2011 Endocrine Jamie 1

Front 1

9 important endocrine glands:

Back 1

1. Pituitary
2. Thyroid
3. Parathyroid
4. Thymus
5. Adrenal
6. Pancreas
7. Testes
8. Ovaries
9. Placenta

Front 2

Anterior Pituatary Hormones (6 major)

Back 2

Anterior Pituatary Hormones (6 major)
1. Growth: causes growth of almost all cells and tissues
2. Adrenocorticotropin:
a. causes adrenal cortex to secrete adrenocortical hormones
b. Cortisol, Aldosterone
3. Thyroid Stimulating:
a. causes thyroid gland to secrete thyroid hormones
b. triiodothyronine (T3) & Thyroxine (T4)
4. Follicle Stimulating:
a. causes growth of follicles in ovaries prior to ovulation
b. formation of sperm in testes
5. Luteinizing:
a. important role in ovulation
b. causes secretion of female sex hormones by ovaries
c. testosterone from the testes
6. Prolactin:
a. Promotes development of the breasts
b. Secretion of mild during lactation

Front 3

Adrenocorticotropin: causes

Back 3

a. causes adrenal cortex to secrete adrenocortical hormones
b. Cortisol, Aldosterone

Front 4

Thyroid Stimulating: causes

Back 4

a. causes thyroid gland to secrete thyroid hormones
b. triiodothyronine (T3) & Thyroxine (T4)

Front 5

Follicle Stimulating: 2x

Back 5

causes growth of follicles in ovaries prior to ovulation

formation of sperm in testes

Front 6

Luteinizing:

Back 6

important role in ovulation

causes secretion of female sex hormones by ovaries

testosterone from the testes

Front 7

Prolactin:

Back 7

Promotes development of the breasts
Secretion of mild during lactation

Front 8

Posterior Pituitary Hormones (2)

Back 8

1. ADH (Vasopressin)

2. Oxytocin

Front 9

Adrenal Gland Hormones

2 ADRENAL CORTEX

Back 9

1. Cortisol

2. Aldosterone

Front 10

ADRENAL MEDULLA

2

Back 10

Catecholamine hormones

a. Adrenaline (Epinephrine)
b. Noradrenaline (Norepinephrine)

Front 11

Placenta
4 hormones

Back 11

1. Human Chorionic Gonatropin (HCG
2. Estrogen
3. Progesterone
4. Human Somatomammotropin

Front 12

Human Chorionic Gonatropin (HCG)

2x

Back 12

Promotes growth of corpus luteum


Promotes secretion of estrogen & progesterone by corpus luteum

Front 13

Estrogen

Back 13

Promotes growth of mothers sex organs

Promotes growth of fetal tissues

Front 14

Progesterone

3x

Back 14

a. Development of uterine endometrium in advance of implantation of fertilized ovum
b. Renal tissue & organ development
c. Development of secretory apparatus of mothers breasts

Front 15

Human Somatomammotropin
2x

Back 15

Promotes growth of some fetal tissues

Aides in development of mothers breasts

Front 16

General hormones 4

Back 16

Epinephrine
Norepinephrine
Growth Hormone
Thyroid Hormone

Front 17

Local hormones: only have specific local effect

3

Back 17

ACTH (Adrenal gland)

TSH (Thyroid gland)

Luteinizing Hormone (Ovaries & Testes)

Front 18

Steroid Hormones: Chemical structure

Back 18

based on steroid nucleus similar to cholesterol

Front 19

Steroid Hormones:
released by 3 areas

Back 19

adrenal cortex, ovaries, and testes

Front 20

5 Steroid Hormones:

Back 20

Cortisol, Aldosterone, Estrogen, Progesterone, Testosterone

Front 21

Steroid Hormones

• Storage

Back 21

: compartmentalized in small amounts inside glandular cells, larger amts in precursor molecules

Front 22

Steroid Hormones: • MOA:

Back 22

Intracellular- small w/ high lipid solubility so penetrate membrane easily entering cytoplasm & binds with DNA effectively amplifying or suppressing action of hormone

