Med Surg Exam 4 Flashcards
1
Q
type 2 DM association
A
old age and obesity
***progresses slowly
2
Q
insulin resistance
A
-means that insulin is less effective at stimulating glucose uptake
3
Q
T2DM
A
*typically enough insulin present to prevent breakdown of fat, so DKA does not typically occur in T2DM
4
Q
gestational diabetes
A
- placental hormones cause insulin resistance
- after delivery, BG returns to normal
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
6
Q
3 P’s of DM
A
(1) polyuria (excessive urination/induced diuresis)
(2) polyphagia (increased appetite)
(3) polydipsia (excessive thirst)
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)
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
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)
10
Q
A1C
A
greater than 6.5% = DM criteria
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
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
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)
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
15
Q
self-monitoring of blood sugars
A
-2-4x a day (before meals and at bedtime)
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)
17
Q
IV insulin
A
regular insulin is the only insulin that can be given intravenously (double check with TWO nurses)
18
Q
rapid-acting insulins
A
- lispro (Humalog)
- aspart (Novolog)
- glulisine (Apidra)
*15 min onset, 1h peak, 3-5 hr duration
“meal-time insulin”
19
Q
short-acting insulins
A
- regular (Humulin-R, Novolin-R)
- 4-6 hr duration
**usually given before meal
20
Q
intermediate acting insulins
A
-NPH (Humulin N, Novolin N)
- 12-16 hr duration
- *usually taken after food
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”
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
23
Q
rotating injection sites
A
prevents lipodystrophy (alters absorption)
**do not massage injection–alters absorption
24
Q
insulin pumps
A
- change every 2-3 days
* rapid-acting secreted constantly and boluses calculates @ meals
25
resistance to injected insulin
-fat cells impair insulin resistance (r/t obesity)
26
fasting hyperglycemia
-@ night (high glucose)
27
non-insulin antidiabetic agents
- if beta cells continue to decline in time, these will not be enough to control DMT2
* doesn't work for T1DM
28
biguanides
- 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
29
ADRs of biguanides (Metformin)
- metformin-induces lactic acidosis (more common if drink alc)
- kidney injury
- hypoglycemia (if used in combo w/ insulin or other antidiabetic agents)
30
contraindications Metformin
- alcohol abuse
| - kidney impairment
31
education on Metformin
- should not be administered w/in 2 days of contrast agent
| - avoid alc
32
hypoglycemia range
50-60 or below
33
hypoglycemia s/s
- diaphoresis, tremors, tachy, palpitations, anxiety, hunger
- confusion, slurred speech, impaired coordination, irrational behavior, drowsy
- seizures, LOC
34
the brain and glucose
- 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
35
hypoglycemia tx
-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.
36
IM glucagon injection can be administered
-transiently raises BG so need something else after
37
IV tx hypoglycemia
50% dextrose in water can be pushed via IV if IV available
38
DKA patho
- 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
39
DKA labs
- 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
40
DKA s/s
- 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
41
DKA tx
- 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
42
sick day rules
-test blood glucose and urine ketones every 3-4 hrs
43
Hyperglycemia Hyperosmolar Nonketotic Syndrome (HHNS)
- 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
44
HHNS risk
-older T2DM pts
45
HHNS labs
- hyperosmolality (at least 340)
- hyperglycemia (at least 600)
- ketones NOT present and acidosis does NOT occur
46
clinical manifestations of HHNS
- profound dehydration & dry mucous membranes
- hypotension and tachy
- seizures
- mental status changes
47
HHNS tx
- fluids
- correct electrolyte imbalances
- insulin admin
48
precipitating event DKA vs HHNS
DKA--omission of insulin or physio stress like infection, stroke, surgery, MI
HHNS--physio stress
49
macrovascular long-term complications of DM
- CAD
- PVD
- stroke
50
microvascular long-term complications of DM
- neuropathy
- nephropathy
- retinopathy (tiny BVs leak fluid into retina)
51
autonomic neuropathy
- silent MI, painless cardiac ischemia
- decreased gastric emptying
- urinary retention
- sexual dysfxn
52
wash feet (DM neuropathy)
- do not soak feet
- warm, not hot
- use thermometer or elbow to check water temp
53
keep skin soft and smooth (DM neuropathy)
- 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
54
the master gland
- Pituitary gland (regulates MANY hormones)
| * located underneath hypothalamus and divided into posterior/anterior lobes
55
pituitary tumors s/s
- HA
- vision changes
- various symptoms depending on over/undersection of hormone affected
56
tx of pituitary tumor
- hypophysectomy
| - admin of hormones
57
hypophysectomy
- 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
58
cererbrospinal fluid leak
- Halo ring test (fluid leaking tested, outer ring clear fluid)
- a positive beta-2-transferrin test (indicates CSF fluid is present)
59
ADH
(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
60
diabetes insipidus
-dz of posterior lobe of pituitary gland characterized by deficiency of ADH
61
s/s diabetes insipidus
- 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
62
diabetes insipidus tx/management
- replace ADH (desmopressin)
- hydrate!!!!
