Renal & Endo Flashcards
function of feedback loops
maintain homeostasis
what connects 2 lobe of thyroid gland
isthmus
function of thyroid
Hormone that regulates cellular metabolism, growth, body system functions, & regulation of Calcium Levels
what does the thyroid store
thyroid hormone (sequesters circulation Iodine)
thyroidal secretion is mostly ____________
the prohormone T4
T3:T4 Ratio of secretion
1:10
80% of T3 deiodination of T4 by body tissues
elimination time of T3 and T4
T4 (7 days)
T3 (24-30 hours)
which is more potent: T3 or T4
T3 is 3-4 times more potent than T4
T3 and T4 protein binding
T3 & T4 are mostly protein bound.
Free & biologically active = T3 (0.3% of total T3)
Free & biologically active = T4 (0.03% of total T4)
functions of T3 and T4
- 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
thyroid function is regulated by… (3)
TSH
TRH
T3, T4 & circulating levels of Iodine
where is TSH produced
anterior pituitary gland
function of TSH (2)
- enhances/regulates iodine uptake
- T3/T4 production/secretion by thyroid gland
TRH location of production and function
produced in hypothalamus & promotes TSH secretion
High (or low) T3/T4 levels in the hypothalamus/anterior pituitary gland regulate ____________
secretion of TRH & TSH.
what do high iodine levels do to T3/T4 production
down-regulate T3/T4 production
how are T3/T4 produced?
Thyroid hormone is produced and activated by____________
Iodine in the Thyroid Gland
Dietary intake of Iodine is ____________
reduced to Iodide in the GI tract ➔ Iodide is absorbed by the thyroid gland
Iodide bounds with ____________ ➔ forms ____________ ➔ ____________ & ____________ couple with____________ to form T3 & T4
Iodide bounds with Tyrosine ➔ forms Iodotyrosine ➔ Monoidotyrosine & Diiodotyrosine couple with thyroperoxalase to form T3 & T4
T3 & T4 attach to ____________ and are stored in the gland as ____________
thyroglobulin and are stored in the gland as a colloid
T3 & T4 are released into circulation after ____________
proteolysis from colloid thyroglobulin
function on parathyroid glands
Secrete calcitonin in response to high Ca++ levels, which decrease levels of calcium & phosphorus
calcitonin inhibits: (2)
- Osteoclast activity
- Renal reabsorption of calcium and phosphorus
⭐️ ____________ is secondary to the inadvertent removal of all (4) parathyroids during thyroidectomy ⭐️
hypoparathyroidism
3 forms of plasma calcium
- 50% - Protein - bound calcium
- 45% - Ionized fraction (physiologically active & homeostatically regulated)
- 5% - non-ionized fraction bound with phosphate, bicarbonate, & citrate
normal calcium value
8.8-10.4 mg/dL
⭐️
what is calcium important for? (4)
- muscle contraction
- coagulation
- neurotransmitter release
- endocrine secretion
how does albumin affect Ca++ levels
Albumin binds (90%) protein-bound calcium
for every 1g/dL change in Albumin == 0.8 mg/dL in Ca++ level
what tightly controls Ca++ levels?
- Parathyroid hormone through a negative-feedback mechanism
- low Ca++ increases PTH to stimulate bone reabsorption/release of Ca++ and renal Ca++ reabsorption
what suppresses parathyroid hormone release?
