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Special Pop Exam 3 > Renal & Endo > Flashcards

Renal & Endo Flashcards

1
Q

function of feedback loops

A

maintain homeostasis

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2
Q

what connects 2 lobe of thyroid gland

A

isthmus

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3
Q

function of thyroid

A

Hormone that regulates cellular metabolism, growth, body system functions, & regulation of Calcium Levels

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4
Q

what does the thyroid store

A

thyroid hormone (sequesters circulation Iodine)

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5
Q

thyroidal secretion is mostly ____________

A

the prohormone T4

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6
Q

T3:T4 Ratio of secretion

A

1:10

80% of T3 deiodination of T4 by body tissues

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7
Q

elimination time of T3 and T4

A

T4 (7 days)
T3 (24-30 hours)

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8
Q

which is more potent: T3 or T4

A

T3 is 3-4 times more potent than T4

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9
Q

T3 and T4 protein binding

A

T3 & T4 are mostly protein bound.

Free & biologically active = T3 (0.3% of total T3)
Free & biologically active = T4 (0.03% of total T4)

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10
Q

functions of T3 and T4

A
  • Promote gene transcription & basal cell metabolism.
  • Intestinal absorption of glucose & insulin transport of glucose into cells.
  • Enhance hepatic gluconeogenesis & glycogenolysis
  • Increase Lipid utilization from adipose tissue
  • Increases β-adrenergic receptors & sensitivity to catecholamines ➔ increases myocardial contractility, decreases SVR, and increases systemic volume.
  • Promote in-utero brain development.
  • Thermogenesis
  • heat from body’s vital processes
  • adaptive thermogenesis
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11
Q

thyroid function is regulated by… (3)

A

TSH
TRH
T3, T4 & circulating levels of Iodine

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12
Q

where is TSH produced

A

anterior pituitary gland

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13
Q

function of TSH (2)

A
  • enhances/regulates iodine uptake
  • T3/T4 production/secretion by thyroid gland
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14
Q

TRH location of production and function

A

produced in hypothalamus & promotes TSH secretion

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15
Q

High (or low) T3/T4 levels in the hypothalamus/anterior pituitary gland regulate ____________

A

secretion of TRH & TSH.

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16
Q

what do high iodine levels do to T3/T4 production

A

down-regulate T3/T4 production

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17
Q

how are T3/T4 produced?

A
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18
Q

Thyroid hormone is produced and activated by____________

A

Iodine in the Thyroid Gland

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19
Q

Dietary intake of Iodine is ____________

A

reduced to Iodide in the GI tract ➔ Iodide is absorbed by the thyroid gland

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20
Q

Iodide bounds with ____________ ➔ forms ____________ ➔ ____________ & ____________ couple with____________ to form T3 & T4

A

Iodide bounds with Tyrosine ➔ forms Iodotyrosine ➔ Monoidotyrosine & Diiodotyrosine couple with thyroperoxalase to form T3 & T4

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21
Q

T3 & T4 attach to ____________ and are stored in the gland as ____________

A

thyroglobulin and are stored in the gland as a colloid

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22
Q

T3 & T4 are released into circulation after ____________

A

proteolysis from colloid thyroglobulin

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23
Q

function on parathyroid glands

A

Secrete calcitonin in response to high Ca++ levels, which decrease levels of calcium & phosphorus

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24
Q

calcitonin inhibits: (2)

A
  • Osteoclast activity
  • Renal reabsorption of calcium and phosphorus
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25
Q

⭐️ ____________ is secondary to the inadvertent removal of all (4) parathyroids during thyroidectomy ⭐️

A

hypoparathyroidism

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26
Q

3 forms of plasma calcium

A
  • 50% - Protein - bound calcium
  • 45% - Ionized fraction (physiologically active & homeostatically regulated)
  • 5% - non-ionized fraction bound with phosphate, bicarbonate, & citrate
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27
Q

normal calcium value

A

8.8-10.4 mg/dL

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28
Q

⭐️
what is calcium important for? (4)

A
  • muscle contraction
  • coagulation
  • neurotransmitter release
  • endocrine secretion
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29
Q

how does albumin affect Ca++ levels

A

Albumin binds (90%) protein-bound calcium

for every 1g/dL change in Albumin == 0.8 mg/dL in Ca++ level

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30
Q

what tightly controls Ca++ levels?

A
  • Parathyroid hormone through a negative-feedback mechanism
  • low Ca++ increases PTH to stimulate bone reabsorption/release of Ca++ and renal Ca++ reabsorption
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31
Q

what suppresses parathyroid hormone release?

A

high Ca++ levels

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32
Q

Protein binding of Ca++ affected by ____________ (2)

A

temperature and pH

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33
Q

how does acidosis affect Ca++(2)

A
  • decreases protein binding of Ca++
  • increases ionized Ca++ levels in the blood
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34
Q

how does alkalosis affect Ca++

A
  • increases protein binding of Ca++
  • decreases ionized Ca++ levels in the blood
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35
Q

when are s/s of hypocalcemia due to parathyroidectomy seen

A

Signs & Symptoms seen in (24-96h) post-op from acute parathyroid removal and the hypocalcemia that develops

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36
Q

⭐️
First signs of Hypocalcemic Tetany (2)

A
  • laryngeal stridor
  • laryngospasm
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37
Q

Serum Thyroxine (T4) Levels

A
  • evaluates thyroid function
  • 90% of hyperthyroid pt’s have elevated levels
  • 85% of hypothyroid pt’s have low levels
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38
Q

Serum Triiodothyronine

A
  • measures serum T3 levels
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39
Q

