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Med Surg > Med Surg Exam 4 > Flashcards

Med Surg Exam 4 Flashcards

1
Q

type 2 DM association

A

old age and obesity

***progresses slowly

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2
Q

insulin resistance

A

-means that insulin is less effective at stimulating glucose uptake

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3
Q

T2DM

A

*typically enough insulin present to prevent breakdown of fat, so DKA does not typically occur in T2DM

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4
Q

gestational diabetes

A
  • placental hormones cause insulin resistance

- after delivery, BG returns to normal

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5
Q

risk factors DM

A
  • obesity–BMI at least 25
  • 45 or older
  • AA, native american, pacific islanders
  • HTN (140/90)
  • HDL cholesterol level at least 35 or triglyceride level at least 250
  • hx of gestational dm, delivery of babies over 9 lb
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6
Q

3 P’s of DM

A

(1) polyuria (excessive urination/induced diuresis)
(2) polyphagia (increased appetite)
(3) polydipsia (excessive thirst)

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7
Q

other clinical manifestation of DM

A
  • dehydration
  • weight loss (cells can’t pick up insulin)
  • vision changes (refractory error w/ vision)
  • fatigue
  • SLOW wound healing
  • recurrent infections (hyperglycemia impairs immune fxn)
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8
Q

immune fxn

A

-hyperglycemia decreases WBC fxn, promotes inflammation, increases blood viscosity and favors growth of yeast organisms, & associated w/ changes in BV walls…resulting in increased risk for infection, microvascular/macrovascular complications, and foot ulcers

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9
Q

labs in uncontrolled glucose levels

A
  • ketones in urine (fat breakdown)
  • glucose in urine (180-200, glucose in urine)
  • elevated A1C (measures glucose over 2-3mo)
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10
Q

A1C

A

greater than 6.5% = DM criteria

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11
Q

why increase in DM in older adults?

A
  • changes in metabolism
  • poor diet
  • physical inactivity
  • altered insulin secretion or resistance

**also more likely to have comorbidities

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12
Q

carbs

A

-main nutrients in food that influence blood glucose levels (because carb broken down into blood sugars) so carb counting is sometimes utilized to help manage

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13
Q

diet for DM

A
  • low carb
  • high protein (has minimal impact on BG levels)
  • moderation of alc intake (alcohol increases insulin sensitivity, causing hypoglycemia)
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14
Q

exercise and DM

A

-lowers BG levels by increasing uptake of glucose and improving insulin utilization (hypoglycemia can occur during or after exercise)

**AVOID TRAUMA TO LOWER EXTREMITIES IN PTs WITH NEUROPATHY

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15
Q

self-monitoring of blood sugars

A

-2-4x a day (before meals and at bedtime)

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16
Q

stress response

A

-results in hyperglycemia because activates sympathetic NS which increases catecholamines increases hepatic glycogenolysis and release of large quantities of glucose in bloodstream while inhibiting release of insulin (stressed pts=at risk for hyperglycemia)

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17
Q

IV insulin

A

regular insulin is the only insulin that can be given intravenously (double check with TWO nurses)

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18
Q

rapid-acting insulins

A
  • lispro (Humalog)
  • aspart (Novolog)
  • glulisine (Apidra)

*15 min onset, 1h peak, 3-5 hr duration

“meal-time insulin”

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19
Q

short-acting insulins

A
  • regular (Humulin-R, Novolin-R)
  • 4-6 hr duration

**usually given before meal

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20
Q

intermediate acting insulins

A

-NPH (Humulin N, Novolin N)

  • 12-16 hr duration
  • *usually taken after food
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21
Q

long-acting insulins

A
  • glargine (Lantus, Basaglar)
  • glargine U-300 (Toujeo)
  • detemir (Levemir)
  • degludec (Tresiba)

**continuous, no defined onset or peak (24 hr duration)

“used for basal dose”

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22
Q

what insulins can you mix

A

-can mix short-acting and intermediate acting (draw up clear first [short-acting] and cloudy next [intermediate acting])

**DO NOT mix long-acting w/ anything

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23
Q

rotating injection sites

A

prevents lipodystrophy (alters absorption)

**do not massage injection–alters absorption

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24
Q

insulin pumps

A
  • change every 2-3 days

* rapid-acting secreted constantly and boluses calculates @ meals

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25
Q

resistance to injected insulin

A

-fat cells impair insulin resistance (r/t obesity)

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26
Q

fasting hyperglycemia

A

-@ night (high glucose)