high Ca++ levels
Protein binding of Ca++ affected by ____________ (2)
temperature and pH
how does acidosis affect Ca++(2)
- decreases protein binding of Ca++
- increases ionized Ca++ levels in the blood
how does alkalosis affect Ca++
- increases protein binding of Ca++
- decreases ionized Ca++ levels in the blood
when are s/s of hypocalcemia due to parathyroidectomy seen
Signs & Symptoms seen in (24-96h) post-op from acute parathyroid removal and the hypocalcemia that develops
⭐️
First signs of Hypocalcemic Tetany (2)
- laryngeal stridor
- laryngospasm
Serum Thyroxine (T4) Levels
- evaluates thyroid function
- 90% of hyperthyroid pt’s have elevated levels
- 85% of hypothyroid pt’s have low levels
Serum Triiodothyronine
- measures serum T3 levels
____________ is used to detect disease in pt’s with clinical S/S of hyperthyroidism
Serum Triiodothyronine
first test in evaluating suspected thyroid dysfunction is ____________
TSH Level
normal TSH range
0.4-0.5
Radioactive Iodine Uptake Test
- measures the amount of thyroid uptake of iodine & thyroid activity
- scan after p.o. ingestion and measure amount of thyroid activity
most common cause of hyperthyroidism
Grave’s Disease
patho of Grave’s disease
- Autoimmune multinodular (goiter) disease
- Thyroid Gland Hypertrophy
- Due to IgG antibodies attacking the TSH receptor
who is Grave’s disease associated with
- Commonly seen in females (20-40 yrs)
- Commonly seen with Myasthenia Gravis
other s/s Grave’s disease
exophthalmos (bulging eyes)
Thyroid Adenoma
- Autonomic functioning thyroid tissue that is not down-regulated by increased TSH
- (2nd most common cause)
thyroiditis
Inflammatory process after acute URI with flu-like symptoms and treated with NSAIDS
⭐️
Amiodarone
iodine rich drug that can produce thyrotoxicosis (hyperthyroid disease)
hyperthyroidism signs
treatment of hyperthyroidism
Radioactive Iodine Ablation
pharmacologic treatment of hyperthyroidism (3)
- 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
surgical resection for hyperthyroidism is indicated in… (3)
- thyroidectomy – large symptomatic goiter or refractory to pharmacologic
- thyroid cancer
- obstructive symptoms (airway compressed, deviated, or obstructed)
Primary goal of anesthesia mgmt during thyroid surgery
euthyroid (normal thyroid function tests) prior to surgery
anesthetic considerations/pharmacologic treatment in thyroid patient prior to surgery
- 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
intraop anesthetic considerations for thyroid patient (3)
- 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).
potential surgical complications and risks in thyroid patient (4)
- 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
intraop treatment for hypotension in thyroid patient
direct - acting vasoconstrictors (phenylephrine)
intraop treatment for tachycardia in thyroid patient
esmolol
frequently, thyroid patients are ____________ and ____________
hypovolemic & vasodilated (give slowly & titrate all IV meds)
Neuromonitoring during thyroid surgery
- 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
1 sided RLN injury
1 - sided voice hoarseness (vocal cord paralysis)
bilateral RLN injury
- vocal cords (reintubation is necessary)
- stridor
- aphonia
- respiratory distress from closed vocal cords
anesthetic mgmt for thyroid surgery
⭐️
what is thyroid storm
Life threatening, acute exacerbation of hyperthyroidism
when is thyroid storm most commonly seen?
undiagnosed or under-treated hyperthyroidism because of surgical stress or non-thyroid illness
what else can provoke thyroid storm?
Can be provoked by surgery on an acutely hyperthyroid gland
s/s thyroid storm
- hyperthermia
- tachycardia/dysrhythmias
- myocardial ischemia / CHF
- agitation
- confusion
- hypertension
differential diagnosis of thyroid storm (3)
- pheochromocytoma
- malignant hyperthermia
- light anesthesia
diagnosis for thyroid storm
T4 levels may be elevated, but no lab test is diagnostic for this, diagnosis of exclusion
treatment of thyroid storm
- 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
what to avoid in thyroid storm (2)
salicylates & Lasix – both can increase thyroid hormone levels
take home point of management of thyroid storm under anesthesia
If the patient is under anesthesia, we want to stop all of the hypermetabolic activity and manage the associated symptomology we are seeing.
mortality rate of thyroid storm
10-75%
when else can thyroid storm present
Can present 6-18 hours post-operatively as well!