____________ is used to detect disease in pt’s with clinical S/S of hyperthyroidism

A

Serum Triiodothyronine

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40
Q

first test in evaluating suspected thyroid dysfunction is ____________

A

TSH Level

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41
Q

normal TSH range

A

0.4-0.5

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42
Q

Radioactive Iodine Uptake Test

A
  • measures the amount of thyroid uptake of iodine & thyroid activity
  • scan after p.o. ingestion and measure amount of thyroid activity
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43
Q

most common cause of hyperthyroidism

A

Grave’s Disease

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44
Q

patho of Grave’s disease

A
  • Autoimmune multinodular (goiter) disease
  • Thyroid Gland Hypertrophy
  • Due to IgG antibodies attacking the TSH receptor
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45
Q

who is Grave’s disease associated with

A
  • Commonly seen in females (20-40 yrs)
  • Commonly seen with Myasthenia Gravis
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46
Q

other s/s Grave’s disease

A

exophthalmos (bulging eyes)

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47
Q

Thyroid Adenoma

A
  • Autonomic functioning thyroid tissue that is not down-regulated by increased TSH
  • (2nd most common cause)
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48
Q

thyroiditis

A

Inflammatory process after acute URI with flu-like symptoms and treated with NSAIDS

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49
Q

⭐️
Amiodarone

A

iodine rich drug that can produce thyrotoxicosis (hyperthyroid disease)

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50
Q

hyperthyroidism signs

A
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51
Q

treatment of hyperthyroidism

A

Radioactive Iodine Ablation

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52
Q

pharmacologic treatment of hyperthyroidism (3)

A
  • Antithyroid agents: Tapazole (methimazole), PTU - propylthiouracil
  • Β-Blockers - propranolol (decreases the conversion of T4 to T3 but takes up to 2-weeks for this response), metoprolol
  • Glucocorticoids – (dexamethasone, hydrocortisone) inhibits peripheral conversion of T4 to T3
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53
Q

surgical resection for hyperthyroidism is indicated in… (3)

A
  • thyroidectomy – large symptomatic goiter or refractory to pharmacologic
  • thyroid cancer
  • obstructive symptoms (airway compressed, deviated, or obstructed)
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54
Q

Primary goal of anesthesia mgmt during thyroid surgery

A

euthyroid (normal thyroid function tests) prior to surgery

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55
Q

anesthetic considerations/pharmacologic treatment in thyroid patient prior to surgery

A
  • minimum time 10-14 days but up to 8 weeks preop treatment
  • PTU inhibits conversion of T4 to T3
  • methimazole inhibit organification of Iodide and blocks T3/T4 synthesis
  • Β-Blockers – decrease SNS activity
  • Steroids – continued through day of surgery, may need stress dose
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56
Q

intraop anesthetic considerations for thyroid patient (3)

A
  • Maintain adequate anesthetic depth to block SNS response from surgical stimulation
  • prevent exaggerated highs/lows in hemodynamics
  • avoid the use of SNS - stimulating drugs (ketamine or Pancuronium).
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57
Q

potential surgical complications and risks in thyroid patient (4)

A
  • Airway compression or compromise from goiter (continuously evaluate for high airway pressures during surgery) – consider awake fiberoptic intubation with a very large thyroid gland
  • Cardiac arrhythmias
  • Potential Hyperthermia
  • Myasthenia Gravis incidence increased – initial dose of paralytic should be lowered and TOF twitch monitor required
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58
Q

intraop treatment for hypotension in thyroid patient

A

direct - acting vasoconstrictors (phenylephrine)

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59
Q

intraop treatment for tachycardia in thyroid patient

A

esmolol

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60
Q

frequently, thyroid patients are ____________ and ____________

A

hypovolemic & vasodilated (give slowly & titrate all IV meds)

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61
Q

Neuromonitoring during thyroid surgery

A
  • NIMS ETT tubes are commonly used ➔ will prohibit use of NMDBs (if used for intubation must be reversed)
  • Surgeons will monitor recurrent laryngeal nerve (RLN) function
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62
Q

1 sided RLN injury

A

1 - sided voice hoarseness (vocal cord paralysis)

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63
Q

bilateral RLN injury

A
  • vocal cords (reintubation is necessary)
  • stridor
  • aphonia
  • respiratory distress from closed vocal cords
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64
Q

anesthetic mgmt for thyroid surgery

A
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65
Q

⭐️
what is thyroid storm

A

Life threatening, acute exacerbation of hyperthyroidism

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66
Q

when is thyroid storm most commonly seen?

A

undiagnosed or under-treated hyperthyroidism because of surgical stress or non-thyroid illness

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67
Q

what else can provoke thyroid storm?

A

Can be provoked by surgery on an acutely hyperthyroid gland

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68
Q

s/s thyroid storm

A
  • hyperthermia
  • tachycardia/dysrhythmias
  • myocardial ischemia / CHF
  • agitation
  • confusion
  • hypertension
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69
Q

differential diagnosis of thyroid storm (3)

A
  • pheochromocytoma
  • malignant hyperthermia
  • light anesthesia
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70
Q

diagnosis for thyroid storm

A

T4 levels may be elevated, but no lab test is diagnostic for this, diagnosis of exclusion

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71
Q

treatment of thyroid storm

A
  • Cardiovascular & Ventilatory Support
  • Immediate cooling
  • Keep HR < 100/min
  • High FiO2
  • Stop precipitating factor
  • β-Blockers (Esmolol drip or propranolol)
  • Corticosteroids ➔ hydrocortisone (50-100mg IV q6h)
  • Antithyroid Meds (PTU)
  • Sodium Iodide 250 mg IV q6h
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72
Q

what to avoid in thyroid storm (2)

A

salicylates & Lasix – both can increase thyroid hormone levels

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73
Q

take home point of management of thyroid storm under anesthesia

A

If the patient is under anesthesia, we want to stop all of the hypermetabolic activity and manage the associated symptomology we are seeing.