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27
Q

non-insulin antidiabetic agents

A
  • if beta cells continue to decline in time, these will not be enough to control DMT2
  • doesn’t work for T1DM
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28
Q

biguanides

A
  • Prototype: Metformin
  • Action: inhibits production of glucose by liver and increases body’s sensitivity to insulin

**no effect on beta cells so not used for T1DM

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29
Q

ADRs of biguanides (Metformin)

A
  • metformin-induces lactic acidosis (more common if drink alc)
  • kidney injury
  • hypoglycemia (if used in combo w/ insulin or other antidiabetic agents)
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30
Q

contraindications Metformin

A
  • alcohol abuse

- kidney impairment

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31
Q

education on Metformin

A
  • should not be administered w/in 2 days of contrast agent

- avoid alc

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32
Q

hypoglycemia range

A

50-60 or below

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33
Q

hypoglycemia s/s

A
  • diaphoresis, tremors, tachy, palpitations, anxiety, hunger
  • confusion, slurred speech, impaired coordination, irrational behavior, drowsy
  • seizures, LOC
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34
Q

the brain and glucose

A
  • the brain relies almost entirely on glucose for energy
  • since brain cannot synthesize or store more than a few minutes supply of glucose, symptoms of cerebral fxn deterioration are noted with hypoglycemia
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35
Q

hypoglycemia tx

A

-administer 15g of fast acting glucose (4-6 oz juice/soda, 2-3 tsp of sugar/honey, 3-4 glucose tabs)

**after admin, retest CBG in 15 min.

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36
Q

IM glucagon injection can be administered

A

-transiently raises BG so need something else after

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37
Q

IV tx hypoglycemia

A

50% dextrose in water can be pushed via IV if IV available

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38
Q

DKA patho

A
  • kidneys attempt to excrete excess glucose and osmotic diuresis occurs, leading to dehydration and loss of electrolytes
  • body breaks down fat and byproduct is ketones, which leads to metabolic acidosis
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39
Q

DKA labs

A
  • low pH (6.8-7.3)
  • ketones and glucose in urine
  • abnormal levels serum electrolytes (Na, K, Cl)
  • high anion gap
  • elevated beta-3-hydroxybutyrate
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40
Q

DKA s/s

A
  • polyuria, polydipsia
  • weakness,malaise
  • blurred vision
  • decreased skin turgor & warm/dry skin
  • flat neck veins
  • tachy and HYPOtension
  • anorexia
  • n/v
  • Kussmaul respirations
  • mental status changes
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41
Q

DKA tx

A
  • FLUIDS FLUIDS FLUIDS
  • hourly BG checks
  • IV insulin administered at slow rate
  • avoid rapid drops in BG
  • monitor electros, esp K
  • REVERSE acidosis, do not simply lower BG
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42
Q

sick day rules

A

-test blood glucose and urine ketones every 3-4 hrs

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43
Q

Hyperglycemia Hyperosmolar Nonketotic Syndrome (HHNS)

A
  • insulin produced but level too low to prevent hyperglycemia
  • osmotic diuresis occurs and hyperosmolarity of blood occurs
  • GRADUAL development and has VERY high mortality rate
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44
Q

HHNS risk

A

-older T2DM pts

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45
Q

HHNS labs

A
  • hyperosmolality (at least 340)
  • hyperglycemia (at least 600)
  • ketones NOT present and acidosis does NOT occur
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46
Q

clinical manifestations of HHNS

A
  • profound dehydration & dry mucous membranes
  • hypotension and tachy
  • seizures
  • mental status changes
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47
Q

HHNS tx

A
  • fluids
  • correct electrolyte imbalances
  • insulin admin
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48
Q

precipitating event DKA vs HHNS

A

DKA–omission of insulin or physio stress like infection, stroke, surgery, MI

HHNS–physio stress

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49
Q

macrovascular long-term complications of DM

A
  • CAD
  • PVD
  • stroke
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50
Q

microvascular long-term complications of DM

A
  • neuropathy
  • nephropathy
  • retinopathy (tiny BVs leak fluid into retina)
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51
Q

autonomic neuropathy

A
  • silent MI, painless cardiac ischemia
  • decreased gastric emptying
  • urinary retention
  • sexual dysfxn
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52
Q

wash feet (DM neuropathy)

A
  • do not soak feet
  • warm, not hot
  • use thermometer or elbow to check water temp
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53
Q

keep skin soft and smooth (DM neuropathy)

A
  • rub thin coat lotion over tops and bottoms of feet but not between toes
  • trim corns/calluses
  • inspect toenails (podiatrist specialist needed)
  • wear socks at night if feet get cold
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54
Q

the master gland

A
  • Pituitary gland (regulates MANY hormones)

