Endocrine Extra Flashcards
Posterior pituary gland
- “Neurohypophysis”
- Stores & releases ADH, Oxytocin synthesized by hypothalamus
Where is aldosterone released from
Adrenal cortex
DKA Dx
- T1DM new Dx common
- Often caused by increased need for insulin d/t illness, stress.
- more common than HHS
Dx:
1. GLU >250
2. Ketones
3. pH <7.3 & bicarb <18
4. Dehydration d/t to osmotic diuresis and vomiting
K+ and DKA
Serum levels of K are high:
- Insulin facilitates transport of K into cells
- Acidosis: During DKA, H+ ions move into cells to buffer the acidotic state. When this happens, K+ ions shift out of cells into blood to maintain electroneutrality.
BUT total body potassium may be at a deficit:
- Osmotic diuresis; K lost along w Na & H2O
- Vomiting common symptom.
THUS when Tx, beware of hypokalemia
When insulin introduced, K+ goes back into cells
HHS Dx
GLU > 600mg/dL
Serum osmolarity >320 mOsm/kg
pH > 7.3, Bicarb >18mEq/L
Severe dehydration
Minimal ketosis d/t presence of some insulin inhibiting ketogenesis
Altered mental status - lethargy to coma d/t hyperosmolarity
HHS Tx
- Fluid replacement; gradually to prevent cerebral edema
- Correct electrolytes: K+ typically added to IV fluids to avoid hypokalemia during insulin Tx. Sodium supplemented too.
- Insulin: Start low-dose. Aim to gradually lower glucose (50-75 mg/dL per hour) to prevent complications. Switch to subcut insulin once GLU <300mg/dL and pt stable.
Why slow lower? GLU lowered too quick —> serum osmolarity drops too quick —> cerebral edema
Also risk for too abrupt shift in K+ due to insulin. - Address underlying cause: infection? MI? Etc
DKA patho, Sx
Patho:
1. No insulin, cells break down fat
2. fat —> free fatty acids —liver—> ketone bodies —> metabolic acidosis
3. Gluconeogenesis increases b/c no insulin & counter-regulatory hormones (glucagon, cortisol, epinephrine, GH)
4. Osmotic diuresis
Sx:
- hypoglycemia Sx; polyuria, polydipsia, weight loss, fatigue/weak
- nausea, vomit, abdominal pain
- Kussmaul respirations compensate for acidosis
- fruity breath
- dehydration signs (tachycardia, hypotension, skin)
- ALOC
- Na low
- Serum K high or normal but total body K low
- high serum osmolality
DKA Tx
- Fluid replacement
- add dextrose when GLU drops to ~200 to avoid hypoglycemia - IV insulin continuous
- after K is >= 3.3mEq/L
- goal: reduce glucose by 50-75 mg/dL per hour
- transition to subcut once GLU 200 mg/dL and acidosis resolves - Replace K+; monitor
Cerebral edema possible if too rapid correction
Why cortisol increases fat synthesis?
Cortisol’s primary function is to increase blood glucose to make it readily available for brain/heart.
Systematically, it is an insulin antagonist, reducing glucose uptake in peripheral cells.
But in specific areas (trunk & face), it increases insulin sensitivity and lipogenesis.
To promote VISCERAL fat storage. (It decreases fat storage in periphery).
Visceral fat is more metabolically active than subcutaneous fat; more quickly broken down into FFAs for energy when needed to be used by vital organs. This happens during prolonged starvation.
In ancient times, chronic stress often meant starvation. So cortisol—>visceral fat storage—>eventual lipolysis for energy was a protective mechanism. These days, we never get to the eventual lipolysis part.
Difference b/t endocrine & exocrine glands?
Endocrine release directly into bloodstream
Exocrine use ducts (salivary, lacrimal, pancreatic duct, sweat)
4 levels of endocrine gland disorder
Primary - dysfunction of endocrine gland itself
Secondary - dysf anterior pituitary gland
Tertiary - dysf hypothalamus
Quarternary - dysf target tissue; can’t respond to hormone
Adrenal gland
- hormone? Where released? their functions
Adrenal cortex:
- glucocorticoids (cortisol); GLU availability for brain & heart, suppress inflammatory responses
- mineralocorticoids (aldosterone); increase Na+ reabsorption & K+ excretion in kidneys
Adrenal medulla:
- catecholamines (epi & norepi); ^SNS
How regulate blood calcium lvls?
Thyroid —> calcitonin —> Ca+ lvls drop
(Decr bone resorption, decr reabsorption Ca+ in kidneys and intestines)
Parathyroids —> PTH —> Ca+ lvls rise
(Incr bone resorption, Incr reabsorption of Ca+ in kidneys and intestines)
GH function
Aka somatotropin
Maintain bone density, cartilage growth
Facilitate protein synthesis
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Insulin antagonist (decreases cell glucose use) in peripheral tissues.
Increase use of fatty acids
