EXAM 3 Study guide Flashcards
1
Q
negative feedback
A
Most common
regulation self limiting prevents over-excitation
2
Q
positive feedback
A
is rare
explosive and self-reinforcing a hormone has biologic action that causes more secretion of the hormone
-example: LH surge before ovulation - result of positive fb of estrogen on anterior pituitary. LH then acts on ovaries and causes secretion of estrogen.
also seen in blood clotting and labor pain
3
Q
A
- A = Progesterone is secreted during the luteal phase of the menstrual cycle
- B = Estradiol from the Ovary (the ovarian granulosa cells contain high concentrations of aromatase and convert testosterone to estradiol
- C = Estradiol dudring the luteal phase of the cycle; Corpus Luteum is the source of the estradiol; as it prepares the uterus to receive a fertilized egg.
- D = Postive feedback of ESTROGEN on the anterior pituitary. Show the LH surge that initiates ovulation at mid-cycle. The LH surge is caused by increasing estrogen levels from the developing ovarian follicle. increased estrogen (by + fb) stimulatees the anterior pituitary to secrete LH and FSH.
4
Q
X =
A
X = indicated the peak level of HCG (human chorionic gonadotropin) at week nine which then declines. The source of HCG is placenta.
5
Q
PDE inhibitors:
A
caffeine
theophylline
aminophylline
**results in increased cAMP levels
6
Q
ativation of tyrosine kinase:
A
insulin
IGF - 1
7
Q
mechanism of action for:
Nitric oxide
Atrial natriuretic peptide (ANP)
A
cGMP
8
Q
Anterior pituitary supplied by:
A
Artery: hypothalamic hypophysial portal vessels
9
Q
what plexus brings blood to anterior pituitary?
A
primary capillary plexus
10
Q
Posterior pituitary communication from the paraventricular nucleaus via the
A
by neurons via the hypothalamic hypophysial tract
11
Q
the active gland and the storage site of the pituitary system
A
Active gland = anterior pituitary
Storage = posterior pituitary (secretions come from hypothalamus via supra optic and paraventricular nuclei
12
Q
patient complains of visual disturbances with pituitary tumor, why?
A
compression of optic chiasm / optic tract
13
Q
rathke’s pouch - what is it developing?
A
== gives rise to anterior pituitary
- depression in the roof of developing mouth in front of the buccopharyngeal membrane…
- present during embryogenesis
- the dorsal half of Rathke’s pouch forms intermediate lobe
14
Q
pituitary gland (hypophysis) located in
A
sella turcica of sphenoid bone
15
Q
hypopituitarisim causes:
A
all or some pituitary hormones may be absent
MCC: pituitary tumors
pituitary infart; sheehan’s syndrome
trauma
Radiation
Surgery
Infiltrative dx (TB, sarcoid, hemochromatosis)
16
Q
Sheehan’s syndrome is:
A
anterior pituitary infarct during childbirth
due to PPHemorrhage
17
Q
Clinical features of Hypopituitarism:
A
- Low GH - growth failure; low muscle mass
- Low ACTH - adrenal insufficiency
- Low Prolactin - unable to lactate
- Low TSH - hypothyroidism
- Low FSH/LH - impotence, testicular/uterine/ovary atrophy, amenorrhea
- Low MSH - pallor of skin and hair (decreased pigmentation)
18
Q
Hormones of Anterior Pituitary
A
- GH,
- Prolactin
- THS
- LH
- FSH
- ACTH
- beta-lipoprotein
19
Q
hormones of posterior pituitary
A
- Antidiuretic Hormone (ADH) or AVP
- Oxytocine
20
Q
Growth Hormone (Somatotropin)
- is the most important H for normal growth
- Released in pulsatile fashion
- What factors INCREASE secretion?
- What factors DECREASE secretion?
