Exam 2 Part 1 Flashcards
myasthenic crisis = too much or too little ach? what drug do we treat with?
myasthenic crisis = too little ACH
- treatment: neoStigmine
–> increase secretions
cholinergic crisis = too much or too little ach? what drug do we treat with?
cholinergic crisis = too much ACH
- treatment = Atropine
–> dries up secretions, can’t pee with an atropeen
which neuro disorder uses tensilon test? how does the test work?
Tensilon = MG
- give endrophonium –> prevents breakdown of ACH –> increase ACH in body–> increase secretions
- if drug (endrophonium) increase muscle strength = MG diagnosis
- is drug (endrophonium) causes NO CHANGE = NOT MG
Reg ICP =
10-15
Reg CCP = ____
> 70
Reg MAP = _______
> 65
how do you calculate map
2 x (diastolic) + systolic / 3
how do you calculate the CPP? how do you calculate ICP?
map - icp
- icp is given!
Which theses is autoimmune:
MS
MG
ALS
GBS
- MS
- MG
- GBS
NOT autoimmune = ALS
which of these usually follows and infection or virus:
MS
MG
ALS
GBS
GBS
which of these do people usually recover from but in severe forms it can be fatal:
MS
MG
ALS
GBS
GBS
Name this neuro disease:
-Immune system attacks myelin sheaths and destroys.
–>Messages from brain and spinal cord are delayed or stopped.
MS
name this neuro disease:
-Degeneration of motor nerve cells in brain and spinal cord.
–>Muscle weakness and atrophy.
ALS
name this neuro disease:
Immune system attacks nerves, damaging myelin sheaths.
–>Inflammation of nerves causing muscle weakness and loss of sensation.
GBS
name this neuro disease:
- Antibodies form against acetylcholine receptors at neuromuscular junction of voluntary muscles.
–>Causes muscle fatigue and weakness.
MG
which of these causes voluntary muscle loss?
ALS and MG
4 main changes in MS
-Visual disturbances
-Mobility issues
-Sensory alteration
-Cognition/Mental health Changes
–> bowel and bladder
2 main changes in ALS
weakness
muscle atrophy (voluntary)
5 main issues of GBS
- pain
-numbness
-tingling
-weakness
-breathing issues
4 main changes of MG
-Ocular Myasthenia (weakened eye muscles)
-Drooping Eyelids
-Double Vision
-Facial expression difficulty
which neuro diseases cause dysphagia and dyarthria?
MS
MG
ALS
GBS
all of those!
which neuro diseases cause uncontrollable laughing or crying?
MS
ALS
1 cause of death from ALS?
resp failure! top MS complication
top MS complication
infection! (uti, asp. PNA, immunosuppression from drugs)
which 2 can use plasmapheresis as treatment:
MS
MG
ALS
GBS
MG
GBS
4 drugs for MS
-Immunomodulators
-NSAIDs
-Interferon Beta
- Antispasmodics
2 drugs for GBS
IVIG
pain relief
4 drugs for MG
- Cholinesterase inhibitors-(Pyridostigmine)
- Corticosteroids
- Immunosuppressants
- IVIG
True or False: ALS effects bladder and sensory function
FALSE- ALS does NOT cause changes in sensory or bladder fxn
Which neuro disease is characterized by phases : progressive, plateau, and recovery
GBS
In GBS the paralysis onset is ______ and during recovery the paralysis is _______
ascending, descending (whats goes up must come down)
MG will ______ with activity and _______ with rest
worsen, improve
type of MS that allows for remyelination
Relapsing Remitting
MG can have involvement of which endocrine organ?
Thymus
Addisons and Cushings- which is high and which is low steroid levels?
Addisons = low (need to add some steroid)
Cushings = high
speaking of cushings, what is cushings triad?
widening pulse pressure
bradycardia
change in resp pattern
it has nothing to do with endocrine system
Addisons s/s
LOW:
-BP
-Weight (water loss)
-temp
-hair (alopecia)
-mood
-energy
-SODIUM
-glucose
-absent period
HIGH (2):
-pigmentation –> bronze
-*POTASSIUM –> muscle spasms, peaked T wakes/ ST elevations
double p’s for the double d’s in addisons
cushings s/s:
HIGH/BIG
-BP
-SODIUM
-glucose
-truncal obesity
-moon face
-buffalo hump
-hirsutism
-purple striae
-rosy cheeks
-infection (slow wound healing)
-*risk for fractures
whats up with sodium and glucose in addisons and cushings?
addisons = low Na, low glucose
cushings = big Na, big glucose
what does aldosterone do?
keeps salt and water, lets go of K
top primary and secondary causes of addisons?
primary = autoimmune
secondary = cessation fo long term steroids
top causes of cushings?
-long term steroid use
-pituitary/adrenal tumor
-small cell lung cancer
addisons interventions
-report stress to provider (increase dose)
-don’t stop taking steroid abruptly –> addison’s crisis
-no cure- need to be on hormone replacement therapy for life
-monitor glucose –> hypoglycemia risk
cushings interventions
-report weight gain
-infection signs
-manage hyperglycemia
-fall precautions - risk for fractures
-risk for cataracts
-increase dose of meds during stress
re: addison’s crisis: hyperkalemia interventions
-restrict K
-K kinding drugs (insulin, kayexelate)
- no K sparing diuretic (furosemide) –> give thiazide or loop
-Tele
-VS
cushings treatment:
cut it out + life long hormone replacement and do not stop them –> lead to addison crisis
addisonian crisis- what happens> priority intervention?
hypotensive shock!