- correct underlying patho
- daily weights
- strict I&O
63
SIADH
(Syndrome of Inappropriate Antidiuretic Hormone)
-excessive secretion of ADH
64
risk factors SIADH
- malignancy/carcinomas
- head injury
- infection
- meds
65
s/s SIADH
- dilutional hyponatremia
- cerebral edema
- fluid volume overload
- decreased UO & concentrated urine
- decreased serum osmolality
66
managing SIADH
- fluid restriction and diuretics
- correct hyponatremia SLOWLY
- I&O
- daily weight (report weight gain over 1kg)
- serial labs
- seizure precautions!!!!
67
Thyroid Hormone (TH)
-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
68
Iodine
****needed for production of thyroid hormone
69
hypothryoidism
-dz caused by insufficient levels of thyroid hormone and subsequent decreased response to catecholamines
(increased TSH and decreased T3, T4)
70
most common cause hypothyroidism
*autoimmune thyroiditis (Hashimoto dz)
* **but can also be caused by:
- head/neck radiation
- thyroidectomy
- pts taking antithyroid meds for hyperthyroidism
71
s/s hypothyroidism
- coarse, brittle, dry hair & loss of lateral eyebrows
- peripheral edema
- pallor, puffy face
- slow pulse, enlarged heart
- lethargy, impaired mem
- muscle weakness
- menorrhagia
- constipation
72
management hypothyroidism
- Levothyroxine/Synthroid
- tx of atherosclerosis or CAD
- provide extra clothing/blankets but avoid heating pads
73
advanced hypothyroidism
- profoundly hypothermic
| - abnormally sensitive to sedative/opioids/anesthetics (closely monitor VS if given)
74
actions of levothyroxine
-increase metabolic rate, protein synthesis, cardiac output, renal perfusion, body temp, and growth processes
75
severe hypothyroidism associated w/
- elevated cholesterol
- atherosclerosis/CAD
- poor left ventricular fxn
- pericardial effusion
76
Myxedema coma
- patient is hypothermic & unconscious
| - increasing lethargy may progress to stupor and then coma
77
hypoglycemia
-can also be seen with hypothyroidism (sluggish liver, increasing patient's susceptibility to low blood sugar)
78
hyperthyroidism
-INCREASED response to catecholamines
| increased T3/T4, decreased TSH
79
common cause of hyperthyroidism
-Graves disease
80
s/s hyperthyroidism
- 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
81
hyperthyroidism management
- radioactive iodine
- PTU (antithyroid agent)
- surgery
- symptoms tx
82
thionamides
- 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
83
thyroidectomy nursing care
- 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
84
hyperthyroidism interventions
- provide small/frequent meals
- monitor fluids/electrolytes
- cool, comfortable room
- cool baths/cool fluids but avoid shivering
- eye care to protect cornea
85
hyperthyroidism complications
- heart failure
| - thyroid storm
86
thyroid storm
- 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
87
thyroid storm s/s
- high fever
- extreme tachy
- exaggerated symptoms of hyperthyroidism
- altered mental state (delirium/psychosis/coma)
88
thyroiditis causes and s/s
-infection
S/S
* pharyngitis
* swelling of thyroid gland
* pain in neck
* alterations in thyroid hormone
89
management of thyroiditis
- 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
thyroid tumor/cancer (goiter) most common cause
- 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
s/s thyroid goiter
- neck enlargement
- pressure on neck
- difficulty swallowing
92
tx of thyroid tumors
- small, benign tumors do not require tx
- iodine & thyroid hormone given to reduce thyroid growth
- thyroidectomy (malignant)
93
nursing care w/ thyroid tumor
- high calorie diet
- monitor airway (laryngeal edema post-surgery)
- hydration
- talk as little as possible
- provide SOFT food