A
- Increase:
- exercise
- hypoglycemia
- puberty
- sleep
- stress
- starvation
- Decrease:
- hyperglycemia
- obesity
- pregnancy
21
Q
GH deficiency:
A
- growth stunt
- mild obestiy
- delayed puberty
caused by: lack of GH, hypothalamic dysfunction, GH receptor deficiency (end organ deficiency)
22
Q
Excess GH:
- causes
- presentation
A
- Causes:
- pituitary adenoma producing GH
- Before puberty - Gigantism
- After puberty - Acromegaly
- causes glucose intolerance,
- increased bone growth,
- increased organ size
23
Q
Acromegaly presentation:
A
increased GH after puberty - pituitary adenoma
- enlarged features (hands feet, nose, orbits, jaw bone) TONGUE and organs
- Hyperglycemia = Increased IGF-1,
- Tunnel vision “ bitemporal hemianopia” from compression of optic chiasm
24
Q
tx for acromegaly
A
Octreotide (somatostain) to supress GH
- radiation
- transphenoidal resection
25
Prolactin is inhibited by
dopamine
negative feedback control
26
prolactin inhibits ovulation by decreasing synthesis and release of
gonadotropin releasing hormone (GnRH) - no FSH/LH
27
Bromocriptine:
dopamine agonist reduces prolactin secretion when in excess
28
Factors that Increase and decrease prolactin secretion:
* Increase:
* estrogen (pregnancy)
* breast feeding
* sleep
* stress
* TRH
* Dopamin antagonist (antipsyhotic meds)
* Decrease:
* dopamine
* Bromocriptine (dopamine agonist)
* somatostatin
29
ADH and oxytocin are synthesized where?
-supraoptic and paraventricular hypothalamic nuclei
30
Increased serum osmolarity increases:
examples
ADH
* Increased ADH Secreation
* volume contraction
* Pain
* PEEP
* Beta Agonists
* Stress/anxiety
* Nausea (POWERFUL Stimulant)
* hypoglycemia
* hypoxia
* Hyperthermia
* Nicotine
* Opiates
* Histamine releaseing stimulus
31
Decreased serum osmolarity decreases:
examples
ADH
* Decreased serum osmolarity
* Atrial Natriuretic peptide (ANP)
* Alphaagonist
* Ethanol
32
ADH regulation:
v1, v2, v3
* V1 - vasoconstrictor (IP3/ Ca++ moa)
* V2- increases H2O reabsorption (cAMP moa)
* from distal tubules and collecting ducts
* V3-ACTH release; increase intracellular ca when activated
* in pituitary
33
DI results from:
Clinical features:
TX:
* underproduction of ADH
* Polyuria, hypernatremia, hypotension, dehydration
* Tx:
* Deesmopressin (dDAVP)
* Chlorpropamide (oral hypoglycemic drug)
* _Nephrogenic DI TX - **thiazide** diuretics_
34
OVERproduction of ADH leads to:
- Clinical features:
- TX:
* **SIADH** (due to porphyria, hypothyroidism, CNS injury, Pulmonary dx like small cell carinoma)
* Features: Hyponatremia (dilutional), edema (brain, orbital), seizures
* Not urinating much; **water retention**!
* TX:
* remove underlying cause
* fluid restriction
* Lithium
* Demeclocycline (antagonizes ADH on renal tubules)
* hyperosmotic saline (3%NaCl)
* Loop diuretics (to release Na)
* Non-peptide vasopressin antagonists (vaptans)
* conivaptan, Tolvaptan
35
\*\*Diagnosis of Central vs. Nephrogenic DI is done by the Desmopressin (ADH) challenge test. After the small test dose what happens and how do you determine dx of Central vs Nephrogenic?
- Central DI: Increased urine osm after test dose
- Nephrogenic DI: No change in urine osm after test dose
36
lithium can cause
**Nephrogenic DI**
- SE *underproduction* of ADH
- Used in tx SIADH to reduce levels of ADH
37
what is the "Power axis" of the thyroid gland?
THINK "HAT"
1. Hypothalamus
1. TRH (+)
2. Anterior Pituitary
1. TSH (+)
3. Thyrois
1. T3, T4 (- fb to AP)
38
TSI - thyroid stimulating Immunoglobulin:
* **Ig**_G_**** type
* released from reticuloendothelial system
* binds to TSH -R on thyroid
* *ACTS like TSH* by stimulating thyroid to secrete T3 and T4
* Present in high concentration in *Grave's Dx* (high T3/4 and low TSH)
39
Hyperthyroidism mneumonic
THYROIDISM:
Tremor
Heart rate up
Yawning [fatigability]
Restlessness
Oligomenorrhea & amenorrhea
Intolerance to heat
Diarrhea
Irritability
Sweating
Musle wasting & weight loss
40
TSH level in hypothyroid?
