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Med surg 2 > Final > Flashcards

Final Flashcards

1
Q

How to calculate MAP

what do we need in order to perfuse organs?

A

SBP+2DBP/3

Above 60

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2
Q

What are the two heart dysrhythmias we need to call a code on

A

Ventricular tachy w/o pulse and ventricular fib

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3
Q

What are the complications of MI

A

DysR, cardiogenic shock- severe L vent fail, Papillary mm dysfunction, Ventricular aneurism, Acute pericarditis, dresslers- plural effussion with pericarditis

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4
Q

3 signs of sinus bradycardia

A

Confusion, disorientation, SOB

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5
Q

What do we do with vent tachy vs vent fib?

A

Vent tachy- unstable no pulse cpr defib

Vent fib -CPR and defib

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6
Q

What do we like to defib

A

VFib and V tachy

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7
Q

2 Thinks about defib

A

Within 2 mins

and start CPR right away

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8
Q

When do we use Sync? and one thing not to do

A

VT with a pulse or supraventricular tachy aka a fib with rapid vent response
Use on t wave

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9
Q

PR interval

A

time of spread of electrical impulse right before vent contraction

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10
Q

ST segment

A

Time from vent depolarization to repolarization

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11
Q

t wave

A

ventricular repolarization

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12
Q

What is a premature atrial contraction mean and one thing that shows up

A

Location other than SA node distorted p wave

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13
Q

Atrial flutter 2 things

A

saw tooth and cant measure PR interval

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14
Q

A fib

A

Disorganized electrical activity from multiple ectopicfoci

Chaotic waves replace p waves so no p wave

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15
Q

AV block

A

no atrial pulses to vents p wave and qrs have no relationship
cant measure pr

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16
Q

PVC

A

early QRS that are wide and bizzare no p wave with pvc

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17
Q

Vent tachy

A

3 or more PVC in a row

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18
Q

vent fib

A

Cant measure anything

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19
Q

What is ACS 2 and three groups

A

Ischemia that is prolonged and not immediately reversed. It is a coronary art that is part or all the way occluded with thrombus.
UA, STEMI and NSTEMI

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20
Q

One thing about chest pain with NSTEMI

A

20 mins or longer

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21
Q

s/s of NSTEMI

A

maybe s3 s4 heart fail issues valve dysfunction issues

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22
Q

order of management for ACD and what is gold star for diagnostic test

A

12 lead, semi fowler, 02, Nitro asa, morphine, troponin

Angiography

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23
Q

how much time on a small box EKG

A

0.20 seconds

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24
Q

a flutter vs a fib

A

a flut is saw tooth a fib is no p wave

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25
Q

Vent tachy
vent fib
3rd heart block

A

someone looks like they are drawing tall sqiggles
crazy cant make out anything-QRS not measurable
rate less than 40, p no connection to QRS PR not measurable qrs normal to wide

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26
Q

NSTEMI

A

Partial occlusion of coronary art. Chest pain may resolve, st depression or no change, troponin increase
sudden onset chest pain, pressure, heaviness, tightness, fullness, SOB, burning, radiating- may be relieved with nitrates

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27
Q

STEMI

A

ST elevation means 100% occluded chest pain greater than 20mins
immobilizing chest pain not relieved by rest, position change, or nitrate pain is for 20mins or longer and more severe than normal angina.

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28
Q

Rheumatic fever and rheumatic disease

A

inflam disease from abnormal immune response to group A strep after about 3 weeks affects skin, joints, cns

chronic scaring and deformity of heart valves vegetations

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29
Q

Manifestations of rhematic fever 7

A

Erythemia marg, arthritis, carditis, subcut nodules, sydenhams chorea, increase in esr and cpr prolonged PR,

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30
Q

What is the most common thing that rheumatic fever will lead to

A

mitral valve stenosis or other valve disease

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31
Q

2 things about RF

A

Antibiotics for 5 yrs maybe life and assess for pulmonary edema and clear lung sounds

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32
Q

Aortic Valve regurg caused by

A

Syphalyis, connective tissue disorder, post surg

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33
Q

Manifestations 1 acute

and 3 others aortic regerg

A

Sudden vascular colapse
hammer pulse
soft or absent s1
diastolic murmur

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34
Q

s/s of respiratory acidosis 7

A

skin pale, HA, Hyperk, Dysr, drowsiness, mm weaknees, hyperreflexia

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35
Q

s/s of repiratiory alk 9

A

tachy, low to normal bp, hypok, numbness and tingling, hyper reflexes, mm cramping, seixures, anxiety, tremmors,

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36
Q

MEtabolic acidosis 8

A

HA, hyper k, mm twitching, warm flushed skin, NV, decreased mm tone, decreased reflexes, kussumal

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37
Q

Metabolic acidosis s/s 9

A

confusion, dysr, dizzy, n/v/d/ seixures, tremors, mm cramps, tingling, decreased ca

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38
Q

s/s of PE 3

A

Cough, crackles, wheezing, fever,

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39
Q

complications from PE 2

A

Abcess, pleural effusion,

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40
Q

Best test for PE

A

CT

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41
Q

What is the movement with fillet chest?

