- mist be 2 or more increase RR increase or decrease WBC heart rate over 90 increase or decrease temp

Exam 3 Tutoring Notes Flashcards by Lani Manners

kehrs sign

left shoulder pain

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kehr may indicate

spleen injury

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hemothorax percussion

dullness

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fat emobilsim s/s

non balancing skin petechiae (hours to 4 days)

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aortic injury common in

shearing forces
- rapid deceleration, frontal or side impacts, or high falls

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what part of the aorta is vulnerable

proximal

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SIRS criteria

mist be 2 or more
increase RR
increase or decrease WBC
heart rate over 90
increase or decrease temp

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difference between SIRS and sepsis

sepsis is always SIRS but SIRS isn’t always sepsis

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SIRS with an expected source of infection

sepsis

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hyper metabolism for 14-21 days

lead to auto catabolism
- damage GI and biliary

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primary MODS

clear orginal insult that led to other organs being effected

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secondary MODS

resulting from SIRS or sepsis

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s/s neurogenic shock

loss of sympathetic tone
Brady cardia
- spinal cord injury

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s/s anaphylactic

antigen/abtibody
give epi (IM orSQ)

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septic s/s

warm
flushed
achy
resp alk
confusion

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s/s if cardiac tamponade

JVD
low map
paradoxical pulse
narrow pulse pressure
muffled sounds

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ten pneumo percusion

hyperresonace

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hypovolemic shock s/s

cool clammy skin
fluid volume deficit
increase ADH (compensatory)

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causes of cardiogenic

MI, ACS, overdose, myocarditis, valvulopathy, myocardial contusion

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cardiogenic shock CO

decreased

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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.

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ADH/vasopresison does what

regulates water in the body/kidneys

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DI s/s

increase urine output
increase thirst
decrease urine specific gravity
decrease ADH
hypernatremia
clear urine

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what med is used for DI

desmopressin

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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

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

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