patho of hypothyroidism
- 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
⭐️
most cases of hypothyroidism
primary hypothyroidism (95% of cases)
patho of primary hypothyroidism
decreased production of thyroid hormone despite normal levels of TSH
causes of primary hypothyroidism
- surgical resection
- Iodine (or I-131 tx) or amiodarone treatment
- Lithium use – blocks thyroid hormone synthesis & release
- Hashimoto disease – autoimmune thyroid gland destruction
secondary hypothyroidism causes
- 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
s/s hypothyroidism (8)
lethargy
slow mental functioning
cold intolerance/hypothermia
slow movements
depression
obesity
hyperlipidemia
reduced metabolic activity
treatment of hypothyroidism
Thyroid hormone replacement (levothyroxine)
t/f mild-moderate hypothyroid disease is safe for elective surgery
TRUE
⭐️
in severe hypothyroidism, patients need to be ____________ before surgery
✨euthyroid✨
hypothyroidism with CAD
increased risk of MI during euthyroid treatment due to increased HR and myocardial O2 demands
emergency surgery with severe hypothyroidism
aggressive treatment based on patient’s clinical status
goals for hypothyroid patient are to protect from…
- respiratory depression
- hypovolemia
- hypoglycemia
- hyponatremia
- hypothermia
hypothyroidism pre-op medications
Continue levothyroxine
has a ½ life of 5-7 days, but needs to be continued during the operative period
hypothyroid patients have a heightened sensitivity to ____________
respiratory depressant sedatives
GI changes with hypothyroidism
delayed gastric emptying
consider ____________ with delayed gastric emptying
- GI ultrasound scan, especially if they are on GLP-1 agonists
- H2 antagonists
- Reglan
- Rapid sequence induction
- non-particulate antacid
hypothyroidism intraop considerations
- 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
Hypothyroidism
Postop Care & Recovery
recovery may be delayed!
possibly prolonged PACU Stage 1
Pain mgmt for hypothyroidism
Toradol (NSAIDs) and peripheral neuraxial anesthesia are preferred!
If narcotics are used, use short acting like fentanyl, not dilaudid
Ensure your patient with Hypothyroidism is ___ prior to extubation.
normothermic
Assessing recovery of NMB in a hypothyroid patient
quantitative monitoring is best
TOF may be delayed recovery
ensure full muscle recovery/strength before extubation
Myxedema is an extreme form of
hypothyroidism
Diagnosed by very low-levels of T3/T4
Myxedema
Diagnosed by
very low-levels of T3/T4
T/F:
Myxedema is a surgical emergency.
False
Medical emergency
Only life-saving surgery should be performed
⭐️
A pt diagnosed with Myxedema can only go to surgery if…
its a life saving procedure
Only life-saving surgery should be performed
Myxedema Mortality = 25-50%.
What are the strong predictors of mortality?
- Low MAP
- Need for mechanical ventilation d/t hypoventilation
- Concurrent Sepsis
Myxedema
treatment agent
IV thyroid hormone replacement T4 (levothyroxine)
Diagnosed by very low-levels of T3/T4
Myxedema Signs & Symptoms
- 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)
Myxedema
Treatment, aside from primary agent
- ETT & MV
- CV support (inotropes, pressors, etc.)
- IV thyroid hormone
- Steroids (treat adrenal insufficiency)
- 0.9 NaCl IVF
- Glucose
- Gradually correct both: hypothermia & hypoNa
Myxedema
What happens if we treat hypothermia & hyponatremia too quickly?
hypothermia: CV collapse
hypoNa: central pontine demyelination
CAUTION: Treatment of myxedema is aggressive replacement of ___, which can cause ___.
thyroid hormone
MI
Hyperparathyroidism
As Calcium levels rise to __, EKG changes can progress to heart block
20 mg/dL
Primary Hyperparathyroidism causes ___calcemia
hyper
Hypoparathyroidism = Ca++ Levels < 8 mg/dL
Causes of Primary Hyperparathyroidism
- 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)
Hyperparathyroidism (Primary) in OB
(50%) maternal/fetal mortality
can cause spontaneous abortion
Hyperparathyroidism (Primary) symptoms are mainly caused by
hypercalcemia
Hyperparathyroidism (Primary)
Symptoms
- nephrolithiasis MOST common (60-70%)
- depression
- confusion, memory loss,
- hypertension
- Ekg changes, heart block (if Ca very high)
Hyperparathyroidism (Primary)
diagnosis
elevated serum Ca++ levels
T/F:
Secondary Hyperparathyroidism may result from ectopic production of PTH or analog-like substances from malignancies
False
primary
Hyperparathyroidism (Primary)
malignancies that can ectopicly produce PTH or analog-like substances
- lungs
- genitourinary
- breast
- GI
- lymphatic system
Tumors can produce hypercalcemia through …
direct bone reabsorption mechanisms
Secondary Hyperparathyroidism
Increase in parathyroid function d/t diseases that cause:
1. hypocalcemia
(↓ Vit. D metab, GI disorders interrupt absorption)
- hyperphosphatemia (ESRD)
due to decreased renal phosphate excretion
How is hypoCa r/t Secondary Hyperparathyroidism?