A

Paradoxical

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42
Q

What is a spontaneous pneumo

A

Rupture of blebs on surfece of lungs- little air sacs

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43
Q

What is a tension pneumo and one thing about it

A

air can get in but not out

EMERGENCY

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44
Q

Where does a chest tube go in?

A

4th or 5th space anterior to midaxil

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45
Q

how is tube secured in chest tube

A

Heavy no absorbant sutur

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46
Q

What to wrap chest tube in

A

petrolium gauze and sponge gauze

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47
Q

What is suction on for chest tube?

A

80

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48
Q

Submurge in how much water for chest tube

A

250ml

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49
Q

flail chest

A

Flail chest — defined as two or more contiguous rib fractures with two or more breaks per rib

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50
Q

What do normal cells do? 3

A

They respect boundaries (increase contact inhibition)
neighboring cells inhibit cell growth-through the cell membrane
rate of growth in each cell is different depending on location
rapid areas include bone marrow, epithelial tissue, hair/skin/nails

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51
Q

What are protoncogogenes 4

A

Genes that regulate cell growth but can become unlocked from carcinogens or oncogenetic viruses
once they become unlocked they work like oncogenes-tumor inducing
this means the ability and properties that the cell had in fetal development are now active
it is immature, dedifferentiated, change from normal to make
and can make new proteins

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52
Q

Oncogene proteins
are located?
2 ex
and one more thing they produce

A

Located on the cell membrane
in blood tests
CEA and Fetalprot
produce hormones

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53
Q

What are tumor decreasing genes
What happens to them during cancer
Two examples and about them

A

They regulate growth by not letting cells go through the cell cycle
Are mutated or turned off
BRAC1 and BRAC 2 have inherited mutations for breast and cervical cancer

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54
Q

What is ACP gene

A

Tumor suppressor gene that can have a Family mutation gene for adenomatous
polyposis- colorectal cancer

55
Q

Model of development of cancer

A

Initiation- Inherited or acquired
Promotion- Reversible proliferation
Progression-possible metastasis tumor growth

56
Q

Initiation
What is it?
What about inherited?
What about acquired- 3 examples

A

Any change or mutation in usual DNA sequencing
if inherited -sm risk but high risk
carcinogens- Alkylating drugs or immunosuppressants can cause secondary leukemia that is resistant to chemo
Radiation- Atomic bomb and UV
Viral- Epstein barr, HIV, Hep B, HPV

57
Q

CEP

FP

A

Carcenoembryonic antigen is a tumor cell protein

Alpha fetoprotein

58
Q

What are the oncofetal antigens and how do we use them what are they 2

A

Tumor antigens from cell in the fetal state
use them as tumor markers
CEA and AFP

59
Q

Thrombocytopenia numbers

A

tcp-150,000
bleed risk prolonged- 50,000
spontaneous bleed 20,000

60
Q

What is polycythemia?

Two types and about them

A

The production on presence of increased numbers of RBC
Primary (vera) or secondary
P- chronic-all BC involved=viscosity and volume= meglys and clotting
S-hypoxia driven or independent
driven-Hypoxia stimulates EPO
S-independent- tumor is making EPO
There is no splenomeg with secondary

61
Q

S/S of primary polycythemia

A

HA, vertigo, tinnitus, visual changes
pruitus, paresthesia, erythromelagia-buring and red of hands and feet
angina, HF, intermittent claudication, clot issues hypoxia and stroke
Hyperuricemia, hemorrhage, ulcers, meylofibrosis, leukemia,