increase K, decrease Na
-IV push steroids
-IVF- NS or dextrose
top 3 anterior pituitary hormones (+ others)
-Corticotropin –Adrenocorticotropic Hormone (ACTH)
-Growth Hormone (GH)
-Thyrotropin – Thyroid Stimulating Hormone (TSH)
Luteinizing Hormone (LH)
Prolactin (PL)
Mylenocyte Stimulating Hormone (MSH)
Follicle Stimulating Hormone (FSH)
does the posterior pituitary make ADH and oxytocin?
no the hypothalamus does, posterior pituitary just stores them
what does ACTH do? where does it come from
comes from anterior pituitary - tells adrenal glands to make cortisol
what does Thyroid Stimulating Hormone (TSH) do? where is it made?
tells thhyroid to make T4/T3/Calcitonin
made in anterior pituitary
what does ADH do?
aka vasopressin
-tell kidneys to hold onto water
deficiencies of which 2 pituitary hormones are the most serios?
thyroid stimulating and ACTH
hypopituitarism types
selective (1 hormone) , pan (all hormones deificient)
causes of hypopituitarism vs hyperpituitarism
hypo: tumor, head trauma/infection/ischemia, idiopathic, sheehan syndrome (infarction)
hyper:tumors, hyperplasia
Gonadotropic deficiency (LH, FSH) (hypopituitarism)
hair loss, depressed sex organs
adult vs child grwoth hormone deficiency (hypopituitarism)
Adult- decrease bone density/muscle mass, weight gain, fatigue, temp sensitivity, short stature
child- slow puberty, delayed tooth development, increase fat in the face and ABD
diagnostics for hypopituitarism - what kind of labs? (general)
Some hormone levels can be measured directly or may be measured by the effects of the hormone.
Example:
Thyroid Stimulating Hormone
Measure T3, T4…
Gonadotropins
Testosterone, Estradiol, Prolactin
interventions for hypopituitarism?
hormone replacement therapy
testosterone: gynecomastia
estrogen: thrombosis
growth hormone = SQ injection
compliations of hyperpiuitarism tumors?
compress brain tissue: increase ICP, headaches, vision/neuro change
overproduction of growth hormone =
what are the assessment findings for it?
acromegaly
-slow progression
-enlarged bones/organs/features
-hyperglycemia
–> can reverse soft tissue but not skeletal changes
hyperpituiarism with excess ACTH can lead to…
cushings!
what is suppression testing used for? how does it work?
diagnose hyperpituitarism
=Give glucose to induce hyergylcemia, high glucose will suppress G
–> if you have high levels of GH (>1) then you will have a high chance of hyperpituitarism .
-Want GH to be less <1
drugs we give for hyperpituirism related to GH?
-somastatin analogs
-ocoreotide
—> decrease GH
-GH receptor blockers
-Pegvisomant
-Dopamine agonists
- Bromocriptine
- Cabergoline
–> Stimulate dopamine receptors in the brain and slow release of GH and Prolactin
side effects of dopamine agonists (treat GH oversecretion)
Orthostatic hypotension
GI irritation
Given with food
HA’s
Dysrhythmias (rare)
CSF leakage (rare)
if the entire pituitary is removed the patient will require….
life long HRT
ps pituitary removal =Hypophysectomy
What is DI ? causes?
Disorder of the POSTERIOR pituitary
too little ADH (neurogenic- primary) or kidneys don’t respond to ADH (nephrogenic- secondary)
causes: head injury, meds, pituitary problems
drug that might cause DI
lithium anddemeclocycline interfere with kidney’s ability to respond to ADH.
DI assessment findings
-hypotension
-tachcardia
-peeing a lot
-dehydration (dry membranes/poor skin turgor)
-decreased loc
-increased thirst
-hypovolemic shock
HIGH
NA, Serum Osmo >300
LOW
Urine osmo (urine spcific gravity <1.005)
DI urine output I&O diagnosis
DI if >4L UOP and > ingested oral intake
DI can be 4L-30L output/day
interventions for DI?
maintain hydration! -½ NS or NS (if NA levels are normal ish)
-desmopressin (synthatic ADH)
education for DI?
If permanent, education!! – sxs of dehydration, daily weight, nocturia/polyuria/dipsia, how to take desmopressin if its permanent
SIADH- too little or too much ADH?
what happens?
too much ADH
ADH is secreted despite osmolarity being low or normal.
Water retention –>Low Na due to dilution –>Fluid Overload –> peeps not coming out
(3) causes of SIADH?
-Cancer therapy
-Pulmonary infection or impairment
-Certain drugs (SSRIs….)
assessment findings for SIADH
- fluid overload- bounding pulse
-Low LOC
-Low urine output
-risk of seizures
-no dependent edema though (not in the interstitial space because salt is not retained but have high fluid levels)
HIGH
urine osmo
LOW
serum Na, serum osmo
SIADH interventions: how much do we restrict fluids?
500-1000 mL/24 hours
SIADH interventions in general:
restrict fluid
replace sodium
daily weight
mouth care
monitor for fluid overload
what are the Vapta drugs for SIADH?
how do they work and whats our side effects (3)?
Vasopressin ANTAGONIST
“Vaptans”
Tolvaptan PO
Conivaptan IV
–>Promote water excretion, retain sodium
Side effects:
* Rapid increase Na demyelination can occur
* Liver Failure
* Death
drug interventions for SIADH which one for which Na level?
vasopressin antagonist (low Na)
diuretics (normal Na)
hypertonic saline (low Na)
side effects of hypertonic saline?
Can cause HF and preexisting overload worse
Side effects
* Pulm edema
* HF
* Overload
Na less <120 can lead to seizures and….
demyelination
sodium should be changes slowly, no more than ____/24 hours
8mmol/L in 24 hours
