Proteins and polypeptides

Steroids

Derivatives of the Amino Acid Tyrosine

Adrenal Medulla, (80%)

In the abdomen

associated with sympathetic ganglia.

The organ of Zuckerkandl-- (These are small masses of chromaffin cells found near sympathetic ganglia along the abdominal aorta.) and is the most common extra-adrenal site.

-Involve both adrenal glands in 10% of pts

- Approx 10% of tumors arise from extraadrenal

     Chromaffin cells

- Approx. 10% of tumors effect children

-  malignant spread of pheochromocytomoa happens in less than 10% of cases.

Fill in the blanks:

Malignant pheochromocytomas are more often ____________ and secrete _______________

exclusively.

Extraadrenal

Norepinephrine

Headache,

Diaphoresis,

Tachycardia

Other symptoms: HTN (duh), tremors, and cardiac palpitations.

-Surgical Manipulation

- Medications

- urination and defication in some pts. (dependent on tumor location)

-poking it with a stick

True or false:

Psychological Stress can exacerbate pheochromocytoma release of catecholamines

The increase in catecholamines:

- increases cardiac output

- heart rate

- inc. myocardial oxygen consumption

- Coronary artery spasms.

-inc. heart work can result in myocardial ischemia, infarction or CHF even w/o CAD

Much like hyperthyroidism,

the increased metabolism and oxygen consumption

can cause this:

In pheochromocytoma,

the release of catecholamines causes peripheral vasoconstiction.  What can happen as a result of this?

Use a-methyl tyrosine- an agent that inhibits the enzyme tyrosine hydroxylase (the rate limiting step in catecholamine biosynthesis)

This is used in combination with alpha-adrenergic blocking agents.

This produces a "significant" reduction in catecholamine biosynthesis.

-Use of alpha blockers (primarily phenoxybenzmine)

-Use of fluids

How long does a pt. with pheochromocytoma have to be pretreated with alpha blockade?

How do we know if pretreatment is successful?

7-60 days. 

Pretreatment is deemed successful when:

- no inhospital BP > 160/90 24 hr prior to surgery

- No orthostatic hypotension <80/ 45 upon standing

- no new ST segment or t-wave abnormality on ECG

-No marked symptoms of catecholamine release

-  PVC rate of less than 1 per 5 minutes

True or false:

It's important to give Beta Blockers prior to Alpha blockers when pretreating pts for pheochromocytoma surgical intervention.

False.

B-Blockers can be used as adjuncts, however, Administration of Beta Blockers prior to Alpha blockers may cause unopposed alpha stimulation and hypertensive exacerbation.   Blockage of Beta receptor mediated vasodilation in skeletal muscle is the causative factor.

- nitroprusside

-Nitroglycerin

- fenaldopam

- phentalomine

-morphine

-atracurium

-atropine

-pancuronium

-succinylcholine

-droperidol

-reglan

-ephedrine

-Halothane

Ligation of the venous drainage of the tumor.

Catecholamines stop getting pumped into the bloodstream, and the real fun begins.

Pheochromocytoma:

Most common cause of death and most dangerous complication postop?

Hypotension

d/t

1) Low catecholamines

2) Third spacing of fluid

3) residual effects of alpha blockade/ and or a-methyltyrosine (may last up to 36 hours)

After removal of pheochromocytoma,

When do catecholamines return to normal levels?

Postoperatively in pheochromocytoma,

Why can hypoglycemia occur?

23. How is the larynx innervated?

By the recurrent laryngeal nerve. The internal branch of the superior laryngeal nerve. The external branch of the superior laryngeal nerve. All are derived from the vagus nerve!

24. Describe the motor innervation of the larynx.

The external branch of the superior laryngeal nerve supplies the circothyroid muscle. The recurrent laryngeal nerve supplies the rest!

25. Describe the sensory innervation of the larynx.

The internal branch of the superior laryngeal nerve is the major sensory nerve of the larynx supplying laryngeal tissue from the vocal cords up.

The recurrent laryngeal nerve supplies the sensory innervation to the mucosa inferior to the vocal cords.

26. What happens when you have damage to the external branch of the superior laryngeal nerve?

Unilateral right recurrent laryngeal nerve damage?

Bilateral recurrent laryngeal nerve damage?

Damage to the external branch of the superior laryngeal nerve:

This produces weakness and huskiness of the voice. The cricothyroid muscle cannot produce tension or the cricothyroid muscle is paralyzed.

Unilateral right recurrent laryngeal nerve damage is common after a thyroidectomy. This is characterized by hoarseness and a paralyzed cord that assumes an intermediate position.

Bilateral recurrent laryngeal nerve damage results in airway obstruction and aphonia. This causes the cords program flop together during inspiration. Intubation is required.

27. What is the function and innervation of the following muscle: posterior cricoarytenoid

function:

28. What is the function and innervation of the following muscle: lateral cricoarytenoid

function:

29. What is the function and innervation of the following muscle: transverse arytenoid

function:

30. What is the function and innervation of the following muscle: oblique arytenoid

function:

31.What is the function and innervation of the following muscle: aryepiglottic

Function:

32. What is the function and innervation of the following muscle: vocalis

Function:

33. What is the function and innervation of the following muscle: thyroarytenoid

Function:

34. What is the function and innervation of the following muscle: cricothyroid

function:

True or False:

Oxytocin and Antidiuretic hormone are made in the posterior pituitary.

Nay my intrepid Endocrine explorer.  The posterior pituitary is merely a storage vessel  Such hormones are produced in the hypothalamus. 

ADH= primarily made in supraoptic nuclei of hypothalamus

Oxytocin= paraventricular nuclei of hypothalamus\

However, each of these nuclei can synthesize small amount of the second hormone.

Maternal water intoxication

Uterine Tetany (therefore fetal distress d/t hyperstimulation)

Transient hypotension d/t relaxation of vascular smooth muscle

reflex tachycardia

I am an osmoreceptor. 

I make my decision based on osmolarity of the blood.

1) Stretch receptors in the atria:

These receptors are excited by overfilling- therefore when underfilled= unexcited.  Lack of excitement results in profound release of ADH. 

(Dude I'm bored..... Let's call ADH and see what he is up to.  Alright- but he always makes my blood pressure go up....)

2) Decrease stretch receptor stimulation of baroreceptors

Where are the baroreceptors located? 

What are the Afferent and Efferent limbs of each?

Baroreceptors are located in the carotid and aortic bodies.

Carotid baroreceptors: 

Afferent: Via Herring's nerve to tractus solitarius of the medulla

Efferent: from medulla excitation of parasympathetic vagal centers

Aortic baroreceptors:

Afferent: via vagus nerve to tractus solitarius of the medulla

Efferent: from medulla excite vagal parasympathetic center.

What is Diabetes insipidus and what are the 2 types?

Diabetes insipidus is the absence of vasopressin due to:

1) Destruction of post. pituitary (neurogenic DI)

2) Failure of the renal tubes to respond to ADH (nephrogenic)

1) Polydipsia

2) increased serum osmolarity

3) Decreased urine osmolarity

4) High urine output

1) General Anesthesia

2) tumors

3) hypothyroidsim

4) porphyria

5) small cell lung carcinomas

1) decreased serum osmolarity

2) Hyponatremia

3) Increased urine osmolarity

4) symptoms assoc. with hyponatremia.

At what sodium levels (hyponatremic) do pts develop EKG changes?

Seizures?

Coma? 

Death?

EKG changes approx: 115 meq/l

Seizures/Coma:  approx 110 meq/l

DEATH!!!!!:  102 meq/l