62
Q

One lab difference between primary and secondary poly

Tx

A

Primary-Low to normal EPO
secondary- high
Phlebotomy to normalize Hematocrit

63
Q

Types of pneumo

A

● Spontaneous- Rupture of bleb – Primary (idiopathic) & Secondary (to lung disease→COPD)
● Iatrogenic - Caused by medical procedures
● Traumatic penetrating (open)
● Traumatic blunt (closed)
● Hemothorax
o Blood in pleural space
o Treat with chest tube
● Hemopneumothorax
● Chylothorax
o Lymphatic fluid in pleural space
o Treat conservatively, with meds, surgery, or pleurodesis.
● Tension Pneumothorax - medical emergency
o Accumulation of air in pleural space that does not escape
o Causes mediastinal shift and hemodynamic instability.
o Can occur with penetrating (open) or blunt (closed) pneumothorax.
o tracheal deviation!
● S/S of pneumothorax
o dyspnea
o anxiety
o tachycardia
o pleural pain
o asymmetrical chest wall expansion
o diminished breath sounds

64
Q

thorancentesis

A

● Used to obtain specimen of pleural fluid for dx, removal, or giving meds
● complications = Hypoxia, pneumothorax
● Don’t remove fluid too quickly = hypotension, hypoxemia, reexpansion, pulm. edema, spasms?
● X-ray after to check for pneumothorax

65
Q

Tumor Lysis Syndrome

A

● Hyperuricemia
● Hyperphosphatemia
● Hyperkalemia
● hypocalcemia. p262 table 15.19
● Occurs 24-48 hrs after starting chemo. May last 5-7 days. Can lead to acute kidney injury (↑BUN & Cr)
● Patient safety: monitor f/e and cardiac function. Anything else?

66
Q

HITT

A

● platelets reduced by 50% (below 150,000)
● 5-10 days after trt.
● DVT, PE, venous thrombosis (the m/c problem), arterial vascular infarcts - leads to stroke, kidney damage
● Platelet destruction and vascular endothelial injury are the 2 major responses to an immune-mediated response to heparin
● Antibodies are created against the PF4-platelet-heparin complex which are removed prematurely from circulation, leading to thrombocytopenia and platelet-fibrin thrombi
● this is basically like having an allergy to heparin; the patient should NOT take heparin, ever

67
Q

labs

A
68
Q

TACO

A

● Fluid given faster than circulation can handle; blood products are hypertonic
● Cough, dyspnea, pulmonary congestion, headache, hypertension, tachycardia, distended neck veins
● Patient HOB raised, diuretics, oxygen
● May be able to continue the transfusion depending on situation

69
Q

Acute Hemolytic

A

● ABO incompatibility
● Antibodies in patient’s plasma attach to antigens on transfused RBCs causing lysis of cells
● Symptoms usually occur quickly after blood started: Chills, fever, low back pain, hemoglobinuria, flushing, tachycardia, tachypnea, hypotension, jaundice, acute renal failure
● Stop the blood but keep IV patent. Treat shock, draw blood for testing, insert Foley, renal dialysis

70
Q

Transfusion Related Acute Lung Injury (TRALI)

A

● Occurs when donor plasma contains WBC antibodies. Causes fluid leak into lungs Þ pulmonary edema
● Dyspnea, hypotension, and fever usually begin 1-2 hours after the transfusion, but possibly up to 6 hrs later; can have pulmonary edema and acute resp distress
● Ventilatory support may be needed for several days

71
Q

Febrile Non-hemolytic

A

● Sensitization to donor WBCs, platelets, or plasma proteins
● Most common transfusion reaction
● Sudden chills and fever, headache, flushing, anxiety, muscle pain
● stop the infusion!
● Give antipyretics

72
Q

how do we treat right away for DKA?

A

O2, then IV- 0.45-0.9 NS, add dextrose if below 250-SLOWWW, short acting insulin, and k+ because of insulin at 0.1 units and increased output, possibly bicarb, Cardiac monitor, labs

73
Q

What is hyperosmolar hyperglycemia

A

Its an emergency with 600+ BG levels, and severe osmotic diuresis caused by infection or newly diagnosed DM11

74
Q

What are we concerned about hypersomolar hyperglycemia

What can that lead to

A

Hypovolemia, Hypoelectrolytes, dehydration, Hemoconcentraition, renal perfussion, tissue anoxia (Lactic levels increased)
Seizure, shock, coma, death

75
Q

S/s of hyperos hypergly

A

Hypovolemia s/s, dehydration s/s, shock s/s, high urine output to low urine output, seizure, high bg, stroke- similarities. LOV issues, s/s of hypoglycemia- mimic alcohol.

76
Q

Management of Hyperos hypergly

A

Similar to DKA, more fluid, might need a foley, breath sounds, IV- normal half normal, add dextrose at 250, insulin electrolytes, watch cardiac, renal, Mental status.

