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posterior pituitary Flashcards

1
Q

oxytocin: effect on uterus

A

-Stimulates contraction of the smooth muscle cells of the uterus
-Uterine sensitivity increases throughout pregnancy
-Plasma levels do not increase sharply during parturition
-Role of oxytocin in the initiation of labor is unclear

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2
Q

oxytocin: effect on breast

A

-Myoepithelial cells
-Suckling stimulates the production of oxytocin
-Cells surround the alveoli of the mammary gland → contraction causes milk to move from the alveoli to large sinuses for ejection
-Letdown reflex

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3
Q

ADH action

A

action
- water conservation by increasing the permeability of the distal tubular epithelium to water
-At high concentrations: ADH causes vasoconstriction

Plays an important role in maintaining fluid homeostasis and vascular and cellular hydration

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4
Q

ADH stimulation and inhibition

A

Main stimulus for ADH release: Increased osmotic pressure of water in the body***

Other stimulus: Volume depletion
-Sensed by baroreceptors in the left atrium, pulmonary veins, carotid sinus, and aortic arch
-Transmitted to the CNS through the vagus and glossopharyngeal nerves

Other stimulants for ADH release include:
-Pain, stress, emesis, hypoxia, exercise, hypoglycemia, cholinergic agonists, β-blockers, angiotensin, and prostaglandins

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5
Q

Inhibitors of ADH release

A
  • alcohol
  • α-blockers
  • glucocorticoids
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6
Q

Central diabetes insipidus

A

Deficiency of ADH due to a hypothalamic-pituitary disorder

-Primary
-Secondary

Pathology of CDI:
- always involves the supraoptic and paraventricular nuclei of the hypothalamus or a major portion of the pituitary stalk
- Hypothalamic nuclei and part of the neurohypophyseal tract need to be intact

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7
Q

Nephrogenic Diabetes Insipidus:

A

definition:
- Inability to concentrate urine due to impaired renal tubule response to ADH
- Inability of kidney to respond normally to ADH
-Inherited or secondary to impairment of renal concentration

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8
Q

Nephrogenic Diabetes Insipidus: sx, dx

A

sx:
-Excretion of large amounts of dilute urine
-Polyuria
- hypernatremia**
- dehydration but good thirst response**

Diagnosis :
– water deprivation test and/or administration of exogenous ADH
- DDx with CDI with exogenous ADH test

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9
Q

Lack of ADH: other pathologies

A

Vasopressinase-induced DI

Removal of the pituitary gland:
- does NOT result in permanent diabetes insipidus
- some of the remaining hypothalamic neurons produce small amounts of ADH

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9
Q

Nephrogenic Diabetes Insipidus: tx

A
  • adequate free water intake (prevent dehydration)
  • thiazide diuretics (reduces urine volume)
  • NSAIDs
  • low-salt, low-protein diet

Goal: reduce urine output and increase ability to concentrate urine

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10
Q

Differential for polyuria

A

Differential for polyuria:
-CDI
-NDI
- compulsive or habitual water drinking (psychogenic polydipsia)
-DM

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11
Q

diabetes insipidus (DI) main sx and dx

A

Sx:
-Polyuria
-Polydipsia

Diagnosis:
-Water deprivation test: Failure to maximally concentrate urine
-ADH levels and response to exogenous ADH help distinguish CDI from NDI

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12
Q

diabetes insipidus (DI) tx

A

-intranasal desmopressin or lypressin
-Nonhormonal treatment:
diuretics (MC: thiazides)
-ADH-releasing drugs: chlorpropamide

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13
Q

primary central diabetes insipidus

A

-Marked decrease in the hypothalamic nuclei of the neurohypophyseal system
- Genetic abnormalities of the ADH gene on chromosome 20
- Idiopathic

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14
Q

secondary (acquired) central diabetes insipidus

A

Various lesions:
-Hypophysectomy
-Cranial injuries (particularly basal skull fractures)
-Suprasellar & intrasellar tumors (primary or metastatic)
-Granulomas (sarcoidosis or TB),
-Vascular lesions (aneurysm and thrombosis)
-Infections (encephalitis or meningitis)

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15
Q

DI onset and sx of primary vs secondary

A

Onset:
- insidious or abrupt
-Occurring at any age

Primary CDI:
- ONLY SX: polydipsia & polyuria

Secondary CDI:
- S&S of the associated lesions

16
Q

DI signs

A

Large quantities of fluid
ingested + Excreted
-3 to 30 L/day of dilute urine excreted
-Sp.gravity usually < 1.005 (nml 1.030)
-Osmolality < 200 mOsm/L (nml 280-285mOsm/L)
-Nocturia almost always occurs
-Dehydration and hypovolemia

17
Q

tests for DI

A

-All tests for CDI &NDI based on the principle that:
-Increasing the plasma osmolality in normal people – will lead to decreased excretion of urine
-Water deprivation test:
-Simplest
-Most reliable method
-Patient needs constant supervision*
-Serious dehydration may result *

18
Q

water deprivation test: what does it entail

A

Pt is weighed, Electrolyte concentrations are obtained from plasma and urine
Dehydration begins and urine is collected hourly with specific gravity or osmolality measured

Dehydration is continued until:
-Orthostatic hypotension
-Postural tachycardia appear
-≥ 5% of the initial body weight has been lost
-OR
-Urinary concentration does not increase > 0.001 sp gr or > 30 mOsm/L in sequentially voided specimens

After:
-Serum electrolytes and osmolality are obtained
-5 units of aqueous vasopressin injected sc.
-Urine for sp gr or osmolality measurement collected one final time 60 min post injection