Low Ca ➡️ increased PTH secretion
(secondary increase in parathyroid activity)
Parathyroid Surgical Treatment - Preop
- Correction of intravascular volume & electrolyte disturbances
- Emergency treatment of hypercalcemia before surgery
Chronic hypercalcemia patients need:
* EKG / Cardiac clearance
* CNS evaluations
* Renal system evaluations
Parathyroid Surgery
Emergency treatment of hypercalcemia before surgery
- 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
Parathyroidectomy Anesthetic
GETA most common
TIVA remi/prop
NIMS ETT
T/F:
Parathyroidectomy is chosen over any other type of treatment modality for hyperparathyroidism because it is curative.
True
Which nerve are we monitoring with the NIMS tube during a Parathyroidectomy?
RLN
T/F:
The RLN is at greater risk of injury during a Thyroidectomy than a Parathyroidectomy.
False
equal risk
IV acess in Parathyroidectomy
must be 2nd free back-flowing IV for intraop Ca++ and PTH levels
serial draws typically 5 mins apart
Chvostek’s and Trousseau sign are seen with (hypo/hyper)calcemia
hypo
Chvostek Trousseau
Hypoparathyroidism is seen when Ca is below
8 mg/dL
Hypoparathyroidism
MOST common cause
+
other causes
surgical removal w Thyroidectomy
other causes: neck trauma, malignancy, granulomatous disease
Hypoparathyroidism
S/S
- neuronal irritability
- skeletal spasms, twitching, tetany, seizures
- Chvostek’s sign
- Trousseau sign
T/F:
Chvostek’s & Trousseau sign are valid tools to help diagnose Hyperparathyroidism.
FALSE
HyPOparathyroidism
↓ PTH = ↓Ca = Chvostek’s & Trousseau
Hypoparathyroidism (hypocalcemia)
symptoms
CV: CHF, hypoTN, insensitivity to β-Blockers, prolonged QT
fatigue
skeletal muscle cramps
depression
The hypocalcemic patient may be insensitive to this drug in our anesthesia omnicell
β-Blockers
Hypoparathyroidism
Treatment
electrolyte replacement before surgery
(hypocalcemia)
if Severe symptomatic: IV Ca gluconate then elemental Ca drip
Adrenal Cortex
Function is to secrete 3-types of hormones:
- Glucocorticoids (cortisol)
- Mineralocorticoids (aldosterone)
- Androgens
Abnormal functioning of the adrenal cortex could render the patient …
unable to respond appropriately during a period of stress, surgery, or illness
Where are 2 of the adrenal cortex hormones produced?
Glucocorticoids (cortisol): inner portion of the adrenal cortex
Mineralocorticoids (aldosterone): adrenal gland
Cortisol
fxn
- immediate effects on the metabolism of carbohydrates, proteins, and fatty acids.
- immune and circulatory functions
Cortisol is the most “potent” ___
glucocorticoid
Cortisol excretion
inactivated by the liver and excreted in the urine
Aldosterone
major function
regulate ECF volume and potassium homeostasis through the reabsorption of Na+ and secretion of K+ by tissues
Androgens
fxn
sex organ development and changes that manifest during puberty
Cushing’s Syndrome
causes
- overproduction of cortisol by the adrenal cortex
- overdosing of exogenous glucocorticoid
- neoplasm
Cushing’s Syndrome
Symptoms
- truncal obesity, hyperglycemia, abdominal striae
- HTN, intravascular volume increase
- decreased K+
- fatiguability, muscle weakness
- osteoporosis
Cushing’s Syndrome
Management
- Preop: treat diabetes, fluid mgmt, HTN, electrolytes
- Spironolactone diuresis – mobilizes excess fluid
- if bilateral adrenalectomy, need glucocorticoid replacement
⭐️
Cushing’s Syndrome
doesnt have a specific anesthesia plan but….