* located underneath hypothalamus and divided into posterior/anterior lobes

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55
Q

pituitary tumors s/s

A
  • HA
  • vision changes
  • various symptoms depending on over/undersection of hormone affected
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56
Q

tx of pituitary tumor

A
  • hypophysectomy

- admin of hormones

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57
Q

hypophysectomy

A
  • after surgery, avoid coughing, blowing nose, sucking thru straw, or sneezing as CSF leak can occur (SINUS PRECAUTIONS)
  • if sublabial approach is used, do not brush teeth until incision above teeth is healed
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58
Q

cererbrospinal fluid leak

A
  • Halo ring test (fluid leaking tested, outer ring clear fluid)
  • a positive beta-2-transferrin test (indicates CSF fluid is present)
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59
Q

ADH

A

(vasopressin)

  • controls plasma osmolality and is produced by posterior pituitary gland
  • ADH acts on renal tubules to increase water reabsorption and concentrate urine, which reduces serum osmolality and impacts urine specific gravity
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60
Q

diabetes insipidus

A

-dz of posterior lobe of pituitary gland characterized by deficiency of ADH

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61
Q

s/s diabetes insipidus

A
  • daily urine output of very dilute urine (3-20L)
  • fluid volume deficit signs
  • excessive thirst
  • low urine specific gravity
  • elevated serum sodium levels
  • weight loss
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62
Q

diabetes insipidus tx/management

A
  • replace ADH (desmopressin)
  • hydrate!!!!
  • correct underlying patho
  • daily weights
  • strict I&O
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63
Q

SIADH

A

(Syndrome of Inappropriate Antidiuretic Hormone)

-excessive secretion of ADH

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64
Q

risk factors SIADH

A
  • malignancy/carcinomas
  • head injury
  • infection
  • meds
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65
Q

s/s SIADH

A
  • dilutional hyponatremia
  • cerebral edema
  • fluid volume overload
  • decreased UO & concentrated urine
  • decreased serum osmolality
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66
Q

managing SIADH

A
  • fluid restriction and diuretics
  • correct hyponatremia SLOWLY
  • I&O
  • daily weight (report weight gain over 1kg)
  • serial labs
  • seizure precautions!!!!
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67
Q

Thyroid Hormone (TH)

A

-TSH acts on thyroid gland to stimulate release of T3 and T4 (the thyroid hormones)

Functions (metabolic, neurologic, cardio, and resp fxn):

  • controls cell metabolism
  • alters protein, fat, and glucose metabolism & so heat production/oxygen consumption
  • impacts integrity of skin, nails, hair
  • impact cardiac fxn
  • stimulates bone resorption
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68
Q

Iodine

A

**needed for production of thyroid hormone

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69
Q

hypothryoidism

A

-dz caused by insufficient levels of thyroid hormone and subsequent decreased response to catecholamines

(increased TSH and decreased T3, T4)

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70
Q

most common cause hypothyroidism

A

*autoimmune thyroiditis (Hashimoto dz)

  • **but can also be caused by:
  • head/neck radiation
  • thyroidectomy
  • pts taking antithyroid meds for hyperthyroidism
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71
Q

s/s hypothyroidism

A
  • coarse, brittle, dry hair & loss of lateral eyebrows
  • peripheral edema
  • pallor, puffy face
  • slow pulse, enlarged heart
  • lethargy, impaired mem
  • muscle weakness
  • menorrhagia
  • constipation
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72
Q

management hypothyroidism

A
  • Levothyroxine/Synthroid
  • tx of atherosclerosis or CAD
  • provide extra clothing/blankets but avoid heating pads
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73
Q

advanced hypothyroidism

A
  • profoundly hypothermic

- abnormally sensitive to sedative/opioids/anesthetics (closely monitor VS if given)

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74
Q

actions of levothyroxine

A

-increase metabolic rate, protein synthesis, cardiac output, renal perfusion, body temp, and growth processes

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75
Q

severe hypothyroidism associated w/

A
  • elevated cholesterol
  • atherosclerosis/CAD
  • poor left ventricular fxn
  • pericardial effusion
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76
Q

Myxedema coma

A
  • patient is hypothermic & unconscious

- increasing lethargy may progress to stupor and then coma

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77
Q

hypoglycemia

A

-can also be seen with hypothyroidism (sluggish liver, increasing patient’s susceptibility to low blood sugar)

