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Kol- 410 Med Surg II > Exam 2 Part 1 > Flashcards

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

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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

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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
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4
Q

Reg ICP =

A

10-15

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5
Q

Reg CCP = ____

A

> 70

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6
Q

Reg MAP = _______

A

> 65

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7
Q

how do you calculate map

A

2 x (diastolic) + systolic / 3

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8
Q

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

A

map - icp

  • icp is given!
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9
Q

Which theses is autoimmune:

MS
MG
ALS
GBS

A
  • MS
  • MG
  • GBS

NOT autoimmune = ALS

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10
Q

which of these usually follows and infection or virus:

MS
MG
ALS
GBS

A

GBS

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11
Q

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

MS
MG
ALS
GBS

A

GBS

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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

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13
Q

name this neuro disease:

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

–>Muscle weakness and atrophy.

A

ALS

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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

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15
Q

name this neuro disease:

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

–>Causes muscle fatigue and weakness.

A

MG

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16
Q

which of these causes voluntary muscle loss?

A

ALS and MG

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17
Q

4 main changes in MS

A

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

–> bowel and bladder

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18
Q

2 main changes in ALS

A

weakness
muscle atrophy (voluntary)

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19
Q

5 main issues of GBS

A
  • pain
    -numbness
    -tingling
    -weakness
    -breathing issues
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20
Q

4 main changes of MG

A

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

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21
Q

which neuro diseases cause dysphagia and dyarthria?

MS
MG
ALS
GBS

A

all of those!

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22
Q

which neuro diseases cause uncontrollable laughing or crying?

A

MS
ALS

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23
Q

1 cause of death from ALS?

A

resp failure! top MS complication

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24
Q

top MS complication

A

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

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25
Q

which 2 can use plasmapheresis as treatment:

MS
MG
ALS
GBS

A

MG
GBS

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26
Q

4 drugs for MS

A

-Immunomodulators
-NSAIDs
-Interferon Beta
- Antispasmodics

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27
Q

2 drugs for GBS

A

IVIG
pain relief

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28
Q

4 drugs for MG

A
  • Cholinesterase inhibitors-(Pyridostigmine)
  • Corticosteroids
  • Immunosuppressants
  • IVIG
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29
Q

True or False: ALS effects bladder and sensory function

A

FALSE- ALS does NOT cause changes in sensory or bladder fxn

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30
Q

Which neuro disease is characterized by phases : progressive, plateau, and recovery

A

GBS

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31
Q

In GBS the paralysis onset is ______ and during recovery the paralysis is _______

A

ascending, descending (whats goes up must come down)

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32
Q

MG will ______ with activity and _______ with rest

A

worsen, improve

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33
Q

type of MS that allows for remyelination

A

Relapsing Remitting

34
Q

MG can have involvement of which endocrine organ?

A

Thymus

35
Q

Addisons and Cushings- which is high and which is low steroid levels?

A

Addisons = low (need to add some steroid)
Cushings = high

36
Q

speaking of cushings, what is cushings triad?

A

widening pulse pressure
bradycardia
change in resp pattern

it has nothing to do with endocrine system

37
Q

Addisons s/s

A

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
Q

cushings s/s:

A

HIGH/BIG
-BP
-SODIUM
-glucose
-truncal obesity
-moon face
-buffalo hump
-hirsutism
-purple striae
-rosy cheeks
-infection (slow wound healing)
-*risk for fractures

39
Q

whats up with sodium and glucose in addisons and cushings?

A

addisons = low Na, low glucose
cushings = big Na, big glucose

40
Q

what does aldosterone do?

A

keeps salt and water, lets go of K

41
Q

top primary and secondary causes of addisons?

A

primary = autoimmune
secondary = cessation fo long term steroids

42
Q

top causes of cushings?

A

-long term steroid use
-pituitary/adrenal tumor
-small cell lung cancer

43
Q

addisons interventions

A

-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
Q

cushings interventions

A

-report weight gain
-infection signs
-manage hyperglycemia
-fall precautions - risk for fractures
-risk for cataracts
-increase dose of meds during stress

45
Q

re: addison’s crisis: hyperkalemia interventions

A

-restrict K
-K kinding drugs (insulin, kayexelate)
- no K sparing diuretic (furosemide) –> give thiazide or loop
-Tele
-VS

46
Q

cushings treatment:

A

cut it out + life long hormone replacement and do not stop them –> lead to addison crisis

47
Q

addisonian crisis- what happens> priority intervention?