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74
Q

mortality rate of thyroid storm

A

10-75%

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75
Q

when else can thyroid storm present

A

Can present 6-18 hours post-operatively as well!

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76
Q

patho of hypothyroidism

A
  • common disease (0.3 to 5% of the population)
  • inadequate circulating levels of T4, T3, or both
  • onset slow and progressive, often with confusing symptoms
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77
Q

⭐️
most cases of hypothyroidism

A

primary hypothyroidism (95% of cases)

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78
Q

patho of primary hypothyroidism

A

decreased production of thyroid hormone despite normal levels of TSH

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79
Q

causes of primary hypothyroidism

A
  • surgical resection
  • Iodine (or I-131 tx) or amiodarone treatment
  • Lithium use – blocks thyroid hormone synthesis & release
  • Hashimoto disease – autoimmune thyroid gland destruction
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80
Q

secondary hypothyroidism causes

A
  • caused by hypothalamic or pituitary disease
  • often associated with other pituitary pathology (postpartum pituitary necrosis, pituitary mass, surgical resection, intracranial radiation therapy
  • consider hydrocortisone stress dose, especially if they have adrenal insufficiency
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81
Q

s/s hypothyroidism (8)

A

lethargy
slow mental functioning
cold intolerance/hypothermia
slow movements
depression
obesity
hyperlipidemia
reduced metabolic activity

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82
Q

treatment of hypothyroidism

A

Thyroid hormone replacement (levothyroxine)

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83
Q

t/f mild-moderate hypothyroid disease is safe for elective surgery

A

TRUE

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84
Q

⭐️
in severe hypothyroidism, patients need to be ____________ before surgery

A

✨euthyroid✨

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85
Q

hypothyroidism with CAD

A

increased risk of MI during euthyroid treatment due to increased HR and myocardial O2 demands

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86
Q

emergency surgery with severe hypothyroidism

A

aggressive treatment based on patient’s clinical status

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87
Q

goals for hypothyroid patient are to protect from…

A
  • respiratory depression
  • hypovolemia
  • hypoglycemia
  • hyponatremia
  • hypothermia
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88
Q

hypothyroidism pre-op medications

A

Continue levothyroxine

has a ½ life of 5-7 days, but needs to be continued during the operative period

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89
Q

hypothyroid patients have a heightened sensitivity to ____________

A

respiratory depressant sedatives

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90
Q

GI changes with hypothyroidism

A

delayed gastric emptying

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91
Q

consider ____________ with delayed gastric emptying

A
  • GI ultrasound scan, especially if they are on GLP-1 agonists
  • H2 antagonists
  • Reglan
  • Rapid sequence induction
  • non-particulate antacid
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92
Q

hypothyroidism intraop considerations

A
  • Potential difficult airway if they have a large goiter
  • Exaggerated response to cardio-depressant drugs
  • Prolonged NMBDs relaxation
  • Hypocarbia
  • Hyponatremia
  • Hypoglycemia
  • Congestive Heart Failure
  • Refractory Hypotension – may have adrenal insufficiency (steroid dose)
  • Severe disease invasive monitoring
  • Keep patient warm, increase room temp, fluid warmers
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93
Q

Hypothyroidism
Postop Care & Recovery

A

recovery may be delayed!
possibly prolonged PACU Stage 1

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94
Q

Pain mgmt for hypothyroidism

A

Toradol (NSAIDs) and peripheral neuraxial anesthesia are preferred!

If narcotics are used, use short acting like fentanyl, not dilaudid

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95
Q

Ensure your patient with Hypothyroidism is ___ prior to extubation.

A

normothermic

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96
Q

Assessing recovery of NMB in a hypothyroid patient

A

quantitative monitoring is best

TOF may be delayed recovery

ensure full muscle recovery/strength before extubation

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97
Q

Myxedema is an extreme form of

A

hypothyroidism

Diagnosed by very low-levels of T3/T4

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98
Q

Myxedema
Diagnosed by

A

very low-levels of T3/T4

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99
Q

T/F:
Myxedema is a surgical emergency.

A

False
Medical emergency

Only life-saving surgery should be performed

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100
Q

⭐️
A pt diagnosed with Myxedema can only go to surgery if…

A

its a life saving procedure

Only life-saving surgery should be performed

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101
Q

Myxedema Mortality = 25-50%.
What are the strong predictors of mortality?

A
  • Low MAP
  • Need for mechanical ventilation d/t hypoventilation
  • Concurrent Sepsis
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102
Q

Myxedema
treatment agent

A

IV thyroid hormone replacement T4 (levothyroxine)

Diagnosed by very low-levels of T3/T4

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103
Q

Myxedema Signs & Symptoms

A
  • Impaired LOC / Seizures
  • Loss of deep tendon reflexes (DTRs)
  • Hypoventilation
  • Hypothermia
  • Hyponatremia
  • Hypoglycemia
  • Bradycardia, low EKG voltage, non-specific ST/T –wave changes
  • CHF (cardiac pts)
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104
Q

Myxedema
Treatment, aside from primary agent

A
  • ETT & MV
  • CV support (inotropes, pressors, etc.)
  • IV thyroid hormone
  • Steroids (treat adrenal insufficiency)
  • 0.9 NaCl IVF
  • Glucose
  • Gradually correct both: hypothermia & hypoNa
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105
Q

Myxedema

What happens if we treat hypothermia & hyponatremia too quickly?