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78
Q

hyperthyroidism

A

-INCREASED response to catecholamines

increased T3/T4, decreased TSH

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79
Q

common cause of hyperthyroidism

A

-Graves disease

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80
Q

s/s hyperthyroidism

A
  • fine brittle hair and hair loss
  • BULGING eyes
  • enlarged thyroid
  • increased perspiration
  • abnormal heart rhythms
  • enlarged liver
  • n/v/d
  • hand tremors
  • amenorrhea/loss of libido
  • increased appetite
  • intolerance to heat
  • irritable/hyperactive
  • high BS
  • low cholesterol
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81
Q

hyperthyroidism management

A
  • radioactive iodine
  • PTU (antithyroid agent)
  • surgery
  • symptoms tx
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82
Q

thionamides

A
  • Prototype: Propylthiouracil (PTU)
  • Action: block synthesis of thyroid hormones
  • ADRs: overmedication results in s/s hypothyroidism or agranulocytosis
  • Education: abruptly d/c-ing drug can cause thyroid storm
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83
Q

thyroidectomy nursing care

A
  • airway must be monitored because hemorrhage can put pressure on trachea and cause resp. distress
  • complications: hemorrhage, THYROID STORM, airway obstruction, damage to parathyroid gland, nerve damage to vocal cords
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84
Q

hyperthyroidism interventions

A
  • provide small/frequent meals
  • monitor fluids/electrolytes
  • cool, comfortable room
  • cool baths/cool fluids but avoid shivering
  • eye care to protect cornea
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85
Q

hyperthyroidism complications

A
  • heart failure

- thyroid storm

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86
Q

thyroid storm

A
  • sudden large amount of thyroid hormones, caused by uncontrolled hyperthyroidism, or manipulation of thyroid gland (such as during surgery)
  • often precipitated by stress, infection, or trauma as it increases demands of body’s metabolism

**HIGH MORTALITY RATE

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87
Q

thyroid storm s/s

A
  • high fever
  • extreme tachy
  • exaggerated symptoms of hyperthyroidism
  • altered mental state (delirium/psychosis/coma)
88
Q

thyroiditis causes and s/s

A

-infection

S/S

  • pharyngitis
  • swelling of thyroid gland
  • pain in neck
  • alterations in thyroid hormone
89
Q

management of thyroiditis

A
  • usually spontaneously resolves in 1-2 mo but antimicrobial agents, fluids, and NSAIDS can be utilized
  • other meds may be used to tx alterations in thyroid hormone
90
Q

thyroid tumor/cancer (goiter) most common cause

A
  • lack of iodine
  • w/out iodine, thyroid hormone isn’t produced, and body makes more TSH which stimulates thyroid enlargement
  • too MUCH iodine can also cause goiter as gland oversecretes TH
91
Q

s/s thyroid goiter

A
  • neck enlargement
  • pressure on neck
  • difficulty swallowing
92
Q

tx of thyroid tumors

A
  • small, benign tumors do not require tx
  • iodine & thyroid hormone given to reduce thyroid growth
  • thyroidectomy (malignant)
93
Q

nursing care w/ thyroid tumor

A
  • high calorie diet
  • monitor airway (laryngeal edema post-surgery)
  • hydration
  • talk as little as possible
  • provide SOFT food
94
Q

parathyroid hormone

A

-regulates serum calcium concentration

**when ionized calcium levels fall, PTH secretes which increases calcium concentration by releasing calcium from bones

-PTH also acts on kidney to INCREASE calcium reabsorption and decrease phosphate reabsorption

95
Q

hyperparathyroidism

A

**excess PTH leads to markedly elevated serum calcium

96
Q

risk factors hyperparathyroidism

A
  • tumor of parathyroids

- CKD

97
Q

s/s hyperparathyroidism

A
  • may be asymptomatic
  • high Ca levels
  • elevated PTH
  • signs of hypercalcemia
98
Q

management of hyperparathyroidism

A
  • parathyroidectomy
  • hydrate
  • encourage mobility
  • restrict dietary Ca
  • manage hypercalcemic crisis (potential complication)
99
Q

hypercalcemic crisis

A
  • causes neurologic, cardio, and renal symptoms that can be life-threatening
  • Tx: fluids, diuretics, phosphate therapy, calcitonin, dialysis, corticosteroids, bisphosphonates
  • death usually results from cardiac dysthymias that progress to cardiac arrest
100
Q

hypoparathyroidism

A

-causes hypocalcemia and hyperphosphatemia

101
Q

hypoparathyroidism risks

A
  • surgical removal of parathyroid gland during thyroidectomy
  • parathyroidectomy
  • radical neck dissection
102
Q

s/s hypoparathyroidism

A
  • hypocalcemia
  • tetany
  • seizures
  • bronchospasm
  • Trousseaus sign
  • Chvostek sign (touching cheek and spasm)
  • increased bone density (blood pressure cuff on arm) `
103
Q

diet hypoparathyroidism

A

Eat:

  • rice milk/nondairy creamer
  • refined white bread
  • green beans/broccoli/cucumbers
  • fish

do NOT eat:

  • egg yolks
  • milk/milk products (high levels of phosphorus in attention to high calcium)
  • spinach
104
Q

adrenal gland fxn

A
  • releases glucocorticoids when body is under stress (cortisol being the most potent of these)
  • glucocorticoids suppress immune rxns, increase blood glucose levels, and potentiate effects of catecholamines
105
Q

pheochromocytoma

A

-benign tumor of adrenal gland that causes massive release of catecholamines

106
Q

s/s pheochromocytoma

A
  • severe hypertension
  • HA
  • hyperhydrosis
  • hypermetabolism
  • hyperglycemia

**the FIVE H’s

107
Q

managing/tx of pheochromocytoma

A
  • monitor vital signs
  • remove tumor
  • admin of alpha-adrenergic blockers or smooth muscle relaxants to lower BP
  • insulin (if hyperglycemic)
108
Q

complications of pheochromocytoma

A

-hypertensive crisis

109
Q

aldosterone

A
  • part of RAAS system that promotes reabsorption of Na and H2O in kidney to raise BP
  • promotes excretion of K+

(excreted by adrenal glands)

110
Q

Addison disease

A

-adrenal insufficiency (primary OR secondary) results in inadequate production of cortical hormones

111
Q

risk factors of Addison dz

A
  • surgical removal of both adrenal glands

- infection of adrenal glands

112
Q

what does Addison dz affect?

A

-glucocorticoids (cortisol), mineralcorticoids (aldosterone), and androgens (sex hormones)

113
Q

Addison disease s/s

A
  • GI disturbances
  • /hypotension
  • hyperpigmentation
  • muscle weakness
  • hypoglycemia
  • weight loss
  • hyperkalemia (potassium retention)
114
Q

Addison disease tx

A
  • fluids
  • corticosteroid admin (hydrocortisone IV)
  • 5% dextrose in normal saline
  • tx of hyperkalemia
  • long term oral corticosteroid replacement
115
Q

Addisonian crisis

A

**COMPLETE circulatory collapse and shock

  • triggers: cold, overexertion, infection, emotional stress
  • tx: fluids, glucose, electrolytes, steroid hormone replacement, vasopressors
116
Q

pt education for Addison’s disease

A
  • high sodium diet
  • lifelong replacement of adrenal cortex hormones (steroids)
  • body can’t respond to stress/illness as effectively
  • carry dose of injectable corticosteroid
117
Q

signs of Addisonian crisis

A
  • prolonged fatigue/lethargy/coma
  • dehydration (from severe d/v)
  • low Na, high K
  • HA/dizziness
  • low BP/BS
  • seizures
118
Q

Cushing syndrome

A

-hypercortisolism (high levels of serum cortisol)

119
Q

causes of Cushing syndrome

A
  • pituitary tumor
  • adrenal tumor
  • long term glucocorticoid therapy
120
Q

Cushing gender

A

-more common in females

121
Q

Cushing syndrome s/s

A
  • fat pads (BUFFALO HUMP and in stomach)
  • Moon Face & red
  • hypertension
  • thin, wrinkled skin that bruises easily
  • poor wound healing
  • muscle weakness/muscle wasting/osteoporosis
  • abdominal striae
122
Q

management of Cushing syndrome

A
  • removal of pituitary tumors or adrenalectomy for patients w/ primary adrenal hypertrophy
  • adrenal enzyme inhibitors
  • if due to corticosteroids, attempt made to reduce or taper meds to minimum dosing
123
Q

Cushing syndrome patient education

A
  • falls prevention
  • avoid exposure to infection
  • moderate activity can help prevent immobility from weakness/fatigue
  • rest throughout day
  • prevent trauma to fragile skin
  • do not d/c steroids abruptly
124
Q

Primary Aldosteronism

A

-too much aldosterone production due to adrenal tumor

125
Q

s/s primary aldosteronism

A
  • low K+
  • HTN
  • normal or elevated Na
  • weakness/cramping/fatigue
  • glucose intolerance
126
Q

management of primary aldosteronism

A
  • surgical removal of adrenal tumor (adrenalectomy)
  • tx hypokalemia and hyperglycemia
  • spironolactone to tx HTN
127
Q

primary vs secondary head injury

A
  • primary (initial incident damages brain parenchyma or vessels)
  • secondary (occurs over next hrs or days due to cerebral edema, hypoxia, seizures, hyperthermia, infection, or hypovolemia)
128
Q

skull fractures can be…

A

…linear, comminuted, basilar, or depressed

129
Q

s/s skull fracture

A
  • pain
  • bleeding from nose, ear, mouth
  • CSF leakage from nose, ear, mouth
  • Battle’s sign
  • periorbital ecchymosis
130
Q

diagnostics for skull fracture

A
  • CT

- MRI

131
Q

leakage of CSF

A

-@ risk for infections because passes BBB (meningitis or abscess formation or osteomyelitis)