A

hypotensive shock!
increase K, decrease Na
-IV push steroids
-IVF- NS or dextrose

48
Q

top 3 anterior pituitary hormones (+ others)

A

-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
Q

does the posterior pituitary make ADH and oxytocin?

A

no the hypothalamus does, posterior pituitary just stores them

50
Q

what does ACTH do? where does it come from

A

comes from anterior pituitary - tells adrenal glands to make cortisol

51
Q

what does Thyroid Stimulating Hormone (TSH) do? where is it made?

A

tells thhyroid to make T4/T3/Calcitonin

made in anterior pituitary

52
Q

what does ADH do?

A

aka vasopressin
-tell kidneys to hold onto water

53
Q

deficiencies of which 2 pituitary hormones are the most serios?

A

thyroid stimulating and ACTH

54
Q

hypopituitarism types

A

selective (1 hormone) , pan (all hormones deificient)

55
Q

causes of hypopituitarism vs hyperpituitarism

A

hypo: tumor, head trauma/infection/ischemia, idiopathic, sheehan syndrome (infarction)

hyper:tumors, hyperplasia

56
Q

Gonadotropic deficiency (LH, FSH) (hypopituitarism)

A

hair loss, depressed sex organs

57
Q

adult vs child grwoth hormone deficiency (hypopituitarism)

A

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
Q

diagnostics for hypopituitarism - what kind of labs? (general)

A

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
Q

interventions for hypopituitarism?

A

hormone replacement therapy

testosterone: gynecomastia
estrogen: thrombosis
growth hormone = SQ injection

60
Q

compliations of hyperpiuitarism tumors?

A

compress brain tissue: increase ICP, headaches, vision/neuro change

61
Q

overproduction of growth hormone =

what are the assessment findings for it?

A

acromegaly

-slow progression
-enlarged bones/organs/features
-hyperglycemia

–> can reverse soft tissue but not skeletal changes

62
Q

hyperpituiarism with excess ACTH can lead to…

A

cushings!

63
Q

what is suppression testing used for? how does it work?

A

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
Q

drugs we give for hyperpituirism related to GH?

A

-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
Q

side effects of dopamine agonists (treat GH oversecretion)

A

Orthostatic hypotension
GI irritation
Given with food
HA’s
Dysrhythmias (rare)
CSF leakage (rare)

66
Q

if the entire pituitary is removed the patient will require….

A

life long HRT

ps pituitary removal =Hypophysectomy

67
Q

What is DI ? causes?

A

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
Q

drug that might cause DI

A

lithium anddemeclocycline interfere with kidney’s ability to respond to ADH.

69
Q

DI assessment findings

A

-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
Q

DI urine output I&O diagnosis

A

DI if >4L UOP and > ingested oral intake
DI can be 4L-30L output/day

71
Q

interventions for DI?

A

maintain hydration! -½ NS or NS (if NA levels are normal ish)

-desmopressin (synthatic ADH)

72
Q

education for DI?

A

If permanent, education!! – sxs of dehydration, daily weight, nocturia/polyuria/dipsia, how to take desmopressin if its permanent

73
Q

SIADH- too little or too much ADH?

what happens?

A

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
Q

(3) causes of SIADH?

A

-Cancer therapy
-Pulmonary infection or impairment
-Certain drugs (SSRIs….)

75
Q

assessment findings for SIADH

A
  • 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
Q

SIADH interventions: how much do we restrict fluids?

A

500-1000 mL/24 hours

77
Q

SIADH interventions in general:

A

restrict fluid
replace sodium
daily weight
mouth care
monitor for fluid overload

78
Q

what are the Vapta drugs for SIADH?
how do they work and whats our side effects (3)?

A

Vasopressin ANTAGONIST

“Vaptans”
Tolvaptan PO
Conivaptan IV

–>Promote water excretion, retain sodium

Side effects:
* Rapid increase Na  demyelination can occur
* Liver Failure
* Death

79
Q

drug interventions for SIADH which one for which Na level?

A

vasopressin antagonist (low Na)
diuretics (normal Na)
hypertonic saline (low Na)

80
Q

side effects of hypertonic saline?

A

Can cause HF and preexisting overload worse

Side effects
* Pulm edema
* HF
* Overload

81
Q

Na less <120 can lead to seizures and….

A

demyelination

82
Q

sodium should be changes slowly, no more than ____/24 hours

A

8mmol/L in 24 hours

Kol- 410 Med Surg II (27 decks)

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