94
parathyroid hormone
-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
hyperparathyroidism
**excess PTH leads to markedly elevated serum calcium
96
risk factors hyperparathyroidism
- tumor of parathyroids
| - CKD
97
s/s hyperparathyroidism
- may be asymptomatic
- high Ca levels
- elevated PTH
- signs of hypercalcemia
98
management of hyperparathyroidism
- parathyroidectomy
- hydrate
- encourage mobility
- restrict dietary Ca
- manage hypercalcemic crisis (potential complication)
99
hypercalcemic crisis
- 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
hypoparathyroidism
-causes hypocalcemia and hyperphosphatemia
101
hypoparathyroidism risks
- surgical removal of parathyroid gland during thyroidectomy
- parathyroidectomy
- radical neck dissection
102
s/s hypoparathyroidism
- hypocalcemia
- tetany
- seizures
- bronchospasm
- Trousseaus sign
- Chvostek sign (touching cheek and spasm)
- increased bone density (blood pressure cuff on arm) `
103
diet hypoparathyroidism
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
adrenal gland fxn
- 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
pheochromocytoma
-benign tumor of adrenal gland that causes massive release of catecholamines
106
s/s pheochromocytoma
- severe hypertension
- HA
- hyperhydrosis
- hypermetabolism
- hyperglycemia
**the FIVE H's
107
managing/tx of pheochromocytoma
- monitor vital signs
- remove tumor
- admin of alpha-adrenergic blockers or smooth muscle relaxants to lower BP
- insulin (if hyperglycemic)
108
complications of pheochromocytoma
-hypertensive crisis
109
aldosterone
- 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
Addison disease
-adrenal insufficiency (primary OR secondary) results in inadequate production of cortical hormones
111
risk factors of Addison dz
- surgical removal of both adrenal glands
| - infection of adrenal glands
112
what does Addison dz affect?
-glucocorticoids (cortisol), mineralcorticoids (aldosterone), and androgens (sex hormones)
113
Addison disease s/s
- GI disturbances
- /hypotension
- hyperpigmentation
- muscle weakness
- hypoglycemia
- weight loss
- hyperkalemia (potassium retention)
114
Addison disease tx
- fluids
- corticosteroid admin (hydrocortisone IV)
- 5% dextrose in normal saline
- tx of hyperkalemia
- long term oral corticosteroid replacement
115
Addisonian crisis
**COMPLETE circulatory collapse and shock
- triggers: cold, overexertion, infection, emotional stress
- tx: fluids, glucose, electrolytes, steroid hormone replacement, vasopressors
116
pt education for Addison's disease
- 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
signs of Addisonian crisis
- prolonged fatigue/lethargy/coma
- dehydration (from severe d/v)
- low Na, high K
- HA/dizziness
- low BP/BS
- seizures
118
Cushing syndrome
-hypercortisolism (high levels of serum cortisol)
119
causes of Cushing syndrome
- pituitary tumor
- adrenal tumor
- long term glucocorticoid therapy
120
Cushing gender
-more common in females
121
Cushing syndrome s/s
- 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
management of Cushing syndrome
- 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
Cushing syndrome patient education
- 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
Primary Aldosteronism
-too much aldosterone production due to adrenal tumor
125
s/s primary aldosteronism
- low K+
- HTN
- normal or elevated Na
- weakness/cramping/fatigue
- glucose intolerance
126
management of primary aldosteronism
- surgical removal of adrenal tumor (adrenalectomy)
- tx hypokalemia and hyperglycemia
- spironolactone to tx HTN
127
primary vs secondary head injury
- 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
skull fractures can be...