Front 23

Steroid Hormones:

secreted, travel in

Back 23

bloodstream bound to transport proteins (like thyroid hormones), this protects them from metabolism or secretion so half-life longer

Front 24

Peptide or Protein Hormones

Back 24

peptides amino acid chains, proteins large chains of hundreds of amino acids

Front 25

Peptide or Protein Hormones:
• Formed in

Back 25

in the glandular cells

Front 26

Peptide or Protein Hormones:

10

where each is from

Back 26

o Anterior Pituitary: growth, ACTH, FSH, Luteinizing, Prolactin (large polypeptides)
o Posterior Pituitary: ADH, Oxytocin (peptides)
o Insulin, Glucagon, Parathyroid hormone (large polypeptides)

Front 27

Peptide or Protein Hormones: Storage:

Back 27

: active hormone stored in cytoplasmic compartment of endocrine cell

Front 28

Peptide or Protein Hormones
• MOA:

4x

Back 28

o Binds to membrane receptor then 2nd messenger (cAMP) permeates the membrane
o 2nd messenger permeates cell membrane & binds w/receptor intracellular (enzyme stimulation)
o May also act by changing membrane permeability (receptors on postsynaptic membrane) causing ion channels to open or close (Na⁺, K⁺, Ca⁺⁺) which causes subsequent effects on postsynaptic cells
o Acts rapid: seconds to minutes

Front 29

Amine Hormones:

derived from

Back 29

amino acid tyrosine & tryptophan

Front 30

Amine Hormones:

Formed by

Back 30

by actions of enzymes in cytoplasmic compartment of glandular cells until released

Front 31

Amine Hormones:

Secreted by:2x

Back 31

o Adrenal medulla:

o Thyroid:

Front 32

Adrenal medulla:

Epinephrine & Norepinephrine

storage and action

Back 32

 Absorbed in preformed vesicles until signal for release
Duration of action no more than 1-3 minutes

Destroyed rapidly by local tissue enzymes or absorbed into cells

Front 33

Thyroid: Triidothyronine (T3) & Thyroxin (T4)

Stored in

Back 33

large follicles in thyroid until release

Front 34

Amine Hormones

moa

Back 34

Binds to membrane receptor then 2nd messenger permeates the membrane

2nd messenger permeates cell membrane & binds w/receptor intracellular (enzyme stimulation)

Front 35

Feedback control:

Back 35

mechanism for regulation of hormone concentration in the bloodstream

• Hormone concentrations ↑, further production of that hormone inhibited
• Hormone concentrations ↓, further production of that hormone increases

Front 36

Negative feedback:

Back 36

• Endocrine gland has tendency to over-secrete its hormone
• When too much function occurs, that function feeds back to the gland to ↓ its secretory rate

Front 37

Hormone receptors & their activation:

Back 37

: hormones usually combine w/ hormone receptors on surface or inside the cell, this initiates cascade of reactions in cell that progressively get more powerful

Front 38

Receptor locations:3x

Back 38

In or on surface of cell membrane:

In the cell cytoplasm:

In the cell nucleus:

Front 39

Receptor locations:
In or on surface of cell membrane:

Back 39

specific to protein, peptide, & catecholamines, needs 2nd messengers

Front 40

Receptor locations:
In the cell cytoplasm:

2x

Back 40

intracellular, steroid hormones

Front 41

Receptor locations:
In the cell nucleus:

Back 41

metabolic thyroid hormones (T4 & T3)

Front 42

Regulation of Receptors:

Down Regulation:

Back 42

binding of a hormone w/ its target cell receptor usually causes the number of active receptors to ↓

• Inactivation of receptor molecules
• Decreased production of molecules

Front 43

Regulation of Receptors:

Up Regulation:

Back 43

: Hormones induce the formation (↑) of more receptor molecules than normal
Target tissue becomes progressively more sensitive to stimulation effects of hormone (amplified)

Front 44

Assessing Endocrine function:?