**may spontaneously close or require surgery

132
Q

surgery in skull fx

A

-nondepressed do not require, depressed do

133
Q

penetrating injury

A

-surgical debridement of brain and IV abx admin is necessary

134
Q

Monro-Kellie Doctrine

A
  • *brain is a closed vault made of:
    (1) cerebrospinal fluid (10%)
    (2) intravascular blood (12%)
    (3) brain tissue (78%)

-all 3 will impact each other; if anything changes, theres no space for what swells so need to compensate

135
Q

TBIs

A
  • tend to have lasting effects

- increased ICP=decreased perfusion to brain, crushing itself (brain will eventually herniate)

136
Q

s/s concussion

A

(usually resolves w/in 24 hrs)

  • photophobia
  • n/v
  • HA
  • blurry vision

**decrease stimuli which will help w/ symptoms

137
Q

s/s to look for post-concussion and to notify PCP of

A
  • difficulty speaking
  • confusion/seizures
  • SEVERE HA
  • continued vomiting
  • weakness one side of body
138
Q

s/s brain contusion

A
  • difficulty arousing pt
  • cool/clammy skin
  • shallow respirations
  • hypotension
  • hypothermia
139
Q

diffuse axonal injury s/s

A
  • coma
  • posturing (decorticate or decerebrate)
  • global cerebral edema
140
Q

diagnostics diffuse axonal injury

A
  • MRI
  • CT
  • patient presentation
141
Q

s/s epidural hematoma

A
  • classic sign: loss of consciousness followed by brief period of lucidity
  • signs of focal neuro deficits and LOC as compensatory mechanism fails
142
Q

management of epidural hematoma

A
  • burr holes and drain placement
  • craniotomy
  • attempts to decrease ICP
143
Q

causes of subdural hematoma

A
  • trauma
  • rupture of aneurysm
  • coagulopathy

***more often tends to be venous bleed (slow bleed)

144
Q

SDH can be…

A
  • acute (less than 72 hrs)
  • subacute (4-21 days after injury)
  • chronic (21 or more days after injury…around 3 mo.)
145
Q

s/s SDH

A
  • changes in LOC
  • changes in pupil reactivity
  • hemiparesis

**if it is rapidly expanding: coma, high BP, decreased HR may occur

146
Q

SDH tx

A

sx to open dura

147
Q

ICH (intercerebral hemorrhage)

A

**bleeding into parenchyma (tissues) of brain

148
Q

causes of ICH

A
  • trauma
  • aneurysm rupture
  • bleeding disorders
  • tumors
149
Q

s/s ICH

A
  • neurological deficits

- HA

150
Q

management of ICH

A
  • supportive care
  • control of ICP
  • careful admin of fluids
  • antihypertensives (too high BP will promote faster bleeding)

**craniotomy may be possible depending on location

151
Q

patients w/ TBI are…

A

…at increased risk of cervical spine injuries so cervical spine immobilization is recommended

152
Q

preventing secondary brain injury

A

-prevent cerebral edema, hypotension, and respiratory depression

153
Q

LOC change can indicate…

A

…increased ICP

154
Q

CSF

A

little cushion around brain

155
Q

cerebral edema occurs when…

A

…an abnormal accumulation of fluid occurs and the body’s compensatory mechanism can no longer compensate

156
Q

when cerebral blood flow decreases significantly…

A

…a widening pulse pressure and cardiac slowing will occur (can get necrosis)

157
Q

clinical manifestations of increased ICP

A

*FIRST SIGNS: restlessness, confusion, increased drowsiness, and LOC changes

  • pupillary changes
  • impaired extraocular movements
  • unilateral weakness
  • HA
158
Q

impending signs of brain herniation

A

(increased ICP=herniation)

  • Cushing triad:
    (1) bradycardia
    (2) bradypnea (irregular respirations/Cheynes-stoke resp=really high ICP)
    (3) hypertension (widening pulse pressure)
159
Q

normal ICP

A

5-15

160
Q

invasive monitoring of ICP

A

-bolt (only monitors pressure not the fluid)
or
-extra-ventricular drain (EVD)…increased risk for infection