...linear, comminuted, basilar, or depressed
129
s/s skull fracture
- pain
- bleeding from nose, ear, mouth
- CSF leakage from nose, ear, mouth
- Battle's sign
- periorbital ecchymosis
130
diagnostics for skull fracture
- CT
| - MRI
131
leakage of CSF
-@ risk for infections because passes BBB (meningitis or abscess formation or osteomyelitis)
**may spontaneously close or require surgery
132
surgery in skull fx
-nondepressed do not require, depressed do
133
penetrating injury
-surgical debridement of brain and IV abx admin is necessary
134
Monro-Kellie Doctrine
* *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
TBIs
- tend to have lasting effects
| - increased ICP=decreased perfusion to brain, crushing itself (brain will eventually herniate)
136
s/s concussion
(usually resolves w/in 24 hrs)
- photophobia
- n/v
- HA
- blurry vision
**decrease stimuli which will help w/ symptoms
137
s/s to look for post-concussion and to notify PCP of
- difficulty speaking
- confusion/seizures
- SEVERE HA
- continued vomiting
- weakness one side of body
138
s/s brain contusion
- difficulty arousing pt
- cool/clammy skin
- shallow respirations
- hypotension
- hypothermia
139
diffuse axonal injury s/s
- coma
- posturing (decorticate or decerebrate)
- global cerebral edema
140
diagnostics diffuse axonal injury
- MRI
- CT
- patient presentation
141
s/s epidural hematoma
* classic sign: loss of consciousness followed by brief period of lucidity
- signs of focal neuro deficits and LOC as compensatory mechanism fails
142
management of epidural hematoma
- burr holes and drain placement
- craniotomy
- attempts to decrease ICP
143
causes of subdural hematoma
- trauma
- rupture of aneurysm
- coagulopathy
***more often tends to be venous bleed (slow bleed)
144
SDH can be...
- acute (less than 72 hrs)
- subacute (4-21 days after injury)
- chronic (21 or more days after injury...around 3 mo.)
145
s/s SDH
- changes in LOC
- changes in pupil reactivity
- hemiparesis
**if it is rapidly expanding: coma, high BP, decreased HR may occur
146
SDH tx
sx to open dura
147
ICH (intercerebral hemorrhage)
**bleeding into parenchyma (tissues) of brain
148
causes of ICH
- trauma
- aneurysm rupture
- bleeding disorders
- tumors
149
s/s ICH
- neurological deficits
| - HA
150
management of ICH
- 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
patients w/ TBI are...
...at increased risk of cervical spine injuries so cervical spine immobilization is recommended
152
preventing secondary brain injury
-prevent cerebral edema, hypotension, and respiratory depression
153
LOC change can indicate...
...increased ICP
154
CSF
little cushion around brain
155
cerebral edema occurs when...
...an abnormal accumulation of fluid occurs and the body's compensatory mechanism can no longer compensate
156
when cerebral blood flow decreases significantly...
...a widening pulse pressure and cardiac slowing will occur (can get necrosis)
157
clinical manifestations of increased ICP
*FIRST SIGNS: restlessness, confusion, increased drowsiness, and LOC changes
- pupillary changes
- impaired extraocular movements
- unilateral weakness
- HA
158
impending signs of brain herniation
(increased ICP=herniation)
* Cushing triad:
(1) bradycardia
(2) bradypnea (irregular respirations/Cheynes-stoke resp=really high ICP)
(3) hypertension (widening pulse pressure)
159
normal ICP
5-15
160
invasive monitoring of ICP
-bolt (only monitors pressure not the fluid)
or
-extra-ventricular drain (EVD)...increased risk for infection
161
other management of ICP management
- 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
three cardinal findings of brain death
- 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
primary vs secondary spinal cord injury
- 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
incomplete spinal cord lesion
-impacts sensory and motor function or both and may only impact an area of the spinal cord
165
complete spinal cord lesion
-causes total loss of sensation and voluntary muscle control below the lesion
166
paraplegia
paralysis of lower body
167
tertraplegia
-paralysis of all 4 extremities
168
worry about breathing when...
...spinal cord injury C4 or above (brainstem problems)
169
complications of SCI
- neurogenic shock
- DVT
- orthostatic hypotension
- autonomic dysreflexia
170
neurogenic shock
- warm, flushed skin
- bradycardia (PNS activated)
- hypotension
- tachypnea
171
autonomic dysreflexia
-exaggerated sympathetic nervous system response occurs due to stimuli
172
s/s autonomic dysreflexia
- HA
- HTN
- diaphoresis (can lead to rupture of cerebral blood vessels or increased ICP)
- nausea
173
common triggers of autonomic dysreflexia
- distention of bladder or bowel
- pressure ulcers
- thermal stimuli
174
types of shock
- obstructive
- cardiogenic
- hypovolemic (hemorrhagic)
- distributive
175
types of distributive shock
(pipe problem)
- septic
- neurogenic
- anaphylactic
176
tissue perfusion determined by...