SEVERE Cushing’s can be temporized w/ Etomidate
it will inhibit steroid synthesis (adrenal suppression)
Adrenal Problems
Mineralocorticoid Excess
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
Addison’s Disease
undersecretion of adrenal steroid hormones (decrease of ACTH)
Addison’s Disease is not apparent until
90% adrenal cortex has been destroyed
Addison’s Disease
causes
(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
Addison’s Disease
S/S
weight loss, N/V, diarrhea, chronic fatigue, hypotension
Addison’s Disease
Acute crisis
- abdominal pain
- severe vomiting, diarrhea
- low BP, decreased LOC, shock symptoms
- severe hyperkalemia (life-threatening arrhythmias)
doA of:
decadron
prednisone
hydrocortisone
decadron = long
prednisone = short
hydrocortisone = short
HTN and hypokalemia can be controlled by
Na+ intake restriction
the adrenal ____ synthesizes catecholamines
medulla
⭐️
The adrenal medulla produces epi and norepi in what %
80% - epinephrine
20% - norepinephrine
⭐️
Catecholamines are derived from
Tyrosine
⭐️
Pheochromocytoma
Rare but interesting disease
tumors that arise in the chromaffin cells of the adrenal medulla
secrete epinephrine & norepinephrine
Paragangliomas
extra-adrenal pheochromocytomas
pheochromocytomas= chromaffin cells of the adrenal medulla
Most Pheochromocytomas (75%) follow which pattern?
solidary and found in the right adrenal gland
Pheochromocytomas are usually optimized by the time we see them in the OR, so why do we care?
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.
T/F:
Unreated Pheochromocytoma will kill you.
True
Pheochromocytoma
Diagnosis
excess catecholamine or metabolite level
Pheochromocytoma
S/S
- headache
- HTN
- hyperglycemia
- catecholamine-induced cardiomyopathy
- palpitations, tremors, sweating, anxiety
Pheochromocytoma⭐️
Paroxysmal catecholamine release
- stimulation, laryngoscopy, tumor manipulation, abdomen insufflation
- Tyramine foods (aged cheeses, cured meats)
- TCA’s and metoclopramide (Reglan)
- Micturition – when there is a bladder tumor
Pheochromocytoma can masquerade as
malignant hyperthermia
⭐️
Pheochromocytoma
excision mortality decreased from 50% to 0-3% with the preop use of:
A-antagonism (must be blocked first)
β-antagonism (used in pt’s with dysrhythmias/tachycardias) – blocked 2nd
Pheochromocytoma
⍺-antagonism
-fxn
-agents
(must be blocked first)
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
Pheochromocytoma
β-antagonism
-fxn
-agents
used in pt’s with dysrhythmias/tachycardias
(blocked 2nd)
Propanolol, atenolol, metoprolol
⭐️
How to time alpha and beat blockade in Pheochromocytoma?
Why is it important?
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
Pheochromocytoma
____ mandatory started prior to induction
Arterial BP
- Pheochromocytoma
- Intraop monitoring
- 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
Pheochromocytoma
To achieve adequate anesthesia depth before laryngoscopy, use
- 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!!)
Pheochromocytoma
Excision can be performed via:
laparoscopic (robotic)
open procedure
⭐️
T/F:
Manipulation of the Pheochromocytoma, despite ⍺- & β-blockade will still release catecholamines.
True
expect it and you will be prepared, wild BP and HR changes
Pheochromocytoma
post-tumor excision
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.
Diabetic & Pre-Diabetic
fasting glucose & HbA1c
Diabetic: fasting glucose levels > 126 mg/dL (HbA1c ≥ 6.5%)
Pre-Diabetic: fasting glucose 100-125 mg/dL (HbA1c ≥ 5.7-6.4%)
DM Types
Type 1 DM
Type 2 DM
Gestational DM
Diabetes due to other causes
Diabetes – Type 1 DM
- 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
Type 1 DM
aossicated disease processes/risks
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
Type II DM
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
Anesthetic Management in DM
Determine end-organ damage by examining full H&P:
EKG
BP
Serum BUN, Cr, Blood sugar
Anesthetic Management in DM
End-organ complications
- 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
HHNC is a BG level of > ______
600
T/F HHNC patients experience ketoacidosis
FALSE
What precipitates HHNC? How should you treat it? Why?
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***
clinical manifestations of DKA include:
ketonemia, hyperglycemia, & acidemia
Blood glucose level: 250-500 mg/dL range
ALWAYS dehydrated due to hyperglycemic osmotic diuresis, nausea, vomiting.
DKA Tx
fluids, insulin, and electrolyte replacement
What is the Whipple triad? What is it a/w?