A

hypothermia: CV collapse

hypoNa: central pontine demyelination

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106
Q

CAUTION: Treatment of myxedema is aggressive replacement of ___, which can cause ___.

A

thyroid hormone

MI

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107
Q

Hyperparathyroidism

As Calcium levels rise to __, EKG changes can progress to heart block

A

20 mg/dL

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108
Q

Primary Hyperparathyroidism causes ___calcemia

A

hyper

Hypoparathyroidism = Ca++ Levels < 8 mg/dL

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109
Q

Causes of Primary Hyperparathyroidism

A
  • parathyroid adenoma (90%)
  • hyperplasia (9%) – usually affects all (4) glands
  • rarely parathyroid carcinoma
  • can exist as part of MEN – multiple endocrine neoplasia

Secondary Hyperparathyroidism: Increased PTH function from diseases that cause:
hypoCa & hyperphosphatemia (ESRD)

110
Q

Hyperparathyroidism (Primary) in OB

A

(50%) maternal/fetal mortality

can cause spontaneous abortion

111
Q

Hyperparathyroidism (Primary) symptoms are mainly caused by

A

hypercalcemia

112
Q

Hyperparathyroidism (Primary)
Symptoms

A
  • nephrolithiasis MOST common (60-70%)
  • depression
  • confusion, memory loss,
  • hypertension
  • Ekg changes, heart block (if Ca very high)
113
Q

Hyperparathyroidism (Primary)
diagnosis

A

elevated serum Ca++ levels

114
Q

T/F:
Secondary Hyperparathyroidism may result from ectopic production of PTH or analog-like substances from malignancies

A

False
primary

115
Q

Hyperparathyroidism (Primary)

malignancies that can ectopicly produce PTH or analog-like substances

A
  • lungs
  • genitourinary
  • breast
  • GI
  • lymphatic system
116
Q

Tumors can produce hypercalcemia through …

A

direct bone reabsorption mechanisms

117
Q

Secondary Hyperparathyroidism

A

Increase in parathyroid function d/t diseases that cause:
1. hypocalcemia
(↓ Vit. D metab, GI disorders interrupt absorption)

  1. hyperphosphatemia (ESRD)
    due to decreased renal phosphate excretion
118
Q

How is hypoCa r/t Secondary Hyperparathyroidism?

A

Low Ca ➡️ increased PTH secretion

(secondary increase in parathyroid activity)

119
Q

Parathyroid Surgical Treatment - Preop

A
  • Correction of intravascular volume & electrolyte disturbances
  • Emergency treatment of hypercalcemia before surgery

Chronic hypercalcemia patients need:
* EKG / Cardiac clearance
* CNS evaluations
* Renal system evaluations

120
Q

Parathyroid Surgery

Emergency treatment of hypercalcemia before surgery

A
  • Ca++ exceeding 15 mg/dL
  • Expand intravascular volume with 0.9 Saline IVF
  • Promote sodium diuresis with Lasix promotes Na+ and Ca++ excretion
  • Correct hypophosphatemia if present
  • Hemo/peritoneal dialysis if above are contraindicated
121
Q

Parathyroidectomy Anesthetic

A

GETA most common
TIVA remi/prop
NIMS ETT

122
Q

T/F:
Parathyroidectomy is chosen over any other type of treatment modality for hyperparathyroidism because it is curative.

A

True

123
Q

Which nerve are we monitoring with the NIMS tube during a Parathyroidectomy?

A

RLN

124
Q

T/F:
The RLN is at greater risk of injury during a Thyroidectomy than a Parathyroidectomy.

A

False
equal risk

125
Q

IV acess in Parathyroidectomy

A

must be 2nd free back-flowing IV for intraop Ca++ and PTH levels

serial draws typically 5 mins apart

126
Q

Chvostek’s and Trousseau sign are seen with (hypo/hyper)calcemia

A

hypo

Chvostek Trousseau

127
Q

Hypoparathyroidism is seen when Ca is below

A

8 mg/dL

128
Q

Hypoparathyroidism
MOST common cause
+
other causes

A

surgical removal w Thyroidectomy

other causes: neck trauma, malignancy, granulomatous disease

129
Q

Hypoparathyroidism
S/S

A
  • neuronal irritability
  • skeletal spasms, twitching, tetany, seizures
  • Chvostek’s sign
  • Trousseau sign
130
Q

T/F:
Chvostek’s & Trousseau sign are valid tools to help diagnose Hyperparathyroidism.

A

FALSE
HyPOparathyroidism

↓ PTH = ↓Ca = Chvostek’s & Trousseau

131
Q

Hypoparathyroidism (hypocalcemia)
symptoms

A

CV: CHF, hypoTN, insensitivity to β-Blockers, prolonged QT
fatigue
skeletal muscle cramps
depression

132
Q

The hypocalcemic patient may be insensitive to this drug in our anesthesia omnicell

A

β-Blockers

133
Q

Hypoparathyroidism
Treatment

A

electrolyte replacement before surgery
(hypocalcemia)

if Severe symptomatic: IV Ca gluconate then elemental Ca drip

134
Q

Adrenal Cortex
Function is to secrete 3-types of hormones:

A
  • Glucocorticoids (cortisol)
  • Mineralocorticoids (aldosterone)
  • Androgens
135
Q

Abnormal functioning of the adrenal cortex could render the patient …

A

unable to respond appropriately during a period of stress, surgery, or illness

136
Q

Where are 2 of the adrenal cortex hormones produced?