161
Q

other management of ICP management

A
  • osmotic diuretics (Mannitol) or hypertonic saline (pull volume out of brain and into vessels)
  • restrict fluids
  • drain CSF and attempt to decrease ICP (too tight C-collar, shivering, decrease stimuli)
  • control fever (increased metabolic demands and associated w/ worse patient outcomes) && seizure prophylaxis
  • maintain BP (above 90 systolic)
  • good oxygenation
  • prevent urinary retention and promote bowel fxn
162
Q

three cardinal findings of brain death

A
  • apnea (draw ABG and turn vent off…hypercapnic?)
  • coma
  • absence of brainstem reflexes

**pt. cannot be under the influence of CNS depressant or paralytic when declared

163
Q

primary vs secondary spinal cord injury

A
  • primary: initial trauma occurs and usually permanent

- secondary: result of swelling and can cause ischemia, hypoxia, edema, and subsequent destruction of myelin and axons

164
Q

incomplete spinal cord lesion

A

-impacts sensory and motor function or both and may only impact an area of the spinal cord

165
Q

complete spinal cord lesion

A

-causes total loss of sensation and voluntary muscle control below the lesion

166
Q

paraplegia

A

paralysis of lower body

167
Q

tertraplegia

A

-paralysis of all 4 extremities

168
Q

worry about breathing when…

A

…spinal cord injury C4 or above (brainstem problems)

169
Q

complications of SCI

A
  • neurogenic shock
  • DVT
  • orthostatic hypotension
  • autonomic dysreflexia
170
Q

neurogenic shock

A
  • warm, flushed skin
  • bradycardia (PNS activated)
  • hypotension
  • tachypnea
171
Q

autonomic dysreflexia

A

-exaggerated sympathetic nervous system response occurs due to stimuli

172
Q

s/s autonomic dysreflexia

A
  • HA
  • HTN
  • diaphoresis (can lead to rupture of cerebral blood vessels or increased ICP)
  • nausea
173
Q

common triggers of autonomic dysreflexia

A
  • distention of bladder or bowel
  • pressure ulcers
  • thermal stimuli
174
Q

types of shock

A
  • obstructive
  • cardiogenic
  • hypovolemic (hemorrhagic)
  • distributive
175
Q

types of distributive shock

A

(pipe problem)

  • septic
  • neurogenic
  • anaphylactic
176
Q

tissue perfusion determined by…

A

-cardiac output AND systemic vascular resistance q

177
Q

cardiac output=

A

stroke volume x HR

178
Q

in shock…

A
  • cells lack adequate blood supply so aren’t well oxygenated
  • cells move into anaerobic cellular respiration and lactic acid levels rise
  • hyperglycemia occurs as part of stress response (need more fuel)
  • cells that are not well perfused die and organ dysfxn occurs
179
Q

increasing lactic acid levels

A

-indicate cells are moving into anaerobic cellular respiration

***higher lactic acid levels are correlated with worse patient outcome (CRITICAL value..report w/in 1 hr)

180
Q

BP readings

A

-alone, they are unreliable indicators of circulatory status, but a single episode of systolic BP less than 80 is associated w/ 18% increase in hospital mortality

181
Q

compensated stage of shock (nonprogressive)

A

-BP is near normal limits because compensatory mechanisms are causing adequate perfusion

  • *COMP mechanisms:
  • increased HR
  • vasoconstriction
  • increased contractibility of heart
182
Q

s/s compensated stage of shock

A
  • tachycardia
  • anxiety
  • vasoconstriction
183
Q

management compensated stage of shock

A
  • identify cause of shock—> tx
  • aggressively support body’s comp mechanisms by fluid replacement and meds to manage BP

**if they are on beta blockers, you may not see tachy occur

184
Q

by the time BP drops in shock…

A

…damage has already occurred at cell and tissue levels

185
Q

hypoperfusion…

A

….tends to impact brain and kidneys 1st

186
Q

uncompensated stage of shock (progressive)

A

**pt loses ability to compensate for injury/infection/insult

187
Q

s/s uncompensated stage of shock

A
  • tachy
  • dyspnea
  • restlessness
  • diaphoresis
  • metabolic acidosis (impacts ability to clot)
  • hypotension
  • prolonged cap refill
  • oliguria
  • decreased LOC
188
Q

management of uncompensated stage of shock

A
  • TWO large bore IV sites initiated to administer fluids, meds, and/or blood products
  • close monitoring in ICU for hemodynamic stability
  • UA monitoring
189
Q

if perfusion does not improve despite aggressive interventions… (PATHO CONCEPT)