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
pituitary location =
located in the base of the brain in Sella Turcica
The pituitary and hypothalamus together form the master control over _____________
the release of all the body’s hormones
hyposecretion of the anterior pituitary is treated with ______ and ______
hormone replacement therapy and stress doses of corticosteroids.
what causes Anterior Pituitary (hyposecretion)?
caused by decrease in ACTH secretion
Anterior Pituitary (hypersecretion) is caused by? what does it produce?
caused by adenoma secondary to Cushing’s
secondary due to increase in ACTH
giantism or acromegaly due to excess growth hormone
secretes vasopressin (antidiuretic hormone ADH) – ECF balance and oxytocin (uterine contractions & breast milk secretion)
Posterior Pituitary
inadequate secretion of ADH or,
renal tubular resistance to ADH (nephrogenic)
DI
DI S/S
polydipsia
hypernatremia **
high output of poorly concentrated urine
hypovolemia **
DI Causes:
destruction of the pituitary gland by trauma (head, subarachnoid hemorrhage, brain death) or surgical injury
DI Tx
Depends on hormone deficiency
DDAVP or vasopressin infusion
Isotonic crystalloid
frequent Na+ serum level measurements
What causes SIADH?
Caused by excessive ADH production:
Head injuries
intracranial tumors
pulmonary infections
lung small cell carcinoma
hypothyroidism
SIADH S/S
hyponatremia
very low urine output
skeletal muscle weakness
confusion/seizures
SIADH Tx
fluid restriction
hypertonic saline infusion (3% NS)
Lasix
Slow correction of hypernatremia
required due to osmotic demyelination of the brain – permanent neurologic injury.
Don’t correct serum sodium levels more than: ________________
9mEq/L in 24 hours ***
describe the position and anatomy of the kidneys.
behind the peritoneum
right is lower than the left
held in place by the inferior mesenteric artery
renal artery enters at the hilum
describe the location + innervation of the bladder.
retropubic space
PNS innervation from T11-L2 & S2- S4 segments
Kidneys receive ____% cardiac output
25
Plasma filtration rates =
125-140 mL/min
The main functions of the renal system are:
waste filtration
endocrine/exocrine function
maintenance of physiologic homeostasis
tight control of Na+, K+, Hydrogen, Bicarb, glucose
2 Major determinants of glomerular filtration pressure are:
glomerular capillary pressure
glomerular oncotic pressure
Renal autoregulation of blood flow is controlled by:
Primarily local feedback signals that regulate glomerular arteriolar tone to protect glomeruli from excessive pressure
determining factor for all our Na+ reabsorption =
Glomerular Filtration
Glomerular Filtration is controlled how?
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
reabsorbs 2/3rd of Na+ filtrate
proximal tubule
ATP drives Na+ into__________ cells, and H2O passively follows
tubular
describe the various urinalysis findings and what they mean.
Cloudy – has WBCs (infection/UTI)
Color-
dark amber (dehydrated)
Red (blood or rhabdomyolysis)
SG – renal concentration ability
decreased output pending renal failure
maintaining adequate MAP during anesthesia will adequately perfuse the kidneys and maintain urine output if _____
pt is euvolemic.
hyponatremia S/S
anorexia, nausea, vomiting, lethargy, seizures, dysrhythmias, coma, death
TURP Syndrome =
hyponatremia caused by excessive ECF overload seen in hysteroscopies, TURP procedures.
Hypo and Hypernatremia Na+ values
Na < 125 mmol/L
Na > 145 mmol/L
hypernatremia S/S
result of dehydrating the brain: headache, confusion, seizures, coma, very low urine output
Hypernatremia Tx
ypernatremia Tx
: IVF (iso/hypotonic) to restore Na to normal levels combined with Lasix, hemodialysis may be necessary if renal function disrupted.
hypernatremia is the result of _________
H2O loss or Na gain
_____ = most common cause of AKI (surgical cause)
ATN (tubular necrosis)
AKI causes high blood levels of what?
causes high levels of creatine & urea in the blood
prerenal AKI causes:
low MAP & hypoperfusion states
AKI is seen in what pt pop?
seen in critically ill pt’s that have high morbidity rates
what is the mortality rate for AKIs
up to 80% - a 20-30 min prolonged period of hypotension can precipitate an AKI.
Prerenal Azotemia =
increased BUN from renal hypoperfusion or ischemia
Intrinsic Acute Kidney Injury =
AKI due to ischemia, nephrotoxins, renal parenchymal diseases
Post-renal AKI =
(Obstructive) some type of downstream obstruction in urinary flow has caused high back pressure into the kidney.
