Exam 3 Tutoring Notes Flashcards

1
Q

kehrs sign

A

left shoulder pain

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2
Q

kehr may indicate

A

spleen injury

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3
Q

hemothorax percussion

A

dullness

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4
Q

fat emobilsim s/s

A

non balancing skin petechiae (hours to 4 days)

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5
Q

aortic injury common in

A

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

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6
Q

what part of the aorta is vulnerable

A

proximal

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7
Q

SIRS criteria

A
  • mist be 2 or more
    increase RR
    increase or decrease WBC
    heart rate over 90
    increase or decrease temp
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8
Q

difference between SIRS and sepsis

A

sepsis is always SIRS but SIRS isn’t always sepsis

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9
Q

SIRS with an expected source of infection

A

sepsis

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10
Q

hyper metabolism for 14-21 days

A

lead to auto catabolism
- damage GI and biliary

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11
Q

primary MODS

A

clear orginal insult that led to other organs being effected

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12
Q

secondary MODS

A

resulting from SIRS or sepsis

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13
Q

s/s neurogenic shock

A

loss of sympathetic tone
Brady cardia
- spinal cord injury

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14
Q

s/s anaphylactic

A

antigen/abtibody
give epi (IM orSQ)

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15
Q

septic s/s

A

warm
flushed
achy
resp alk
confusion

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16
Q

s/s if cardiac tamponade

A

JVD
low map
paradoxical pulse
narrow pulse pressure
muffled sounds

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17
Q

ten pneumo percusion

A

hyperresonace

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18
Q

hypovolemic shock s/s

A

cool clammy skin
fluid volume deficit
increase ADH (compensatory)

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19
Q

causes of cardiogenic

A

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

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20
Q

cardiogenic shock CO

A

decreased

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21
Q

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

A

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22
Q

ADH/vasopresison does what

A

regulates water in the body/kidneys

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23
Q

DI s/s

A

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

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24
Q

what med is used for DI

A

desmopressin

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25
Q

SIADH s/s

A

slow onste
confusion
dilution hyponatremia
low serum osmo
high ADH
concentrated urine

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26
Q

treatment of SIADH

A

restrict water

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27
Q

goal a1c

A

under 7

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28
Q

Novolog insulin aspart

A

onset 5-15, peak 1-2, duration 4-6

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29
Q

NPH

A

onset 2-4
peak 4-10
duration 10-16

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30
Q

Lantus

A

onset: 2-4
peak flat
duration 20-26hr

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31
Q

DKA s/s

A

pH under 7.3
high K
glucose over 250

32
Q

HHS s/s

A

pH over 7.3
serum osmo over 320
glucose over 600

33
Q

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

A

B

34
Q

acute glomerulonephritis s/s

A

hematuria which causes cola colored urine

35
Q

hematuria is also a sign of

A

renal trauma

36
Q

what infection might precede glomerulonephritis

A

group A beta hemolytic streptococcal 2-3 weeks

37
Q

another cause of acute glomerulopnephtirits

A

repeated episodes of acute nephritis syndrome

38
Q

polycystic kidney disease is caused by

A

genetic

39
Q

main sign of acute renal failure

A

oliguria

40
Q

oliguria can also be a sign of

A

organ rejection

41
Q

nephrotic syndrome

A

excess fluid and generalized edema

42
Q

acute tubular necrosis can be caused by

A

-May be caused by nephrotoxic medications and environmental exposures (aminoglycosides, cephalosporins, antineoplastics, phenytoin, contrast, lead, arsenic, mercury, and uranium), sepsis, or prolonged severe hypotension

43
Q

Acute tubular necrosis stages

A

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

44
Q

Acute tubular necrosis stages
- onset phase

A

hours to days

45
Q

Acute tubular necrosis stages
- oliguric phase

A

5-16 days

46
Q

Acute tubular necrosis stages
- diuretic phase

A

7-14 days

47
Q

tx for hyperkalemia

A

Hypertonic glucose, insulin infusion and sodium bicarb

48
Q

s/s of hyperkalemia

A

high, peaked t waves and QRS widening. It may cause V-tach as well.

49
Q

treatment for creatinine over 2

A

acetylcysteine and make sure to hydrate patients before CT contrast is administered

50
Q

nephrosclerosis and ESRD

A

Develops after prolonged high blood pressure and diabetes mellitus

51
Q

calcium acetate

A

-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

52
Q

stage 1

A

GFR over 90

53
Q

stage 2

A

60-89

54
Q

stage 3

A

30-59

55
Q

stage 4

A

15-29

56
Q

stage 5

A

15 or less or on dialysis

57
Q

acute glomerular inflammation is diagnosed by

A

urinalysis

58
Q

Acute glomerular inflammation s/s

A

edema around eyes and flank
bilateral flank tenderness

59
Q

gray turners sign

A

brushing on flank around 11-12th rib

60
Q

gold standard for dialysis

A

fistula

61
Q

should we take blood pressure on AV fistula or graft

A

no can cause clotting

62
Q

how long until stress ulcers develop

A

5-7 days

63
Q

GI ulcer prophylactic meds

A

Famotidine, pantoprazole, lansoprazole

64
Q

portal hypertension

A

narrowed portal vein- decreased blood flow to the liver and increased pressure in the portal vein

65
Q

Asterixis

A

Involuntary flapping of hand
Found in encephalopathy

66
Q

hepatic fector

A

distinct smell

67
Q

Fulminant hepatic failure onset

A

Sudden onset (chronic liver failure is slow onset)

68
Q

Fulminant hepatic failure s/s

A

-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)

69
Q

Fulminant hepatic failure treatment

A

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

70
Q

bilirubin over what is severe

A

3

71
Q

pancreatitis electrolyte

A

Chvostek=Cheek Trousseau= Tension of hand

72
Q

s/s pancreatitis

A

-Hyperglycemia, hypoxemia, ARDS, hypotension,
acute tubular necrosis,

73
Q

tx of pancreatitis

A

NPO

74
Q

Esophageal varices tx

A

TIPPS procedure for tx- creates a channel between systemic and portal venous system to redirect blood flow and decrease portal hypertension

75
Q

diagnosis GI bleed

A

Fiberoptic endoscopy to diagnose