Exam 3 Tutoring Notes Flashcards
kehrs sign
left shoulder pain
kehr may indicate
spleen injury
hemothorax percussion
dullness
fat emobilsim s/s
non balancing skin petechiae (hours to 4 days)
aortic injury common in
shearing forces
- rapid deceleration, frontal or side impacts, or high falls
what part of the aorta is vulnerable
proximal
SIRS criteria
- mist be 2 or more
increase RR
increase or decrease WBC
heart rate over 90
increase or decrease temp
difference between SIRS and sepsis
sepsis is always SIRS but SIRS isn’t always sepsis
SIRS with an expected source of infection
sepsis
hyper metabolism for 14-21 days
lead to auto catabolism
- damage GI and biliary
primary MODS
clear orginal insult that led to other organs being effected
secondary MODS
resulting from SIRS or sepsis
s/s neurogenic shock
loss of sympathetic tone
Brady cardia
- spinal cord injury
s/s anaphylactic
antigen/abtibody
give epi (IM orSQ)
septic s/s
warm
flushed
achy
resp alk
confusion
s/s if cardiac tamponade
JVD
low map
paradoxical pulse
narrow pulse pressure
muffled sounds
ten pneumo percusion
hyperresonace
hypovolemic shock s/s
cool clammy skin
fluid volume deficit
increase ADH (compensatory)
causes of cardiogenic
MI, ACS, overdose, myocarditis, valvulopathy, myocardial contusion
cardiogenic shock CO
decreased
A young male patient has been brought to the emergency department with a knife wound to the abdomen. When the patient’s hands are removed from the area of the wound to facilitate assessment, the patient’s intestine protrudes from the wound. How should the nurse respond to this development?
a) Cover the protruding viscera with saline-soaked, sterile gauze.
b) Apply a pressure dressing to the wound.
c) Irrigate the protruding intestine with sterile water or normal saline.
d) Don sterile gloves and attempt to push the organ back inside the wound.
A
ADH/vasopresison does what
regulates water in the body/kidneys
DI s/s
increase urine output
increase thirst
decrease urine specific gravity
decrease ADH
hypernatremia
clear urine
what med is used for DI
desmopressin
SIADH s/s
slow onste
confusion
dilution hyponatremia
low serum osmo
high ADH
concentrated urine
treatment of SIADH
restrict water
goal a1c
under 7
Novolog insulin aspart
onset 5-15, peak 1-2, duration 4-6
NPH
onset 2-4
peak 4-10
duration 10-16
Lantus
onset: 2-4
peak flat
duration 20-26hr
DKA s/s
pH under 7.3
high K
glucose over 250
HHS s/s
pH over 7.3
serum osmo over 320
glucose over 600
The nurse documents a capillary blood glucose level of 47 mg/dL for a client who is diagnosed with type 2 diabetes mellitus (DM). The client is alert, but clammy and has cool skin to the touch. Which is the nurse’s first action?
Give D50W by IV push immediately
Have the client drink 8 oz juice
Quickly inject glucagon 1 mg by IM injection
Draw blood from a different finger for comparison
B
acute glomerulonephritis s/s
hematuria which causes cola colored urine
hematuria is also a sign of
renal trauma
what infection might precede glomerulonephritis
group A beta hemolytic streptococcal 2-3 weeks
another cause of acute glomerulopnephtirits
repeated episodes of acute nephritis syndrome
polycystic kidney disease is caused by
genetic
main sign of acute renal failure
oliguria
oliguria can also be a sign of
organ rejection
nephrotic syndrome
excess fluid and generalized edema
acute tubular necrosis can be caused by
-May be caused by nephrotoxic medications and environmental exposures (aminoglycosides, cephalosporins, antineoplastics, phenytoin, contrast, lead, arsenic, mercury, and uranium), sepsis, or prolonged severe hypotension
Acute tubular necrosis stages
Onset phase-lasts for hours to days. If treatment is initiated in this stage, irreversible damage may be eliminated
Oliguric/anuric phase- 5-16 days, necrotic cellular debris blocks urine and damage is done to the tubular wall
Diuretic phase- 7-14 days- increasing GFR and polyuria. Monitor for dehydration
Recovery/convalescent phase- even more increase in urine output. BUN and creatinine either increase or stay at their new normal
Acute tubular necrosis stages
- onset phase
hours to days
Acute tubular necrosis stages
- oliguric phase
5-16 days
Acute tubular necrosis stages
- diuretic phase
7-14 days
tx for hyperkalemia
Hypertonic glucose, insulin infusion and sodium bicarb
s/s of hyperkalemia
high, peaked t waves and QRS widening. It may cause V-tach as well.
treatment for creatinine over 2
acetylcysteine and make sure to hydrate patients before CT contrast is administered
nephrosclerosis and ESRD
Develops after prolonged high blood pressure and diabetes mellitus
calcium acetate
-Phosphate binding medication for renal patients with hyperphosphatemia
-Main hyperphosphatemia symptom is pruritus and it may lead to hypocalcemia
-Educate them to take it with meals
stage 1
GFR over 90
stage 2
60-89
stage 3
30-59
stage 4
15-29
stage 5
15 or less or on dialysis
acute glomerular inflammation is diagnosed by
urinalysis
Acute glomerular inflammation s/s
edema around eyes and flank
bilateral flank tenderness
gray turners sign
brushing on flank around 11-12th rib
gold standard for dialysis
fistula
should we take blood pressure on AV fistula or graft
no can cause clotting
how long until stress ulcers develop
5-7 days
GI ulcer prophylactic meds
Famotidine, pantoprazole, lansoprazole
portal hypertension
narrowed portal vein- decreased blood flow to the liver and increased pressure in the portal vein
Asterixis
Involuntary flapping of hand
Found in encephalopathy
hepatic fector
distinct smell
Fulminant hepatic failure onset
Sudden onset (chronic liver failure is slow onset)
Fulminant hepatic failure s/s
-impaired bilirubin conjugation, decreased production of clotting factors (bleeding risk!), decreased glucose synthesis and decreased lactate clearance
-Similar symptoms to cirrhosis (jaundice, ascites, confusion, nausea/vomiting)
Fulminant hepatic failure treatment
goal is to reduce bacterial flora and ammonia levels
Neomycin to reduce the bacterial flora
Lactulose to decrease bacterial growth, causes patient to excrete excess ammonia
bilirubin over what is severe
3
pancreatitis electrolyte
Chvostek=Cheek Trousseau= Tension of hand
s/s pancreatitis
-Hyperglycemia, hypoxemia, ARDS, hypotension,
acute tubular necrosis,
tx of pancreatitis
NPO
Esophageal varices tx
TIPPS procedure for tx- creates a channel between systemic and portal venous system to redirect blood flow and decrease portal hypertension
diagnosis GI bleed
Fiberoptic endoscopy to diagnose
