hypoglycemia pathophys - ANSlow glucose->adrenal medulla knows and releases
adrenaline->liver releases glycogen which is converted into glucose to increase BGL
if block in adrenaline or liver cant convert glycogen into glucose (AKA BETA BLOCKERS)
then CVS s/s wont occur
DKA s/s - ANSonly in insulin dependent diabetics
,BGL 400-900
dehydrated (4-6L lost)
No circulating insulin
+acidosis b/c body breaks down fat into ketones
Kussmaul (inc rate depth to blow off c02)
DKA and HHNK treatment - ANSinsulin gtt
IVF (more for HHNK)
NS 1st- to hydrate vascular compartment
1/2NS to hydrate cell
D51/2NS to prevent hypoglycemia
**for every decrease in pH by 0.1, K+increases by 0.6
HHNK vulnerable population - ANSOLD AGE (pancrease gets tired)
diet controlled diabetics
people on TPN (gets 80% glucose IV->pancreatic fatigue
pancreatitis
HHNK s/s - ANSBGL 1000-2000
Severe dehydration (6-8L lost)
+insulin (prevents breakdown of fat)
No acidosis (baby breaths)
somogyi phenomenon - ANSRapid decrease in serum glucose, usually at night, that generates
the release of glucose-elevating hormones that manifests as an elevated glucose level in the
morning.
dehydration is not a component of this
NPH peak - ANS6-10 hrs
Pancreatitits - ANSobstruction of pancreatic ducts
gallstones
infection
alcoholism
drug toxicity (cyclosporines, steroids, thiazides, tetracyclines)
trauma
s/s of pancreatitis - ANShypocalcemia (pancreas uses Ca+ to break down its fatty organ self)
HHNK
increase amylase levels
l sided pleural effusion
L atelectasis
B rales
ARDS (panc releases phosfolipase A=>lungs =>eats alveoli=> no surfactant production
GI obstructions - ANSsmall bowel: small distention, diarrhea, n/v
large bowel: large distention
how fast is blood filtered through the liver? - ANS1500cc blood/min
Kupper cells - ANSdetoxify blood in liver
Liver - ANScreates bile
synthesis amino acicds
makes albumin, PT, Fibrinogen
converts glucose into glycogen
converts NH3 into urea
How does ascitis happen? - ANSLiver produces albumin, and with decreased
albumin=>decrease in oncotic pressure=>fluid shift to interstitial compartments
hepatic encephalopathy (high ammonia) - ANSdecrease in K+ levels (kidneys hold onto K
and NH3)
increase in BUN (breaks down NH3)
increase proteins (GIB's release NH3)
increase in acids (metabolic acidosis=>low BP, ringers lactate=>lactate=>bicarb by liver
with ESLD, lactate cant be converted to bicarb, so the kidneys convert it to lactic acid instead
Complication of Neomycin Therapy - ANSvitamin deficiency
its not systematically absorbed, stays in the gut in order to destroy bacteria (makes vitamins
and releases NH3)
bilirubin (conjugated or unconjugated) - ANSunconjugated/indirect bili goes to liver to be
'married' and once it leaves the liver, its conjugated/direct bili and then goes to gall bladder
if indirect is high=>liver problem (hepatic failure, liver disease)
if direct is high=>gall bladder problem/biliary tract disease
Kehr's sign - ANSl shoulder pain.
fingers under left rib cage results in neck pain
RUPTURED SPLEEN
Normal GFR - ANS125ml/min or 180L/day
Creatnine clearance reflects GFR-it evaluates the ability of the kidney to filter a waste
product (creatnine) that is neither absorbed nor secreted
What causes excretion of Na+ and H20 and retention of K+? - ANSACE Inhibitors
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