TSH level in Hyperthyroid?
Hypothyroid: TSH is Increased, Low T3, T4
Hyperthyroid: TSH is Decreased; elevated T3, T4
41
Myxedema / Hypothyroidism mneumonic
SLUGGISH
* S = Sleepiness, fatigue, tiredness
* L = Loss of memory
* U = Unusually dry skin
* G = Goiter
* G = Gradual personality change
* I = Increase in body weight
* S = Sensitivity to cold
* H = Hair loss, sparseness of hair
42
tx for hypothyroidism
Levothyroxine T4 Replacement
43
Tx for Hyperthyroidism
- thyroidectomy
- Prophylthiouracil (inhibit TH synthesis by blcoking peroxidase)
- Radioactive Iodine - 131-I to destroy thyroid
- beta blockers
44
Thyroid Binding Globulin (TBG)
-when is it normal, high, or low?
* Normal
* Hyper/Hypothyroidism
* High
* Pregnancy; Estrogens
* Low
* Liver disease
* "L.L." ,\<-- Low in Liver dx
45
Know the Condition and associated Levels of Total/ Free T4,T3 and TSH
46
in conditions of the thyroid, no surgery until the patient is
Euthyroid with medical tx
- sodium iodine to reduce size; reduce r/o bleeding
- beta blocker (esmolol)
Benzodiazepine (sedation)
Antithyroid medication (PTU, methimazole)
47
Intraoperative considerations for Hyperthyroid pt:
- protect eyes from injury, abrasion, ulceration
- Avoid SNS drugs (*ketamine, pancuronium*) b/c of r/o BP and HR elevation
- _Thiopental_ - drug of choice for induction (has some antithyroid activity in high dose)
- caution with muscle relaxants - thyrotoxicosis assoc. w/myopathisa and MG
- **_NO_** change to MAC
48
Thyroid storm post op consideration
- **sudden/excessive release of T3 & T4** (MOST important threat)
- resembles **MH** but _no_ muscular rigidity
- **RLN** *palsy --\> stridor* (assoc. with subtotal thyroidectomy)
49
Hypoparathyroidism may occur by unintential removal of parathyroid glands which can lead to:
- hypocalcemia
- increased NM excitability
- muscular spasm and tetany
50
intraoperative consideration for hypothyroidism
* **make EUTHYROID**
* more susceptible to hypotensive effects of anesthetic agent b/c
* decreased CO
* decreased baroreceptro reflex
* decreased IV Vol
* no MAC changes
* Anticipate difficult airway/intubation d/t tongue size
* hypoglycemia
* anemia
* hypothermia d/t decreased BMR
51
Secretion of adrenocortical hormones by **zones** of adrenal cortex:
Zona **G**lomerulosa (outer layer) = **A**ldosterone / *salt*
Zona **F**asiculata (middle) = **C**ortisol / *sugar*
Zona **R**eticularis (inner) = **A**ndrogen / *sex*
**GFR** - corresponds with salt (na), sugar (glucocorticoids), and sex (androgen)
"The deeper you go... the sweeter it gets"
52
control of glucocorticoid (cortisol) secretion order:
Hypothalamus = CRH (+)
Anterior pituitary =ACTH (+)
Adrenal cortex = cortisol
------
Cortisol then has (-) fb effect on Anterior Pituitary and Hypothalamus
53
Cortisol Stimulation of gluconeogenesis i.e.
formation of glucose from non-carbohydrate sources such as protein and fat .
**-- Increase protein and fat breakdown to synthesize more glucose**
54
Anti-inflammatory effect: Cortisol inhibits formation of:
* prostaglandins (PG) and leukotriene (IL-2)
* release of histamine and serotonin from mast cells and platelets
55
Suppression of immune response: Cortisol inhibits formation of
* IL-2 and T lymphocytes .