Back 44

Radioimmunoassay: measures concentrations of endocrine hormones, highly sensitive & specific

Front 45

ENDOCRINE DISEASE:

2x

Back 45

• characterized by overproduction or underproduction of single or multiple hormones


• alterations in the physiologic responses to stress or changes in hemeostatic mechanisms reflect the impact of excessive or deficient amounts of these hormones

Front 46

PITUITARY GLAND

controlled by

Back 46

HYPOTHALAMUS

Front 47

Inhibiting & releasing hormones secreted in hypothalamus & transported to ant pituitary via

Back 47

the hypophysial portal vessels (housed in pituitary stock)

Front 48

PITUITARY GLAND

size

Back 48

1/2 inch in diameter

1 gram weight

Front 49

PITUITARY GLAND

connected to

Back 49

-at base of brain in sella turcica & connected to hypothalamus by pituitary stalk, outside of BBB

Front 50

Nearby Structures: to pituitary gland 7

Back 50

• Optic chiasma
• Cavernous sinuses
o Oculomotor (3rd)
o Trochlear (4th)
o Trigeminal (5th)
o Abducens (6th)
o Internal carotid arteries

Front 51

Pituitary has 2 portions

separated by

Back 51

Anterior pituitary & posterior pituitary
(Two portions separated by pars intermedia which is highly vascular)

Front 52

Anterior pituitary (adenohypophysis):
• Originates from

Back 52

Rathke’s pouch (an embryonic invagination of the pharyngeal epithelium)

Front 53

Anterior pituitary (adenohypophysis):

6 hormones

Back 53

GH, ACTH, TSH, FSH, LH, Prolactin

Front 54

GH
Principle site of action

Principle processes affected

Back 54

All cells of body

Growth of bones, muscles, organs, lipid & carbohydrate metabolism

Front 55

ACTH

Principle site of action

Principle processes affected

Back 55

Adrenal Cortex

Growth & secretory activity of adrenal cortex, Cortisol & Aldosterone

Front 56

TSH

Principle site of action

Principle processes affected

Back 56

Thyroid

Growth & secretory activity of thyroid gland (T3 & T4)

Front 57

FSH

Principle site of action

Principle processes affected

Back 57

Ovaries & Testes

Ovaries: development of follicles, secretion of estrogen
Testes: Development of sperm

Front 58

LH

Principle site of action

Principle processes affected

Back 58

Ovaries & Testes

Ovaries: ovulation, form corpus luteum, secrete progesterone
Testes: Secretion of testosterone

Front 59

Prolactin

Principle site of action

Principle processes affected

Back 59

Mammary glands, Ovaries

Secretion of milk, maintenance of corpus luteum

Front 60

Posterior pituitary (neurohypophysis):
Outgrowth of

Back 60

of the hypothalamus

Front 61

Posterior pituitary (neurohypophysis):

Linked to hypothalamus by

Back 61

nerve fibers (communicates via nerve fibers)

Front 62

ADH (Vasopressin)-

formed in

Back 62

hypothalamus in supraoptic nuclei

Front 63

ADH (Vasopressin)-

secreted in response to

Back 63

↑ in osmolarity (Na⁺ ion concentration) or ↓ in blood volume or pressure

Front 64

ADH (Vasopressin)-

acts on

Back 64

collecting ducts to ↑ H2O absorption from tubules

Front 65

w/o ADH, tubules

Back 65

tubules are impermeable to water & water loss is excessive, dehydration is provoked

Front 66

ADH (Vasopressin)-

high levels cause

Back 66

systemic vasoconstriction

Front 67

ADH (Vasopressin)-

promotes homeostasis by 2x

Back 67

↑ von Willenbrand factor & factor VIII

Front 68

Oxytocin

formed in

Back 68

hypothalamus in paraventricular nuclei

Front 69

most common type of pituitary tumor

Back 69

Adenomas:

Front 70

Adenomas: most commonly seen

Back 70

seen in middle aged women

Front 71

3 Tumor Classifications: based on hormone secreted from the tumor

Back 71

1. Functioning: secreting
2. Non-functioning: non-secreting
3. Mixed: may secrete more than one hormone

Front 72

Mass effect

Back 72

occurs when tumor size reaches stage where it exerts pressure on surrounding structures