-cardiac output AND systemic vascular resistance q
177
cardiac output=
stroke volume x HR
178
in shock...
- 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
increasing lactic acid levels
-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
BP readings
-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
compensated stage of shock (nonprogressive)
-BP is near normal limits because compensatory mechanisms are causing adequate perfusion
* *COMP mechanisms:
- increased HR
- vasoconstriction
- increased contractibility of heart
182
s/s compensated stage of shock
- tachycardia
- anxiety
- vasoconstriction
183
management compensated stage of shock
- 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
by the time BP drops in shock...
...damage has already occurred at cell and tissue levels
185
hypoperfusion...
....tends to impact brain and kidneys 1st
186
uncompensated stage of shock (progressive)
**pt loses ability to compensate for injury/infection/insult
187
s/s uncompensated stage of shock
- tachy
- dyspnea
- restlessness
- diaphoresis
- metabolic acidosis (impacts ability to clot)
- hypotension
- prolonged cap refill
- oliguria
- decreased LOC
188
management of uncompensated stage of shock
- TWO large bore IV sites initiated to administer fluids, meds, and/or blood products
- close monitoring in ICU for hemodynamic stability
- UA monitoring
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if perfusion does not improve despite aggressive interventions... (PATHO CONCEPT)
...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
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irreversible stage of shock (end-organ dysfunction)
- 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
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management of irreversible stage of shock
-prevent complications and provide comfort
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multiorgan system effects of shock
- ARDS
- acidosis
- acute renal/liver failure
- ileus forms
- stress ulcers
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4 key points in general management of shock
- fluids
- optimal O2 delivery
- vasopressors
- nutrition support
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pulse ox
-less reliable with decreased BP (so use forehead)
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fluid replacement in shock
- isotonic cyrstalloids
- colloids
- blood components
**normal saline for patients who are more stable, trauma patients get LR
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CVL
-central venous line may be inserted to monitor central venous pressure (CVP) ....tells you volume of blood in R atrium
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arterial lines
may be used for accurate BP monitoring
***DO NOT give meds thru these
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vasopressors
-used in shock pts to improve hemodynamic stability when fluids alone can't maintain adequate MAP
* strengthen myocardial contraction
* regulate HR
* initiate vasoconstriction
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vasopressors and lines
***give thru biggest line (CVL)
- they can extravasate and can cause severe tissue damage
- TITRATE the vasopressors (goal is MAP of 65 or higher)
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2 most common causes of cardiogenic shock
- MI
| - dysrhythmias
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cardiogenic shock and fluid
**fluid admin should be closely monitored (its not a fluid volume problem so dont give more because dont want to overload the heart)
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obstructive shock (heart cant pump past something)
- decreased oxygen delivery due to obstructive cause
ex: pericardial tamponade, tension pneumothorax (insert CT), pulmonary embolism, abdominal compartment syndrome
***REVERSE THE CAUSE
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distributive shock examples
- Addison's crisis
- toxic shock syndrome
**alterations in vascular smooth muscle tone causes systemic vasodilation
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s/s septic shock
- fever or hypothermia
- tachy
- leukocytosis or leukopenia
- a left shift (increase in immature WBC)
- infection
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1 hr bundle for septic shock
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
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SIRS
- 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
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neurogenic shock
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)
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management of neurogenic shock
- goal MAP 85
- restore sympathetic tone until stabilization of spinal cord injury
- spinal precautions (log rolls, reverse trendelenburg)
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s/s anaphylactic shock
- hypotension
- angioedema
- pruritus
- flushing
- swelling of tongue/mouth
- wheezing stridor
- GI symptoms
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management of anaphylactic shock
- epi
- H2 agonists (Pepcid....stop release of antihistamines)
- steroids
- Benadryl
- fluids
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MODS
(Multiple Organ Dysfunction Syndrome)
- severe organ dysfxn in two or more organ systems
- Most Commonly: ARDS and acute kidney failure occurs
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MODS--Hepatic
- jaundice
- LFTs
- decreased albumin
- elevated PT
213
MODS--hematologic
- decreased platelets
- elevated PT
- increased D-dimer
214
MODS--CNS
-altered LOC
215
MODS--respiratory
- tachypnea
- hypoxemia
- high PaO2
216
MODS--cardio
- tachy
| - hypotension