A

Glucocorticoids (cortisol): inner portion of the adrenal cortex

Mineralocorticoids (aldosterone): adrenal gland

137
Q

Cortisol
fxn

A
  • immediate effects on the metabolism of carbohydrates, proteins, and fatty acids.
  • immune and circulatory functions
138
Q

Cortisol is the most “potent” ___

A

glucocorticoid

139
Q

Cortisol excretion

A

inactivated by the liver and excreted in the urine

140
Q

Aldosterone
major function

A

regulate ECF volume and potassium homeostasis through the reabsorption of Na+ and secretion of K+ by tissues

141
Q

Androgens
fxn

A

sex organ development and changes that manifest during puberty

142
Q

Cushing’s Syndrome
causes

A
  • overproduction of cortisol by the adrenal cortex
  • overdosing of exogenous glucocorticoid
  • neoplasm
143
Q

Cushing’s Syndrome
Symptoms

A
  • truncal obesity, hyperglycemia, abdominal striae
  • HTN, intravascular volume increase
  • decreased K+
  • fatiguability, muscle weakness
  • osteoporosis
144
Q

Cushing’s Syndrome
Management

A
  • Preop: treat diabetes, fluid mgmt, HTN, electrolytes
  • Spironolactone diuresis – mobilizes excess fluid
  • if bilateral adrenalectomy, need glucocorticoid replacement
145
Q

⭐️
Cushing’s Syndrome
doesnt have a specific anesthesia plan but….

A

SEVERE Cushing’s can be temporized w/ Etomidate

it will inhibit steroid synthesis (adrenal suppression)

146
Q

Adrenal Problems

Mineralocorticoid Excess

A

too much aldosterone = HTN, hypoK alkalosis, weakness & fatigue

Anesthetic considerations:
restore IV fluid volume, electrolyte balance
HTN and hypokalemia can be controlled by Na+ intake restriction

147
Q

Addison’s Disease

A

undersecretion of adrenal steroid hormones (decrease of ACTH)

148
Q

Addison’s Disease is not apparent until

A

90% adrenal cortex has been destroyed

149
Q

Addison’s Disease
causes

A

(on the rise)
* previously TB, now mainly autoimmune destruction of the gland
* Hashimoto’s thyroiditis association

Other causes: bacterial, fungal, advanced HIV, sepsis, and hemorrhage

150
Q

Addison’s Disease
S/S

A

weight loss, N/V, diarrhea, chronic fatigue, hypotension

151
Q

Addison’s Disease
Acute crisis

A
  • abdominal pain
  • severe vomiting, diarrhea
  • low BP, decreased LOC, shock symptoms
  • severe hyperkalemia (life-threatening arrhythmias)
152
Q
A
153
Q
A
154
Q

doA of:
decadron
prednisone
hydrocortisone

A

decadron = long
prednisone = short
hydrocortisone = short

155
Q

HTN and hypokalemia can be controlled by

A

Na+ intake restriction

156
Q

the adrenal ____ synthesizes catecholamines

A

medulla

157
Q

⭐️
The adrenal medulla produces epi and norepi in what %

A

80% - epinephrine
20% - norepinephrine

158
Q

⭐️
Catecholamines are derived from

A

Tyrosine

159
Q

⭐️
Pheochromocytoma

Rare but interesting disease

A

tumors that arise in the chromaffin cells of the adrenal medulla

secrete epinephrine & norepinephrine

160
Q

Paragangliomas

A

extra-adrenal pheochromocytomas

pheochromocytomas= chromaffin cells of the adrenal medulla

161
Q
A
162
Q

Most Pheochromocytomas (75%) follow which pattern?

A

solidary and found in the right adrenal gland

163
Q

Pheochromocytomas are usually optimized by the time we see them in the OR, so why do we care?

A

surgeon stimulating or resecting the adrenal gland = wild swings (highs/lows) in our hemodynamics

wonk: I consider them “angry tumors” and make anesthesia management challenging.

164
Q

T/F:
Unreated Pheochromocytoma will kill you.

A

True

165
Q

Pheochromocytoma
Diagnosis

A

excess catecholamine or metabolite level

166
Q

Pheochromocytoma
S/S

A
  • headache
  • HTN
  • hyperglycemia
  • catecholamine-induced cardiomyopathy
  • palpitations, tremors, sweating, anxiety
167
Q

Pheochromocytoma⭐️

Paroxysmal catecholamine release

A
  • stimulation, laryngoscopy, tumor manipulation, abdomen insufflation
  • Tyramine foods (aged cheeses, cured meats)
  • TCA’s and metoclopramide (Reglan)
  • Micturition – when there is a bladder tumor
168
Q

Pheochromocytoma can masquerade as

A

malignant hyperthermia

169
Q

⭐️
Pheochromocytoma
excision mortality decreased from 50% to 0-3% with the preop use of:

A

A-antagonism (must be blocked first)

β-antagonism (used in pt’s with dysrhythmias/tachycardias) – blocked 2nd

170
Q

Pheochromocytoma
⍺-antagonism

-fxn
-agents

(must be blocked first)

A

prevents HTN from catecholamines
10-14 days preop with IVF replacement to mitigate orthostatic hypotension

Long-acting irreversible drugs: phenoxybenzamine

Short-acting competitive: doxazosin, prazosin, terazosin

171
Q

Pheochromocytoma
β-antagonism

-fxn
-agents

A

used in pt’s with dysrhythmias/tachycardias
(blocked 2nd)

Propanolol, atenolol, metoprolol

172
Q

⭐️
How to time alpha and beat blockade in Pheochromocytoma?
Why is it important?