Front 73

Pituitary apoplexy

Back 73

: sudden hemorrhage & infarction of pituitary gland d/t rapid expansion of tumor
(It is fed by a branch of the internal carotid artery)

Front 74

Adenomas:
Diagnosis

4x

Back 74

• Clinical manifestations of abnormal hormone production
• CT & MRI
• Angiogram to visualize location of internal carotids
• 24° urine to assess pituitary function

Front 75

Pituitary tumor treatment:

3 ways

Back 75

Surgical intervention most common
Radiological therapy if radiosensitive and/or hard to resect
Pharmacological therapy to reduce tumor size

Front 76

Panhypopituitaryism:

Back 76

multiple hormones not being secreted

Front 77

Panhypopituitaryism
Cause

Back 77

tumor or thrombosis of pituitary vessels

Front 78

Panhypopituitaryism

3 S&S

Back 78

Hypothyroidism,
↓production of glucocorticoids by adrenals,
↓ gonadotropic hormones

Front 79

Panhypopituitaryism:

• Treatment:

Back 79

: replacement of specific hormones until intervention can be done

Front 80

Growth Hormone (Hyposecretion from ant pituitary gland):
• ↓ w/ age (70y/o 25% of that as a child), secreted highest at ...

Back 80

at sleep & during exercise

Front 81

Achondroplasia

4 points

Back 81

• Most common type of dwarfism, Men 51”, Women 48”
• Mutation of a single gene (1:27,000 births)
• Trunk length, intelligence, life span normal
• Short limbs, large head w/ prominent forehead, flattened mid-face w/ depressed nasal bridge, prominent mandible

Front 82

Common procedures obtained by patients w/ Achondroplasia:

4 Common procedures obtained by patients

Back 82

1. PE tubes
2. Decompression suboccipital craniotomy
3. CSF shunting
4. Obstetrical

Front 83

Dwarfism (Achondroplasia)

3 Anesthetic Concerns:

Back 83

1. Intubation: d/t instability of first two cervical vertebrae
2. Ventilation: d/t abnormal curvature of spine may impair lung expansion
3. Difficult to get IV access

Front 84

Growth Hormone Hypersecretion

results in

Back 84

Gigantism:

Acromegaly:

Front 85

Gigantism:
• Occurs BEFORE

Back 85

adolescence before growth plates are closed, height can be 8-9’ tall
• Large quantities of GH produced d/t over activity of acidophilic GH producing cell or tumor (20%)
• All body tissues grow rapidly including bones

Front 86

Acromegaly:

Occurs AFTER

ss

Back 86

adolescence & the bones cannot grow taller
• Soft tissue continues to grow & the bones grow in thickness
• Bone enlargement: hands/feet, nose, forehead, suborbital ridges, lower jaw bone causing chin protrudement, portions of vertebra leading to kyphosis & arthritis
• Enlarged internal organs: Tongue, heart, spleen, liver, kidney

Front 87

14 Anesthetic concerns for Acromegaly:

Back 87

1. Mandible ↑ thickness & length= difficult to intubate and ventilate
2. Overgrowth of soft tissue= upper airway tongue & epiglottis
3. Abnormal movement of vocal cords=thickening of cords, paralysis of laryngeal nerve d/t overgrowth stretching of the cartilaginous structures
4. Stridor or dyspnea= suggestive of larynx involvement & subglottic stenosis
5. Subglottic diameter of trachea= can be reduced & nasal turbinates enlarged
6. Peripheral neuropathy= d/t trapping of nerves by skeletal, connective, & soft tissue overgrowth
7. Compromised ulnar artery blood flow w/ carpal tunnel
8. HTN leading to CHF
9. ↑ incidence of CAD, arrhythmias, cardiomegaly
10. Lung volumes ↑ & V/Q mismatch perfusions are increased
11. Glucose intolerance= growth hormone ↓utilization of carbohydrates
Pituitary Diabetes: GH ↓ utilization of carbs, when carb stores are filled, blood glucose ↑
12. Osteoarthritis & Osteoporosis
13. Skeletal muscle weakness
14. Hypo-adrenal status=d/t inhibited ACTH **might need to give stress dose**