77
Q

What is the number for hypoglycemia

A

less than 70

78
Q

Types of DI and about them

A

Central- Interference with ADH production tumors, infections, brain surgery
Neph-kidneys wont respond- Lith, renal damage
primary- Thirst issues

79
Q

Manifestations of di 5 causes with with r/t s/s

A

polydipsia, polyuria,- 2-20 l a day with low SG
Increased plasma osmolality
Sleepy from nocturia
dehydration-thirst, hypo, tachy, shock
Hyperna+ irritable, mental dullness, coma

80
Q

DI and three things to watch for one thing to teach

Specific tx for neph and central-

A

Hyperna+-Watch s/s, hypotonic solutions, dextrose-watch glucose and its diuretic effect.
Increase fluids-DDAVP and aqueous vassopressin
FVD- Thirst- CLor and carban, I and O, Vitals-esspecially volume rt, Specific gravity, daily weights, flushed skin- sign of FVD
Long term mat
Nephro-Fluids and decrease Na+ no hormones, thiazides, indometh-NSAID and increases kid sensitivity.

81
Q

Explain test for DI

A 
Water deprivation test 
before test measure body weight, urine osmo, volume, and sg
no water for 8-12 hr
Give presser 
Central-increse urine osmo
nephro- no increase in urine osmo
82
Q

Myedexema coma

A

Long standing hypothyroidism from acculumulation of hydrophilic monopolysacerides, in dermis and tissue

83
Q

Myedex coma s/s 5

caused by?

A

Puffy face and peri orbital,
coma-mentally slow, drowsy, lathargic
infection, drugs, cold, trauma, stopping tx

84
Q

Manifestaions of My coma 4

A

Subnormal temp, hypotn, hypovolemia, cardiac collapse- hypovent, hypona hypogly lactic acidosis,

85
Q

Care for myex coma

two drugs

A

Mechanical respiration, cardiac monitoring, temp, skin care, vitals weights i LOC
IV thyroid hormone vassopressors

86
Q

Cushings cause
types
Common

A

Over exposure to corticosteroids, iatrogenic- prednisone, ACTH Secreting pituitary adneoma or adrenal tumor
Ectopic-Tumors somewhere else- lungs and pancreas
women 20-40

87
Q

Manifestations that you don’t know of chushings

A

hyperglycemia, mm weak and atrophy, osteoporosis, weak skin, delayed wound healing, hypoK, hypertn, acne, buffalo hump edema, awkward gate, CNS changes, GI increased Acid, bruise and petechiae

88
Q

What tests would you expect with cushings.

A

MRI or CT for tumor, Plasma ACH- low or high, blood penias-white, glucose in urine, hyperca, hypo k and alkolosis

89
Q

TX for cushings

A

Radiation- for those who can’t have surg,
surgery
drugs-destroy adrenal-ketoconazole and mitotane
Mifepristone0 for hypergly

90
Q

What to watch for with cushings

A

Thrombolytic event, medical alert bracelet, no extreme temps, may need more steroids for stress, watch for infection and OSHTN

91
Q

Addisons causes

A

TB, amylodisis, fungal infection, AIDS, meta cancer. chemo, ketoconazole, bilat adrenoectomy, Anticoag therapy

92
Q

pheochromcytoma

A

Tumor in the medulla affecting chromaffin cells aka catecolamines

93
Q

pheochromcytoma s/s 7

A

Severe pounding HA, High BP, tachy, chest pain, diaphoresis ab pain

94
Q

Causes of pheochromcytoma 10

A

direct trauma, stress, sex, alcohol, smoking, drugs antihypertensives, opioidsm contrast, tri antidepressants,

95
Q

tx of pheochromcytoma

A

Alpha and beta blockers sin and lol surg decrease bp and dysr
watch orthp

96
Q

ANION GAP

A

(na+-k+)- (Cl+HCO3)

normal 8-10

97
Q 
stoma colors 
rose to brick pink 
pale
blanching, dark red to purple
small blood
A

Rose- viable stoma mucosa
maybe anemia
inadequate blood supply
when touched is normal from high vascularity

98
Q

bile billy and ammonia

A

Bile salts aid in digestion by making cholesterol, fats, and fat-soluble vitamins easier to absorb from the intestine. Bilirubin is the main pigment in bile. Bilirubin is a waste product that is formed from hemoglobin (the protein that carries oxygen in the blood) and is excreted in bile.
Ammonia is protein breakdown that turns into urea in the liver and leaves

