give if K is low |
Gi bleeding
hypokalemia hypovolemia hypoxia sedatives or tranqu;izers hypoglycemia metab alkalosis infection ( including spontaneus bacterial peritonitis) |
|
|
what to give if K is low in situation wiith hepatic encephalopathy
ventilatory failure and card arhytm |
fast K replacement
hypokaleia may induce hepatioc encephalopathy itself( look for loop diuretuc!) |
|
|
Therapeutic approach to hyperkalemia.
|
The foremost step in the initial clinical management of hyperkalemia is to decide whether a hyperkalemic patient requires immediate treatment to avoid a life-threatening situation (serum potassium concentration >6.0 mEq/l and EKG changes). When the decision for urgent treatment of hyperkalemia is based on EKG changes, an important caveat for clinicians is that absent or atypical EKG changes do not exclude the necessity for immediate intervention. Once an urgent situation has being handled with intravenous push of a 10% calcium salt, the initiation of short-term measures can be launched by either a single or combined regimen of the three agents that cause a transcellular shift of potassium - insulin with glucose, beta(2)-agonist (albuterol), and NaHCO(3)
|
|
|
what is the leading cause of hypophophatemia in hospitalized P
|
cont infusion of glucose
nadir is serum PH may apper in first few days after admission. low serum Ph can impair ATP generation( that need for sceleta muscle to perform the work) andmuscle weaknes could resullt respiratory musc weakness will prevent from weaning from ventilator also low Ph srum may lead to decre of cardiac contractility and chronic low Ph ---> cardiomyopathy. low Ph will lead to depletion of 2.3 diphosphoglycerate and this cause the leftward shift of the curve and as result- oxygen is less readily released to the tissues |
|
hypocalcemia clinical,
|
|
|
|
when hypocal can occur and why
clinical picture what can mimic the hypocalcemia and hw to differen |
|
|
|
hyperkalemia
|
|
|
|
pseudo hypernatremia , associt with
|
|
|
|
when hyperosmolar hyperglycemic state could occur
why could dehydration occur |
|
|
|
do we use Ringer lactate in the initial mng of symptomatic hyponatremia
|
|
|
|
do we administe free water in hypernatremia
|
|
|
|
sign of hypocalcemia
|
|
|
|
;why zink def is often seen in ICU
what bioch proc is zink involved where to lead the def in zink what will we see on DS how to rx the zink def |
|
|
|
l
|
|
|
|
b
|
|
|
|
what will see in osmolarity on true volume depletion and SIADH ( compare)
|
b
|
|
|
how to manage hyperkalemia in patients with hyperosmotic, hyperglycemic syndrome
|
|
|
|
how to calculate th eplasma osmol
what is the nrma |
|
|
|
tx of hypernatremia
|
|
|
|
tinel sign
|
|
|
|
loss of muscle strengh and Na
|
|
|
|
hyponatremia
|
|
|
|
primary polidipsia and NA
|
|
|
|
gullian barre
|
|
|
|
will low Na and K lead to hyperactice deep tendon
|
|
|
|
what drugs could lead to SIADH
|
|
|
|
HHS what is with K and insulin
|
|
|
|
hyponatremia
|
|
|
|
when to admin hyprtonic salin to P with hyponatremia
|
|
|
|
hg
|
|
|
|
hyponatremia... when could occur
when exessive releas of ADH can occur |
|
|
|
mk
|
|
|
|
mild hypermagnesemia will lead to
severe form of it will lead to |
|
|
|
hyponatremia
|
|
|
|
j
|
|
|
|
in high blood glucose, why insulin shouldbe start after water administ
|
|
|
|
SIADH and milf hypernatremia- manag
|
|
|
|
when to admin demeclocycline
|
|
|
|
hyprreflexia,, when could occur( tell me about Ca NA
|
|