Front 88

• MOST COMMON abnormality associated w/ pituitary

Back 88

Prolactin (excessive production):

Front 89

Prolactin (excessive production):

ss

Treatment:

Back 89

• MOST COMMON abnormality associated w/ pituitary

galactorrhea, amenorrhea, infertility, impotence & ↓ libido in men

Surgery, Bromocriptine

Front 90

High levels of ACTH =

Back 90

CUSHINGS DISEASE:

Front 91

CUSHINGS DISEASE:=

Back 91

• High levels of ACTH = leads to adrenal cortex secreting excessive amts of Cortisol

Front 92

CUSHINGS DISEASE:

most common cause

Back 92

• Benign or malignant tumors most common cause

Front 93

CUSHINGS DISEASE:

4 SS

Back 93

Moon face, buffalo hump, purple striae on abdomen

Front 94

• Anesthetic Concerns

CUSHINGS DISEASE:

Back 94

o HTN (85%)
o Hyperglycemia (80%)
o Skeletal muscle weakness (60%)
o Osteoporosis (40%)
o Central Obesity (90%)

Front 95

• Physiological effects of excessive Cortisol:

5

Back 95

o Fluid retention
o Insomnia
o Depression, Mania, Psychosis
o Women manifest a degree of masculinity (hirsuitism, hair thinning, acne, amenorrhea)
o Men manifest a degree of feminism (gynecomastia, impotence)

Front 96

CUSHINGS DISEASE:

Treatment:

Back 96

Transsphenoidal Surgery

Front 97

Transsphenoidal Surgery

3 Advantages: of surgery

Back 97

↓incidence of DI

Elimination of the frontal lobe retraction (preferred is to shrink & remove)

Magnified visualization

Front 98

Transsphenoidal Surgery

major Disadvantage

Back 98

Accumulatin of blood & tissue debris in pharynx & stomach (NG/OG at end)

Hemorrhage-internal carotids are close by
Inability to visualize structures adjacent to tumors (carotids, Cranial nerves, CSF)
CSF leak (rhinorrhea)
Meningitis
Pituitary hypofunction (glucocorticoids usually given)
DI

Front 99

Posterior Pituitary Abnormalities

SIADH

Back 99

Posterior pituitary excess

High circulating levels of ADH (Vasopressin) relative to plasma osmolarity & Na⁺ concentration

Front 100

SIADH (Syndrome of Inappropriate Anti-Diruetic Hormone):

results in 2x

Back 100

• Results in hyponatremia and fluid retention

Front 101

SIADH (Syndrome of Inappropriate Anti-Diruetic Hormone):

7 etiologys

Back 101

o CNS lesions, trauma, infection
o Drugs: nicotine, narcotics, thiazide diuretics, phenothiazines, vincristine, vinblastine
o Pulmonary infections/disease
o Porphyria
o Hypothyroidism
o Adrenal insufficiency
o Ectopic production of tumors (mostly in lungs)

Front 102

SIADH

Know well
• Clinical features:

Back 102

• Clinical features:
o Water intoxication, hyponatremia, and brain edema
o S&S of Hyponatremia
 Wt gain, weakness, lethargy, headache, nausea, mental confusion→convulsion→coma
Lab findings:
Serum Na⁺ <120
Plasma Osmolarity <270
Low BUN/Cr, Uric acid, albumin
Urine Na⁺ >20

Front 103

Siadh
diagnosis

2x

Back 103

o Evaluate hyponatremia by water loading (pts w/ inappropriate ADH are unable to excrete diluted urine even after water loading)
o Assay of ADH in blood

