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ACCRN REVIEW

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SIADH - ANStoo much ADH low Na, hypo-osmolar, low UOP ADH - ANSmade in hypothalamus stored in pituitary released to kidney and makes kidney hold onto h20 serum osmolarity - ANSNa X2 275-295 low=fluid overloaded high=concentrated SIADH CAUSES - ANSoat cell carcinoma (bronchogenic CA)-makes ...

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  • November 29, 2023
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  • 2023/2024
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A CCRN REVIEW
SIADH - ANStoo much ADH
low Na, hypo-osmolar, low UOP

ADH - ANSmade in hypothalamus
stored in pituitary
released to kidney and makes kidney hold onto h20

serum osmolarity - ANSNa X2
275-295
low=fluid overloaded
high=concentrated

SIADH CAUSES - ANSoat cell carcinoma (bronchogenic CA)-makes its own ADH
Viral PNA
Head Problem
inc. serum osmo, anesthesia, analgesics, stress

COMPLICATIONS OF SIADH - ANSSz's

TREATMENT of SIADH - ANSget rid of causes
fluid restrictions
hypertonic solutions (3%, D5NS, D51/2NS) give 25-50cc/hr d/t CHF

DI - ANSNo ADH (no h20 at kidney)
inc Na+ levels, inc osmolarity, inc. UOP (spec grav 1.001-1.005)

DI Causes - ANShead problems
dilantin

DI Treatment - ANSGive ADH (PItressin or vasopressin)
Give fluids to increase Intravascular volume
monitor UOP
*monitor fo ischemia

Hypoglycemia - ANSCVS s/s
tachycardia, palpitations, diaphoresis, irritable, restlessness
CNS s/s
confusion, lethargy, slurred speech, sz, coma

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

Cullens and Grey Turners Signs - ANSblack/blue umbilicus (Cullens)
black/blue flank/groin (greyturners)

, in Pancreatitis

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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