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OPP 4 midterm > endocrine cases - Ramey > Flashcards

endocrine cases - Ramey Flashcards

1
Q

hypothyroidism etiologies

A
  1. radioactive iodine therapy
  2. thyroid surgery
  3. previous treatment with thiamoid drugs (PTU or methimazole)
  4. autoimmune thyroiditis
  5. iodine deficiency
  6. other pharmaceuticals (lithium, phenylbutazone, and amiodarone)
  7. hypothalamic or pituitary insufficiency (due to head trauma, sinus surgery, or prior radiation treatment for acne)
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2
Q

labs to order for hypothyroidism

A

TSH, free T4

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3
Q

cautions and contraindication with OMM when treating hypothyroidism

A
  1. Do not overtreat and tire the patient. You don’t want to overstress an already stressed system. Less is frequently more.
  2. You may see adrenal dysfunction in combination with thyroid dysfunction. Don’t forget to structurally assess the entire system.
  3. Focus on treating the somatic dysfunction. Don’t chase the pain!
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4
Q

TSH increased and T4 decreased

A

primary hypothyroidism

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5
Q

TSH and T4 both decreased

A

central hypothyroidism

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6
Q

TSH increased and T4 normal

A

subclinical hypothyroidism

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7
Q

TSH and T4 increased

A

can occur with use of oral contraceptives

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8
Q

when to consider T3 level?

A

if suspect impaired T4 conversion to T3 in the liver

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9
Q

what can slightly increase TSH levels?

A

adrenal insufficiency

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10
Q

medical management of hypothyroidism

A
  1. Levothyroxine (T4) 1.6ug/kg/day
  2. Repeat TSH every 6 weeks until stabilized
  3. Consider liothyronine (T3) if no response to levothyroxine (suspect problem with T4 to T3 conversion in liver)
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11
Q

long-term hypothyroidism management

A
  1. Monitor TSH every 6-12 months once stable.
  2. Monitor cardiac status closely in older patients.
  3. Stress the importance of compliance with thyroid replacement therapy.
  4. Achieve/maintain healthy lifestyle including stress reduction (reducing overtraining in athletes), sleep, moderate activity, diet, fluid intake, etc.
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12
Q

lymphatic drainage of thyroid includes? largely drive by? course through?

A
  1. via prelaryngeal, pretracheal, and paratracheal nodes
  2. driven by motion of respiratory diaphragm
  3. courses through the thoracic inlet on the way back to the heart
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13
Q

sympathetics of thyroid arises from? with contribution from?

A
  1. Sympathetics arise from upper thoracic spinal cord segments (T1)
  2. Contributions from superior (located at level of transverse processes of C2 and C3), middle (C6) and inferior cervical (stellate) ganglia (near 1st rib)
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14
Q

sympathetic fibers action on thyroid? parasympathetic fibers action?

A
  1. Sympathetic fibers are vasomotor, not secretomotor

2. Parasympathetic innervation and role not clearly delineated

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15
Q

hypothyroidism OMM treatment

A
  1. Lymphatics - thoracic inlet, respiratory diaphragm and other associated structures
  2. Sympathetics – upper thoracics
    T1 (flexed segment)
    Clinically, may also see compensatory extended segments around T3-4
  3. 1st rib (commonly elevated) – inferior cervical (stellate) ganglion
  4. Cervical spine – remember superior and middle cervical ganglion
  5. Cranial – altered hypothalamic or pituitary function (SBS compression or other strain pattern)
  6. Locally in region of thyroid gland to address fascial restrictions (anterior cervical fascia and attachments)
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16
Q

thyroid Chapman’s point

A
  1. Anterior – intercostal space between the 2nd and 3rd ribs close to sternum bilaterally
  2. Posterior – over the transverse process of T2
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17
Q

dx of metabolic syndrome can be made when 3 or more of the following 5 characteristics are present

A 
1. Abdominal obesity
Men > 102cm (40 in)
Women > 88cm (35 in)
2. BP ≥ 130/85
3. Triglycerides ≥ 150 mg/dl
4. HDL
Men  100
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18
Q

possible etiologies of metabolic syndrome

A
  1. obesity (especially abdominal)
  2. insulin resistance
  3. increasing age
  4. proinflammatory state
  5. genetics
  6. endocrine (postmenopause, possibly andropause, adrenal and thyroid dysregulation)
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19
Q

metabolic syndrome has increased risk of developing?