Front 104

SIADH treatment

3X

Back 104

o Fluid restriction to 500-800mL/day
o IV administration of hypertonic (3%) saline solution of several hours (do not ↑Na⁺ >12mmol in 24 hours or will cause fatal neurological disorder pontine mylinolysis)
o Drugs to block effects of ADH

Front 105

2 Drugs to block effects of ADH

Back 105

Lithium
Demethylchlortetracycline (interferes w/ renal tubules ability to concentrate urine)

Front 106

SIADH

• Anesthetic Concerns:

Back 106

Monitor volume status w/ CVP or PA

Fluid restriction, if tolerated use isotonic solutions

Monitor UOP, urine & plasma osmolarity, serum Na⁺

Front 107

• Posterior Pituitary deficiency

Back 107

DI (Diabetes Insipidus):

Front 108

DI (Diabetes Insipidus):

• Two types of Etiologies:

Back 108

1. Neurogenic DI
o Lack of ADH, inadequate secretion from post pituitary lobe
o Head trauma, neurosurgical procedures, damage to pituitary stalk, brain tumors, infilitrating pituitary lesions
o ADH (desmopressin) concentrates urine in presence of neurogenic only, not nephrogenic!


2. Nephrogenic DI
o Inability of renal collecting duct tubules receptors to respond to ADH
o X-linked inherited trait, Hypkalemia, hypercalcemia, nephrotoxic (ethanol, phenytoin, lithium,etc)

Front 109

Neurogenic DI

Back 109

Lack of ADH, inadequate secretion from post pituitary lobe

Front 110

Nephrogenic DI

Back 110

Inability of renal collecting duct tubules receptors to respond to ADH

Front 111

Neurogenic DI

3 CAUSES

Back 111

Head trauma, neurosurgical procedures, damage to pituitary stalk, brain tumors, infilitrating pituitary lesions

Front 112

Nephrogenic DI

causes

Back 112

X-linked inherited trait, Hypkalemia, hypercalcemia, nephrotoxic (ethanol, phenytoin, lithium,etc)

Front 113

(Hallmark)

DI (Diabetes Insipidus):

Back 113

o Polydipsia

Front 114

Clinical features:

DI 4X

Back 114

o Polydipsia (Hallmark)
o Tremendous urine output of poorly concentrated urine despite ↑ serum Na⁺
o Serum osmolarity >290 d/t tremendous urine output
o Serum Na⁺ concentrations > 145meq/L

Front 115

5 S&S if Hypernatremia

Back 115

Hyperreflexic
Weakness
Lethargy
Seizures
Coma

Front 116

• DI from intracranial trauma:

Back 116

o Doesn’t become apparent until several days after injury
o Spontaneous recovery occurs within 48°

Front 117

• DI from Pituitary surgery (transsphenoidal)

Back 117

o Generally d/t reversible trauma of the posterior pituitary
o Transient

Front 118

DI treatment •

Treatment (depends on extent of deficiency)

Back 118

o Complete ADH deficiency:
Vasopressin (short term)
Desmopressin (long term): 5-10mcg/daily nasally or .5-1mcg bid sq
*be cautious w/ these drugs if CAD, HTN=↓SVR & HR=↓tissue oxygenation*
Surgery-monitor ECG for MI
o Mild-Moderate ADH deficiency:
Only use Vasopressin if osmolarity rises >290
Medications that augment ADH release or ↑receptor response to ADH

Front 119

Anesthesia Implications with DI:

Pre 2x

peri 3x

Back 119

Plasma electrolytes, especial Na⁺, renal function, plasma osmolarity
Restore volume over 24-48°

Surgical management w/ complete DI – vasopressin gtt intra-op (.1-.2 u/hr)
Hourly plasma osmolarity, UOP, serum Na⁺,
Isotonic fluids can be used safely

Front 120

Central Diabetes Insipidus (CDI) Organ Donors:

Back 120

 DI commonly occurs in brain dead organ donors & precedes or follows brain death
 DI’s absence means some blood flow remains to supraoptic & paraventricular regions of brain preserving some release of ADH
 S&S:
o Polyuria
o Dehydration
o Hyperosmolarity
o Hypernatremia