A

…body will shunt blood from organs such as skin, kidneys, and GI tract to brain and heart to ensure adequate blood supply to these organs

  • cool, clammy skin
  • hypoactive bowel sounds
  • UO decreases
190
Q

irreversible stage of shock (end-organ dysfunction)

A
  • acidosis becomes so severe that even vasopressors may be ineffective
  • resp system failure contributes to further organ damage
  • multiple organ dysfxn progresses to complete organ failure & death
191
Q

management of irreversible stage of shock

A

-prevent complications and provide comfort

192
Q

multiorgan system effects of shock

A
  • ARDS
  • acidosis
  • acute renal/liver failure
  • ileus forms
  • stress ulcers
193
Q

4 key points in general management of shock

A
  • fluids
  • optimal O2 delivery
  • vasopressors
  • nutrition support
194
Q

pulse ox

A

-less reliable with decreased BP (so use forehead)

195
Q

fluid replacement in shock

A
  • isotonic cyrstalloids
  • colloids
  • blood components

**normal saline for patients who are more stable, trauma patients get LR

196
Q

CVL

A

-central venous line may be inserted to monitor central venous pressure (CVP) ….tells you volume of blood in R atrium

197
Q

arterial lines

A

may be used for accurate BP monitoring

***DO NOT give meds thru these

198
Q

vasopressors

A

-used in shock pts to improve hemodynamic stability when fluids alone can’t maintain adequate MAP

  • strengthen myocardial contraction
  • regulate HR
  • initiate vasoconstriction
199
Q

vasopressors and lines

A

***give thru biggest line (CVL)

  • they can extravasate and can cause severe tissue damage
  • TITRATE the vasopressors (goal is MAP of 65 or higher)
200
Q

2 most common causes of cardiogenic shock

A
  • MI

- dysrhythmias

201
Q

cardiogenic shock and fluid

A

**fluid admin should be closely monitored (its not a fluid volume problem so dont give more because dont want to overload the heart)

202
Q

obstructive shock (heart cant pump past something)

A
  • decreased oxygen delivery due to obstructive cause
    ex: pericardial tamponade, tension pneumothorax (insert CT), pulmonary embolism, abdominal compartment syndrome

***REVERSE THE CAUSE

203
Q

distributive shock examples

A
  • Addison’s crisis
  • toxic shock syndrome

**alterations in vascular smooth muscle tone causes systemic vasodilation

204
Q

s/s septic shock

A
  • fever or hypothermia
  • tachy
  • leukocytosis or leukopenia
  • a left shift (increase in immature WBC)
  • infection
205
Q

1 hr bundle for septic shock

A

1-measure lactate level
2-obtain blood culture before admin of ABx
3-administer broad-spectrum ABx
4-begin to rapidly administer crystalloid for hypotension or lactate

206
Q

SIRS

A
  • systemic inflammatory response syndrome
  • thought to be caused by release of inflammatory cytokines
  • leads to increased coagulopathy and disrupts essential kidney, heart, and respiratory fxn
207
Q

neurogenic shock

A

vasodilation occurs due to loss of balance between parasymp. NS and symp. NS

**overriding parasymp. stimulation causes decrease in smooth muscle tone and bradycardia (i.e. WARM SHOCK)

-the SNS cannot regulate diameter of blood vessels (so vasodilation occurs because the vessels are just relaxed)

208
Q

management of neurogenic shock

A
  • goal MAP 85
  • restore sympathetic tone until stabilization of spinal cord injury
  • spinal precautions (log rolls, reverse trendelenburg)
209
Q

s/s anaphylactic shock

A
  • hypotension
  • angioedema
  • pruritus
  • flushing
  • swelling of tongue/mouth
  • wheezing stridor
  • GI symptoms
210
Q

management of anaphylactic shock

A
  • epi
  • H2 agonists (Pepcid….stop release of antihistamines)
  • steroids
  • Benadryl
  • fluids
211
Q

MODS

A

(Multiple Organ Dysfunction Syndrome)

  • severe organ dysfxn in two or more organ systems
  • Most Commonly: ARDS and acute kidney failure occurs
212
Q

MODS–Hepatic

A
  • jaundice
  • LFTs
  • decreased albumin
  • elevated PT
213
Q

MODS–hematologic

A
  • decreased platelets
  • elevated PT
  • increased D-dimer
214
Q

MODS–CNS

A

-altered LOC

215
Q

MODS–respiratory

A
  • tachypnea
  • hypoxemia
  • high PaO2
216
Q

MODS–cardio

A
  • tachy

- hypotension

Med Surg (4 decks)

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