99
Q

Manifestations of acute pancreatitis

A

Sudden inflam, edema, necrosis, hemorrhage, fat necrosis, vascular perm, smooth mm contractions, shock, ab pain in LUQ, and mid epi that radiates to shoulder and worse with food, N/V that dosent help pain, low fever, Hypotension, Jaundice, gry turners sign, cullens sign (eccymosis), Hyposctive or no bowel sounds, crackles,

100
Q

Complications of acute pancreatitis

A

plural effusion, atelectasis, pneumonia, ARDS,
Emboli, DIC
Hypotension
hypocalcemia-Tetany
Pseudo cyst- from all the gunk
Ab pain, palpable mass, anorexia, NV, Perf, peritonitis
Abscess- infection of pseudocyst

101
Q

S/S of peritonitis

A

Increased HR, BP, temp, stiff plap belly,

102
Q

Labs for pancreatitis acute

A

Panc enzymes, hypoca+,

Liver, triglycerides, glucose, bilirubin,

103
Q

Chronic pancreatitis and about the two types

A

Irreversible structural damage to the pancreas. This includes fibrotic tissue, strictures, and calcification, Scaring, dilation, stones pass.
Obstructive- Gallstones that cause inflam of sphincter or odi-cancer of amp, duodenum, pancreas, or cystic fibrosis,
Non-obstructive- Inflam and sclerosis in head of pancreases and duct, alcohol abuse

104
Q

manifestations of chronic pancreatitis

A

Swelling, mass, chronic ab pain, or no pain, mal absorption, weight loss, constipation, DM!, increase in cholesterol, heavy burning not relieves by food or antacids, mild jaundice, dark urine-from bile, Steatorrhea

105
Q

Gallbladder disease two types and risks

A

Cholelith-Stones
Cholecys- Inflam of gallbladder usually from cholelith
Balance of chole, bile salts, ca+, and Na+=precipitation
Infections or alterations in metab or chole or stasis
immobility, pregnancy, inflam or obstruction, lesions-all cause obstruction

106
Q

Manifestatons of choelith

A

Pain is severe-none, more pain when stone is moving or obstructing, may be in shoulder or scap, tachy, diaphoresis, tender RUQ pain,- 3-6 hours after meal or when laying down

107
Q

Manifestations of chole sis

A

fat intol, dyspepsia, heart burn, flatulence, inflam with leuko and fever, ab regidity

108
Q

Total gal stone obstruction symptoms

A

Jaundice, dark urine, clay stools, pruritus, intol of fat, bleeding tendencies, steatorrhea

109
Q

Complications of gal bladder disease

A

Cholesis, gangrenous, subphrenic abcess, pancreatitis, cholangitis, billiary ducts, fistulas, bil cirrhosis, perionitis, choledocholithiasis.

110
Q

Tx for cholecycsitis

A

Pain control, NSAIDS, anticholenergics, antibiotics, choleystestomy, Fluids and electrolytes, NG tube in severe N/V,

111
Q

Surgical tx for choleitis

A

Laperascopic cholecystectomy- Removal through holes, minimal post pain, normal activity in 1 week, few complications, clear lq, same day discharge
or open- removal through right subcostal incision
t-tube-Inserted into the common bile duct,
ESWL

112
Q

esophageal cancer patho history and risks

A

Usually advanced disease by the time of diagnosis, it narrows the esophagus, Risks-Increase with age, BE, smoking, alcohol, Obestiy, abestos, cement dust, achalasia-delayed emtying, gerd, barrets

113
Q

Manifestatons of Esoph cancer

A 
Progressive dysphagia-meat, soft food, lq
Pain is latep substernal epigastric, back that increases with swallowing-even spit, 
Weight loss
Sore throat, choacking 
hoarseness\regur with blood tinged
Hemmorrhage-if trach
May cause obstruction
common metastasis to lungs and liver
114
Q

Diagnosis for esoph cancer

A

Endoscope biops
ultrasound
CT/MRI
Bronchoscopy

115
Q

Tx for Esoph cancer

A

Surg-esophagectomy-removal
esophagastromy -resection to stomach
esophagoenterostomy-resection to colon- lap or open
Photodynamic lasor therapy- no sun 3-6 weeks
Chemo and radiation

116
Q

Post of esoph cancer

A

Watch respiratory, pain control, Chest tube, TPN, Swallow study, HOB 30 and for 2hr after meal

117
Q

Surg risk for esoph cancer

A

DysR, anastomatic leaks, fistulas, edema, respiratory distres, dysruption of medial sternal lymph nodes