A
  1. type 2 diabetes

2. CV problems

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20
Q

metabolic syndrome involves which organs?

A
  1. thyroid gland
  2. adrenal glands
  3. pancreas
  4. liver
  5. kidney
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21
Q

lymphatic drainage of pancreas

A
  1. pancreaticosplenic nodes

2. pre-aortic nodes

22
Q

pancreas sympathetic innervation and action

A
  1. arise from spinal cord segments T6-9.

2. Have vasomotor function

23
Q

pancreas parasympathetic innervation and action

A
  1. derived from vagus and have secretomotor function.
  2. Parasympathetic stimulation results in the secretion of:
    Insulin
    Bicarb
    Somatostatin, glucagon
24
Q

liver functions

A
  1. Metabolizes, detoxifies and inactivates substances
  2. Stores carbohydrate, lipids, vitamins and minerals
  3. Activates some hormones (thyroid T4 conversion to T3) and vitamins
  4. Synthesizes or regulates albumin, glucose, cholesterol, phospholipids and fatty acids for triglycerides
25
Q

lymphatic drainage of liver

A

nodes above and below diaphragm

26
Q

liver sympathetic innervation and action

A
  1. arise from spinal cord segments T6-T9.

2. Sympathetic stimulation promotes breakdown of glycogen to glucose (increased energy)

27
Q

liver parasympathetic innervation and action

A
  1. arise from vagus. 2. Parasympathetic stimulation decreases breakdown of glycogen to glucose (decreased energy)
28
Q

lymphatic drainage of kidney

A

follow course of renal vein to drain toward lateral aortic nodes

29
Q

kidney sympathetic innervation and action

A
  1. arise from spinal cord segments T10-L1.

2. Vasomotor in function. Frequently see somatic dysfunction (flexed segment) in the thoracolumbar region

30
Q

kidney parasympathetic innervation and action

A
  1. role not clearly delineated

2. Fibers probably arise from vagus

31
Q

increased sympathetic tone to kidney can result in

A
  1. Vasoconstriction
  2. Enhanced Na+ reabsorption from proximal tubule cells
  3. Increased renin secretion
  4. Net effect – increased fluid retention and increased blood pressure
32
Q

metabolic syndrome OMM treatment

A
  1. Lymphatics
  2. Autonomics – remember spinal cord segments, associated ganglia (ventral abdominal release) and potential parasympathetic influences
  3. Myofascial and/or osseous restrictions in area of involved organs
  4. Chapman’s reflexes
  5. Goal – improve function, motion and health
33
Q

long-term management of metabolic syndrome

A
  1. Weight reduction to decrease abdominal obesity.
    - Reduce caloric intake – low glycemic index meal plan (Mediterranean or Atkins diet).
    - Increase physical activity.
    - May need to start with simple core exercises (pelvic clock) and proprioceptive retraining (single leg stance and tandem walking). The patient may slowly progress to moderate activity if tolerated and sufficiently motivated.
  2. Stress the importance of compliance with medical therapy.
  3. Blood pressure, lipid and diabetes control.
34
Q

when see primary adrenal insufficiency with thyroid dysfunction, what needs to be done? if not, what might the patient experience?

A
  1. start glucocorticoid replacement before thyroid replacement
  2. can experience Schmidt syndrome
35
Q

labs to order for metabolic syndrome

A
  1. fasting lipids
  2. fasting glucose
  3. HbA1c
  4. liver function tests
  5. free testosterone level
  6. thyroid testing
36
Q

medical management of metabolic syndrome

A

control of:

  1. Dyslipidemia - statins
  2. hypertension - ACEI
  3. insulin resistance/impaired glucose tolerance - metformin
37
Q

etiologies of Addison’s disease

A
  1. Withdrawal of long-term corticosteroid use
  2. Sheehan syndrome
  3. Autoimmune adrenal insufficiency
  4. Tuberculosis
  5. HIV
  6. Waterhouse-Friderichsen Syndrome
  7. Fungal disease
  8. Adrenal hemorrhage or infarction due to anticoagulants
  9. Metastatic disease (lung, breast, kidney, colon, melanoma, lymphoma, Kaposi sarcoma)
  10. Drugs (ketoconazole, etomidate)
  11. Sarcoidosis
  12. Amyloidosis
  13. Adrenoleukodystrophy/Adrenomyelodystrophy
  14. Polyglandular autoimmune endocrine syndromes
38
Q

labs/imaging to order for Addison’s disease

A
  1. Basal plasma cortisol and ACTH level (low cortisol and high ACTH)
  2. ACTH stimulation test – administer cosyntropin IV and measure preinjection, 30 and 60 minute post-injection cortisol levels (low to normal cortisol levels that do no rise ).
39
Q

lab findings for adrenal fatigue

A

normal or low normal cortisol level

40
Q

medical management of Addison’s disease

A
  1. Remember the 5 S’s for managing adrenal crisis – salt, sugar, steroids, support and search for precipitating illness (infection, trauma, recent surgery, not taking prescribed meds)
    2, Addison’s disease - commonly managed with hydrocortisone, fludrocortisone and DHEA
  2. Adrenal fatigue – medical management is controversial
41
Q

long term management of Addison’s disease

A
  1. Search for a cause
  2. Stress reduction
  3. Alter training habits to reduce/prevent overtraining
42
Q

lymphatic drainage of adrenal glands? largely drive by? courses through?

A
  1. para-aortic nodes
  2. largely driven by motion of respiratory diaphragm
  3. courses through thoracic inlet on the way back to heart
43
Q

adrenal glands sympathetic innervation

A
  1. from spinal cord segments T6-L2 (T8-T10 NBOME).
  2. Have vasomotor function. Stimulation also results in secretion of epinephrine and norepinephrine.
  3. Commonly see somatic dysfunction (type 2) in the thoracolumbar region
44
Q

adrenal glands parasympathetic innervation

A
  1. fibers (vagus) may be present

2. role not clearly delineated

45
Q

Addison’s disease OMM treatment

A
  1. Lymphatics - thoracic inlet, respiratory diaphragm and other associated structures
  2. Sympathetics – T6-L2
  3. Parasympathetics – although role not clearly defined, consider treating structures that impact vagal function (temporal bone, occipitomastoid suture compression, OA, AA, C2)
  4. Cranial – altered hypothalamic or pituitary function (SBS compression or other strain pattern)
  5. Ventral abdominal release to improve function of celiac, aorticorenal, superior mesenteric and inferior mesenteric ganglion
  6. Locally in region of adrenal gland to address fascial restrictions (don’t forget psoas major muscle and attachments)
46
Q

adrenal glands Chapman’s points

A
  1. Anteriorly – 2-2.5 inches above and 1 inch lateral to the umbilicus (bilateral)
  2. Posteriorly – Intertransverse spaces between T11 and T12 bilaterally
47
Q

characteristics of Chapman’s relfex

A
  1. changes found in deep fascia as gangliform contractions located at specific points and consistently associated with same viscera
  2. size: one-half the size of a BB shot to that of a small bean
  3. often multiple
48
Q

treatment of Chapman’s reflex

A
  1. pad of finger in contact with locus
  2. firm, gentle contact is maintained
  3. rotary motion imparted to the finger through the arm and hand so as to express the fluid content of the locus into the surrounding tissues
  4. finger is not allowed to slip about, but is held firmly in contact with locus
49
Q

dosage of treatment for Chapman’s reflex

A
  1. do treatment until
    - decrease in edema
    - dissolution of the gangliform contracture
    - subsidence of the tenderness in the anterior reflex areas
  2. actual time of treatment varies from 20sec to 2min
50
Q

kidney’s Chapman’s points

A
  1. anterior: b/l 1 inch above and 1 inch lateral to the umbilicus
  2. posterior: intertransverse space between T12 and L1, b/l
51
Q

pancreas Chapman’s points

A
  1. anterior: intercostal space between 7th and 8th ribs on the R side
  2. posterior: intertransverse space between T7 and T8 on the R side
52
Q

congestion of liver Chapman’s points

A
  1. anterior: intercostal space from mid-mammillary line to sternum on the R side between 6th and 7th ribs
  2. posterior: intertransverse space between T6 and T7 on the R side

OPP 4 midterm (8 decks)

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