Exam 2 Part 1 Flashcards

1
Q

myasthenic crisis = too much or too little ach? what drug do we treat with?

A

myasthenic crisis = too little ACH
- treatment: neoStigmine

–> increase secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

cholinergic crisis = too much or too little ach? what drug do we treat with?

A

cholinergic crisis = too much ACH
- treatment = Atropine

–> dries up secretions, can’t pee with an atropeen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

which neuro disorder uses tensilon test? how does the test work?

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Reg ICP =

A

10-15

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Reg CCP = ____

A

> 70

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Reg MAP = _______

A

> 65

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how do you calculate map

A

2 x (diastolic) + systolic / 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how do you calculate the CPP? how do you calculate ICP?

A

map - icp

  • icp is given!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which theses is autoimmune:

MS
MG
ALS
GBS

A
  • MS
  • MG
  • GBS

NOT autoimmune = ALS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

which of these usually follows and infection or virus:

MS
MG
ALS
GBS

A

GBS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

which of these do people usually recover from but in severe forms it can be fatal:

MS
MG
ALS
GBS

A

GBS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Name this neuro disease:

-Immune system attacks myelin sheaths and destroys.

–>Messages from brain and spinal cord are delayed or stopped.

A

MS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

name this neuro disease:

-Degeneration of motor nerve cells in brain and spinal cord.

–>Muscle weakness and atrophy.

A

ALS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

name this neuro disease:

Immune system attacks nerves, damaging myelin sheaths.

–>Inflammation of nerves causing muscle weakness and loss of sensation.

A

GBS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

name this neuro disease:

  • Antibodies form against acetylcholine receptors at neuromuscular junction of voluntary muscles.

–>Causes muscle fatigue and weakness.

A

MG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

which of these causes voluntary muscle loss?

A

ALS and MG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

4 main changes in MS

A

-Visual disturbances
-Mobility issues
-Sensory alteration
-Cognition/Mental health Changes

–> bowel and bladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

2 main changes in ALS

A

weakness
muscle atrophy (voluntary)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

5 main issues of GBS

A
  • pain
    -numbness
    -tingling
    -weakness
    -breathing issues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

4 main changes of MG

A

-Ocular Myasthenia (weakened eye muscles)
-Drooping Eyelids
-Double Vision
-Facial expression difficulty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

which neuro diseases cause dysphagia and dyarthria?

MS
MG
ALS
GBS

A

all of those!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

which neuro diseases cause uncontrollable laughing or crying?

A

MS
ALS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

1 cause of death from ALS?

A

resp failure! top MS complication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