19
Q

result interpretation

A

Normal:
- Urine is maximally concentrated after dehydration
- Specific gravity > 1.020, Osmolality > 700 mOsm/L
- Osmolality does not increase >5% s/p vasopressin injection

CDI
- unable to concentrate urine to greater than the plasma osmolality
-Able to increase their urine osmolality by > 50% after vasopressin administration

NDI
- unable to concentrate urine to greater than the plasma osmolality
- shows NO response to vasopressin**

Partial CDI
- Often able to concentrate urine to above the plasma osmolality *
- Show a rise in urine osmolality of > 9% after vasopressin administration

20
Q

ADH measurement

A

Measurement of circulating ADH
-Plasma ADH levels are diagnostic after either dehydration or infusion of hypertonic saline
-Most direct method of diagnosing CDI
-ADH difficult to measure; test not routinely available
-Direct measurement of ADH unnecessary

Levels of ADH at the end of the water deprivation test (before the vasopressin injection)
-Low in CDI
-Appropriately elevated in NDI

21
Q

psychogenic polydipsia

A

Compulsatory behavior (anxiety, boredom) to ingest high volumes of fluids (up to 6 L/day)
- Does not present with nocturia and thirst does not wake them up at night
-Life-threatening hyponatremia**
- no response to exogenous ADH after water deprivation

Acute phase:
- pt able to concentrate urine during water deprivation

Chronic phase:
- Long-standing water intake = ↓ tonicity of kidney medulla = kidneys unable to maximally concentrate urine
- No response to exogenous ADH after water deprivation
- Once fluid intake normalizes, concentrating ability returns to normal within weeks

22
Q

tx of DI

A

Hormone replacement and treatment of any correctable cause
-Permanent renal damage can result

Desmopressin:
-Synthetic analog of ADH
-Minimal vasoconstrictive properties
-Prolonged antidiuretic activity lasting for 12 to 24 h
ADR:
– fluid retention; headache; ↑ BP; URI or allergic rhinitis

Diuretics: MC= thiazides
-Primarily as a consequence of reducing ECF volume and increasing proximal tubular resorption
-Urine volumes may fall by 25 to 50%

ADH-releasing drugs
-Chlorprpamide (hypoglycemia)
-Carbamazepine
-Clofibrate

Prostaglandin inhibitors:
-Reduce GFR and renal blood flow
-NOT effective in NDI

Restricting salt intake also ↓ urine output by reducing solute load

23
Q

SIADH criteria

A

Excessive ADH release

Defined as:
-Less than maximally dilute urine in the presence of plasma hypo-osmolality + hyponatremia
-urine is not as dilute as it should be under these conditions
-50% of all diagnosed cases of hyponatremia are due to SIADH

WITHOUT:
-Volume depletion or overload
-Emotional stress
-Pain
-Diuretics or other drugs that stimulate ADH secretion,
-AND WITH normal cardiac, hepatic, renal, adrenal, and thyroid function

24
Q

Before diagnosis of SIADH can be made, MUST R/O

A

MUST R/O:
- thyroid disease
- adrenal insufficiency

25
Q

SIADH causes

A

Drugs
Post OP
Hormone administration
CNS infections
Pulm Disorders **
Malignancy= LUNG*

26
Q

disorders associated with SIADH secretion

A

Malignancy:
-CNS
-Pancreas
-Duodenum
-Lung*
-Lymphoma

Pulmonary disorders:
-Aspergillosis
-Lung abscess
-Pneumonia
-Positive-pressure breathing
-TB

CNS disorders:
-Acute intermittent porphyria
-Acute psychosis
-Brain abscess
-Encephalitis
-Guillain-Barré syndrome

Head trauma:
-Meningitis
-Stroke
-Subdural or subarachnoid hemorrhage

Endocrine disorders:
-Addison’s disease
-Hypopituitarism
-Hypothyroidism

Miscellaneous causes:
-Protein-energy malnutrition
-Surgery

27
Q

symptoms SIADH

A

-Patient may be asymptomatic, especially when the cause is indolent or subacute.

Severe or rapid onset hyponatremia may cause:
-Confusion
-Lethargy
-Vomiting
-Seizures

28
Q

SIADH signs

A

-Hyponatremia*
-Hypo-osmolality (<275 mosm/kg)*
-Euvolemic: normal hydration
-Elevated urinary osmolality (>100 mosm/kg and often at least 300 mosm/kg)

-Normal plasma volume
-Serum uric acid <4 mg/dL
-Normal acid base and potassium balance
-Normal renal function
-Relatively normal creatinine concentration
-Normal adrenal and thyroid function

29
Q

diff dx SIADH

A

-Hypervolemic hypotonic hyponatremia:
-An increase in total body water and sodium with a decrease in the circulating volume (impaired water excretion)
-Characterized by clinical fluid overload with edema
-CHF, liver cirrhosis with ascites, nephrotic syndrome, protein losing enteropathy
-Hypovolemic hypotonic hyponatremia:
-Characterized by fluid volume loss due to underlying disorder
-Non-renal loss of electrolyte-containing fluid (diuretics, burns, severe diarrhea and vomiting)
-Salt losing renal diseases (interstitial nephritis, obstructive nephropathy)
-Mineralocorticoid deficiencies

30
Q

SIADH management

A

First Line Therapy: Fluid Restriction !!!

Resolution of any CNS symptoms
- Achievement of safe Na+ levels (>120mEq/L), but GRADUALLY
Resolution of underlying cause of hypo-osmolality
Discontinue offending drugs
If Refractory to tx:
- Demeclocycline/saline infusion
- Tetracycline: Antagonizes ADH

Endocrine (11 decks)

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