118
Q

Care for E cancer

A

Airway, respiratory, swallow B4 oral fluids, high fowlers, tube feeding tol, pain

119
Q

Lower GI obstruction types

A

Mechanical- Detectable, commonly found in sm intestine, surgical adhesion-small intest and colorectal cancer-Large intest
non mechanical- Paralytic illeus, pseudo- acting like theres an obstruction- critically ill, trauma, burns. vascular- no blood to intestines- a fib, art obstruction, clots, heart valve issues, heart attack, congestive fail

120
Q

Types of lower gi obstruction

A

Adhesions, intessuseption, hernwas, tumors, volvus,

121
Q

Steps of lower obs

A

1.obstruction- build up fluid, gas, intestial contents-prox
Collapse- distal
2. Increase in bowel distension- reabsorption of fluids
3. increase pressure- cap perm, fluids into 3rd space
4. loss of blood volume
5, ischemic bowel no blood supply

122
Q

Sm in lower GI

A

Rapid onset

Early- Colckly, intermit ab pain, NV in large ammounts, projectile vom with bile, if long standing smells like poop

123
Q

Lg in obstruction s/s

A

Gradual onset, vom it rare, ab pain present but low grade, ab distention increased new onset of constipation and no flatulus

124
Q

diagnosis of bowel obstruction

Labs

A

x ray-ct scan
Sigmoidoscopy/colonoscopy
Increase in WBC, H and H, BUN and creatinine

125
Q

Tx for lower GI obstruction

When do you need surgery

A

conservative, NPO, rest, NG tube, IV fluids-NS or lac ringers, Pain control
if strangulated or tx not effective, May need colonosctomy or illiostomy

126
Q

What are the biggest concerns with Lrg bowel obstructions

A

Ischemia, peritinitous, sepsis

127
Q

CFS contents

A
128
Q

Stroke: 1 (make sure you know the screening indicators for tPA use

A

d to produce localized fibrinolysis by binding to the fibrin in the thrombi
● Given IV to prevent cell death with ischemic stroke
● Tissue plasminogen activator (tPA)- Reestablish blood flow, given within 3 to 4.5 hours of onset of clinical signs of ischemic stroke –pts screened carefully
● Patient screening includes: noncontrast CT scan or MRI to rule out hemorrhagic stroke, blood tests for coagulation disorders, GI bleeding, storke, head trauma within the past 3 months, major surgery within 14 days, internal bleeding within 22 days
● Monitor patients VS and neuro status, control BP SBP <185

129
Q

Spinal Shock: 30-60 min after injury

A

Spinal Shock: 30-60 min after injury
● Loss of sensation, decreased reflexes, absent thermoreg, or flaccid paralysis below injury level
● Days to weeks after injury

130
Q

Neurogen shock

A

Neurogenic Shock (injury above T-6)
● Loss of SNS innervation/tone (cervical or high thoracic injury)
● Peripheral vasodilation = venous pooling, low CO
● Give fluids, vasopressors
● Respiratory: hypoventilation, C4= loss of resp fctn
● Cardiovascular: bradycardia
● hypotension- (Neurogenic shock)
● Urinary: neurogenic bladder-atonic bladder initially
● Gastrointestinal: hypomotility
● Temperature: unable to regulate-lack of SNS/nerve disruption to hypothalamus
● Integumentary: pressure ulcers/skin breakdown

131
Q

Autonomic Hyperreflexia (Injury T6 or higher)

A

● Uncompensated cardiovascular response from SNS
● Triggered by stimuli at or below T6-
● Blood vessels constrict
● S/S= HTN, HA, bradycardia, diaphoresis-above level of injury
● piloerection- below level of injury
● PNS responds to B/P- reduces HR but can’t dilate peripheral vessels below level of injury
● Causes: most common-bladder distention, bowel impaction, tight clothes, pressure ulcers, pain

132
Q

Treatment of Autonomic Hyperreflexia

A

● Sit patient upright or elevate HOB 45 degrees
● Identify the cause of stimuli
o Insert catheter/look for kink
o Resolve bowel impaction
o Remove restrictive clothing
● Notify healthcare provider
● Monitor B/P & give B/P meds (vasodilators) if s/s continue
● If left untreated= possible stroke, MI, status epilepticus

133
Q

c4, c6, t6, L1

A

c4-Tetra and paralysis of respiratory, C6-tetra with pa in hands and arms, T6 para below chest, L1-Para below waist

Med surg 2 (18 decks)

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