top MS complication

A

infection! (uti, asp. PNA, immunosuppression from drugs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
which 2 can use plasmapheresis as treatment: MS MG ALS GBS
MG GBS
26
4 drugs for MS
-Immunomodulators -NSAIDs -Interferon Beta - Antispasmodics
27
2 drugs for GBS
IVIG pain relief
28
4 drugs for MG
- Cholinesterase inhibitors-(Pyridostigmine) - Corticosteroids - Immunosuppressants - IVIG
29
True or False: ALS effects bladder and sensory function
FALSE- ALS does NOT cause changes in sensory or bladder fxn
30
Which neuro disease is characterized by phases : progressive, plateau, and recovery
GBS
31
In GBS the paralysis onset is ______ and during recovery the paralysis is _______
ascending, descending (whats goes up must come down)
32
MG will ______ with activity and _______ with rest
worsen, improve
33
type of MS that allows for remyelination
Relapsing Remitting
34
MG can have involvement of which endocrine organ?
Thymus
35
Addisons and Cushings- which is high and which is low steroid levels?
Addisons = low (need to add some steroid) Cushings = high
36
speaking of cushings, what is cushings triad?
widening pulse pressure bradycardia change in resp pattern it has nothing to do with endocrine system
37
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
38
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
39
whats up with sodium and glucose in addisons and cushings?
addisons = low Na, low glucose cushings = big Na, big glucose
40
what does aldosterone do?
keeps salt and water, lets go of K
41
top primary and secondary causes of addisons?
primary = autoimmune secondary = cessation fo long term steroids
42
top causes of cushings?
-long term steroid use -pituitary/adrenal tumor -small cell lung cancer
43
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
44
cushings interventions
-report weight gain -infection signs -manage hyperglycemia -fall precautions - risk for fractures -risk for cataracts -increase dose of meds during stress
45
re: addison's crisis: hyperkalemia interventions
-restrict K -K kinding drugs (insulin, kayexelate) - no K sparing diuretic (furosemide) --> give thiazide or loop -Tele -VS
46
cushings treatment:
cut it out + life long hormone replacement and do not stop them --> lead to addison crisis
47
addisonian crisis- what happens> priority intervention?
hypotensive shock! increase K, decrease Na -IV push steroids -IVF- NS or dextrose
48
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)
49
does the posterior pituitary make ADH and oxytocin?
no the hypothalamus does, posterior pituitary just stores them
50
what does ACTH do? where does it come from
comes from anterior pituitary - tells adrenal glands to make cortisol
51
what does Thyroid Stimulating Hormone (TSH) do? where is it made?
tells thhyroid to make T4/T3/Calcitonin made in anterior pituitary
52
what does ADH do?
aka vasopressin -tell kidneys to hold onto water
53
deficiencies of which 2 pituitary hormones are the most serios?
thyroid stimulating and ACTH
54
hypopituitarism types
selective (1 hormone) , pan (all hormones deificient)
55
causes of hypopituitarism vs hyperpituitarism
hypo: tumor, head trauma/infection/ischemia, idiopathic, sheehan syndrome (infarction) hyper:tumors, hyperplasia
56
Gonadotropic deficiency (LH, FSH) (hypopituitarism)
hair loss, depressed sex organs
57
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
58
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
59
interventions for hypopituitarism?
hormone replacement therapy testosterone: gynecomastia estrogen: thrombosis growth hormone = SQ injection
60
compliations of hyperpiuitarism tumors?
compress brain tissue: increase ICP, headaches, vision/neuro change
61
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
62
hyperpituiarism with excess ACTH can lead to...
cushings!
63
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
64
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
65
side effects of dopamine agonists (treat GH oversecretion)
Orthostatic hypotension GI irritation Given with food HA’s Dysrhythmias (rare) CSF leakage (rare)
66
if the entire pituitary is removed the patient will require....
life long HRT | ps pituitary removal =Hypophysectomy
67
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
68
drug that might cause DI
lithium anddemeclocycline interfere with kidney’s ability to respond to ADH.
69
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)
70
DI urine output I&O diagnosis
DI if >4L UOP and > ingested oral intake DI can be 4L-30L output/day
71
interventions for DI?
maintain hydration! -½ NS or NS (if NA levels are normal ish) -desmopressin (synthatic ADH)
72
education for DI?
If permanent, education!! – sxs of dehydration, daily weight, nocturia/polyuria/dipsia, how to take desmopressin if its permanent
73
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
74
(3) causes of SIADH?
-Cancer therapy -Pulmonary infection or impairment -Certain drugs (SSRIs….)
75
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
76
SIADH interventions: how much do we restrict fluids?
500-1000 mL/24 hours
77
SIADH interventions in general:
restrict fluid replace sodium daily weight mouth care monitor for fluid overload
78
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
79
drug interventions for SIADH which one for which Na level?
vasopressin antagonist (low Na) diuretics (normal Na) hypertonic saline (low Na)
80
side effects of hypertonic saline?
Can cause HF and preexisting overload worse Side effects * Pulm edema * HF * Overload
81
Na less <120 can lead to seizures and....
demyelination
82
sodium should be changes slowly, no more than ____/24 hours
8mmol/L in 24 hours