Endocrine Flashcards
Steroid made from cholesterol absorbed in the blood
Responsible for 90% of mineralocorticoid activity
Aldosterone
Aldosterone
⬆️ Na
⬆️ H2O
⬇️ K
Aldosterone increased release when:
⬇️ renal perfusion
Dehydration
⬆️ angiotensin II
⬆️ K
Where is pancreas located?
In the left upper abdominal quadrant
Two types of pancreatic cells
Exocrine - acini cells - secrete enzymes that are important in digestive process
Endocrine - from islets of Langerhans
Three types of endocrine cells
Alpha - glucagon: opposite of insulin
Beta - insulin: intra cellular transportation of K
Delta - gastrin and somastostatin
Osmolality formula
(Na ✖️ 2) ➕ glucose/18 ➕ BUN/2.8
Normal osmolality values for blood and urine
Blood: 280
Urine: 300
What is osmolality?
It measures concentration
Fluid flows to areas of high osmolality
Arginine vasopressin
Produced by hypothalamus
Stored in posterior pituitary
Allows renal collecting ducts to become more permeable to water
Antidiuretic Hormone (ADH)
ADH
⬇️ Diuretic
Water conservation
Urine concentration
⬇️ UO
What increases ADH secretion?
Osmoreceptors in hypothalamus respond to changes in serum osmolality N/V Stress Morphine Nicotine
Blood glucose
Acute hypoglycemia
Three causes of acute hypoglycemia
Endogenous - within body
Exogenous - diabetic agent
Functional - use all of insulin - status epilepticus
Hypoglycemia causes stimulation of counterregulatory hormones:
E G G G
Epinephrine
Glucagon
Glucocorticoids
Growth hormones
Acute hyperglycemia with acidosis cause by not enough insulin, stress trauma or infection
Hypovolemia due to hypotonic fluid loss
Ketonemia
Anion gap > 14
Diabetic ketoacidosis
Normal anion gap and formula
Normal: 8
Formula: (Na+K) - (HCO3 + Cl)
Pathophysiology of DKA
⬆️ blood glucose ➡️ No insulin is released ➡️ without insulin, glucose just not enter cells and accumulates in the blood ➡️ hyperglycemia
Why is acidosis present in DKA?
The breakdown of lipids lead to ketoacids
Dehydration and shock lead to the formation of lactic acid
Dehydration is caused by osmotic diuresis secondary to hyperosmolality
Increased at first due to acidosis and decreased perfusion
Decreased after insulin is replaced
Potassium
Increase due to sodium chloride infusions and sodium loss
Consider K phosphate or K acetate for replacement fluids
Chloride
Increased only when severely dehydrated
Usually decreased due to urinary losses and dilution of solutes in extra cellular fluid
If dehydrated and hyper, do not lower too quickly due to risk of cerebral Adema
Sodium
Decreased due to osmotic diuresis
Phosphate and Magnesium
Decreased if phosphate replacement was high
Inverse relationship with phosphate
Calcium
Manifestations of DKA
Serum glucose > 300
pH
How can cerebral edema be prevented?
Reduce glucose and osmolality slowly
Avoid sodium bicarb ➡️ bicarb can lead to cerebral edema and increase CO2 production and worsen acidosis
If needed give slowly (0.5-1 mEq/L) over 1 hr
Rehydrate slowly ➡️ second bolus only if pressure is still dropping and shock still presence
Managing DKA
Volume replacement
➡️ NS or LR (if Cl is ⬆️)
➡️ If Na > 145 = 0.45% NS
➡️ If Na
Dilute urine
Not enough ADH
Not able to concentrate urine
Diabetes insipidus (DI)
Three causes of DI
Central ➡️ not enough ADH
(Head injury, neurosurgery, tumor, infection)
Nephrogenic ➡️ lack of renal response to ADH
(Kidney disorders, drug toxicity, electrolyte disturbances, sickle cell, renal dz)
Dipsogenic ➡️ oral intake of large amounts of water suppresses the release of ADH
Manifestations of DI
Dehydration ⬆️ SERUM osmolality > 295 ⬆️ SERUM Na > 145 ⬆️ BUN and Cr ⬇️ URINE osmolality
Management of DI
‼️ Slowly decrease Na by 1-2 mEq/hr over 24 hrs ‼️
Rapid volume expansion with isotonic fluids if in shock
Hypertonic fluid replacement
DDAVP (Desmopressin) ➡️ preferred
Goals: UO 1.010
Too much ADH
Excessive reabsorption of water
⬆️ volume
⬇️ Na
Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
Causes of SIADH
Pulmonary condition ➡️ infection, asthma, pneumothorax, PIP/PEEP (⬆️ pressure in intrathoracic cavity it responds by secreting ADH)
CNS conditions ➡️ infections, drama, hypoxic injuries, hydrocephalus, vascular abnormalities
Medications ➡️ Vasopressin, narcotics, chemo, barbiturates, postop
Manifestations of SIADH
⬇️ SERUM osmolality 300 ⬆️ URINE Na > 20 ⬆️ URINE specific gravity > 1.025 Hypertension Dyspnea on exertion Wt gain without edema
Treatment of SIADH
‼️ Na should rise by 0.5 mEq/L every hr ‼️
Eliminate excess water
NPO immediately
Increased serum osmolality: loop diuretics
Fluid restriction (30-75% of maintenance)
Hypertonic saline for severe cases
Initial goal 125-130
Risk for cerebral demyelination - tx may tear apart brain tissue
Large class of genetic metabolic diseases Synthesis or breakdown of fats, carbs, and/or proteins are affected Most are treatable with modification of the diet
Inborn errors of metabolism
Pathophysiology of inborn errors of metabolism
Usually due to a defect of a single gene that codes for enzyme statuses with the conversion of substances into other products
Symptoms are caused by toxic accumulation of substances
Usually present with a period without symptoms, followed by deterioration
Common signs and symptoms of Inborn errors of metabolism
Developmental delay, FTT Irritability and seizures ‼️ Abnormal odor ‼️ Lethargic and poor feeding Protein or carbohydrates sensitivities Temperature regulation difficulties Apnea/bradycardia Hepatic encepalopathy Hypo or hyperglycemia
Management of inborn errors of metabolism
Amino acids or enzyme cofactors for metabolic deficiencies ➡️ arginine
Dietary modification
What is the purpose of endocrine system?
Maintain body's internal environment Growth Reproduction metabolism Fluid and electrolyte balance Coordination body's stress response