A

start beta AFTER several days of ⍺-blockade

to avoid unopposed ⍺-constriction resulting in severe hypertension, myocardial ischemia, heart failure, and other end-organ hypertensive failure

173
Q

Pheochromocytoma
____ mandatory started prior to induction

A

Arterial BP

174
Q
  • Pheochromocytoma
  • Intraop monitoring
A
  • Large bore (18g or larger) IV’s x 2 or Central Line access
  • 5-Lead EKG: for ischemia/infarction/arrhythmias
  • TEE – if cardiomyopathy
  • Adequate depth before laryngoscopy
175
Q

Pheochromocytoma

To achieve adequate anesthesia depth before laryngoscopy, use

A
  • antihypertensives (nitroprusside, phentolamine, nicardipine)
  • hypotension: neo or norepi
  • tachycardia: esmolol (short-acting better vs. using longer-acting blockers since tumor is being removed)

all meds in your room, drawn-up, on pumps, in-line, and programmed for immediate use (you will need them!!)

176
Q

Pheochromocytoma

Excision can be performed via:

A

laparoscopic (robotic)
open procedure

177
Q

⭐️
T/F:
Manipulation of the Pheochromocytoma, despite ⍺- & β-blockade will still release catecholamines.

A

True
expect it and you will be prepared, wild BP and HR changes

178
Q

Pheochromocytoma
post-tumor excision

A

Expect a precipitous drop in BP (reason to have all pressor agents in-line)

Post-Op: pt’s will typically go extubated to ICU for 24 hrs, then step-down for monitoring.

179
Q

Diabetic & Pre-Diabetic

fasting glucose & HbA1c

A

Diabetic: fasting glucose levels > 126 mg/dL (HbA1c ≥ 6.5%)

Pre-Diabetic: fasting glucose 100-125 mg/dL (HbA1c ≥ 5.7-6.4%)

180
Q

DM Types

A

Type 1 DM
Type 2 DM
Gestational DM
Diabetes due to other causes

181
Q

Diabetes – Type 1 DM

A
  • autoimmune pancreatic β-cell destruction causing absolute insulin deficiency and insulin dependency
  • Hard to maintain blood glucose within normal limits
  • Onset: usually < 20 yrs old
182
Q

Type 1 DM
aossicated disease processes/risks

A

Risk for diabetic ketoacidosis (DKA) and hyperosmolar, hyperglycemic non-ketotic coma (HHNC)

Frequently have complications over their life span, retinopathy /blindness, limb infections/amputations, CV disease, neuropathies

183
Q

Type II DM

A

Adult-onset progressive loss of insulin secretion or developing insulin resistance

Treatment:
* Dietary control
* Lifestyle modification
* Oral hypoglycemics may progress in later disease to need insulin
* can D/C the night before surgery or the morning of and restart after PACU recovery regular meal intake

184
Q

Anesthetic Management in DM

Determine end-organ damage by examining full H&P:

A

EKG
BP
Serum BUN, Cr, Blood sugar

185
Q

Anesthetic Management in DM

End-organ complications

A
  • Atherosclerosis(CV, PVD, Renal Vascular, Cerebal) disease
  • GI dysfunction, slow motility, diarrhea, constipation
  • ESRD – dialysis? (type and schedule) fistula or cath?
  • late ESRD can be difficult to manage
186
Q

HHNC is a BG level of > ______

A

600

187
Q

T/F HHNC patients experience ketoacidosis

A

FALSE

188
Q

What precipitates HHNC? How should you treat it? Why?

A

profound dehydration (need 1-2 L of NS bolus over 1 hr)
Insulin Infusion follows the above rehydration
giving insulin infusion before rehydration will cause CV collapse***

189
Q

clinical manifestations of DKA include:

A

ketonemia, hyperglycemia, & acidemia
Blood glucose level: 250-500 mg/dL range
ALWAYS dehydrated due to hyperglycemic osmotic diuresis, nausea, vomiting.

190
Q

DKA Tx

A

fluids, insulin, and electrolyte replacement

191
Q

What is the Whipple triad? What is it a/w?

A

Symptoms of neuroglycopenia (lack of glucose to the brain/CNS symptoms)

  • Blood glucose < 40 mg/dL
  • Relief of symptoms with glucose administration
  • Clinically significant Hypoglycemia
192
Q

pituitary location =

A

located in the base of the brain in Sella Turcica

193
Q

The pituitary and hypothalamus together form the master control over _____________

A

the release of all the body’s hormones

194
Q

hyposecretion of the anterior pituitary is treated with ______ and ______

A

hormone replacement therapy and stress doses of corticosteroids.

195
Q

what causes Anterior Pituitary (hyposecretion)?

A

caused by decrease in ACTH secretion

196
Q

Anterior Pituitary (hypersecretion) is caused by? what does it produce?

A

caused by adenoma secondary to Cushing’s
secondary due to increase in ACTH
giantism or acromegaly due to excess growth hormone

197
Q

secretes vasopressin (antidiuretic hormone ADH) – ECF balance and oxytocin (uterine contractions & breast milk secretion)

A

Posterior Pituitary

198
Q

inadequate secretion of ADH or,
renal tubular resistance to ADH (nephrogenic)

A

DI

199
Q

DI S/S

A

polydipsia
hypernatremia **
high output of poorly concentrated urine
hypovolemia **

200
Q

DI Causes:

A

destruction of the pituitary gland by trauma (head, subarachnoid hemorrhage, brain death) or surgical injury

201
Q

DI Tx

A

Depends on hormone deficiency
DDAVP or vasopressin infusion
Isotonic crystalloid
frequent Na+ serum level measurements

202
Q

What causes SIADH?

A

Caused by excessive ADH production:
Head injuries
intracranial tumors
pulmonary infections
lung small cell carcinoma
hypothyroidism

203
Q

SIADH S/S

A

hyponatremia
very low urine output
skeletal muscle weakness
confusion/seizures

204
Q

SIADH Tx

A

fluid restriction
hypertonic saline infusion (3% NS)
Lasix

Slow correction of hypernatremia
required due to osmotic demyelination of the brain – permanent neurologic injury.