Front 121

Central Diabetes Insipidus (CDI) Organ Donors:

Treatment:

Back 121

o Hypotonic solutions to replace urine output w/ massive polyuria (>4ml/kg/hr)
o Replacement of therapy w/ ADH should commence to conserve intravascular volume & support vascular tone
o Prevention of acidosis and electrolyte imbalances including
 Hypernatremia
 Hypokalemia
 Hypophosphatemia
 Hypomagnesemia
 Hypercholremia

Front 122

SIADH DI

Serum Osmolarity

Back 122

SIADH
<210

DI
>290

Front 123

SIADH DI

Serum Na⁺

Back 123

SIADH <130

DI >145

Front 124

SIADH DI

Urine Osmolarity

Back 124

SIADH ↑ r/t plasma

DI ↓ r/t plasma

Front 125

SIADH DI

Treatment

Back 125

SIADH
Fluid restriction, hypertonic 3% solution over 24° for Na⁺<120

DI Desmopressin or DDAVP

Front 126

ADRENAL GLANDS/SUPRARENAL GLANDS

Have two components:

Back 126

1. Adrenal Cortex
2. Adrenal Medulla

Front 127

3 layers of Adrenal Cortex:

Back 127

1. Zona Glomerulosa:
2. Zona Fasciculata:
3. Zona Reticularis

Front 128

Zona Glomerulosa:

Back 128

a. Outermost thin layer
b. Secretes mineralcorticoid Aldosterone

Front 129

Zona Fasciculata

Back 129

a. Middle layer, widest layer
b. Secretes Glucocorticoids Cortisol, Corticosterone, & Adrenal androgens & estrogens

Front 130

Zona Reticularis:

Back 130

a. Inner deep layer
b. Secretes adrenal androgens, estrogens and glucocorticoids

Front 131

MOST IMPORTANT regulators of aldosterone

Back 131

K⁺ and Renin-Angiotensin system

Front 132

↑in K⁺ ion concentration in ECF

DOES WHAT

Back 132

↑aldosterone secretion

Front 133

Conn’s Disease: IS

Back 133

Hyperaldosteronism

Mineralcorticoid excess

Front 134

Hyperaldosteronism/Conn’s Disease:

Two primary clinical manifestations:

Back 134

o Hypertension
o Hypokalemia

Front 135

Two types of Hyperaldosteronism:

Back 135

o Primary: ↓ in plasma renin, r/t negative feedback from excessive aldosterone, typically r/t hyperplasia (trtd medically) or mass/tumor (trtd surgically)


o Secondary: ↑ renin secretion leads to ↑ aldosterone. Diseases that cause ↑ renin are CHF, Hepatic cirrhosis, nephrotic syndrome, pheo, coarction of aorta, renal artery stenosis

Front 136

Treatment of Conn’s (Hyperaldosteronism)

3x

Back 136

o K⁺ sparing diuretics
o Spironolactone-slowly ↑ K⁺ levels by action on distal tubules.
o Surgery only an option if hypokalemia no controlled medically.
 Surgical management bilateral adrenalectomy which causes complete adrenal insufficiency which is harder to treat than HTN from Conn’s, so…..
 Unilateral preferred method laparoscopically (fewer complications)

Front 137

Hypoaldosteronism

primary
secondary
mainfestations
treatment

Back 137

Primary: caused by aldosterone deficiency of adrenal cause
Secondary: referred to as renal tubular acidosis Type 4
Manifestations: opposite Conn’s-negative salt, HOTN, Hyperkalemia
Treatment: Fludrocortisone

Front 138

Cortisol
Release regulated

Back 138

by ACTH

Front 139

CUSHING’S SYNDROME- is

Back 139

Cortisol excess

Front 140

CUSHING’S SYNDROME


4 Causes:

Back 140

Extrogenous steroid given to pt
Intrinsic hypo-function of adrenal cortex
ACTH production by non-pituitary tumor
Hypersecretion of pituitary adenoma