Nephrotoxic drugs include:
Aminoglycosides
amphotericin B
cyclosporin A
ACE inhibitors increase risk of AKI
Loop diuretics linked to post-op kidney injury
Nephrotoxins include:
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
what is ESRD?
End-Stage Renal Disease is a state of renal dysfunction that will become fatal without renal replacement therapy (dialysis or transplant)
What is uremic syndrome?
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
Drugs that we give that are eliminate unchanged by the kidneys have a prolonged half-life due to this kidney failure:
NDMB’s
Anticholinesterase inhibitors
antibiotics
Digoxin
Should you adjust the dose of opiods for renal failure pts? If so how?
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
How should NMBs be given with renal failure?
Vecuronium – no infusion
Rocuronium – unpredictable duration
(Cis) & Atracurium: normal duration
How does precedex change with renal failure?
incraesed sedative effects
Which IV anesthetics are OK to use in renal failure?
Ketamine, Propofol, Etomidate are Ok with these pt’s
How are benzos effected in renal failure?
Benzodiazepines – accumulate, prolonging their effects
which diuretics are prone to metabolic acidosis?
Proximal Tubule Diuretics
Mannitol-freely filtered by glomerulus but _______
poorly reabsorbed by renal tubules.
Osmotic diuretics are the primary treatment for ______
increased ICP
Loop diuretics
work at the Loop of Henle
Lasix, Bumex, Torsemide
inhibit electrochemical transporter to prevent NaCl reabsorption
Diuretics site of action
Nephrectomy can be ______
partial or total removal of the kidney
living donor
diseased kidney removal
What is the position for nephrectomy? what are the potential risks?
: lateral decubitus with an extreme break in center of bed to allow more lateral exposure
VQ mismatch
axillary injury
What are the surgical and anesthesia techniques for nephrectomies?
Anesthetic Technique: GETA
Surgical Tech:
Laparoscopic / robotic
open lateral or supine
What additional monitors/access should be considered for nephrectomy?
Foley Cath necessary
Arterial line, if appropriate
2nd IV before positioning – necessary due to higher risk of bleeding
How and why would a Cystectomy be performed?
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
what are the intraop/postop considerations for cystectomy?
Intra Op: high-risk for bleeding and hypovolemia
PostOp: ICU admission is needed due bleeding from this procedure 500-3000 mL blood loss possible)
What all is removed for a male or female undergoing a cystectomy?
Males: bladder, related pelvic structures, prostate, portion of urethra removed
Female: uterus, ovaries, tubes,vaginal vault, bladder removed
Cystoscopy (Ureteroscopy)Procedure
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
describe the blood loss typical for a cysto
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.
what is the difference between a prostatectomy for a malignancy vs non-malignancy?
Non-Malignancy will get TURP
Malignancy – requires radical prostatectomy or robotic prostatectomy (500-1500 mL blood loss average)
what are the considerations for a prostatectomy?
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.
what are the concerns/considerations with TURP procedures?
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)**
S/S of acute hyponatremia
classic presentation of Urolithiasis (Kidney stones) =
pale/ashen gray look, clammy, holding lower back, N/V
hematuria
not all stones are radiopaque
How/where is a Percutaneous Nephrolithotomy performed?
performed with sedation in CT scan or IR
ESWL –shock wave therapy: what is it? what anesthesia and position is used?
soundwave used to break-up stones
supine position
General LMA or ETT
ESWL –shock wave therapy relative CI =
large calcified aortic/renal aneurysms
untreated UTI’s
Obstruction distal to calculi
Pacemaker, AICD, Neurostimulator
Morbid Obesity
ESWL –shock wave therapy absolute CI =
Bleeding disorder/anticoagulation
Pregnancy
____, _____, and _____ all inhibit cyclic-GMP phosphodiesterase type 5 (PDE 5) in vascular smooth muscle – causes penile arteriolar vasodilation in response to sexual stimulation.
Viagra, Cialis, Levitra
impotence meds should be stopped with ______. Whats the exception?
should be stopped with NTG or nitroprusside use – extreme hypotension
exception: do not stop when used for pulmonary HTN or altitude sickness
sudden onset of severe scrotal pain with no history of corresponding injury
What occurs with Testicular Torsion? what are the anesthesia considerations?
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