205
Q

Don’t correct serum sodium levels more than: ________________

A

9mEq/L in 24 hours ***

206
Q

describe the position and anatomy of the kidneys.

A

behind the peritoneum
right is lower than the left
held in place by the inferior mesenteric artery
renal artery enters at the hilum

207
Q

describe the location + innervation of the bladder.

A

retropubic space
PNS innervation from T11-L2 & S2- S4 segments

208
Q

Kidneys receive ____% cardiac output

A

25

209
Q

Plasma filtration rates =

A

125-140 mL/min

210
Q

The main functions of the renal system are:

A

waste filtration
endocrine/exocrine function
maintenance of physiologic homeostasis
tight control of Na+, K+, Hydrogen, Bicarb, glucose

211
Q

2 Major determinants of glomerular filtration pressure are:

A

glomerular capillary pressure
glomerular oncotic pressure

212
Q

Renal autoregulation of blood flow is controlled by:

A

Primarily local feedback signals that regulate glomerular arteriolar tone to protect glomeruli from excessive pressure

213
Q

determining factor for all our Na+ reabsorption =

A

Glomerular Filtration

214
Q

Glomerular Filtration is controlled how?

A

dependent on pressure, where MAP comes into play, low MAP will drop GFR and kidney blood supply
body tells kidney too little Na, stop urinary excretion of Na & if too much tells kidney to dump Na in urine

215
Q

reabsorbs 2/3rd of Na+ filtrate

A

proximal tubule

216
Q

ATP drives Na+ into__________ cells, and H2O passively follows

A

tubular

217
Q

describe the various urinalysis findings and what they mean.

A

Cloudy – has WBCs (infection/UTI)
Color-
dark amber (dehydrated)
Red (blood or rhabdomyolysis)
SG – renal concentration ability
decreased output pending renal failure

218
Q

maintaining adequate MAP during anesthesia will adequately perfuse the kidneys and maintain urine output if _____

A

pt is euvolemic.

219
Q

hyponatremia S/S

A

anorexia, nausea, vomiting, lethargy, seizures, dysrhythmias, coma, death

220
Q

TURP Syndrome =

A

hyponatremia caused by excessive ECF overload seen in hysteroscopies, TURP procedures.

221
Q

Hypo and Hypernatremia Na+ values

A

Na < 125 mmol/L
Na > 145 mmol/L

222
Q

hypernatremia S/S

A

result of dehydrating the brain: headache, confusion, seizures, coma, very low urine output

223
Q

Hypernatremia Tx

ypernatremia Tx

A

: IVF (iso/hypotonic) to restore Na to normal levels combined with Lasix, hemodialysis may be necessary if renal function disrupted.

224
Q

hypernatremia is the result of _________

A

H2O loss or Na gain

225
Q

_____ = most common cause of AKI (surgical cause)

A

ATN (tubular necrosis)

226
Q

AKI causes high blood levels of what?

A

causes high levels of creatine & urea in the blood

227
Q

prerenal AKI causes:

A

low MAP & hypoperfusion states

228
Q

AKI is seen in what pt pop?

A

seen in critically ill pt’s that have high morbidity rates

229
Q

what is the mortality rate for AKIs

A

up to 80% - a 20-30 min prolonged period of hypotension can precipitate an AKI.

230
Q

Prerenal Azotemia =

A

increased BUN from renal hypoperfusion or ischemia

231
Q

Intrinsic Acute Kidney Injury =

A

AKI due to ischemia, nephrotoxins, renal parenchymal diseases

232
Q

Post-renal AKI =

A

(Obstructive) some type of downstream obstruction in urinary flow has caused high back pressure into the kidney.

233
Q

Nephrotoxic drugs include:

A

Aminoglycosides
amphotericin B
cyclosporin A
ACE inhibitors increase risk of AKI
Loop diuretics linked to post-op kidney injury

234
Q

Nephrotoxins include:

A

Drugs
Aminoglycosides
amphotericin B
cyclosporin A
ACE inhibitors increase risk of AKI
Loop diuretics linked to post-op kidney injury
heavy metals
Contrast media (threat to renal perfusion)
NSAIDs (known nephrotoxins)
Antimicrobial & Chemotherapeutic agents – are cellular toxins

235
Q

what is ESRD?

A

End-Stage Renal Disease is a state of renal dysfunction that will become fatal without renal replacement therapy (dialysis or transplant)

236
Q

What is uremic syndrome?

A

an extreme form of renal failure in which GFR decreases below 10% of normal.
kidney can’t regulate volume & composition of ECF
excretion of waste products
pt has low K+ clearance and need continuous dialysis
high risk of life-threatening hyperkalemia, metabolic acidosis, CV complications from fluid overload, HTN, autonomic system hyperactivity, electrolyte disturbances

237
Q

Drugs that we give that are eliminate unchanged by the kidneys have a prolonged half-life due to this kidney failure:

A

NDMB’s
Anticholinesterase inhibitors
antibiotics
Digoxin

238
Q

Should you adjust the dose of opiods for renal failure pts? If so how?

A

Opioids- accumulate with repeated doses, decrease the dose amount
morphine will accumulate
Dilaudid will cause cognitive dysfunction
Codeine prolong narcosis
Fentanyl – best choice, small doses
Remifentanil – decrease elimination of the metabolite

239
Q

How should NMBs be given with renal failure?