Front 141

CUSHING’S SYNDROME-Cortisol excess

5 SS

Back 141

 Protein catabolism: muscle weakness, osteoporosis
Suppressed immune system
↑ glucose
Alterations in fat metabolism: Moon face, hump on back, pendulous abdomen
HTN, ↑Na⁺, ↓K⁺
1-2cm red-purple striae found on abdomen, upper thighs, breast, arms

Front 142

Cortisol can be inhibited by 2 drugs:

Back 142

 Ketoconazole: antifungal, long periods at high doses esp. in immune suppressed

 Etomidate: suppresses adrenal function, inhibits enzymes essential for corticosteroid hormones, long term therapy can lead to significant deficiency

Front 143

ADDISON’S DISEASE is

Back 143

hypocortisol sectretion

Front 144

2 drug Causes of: ADDISON’S DISEASE

Back 144

Ketoconazole: antifungal, long periods at high doses esp. in immune suppressed



Etomidate: suppresses adrenal function, inhibits enzymes essential for corticosteroid hormones, long term therapy can lead to significant deficiency

Front 145

ADDISON’S DISEASE-
hypocortisol sectretion

Back 145

Not apparent until 90% destroyed
Severe fatigue & weakness
Loss of weight
Faintness & ↓B/P
N/V, abdominal pain
Salt cravings, licorice cravings, mouth lesions
Painful muscles & joints

Front 146

ADDISON’S DISEASE

may be triggered in

Back 146

steroid dependent pts who don’t receive ↑ doses during periods of stress

Front 147

ADDISON’S DISEASE

7 S&S:

Back 147

Sudden penetrating pain in lower back, abdomen, legs
LOW B/P *key during anesthesia*
Loss of consciousness
Severe N/V
Difficulty breathing

Front 148

ADDISON’S DISEASE

medical treatment

5meds

Back 148

Hyrdocortisone: 20mg
Dexamethasone .75mg
Prednisone 5mg
Cortisone acetate 25mg
Fludrocortisone ( rx to replace aldosterone) .1mg QD

Front 149

Value of Adrenal Medulla
Organs are stimulated 2 ways simultaneously

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Directly by sympathetic nerves

Indirectly by medullary hormones

Both systems support each other and can substitute for each other*
 Capability of Epinephrine & Norepinephrine to stimulate structures that are not innervated by direct sympathetic fibers (metabolic rate of every cell in body effected)

Front 150

Pheochromocytomas:

Back 150

Tumors occurring anywhere sympathetic nervous tissue is found

Adrenal & extra-adrenal paragangliomas (PGL) produce significant amounts of Catecholamines & give rise to the classic PHEO clinical picture

Front 151

classic PHEO clinical picture

KNOW ON EXAM

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Adrenal & extra-adrenal paragangliomas (PGL) produce significant amounts of Catecholamines & give rise to the

Front 152

Pheochromocytomas:

Arise from

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chromaffin cells of adrenal medulla

Front 153

Neofibromatosis type 1 (NF1)

diagnosis criteria


on test

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Autosomal dominant w/ pheo frequency of .1-.7% but 20-50% in pts w/ HTN
Diagnosis criteria:
>6 café-au-lait spots
>2 neurofibromas
Axillary freckling

Front 154

PHEO
Clinical presenting triad:

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Sudden rise in B/P w/ episodic headache
Palpitations
Sweating

Front 155

Pheo Drug treatment

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Alpha antagonists (phenoxybenzamine), causes reflex tachy for which β-blocker is needed
*β-blocker should NEVER be given before the alpha antagonist

Front 156

Avoid these medications in PHEO:

Halothane: sensitizes

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myocardium to catecholamines

Front 157

Avoid these medications in PHEO:

Desflurane: may cause

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sympathetic stimulation (tachycardia)

Front 158

Intra-operative management:
Periods of greatest danger!
with Pheo

Back 158

Induction/Intubation
Exploration of tumor
After venous ligation of tumor (↑ CVP to 16-18 to avoid)
(More narcotic for induction, make sure relaxed and deep before intubation)