* Its is used to prevent transplant rejection
56
Cortisol upregulates (increases number of receptors) the **a1** receptor on arterioles, increasing their sensitivity to the vasoconstrictor effect of norepinephrine. Thus
* Increase cortisol = Increase BP
* Decrease cortisol = decrease BP.
57
renin-angiotensin system (image)
Mineralocoritcoids (Aldosterone)
-controlled by ACTH and separately regulated by the renin-angiotensin system
58
**\*\* three things aldsoterone does:**
1. increase renal Na reabsorption
2. increases renal K secretion
3. increases renal H secretion
59
Addison's Disease presents as:
* Hypotension (hyponatremic vol contraction)
* Hypoglycemia (low cortisol)
* Hyperpigmentation (ACTH )
* Hyperkalemia
* Hyponatremia
* Metabolic Acidosis
* low aldosterone - *helps retain Na, secretes K and H*
**AdD**ison’s disease is due to **Ad**renocortical **D**eficiency
60
in addison's dx - anesthesia consideration
give steroid coverage
61
**Cushing’s disease** is caused by pituitary adenoma that release
–excessive ACTH
* increase cortisol and androgen
* increase ACTH
* Hyperglycemia
* Protein breakdown and muscle wasting
* poor wound healing
* Na/water retetion
* HTN
* Hypervolemia
* Hypokalemia
* Osteopororsis
* Purple striae
62
**Cushing’s syndrome** is the
Excess of glucocorticoids -
–MCC; prolong intake of steroid
63
**•Primary Hyperaldosteronism ( *Conn’s* syndrome**)
Caused by :
Symptoms:
* increased aldosterone-secreting tumors
1. **Hypertension** ( Aldosterone á Na+ reabsorption; á ECF )
2. **Hypokalemia** ( because aldosterone á K+ secretion)
3. **Hypernatremia**
4. **Metabolic alkalosis** (because aldosterone á H+ secretion)
5. **Low plasma renin** (-ve feedback inhibition by high BP and ECF)
64
•Secondary Hyperaldosteronism
Caused by
**CHF .**
Kidney misperception of low intravascular volume, resulting in an **overactive renin-angiotensin system**. Therefore, it is associated with **high plasma renin**
•_Treatment:_
**Spironolactone** ( aldosterone antagonist)
65
Congential Adrenal Hyperplasia (CAH) is an enzymatic deficiency in cortisol synthesis. What are the most common deficiiencies?
* 21b-hydroxylase deficiency MCC
* 17a hydroxylase deficiency
66
In Cushing's Syndrome patients tend to be
- vol overloaded
- Hypokalemic
- Metabolic Alkalosis
67
Anesthetic considerations for Cushing's Syndrome include:
* K+ replacement
* osteoporosis - r/o fracture during positioning
* Increase sensitivity to NMB
* Give supplemental steroids
* life threatening hypotension without
68
Pheocromocytoma is
Tumor of chromoffins cells of adrenal medulla in adults
* increased secretion from cells:
* Norepinephrine
* Epinephrine
* Dopamine
69
Increased Urinary VMA (Vanillyl mandalic acid) indicates
- Diagnosis of Phenochromocytoma
- normetapinephrines, metanephrines
70
TX for Phenochromocytoma:
* Surgery
* Preop with Alpha blockade
* **Phenooxybenzamine**
\*\*\* Beta blockade w/o alpha blockade in pt with Phenochromocytoma can cause HF.
**♦BLOCK ALPHA FIRST**
71
**Rule of 10** in Pheochromocytoma:
10% malignant
10% bilateral
10% extraadrenal
10% calcify
10% kids
10% familial
72
5 P's of Pheochromocytoma
1. Pressure ( Paroxysmal Hypertension)
2. Pain ( headache)
3. Perspiration\*
4. Palpitation
5. Pallor
\*sweat glands are stimulated by catecholamine even though sweat glands don’t have adrenergic receptors
73
No Dopamine results in :
- Lots of catecholamine = HTN CRISIS
74