A

Vecuronium – no infusion
Rocuronium – unpredictable duration
(Cis) & Atracurium: normal duration

240
Q

How does precedex change with renal failure?

A

incraesed sedative effects

241
Q

Which IV anesthetics are OK to use in renal failure?

A

Ketamine, Propofol, Etomidate are Ok with these pt’s

242
Q

How are benzos effected in renal failure?

A

Benzodiazepines – accumulate, prolonging their effects

243
Q

which diuretics are prone to metabolic acidosis?

A

Proximal Tubule Diuretics

244
Q

Mannitol-freely filtered by glomerulus but _______

A

poorly reabsorbed by renal tubules.

245
Q

Osmotic diuretics are the primary treatment for ______

A

increased ICP

246
Q

Loop diuretics

A

work at the Loop of Henle
Lasix, Bumex, Torsemide
inhibit electrochemical transporter to prevent NaCl reabsorption

247
Q

Diuretics site of action

A
248
Q

Nephrectomy can be ______

A

partial or total removal of the kidney
living donor
diseased kidney removal

249
Q

What is the position for nephrectomy? what are the potential risks?

A

: lateral decubitus with an extreme break in center of bed to allow more lateral exposure
VQ mismatch
axillary injury

250
Q

What are the surgical and anesthesia techniques for nephrectomies?

A

Anesthetic Technique: GETA
Surgical Tech:
Laparoscopic / robotic
open lateral or supine

251
Q

What additional monitors/access should be considered for nephrectomy?

A

Foley Cath necessary
Arterial line, if appropriate
2nd IV before positioning – necessary due to higher risk of bleeding

252
Q

How and why would a Cystectomy be performed?

A

Radical (malignancy): will remove other pelvic organs vs. simple (non-malignancy)
combined with urinary diversion procedures, using a section of the ileum to create a pouch for urine collection (ileal conduit) that drains to the stoma and exterior bag for urine collection.
Appendicitis – difficult to diagnose after this procedure and appendectomy is performed

253
Q

what are the intraop/postop considerations for cystectomy?

A

Intra Op: high-risk for bleeding and hypovolemia
PostOp: ICU admission is needed due bleeding from this procedure 500-3000 mL blood loss possible)

254
Q

What all is removed for a male or female undergoing a cystectomy?

A

Males: bladder, related pelvic structures, prostate, portion of urethra removed
Female: uterus, ovaries, tubes,vaginal vault, bladder removed

255
Q

Cystoscopy (Ureteroscopy)Procedure

A

Cystoscope entered into the urethra to visualize the bladder and kidney.
bladder cancer/TURPs
renal calculi
biopsies
assess urethral patency
Position: lithotomy
Anesthetic Technique: GETA or LMA/General, ERAS

256
Q

describe the blood loss typical for a cysto

A

Blood loss should be minimal for cystoscopy. If a TURP is performed, blood loss will occur, but the amount is very hard to quantify due to the mixture of irrigant and urine.

257
Q

what is the difference between a prostatectomy for a malignancy vs non-malignancy?

A

Non-Malignancy will get TURP
Malignancy – requires radical prostatectomy or robotic prostatectomy (500-1500 mL blood loss average)

258
Q

what are the considerations for a prostatectomy?

A

Intraop: similar to cystectomy and 2-large bore IV’s for blood loss
PostOp: radical patients may need ICU; TURP patients can be same-day outpatients or 23h obs.
Complications: sensory nerve injury and muscle weakness from operative procedure.
Steep Trendelenburg positioning complications.

259
Q

what are the concerns/considerations with TURP procedures?

A

done for resection of BPH
positioning concerns – older pt’s make sure padded and well positioned to prevent injury
Anticoagulant therapy: older pt’s may be on this, risk v. benefit of stopping the therapy – needs cardiac & medical clearance.
Neuraxial or General can be used
Hypothermia risk ( 1℃ / hr)
Bloodloss: 2-4 mL/min
Cold glycine/saline fluids used and pt in cold OR
TURP syndrome (Fluid overload)**

260
Q

S/S of acute hyponatremia

A
261
Q
A
262
Q
A
263
Q

classic presentation of Urolithiasis (Kidney stones) =

A

pale/ashen gray look, clammy, holding lower back, N/V
hematuria
not all stones are radiopaque

264
Q

How/where is a Percutaneous Nephrolithotomy performed?

A

performed with sedation in CT scan or IR

265
Q

ESWL –shock wave therapy: what is it? what anesthesia and position is used?

A

soundwave used to break-up stones
supine position
General LMA or ETT

266
Q

ESWL –shock wave therapy relative CI =

A

large calcified aortic/renal aneurysms
untreated UTI’s
Obstruction distal to calculi
Pacemaker, AICD, Neurostimulator
Morbid Obesity

267
Q

ESWL –shock wave therapy absolute CI =

A

Bleeding disorder/anticoagulation
Pregnancy

268
Q

____, _____, and _____ all inhibit cyclic-GMP phosphodiesterase type 5 (PDE 5) in vascular smooth muscle – causes penile arteriolar vasodilation in response to sexual stimulation.

A

Viagra, Cialis, Levitra

269
Q

impotence meds should be stopped with ______. Whats the exception?

A

should be stopped with NTG or nitroprusside use – extreme hypotension
exception: do not stop when used for pulmonary HTN or altitude sickness

270
Q

sudden onset of severe scrotal pain with no history of corresponding injury

A
271
Q

What occurs with Testicular Torsion? what are the anesthesia considerations?

A

spermatic cord twists the testicular, and venous outflow is obstructed with resultant testicular ischemia and infarction
Requires emergency surgical with RSI induction
Patients typically will not be NPO
Survival of the testicular is dependent on the time from onset of the symptoms

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