Endocrine Flashcards

(40 cards)

1
Q

Steroid made from cholesterol absorbed in the blood

Responsible for 90% of mineralocorticoid activity

A

Aldosterone

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2
Q

Aldosterone

A

⬆️ Na
⬆️ H2O

⬇️ K

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3
Q

Aldosterone increased release when:

A

⬇️ renal perfusion
Dehydration
⬆️ angiotensin II
⬆️ K

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4
Q

Where is pancreas located?

A

In the left upper abdominal quadrant

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5
Q

Two types of pancreatic cells

A

Exocrine - acini cells - secrete enzymes that are important in digestive process

Endocrine - from islets of Langerhans

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6
Q

Three types of endocrine cells

A

Alpha - glucagon: opposite of insulin
Beta - insulin: intra cellular transportation of K
Delta - gastrin and somastostatin

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7
Q

Osmolality formula

A

(Na ✖️ 2) ➕ glucose/18 ➕ BUN/2.8

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8
Q

Normal osmolality values for blood and urine

A

Blood: 280

Urine: 300

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9
Q

What is osmolality?

A

It measures concentration

Fluid flows to areas of high osmolality

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10
Q

Arginine vasopressin
Produced by hypothalamus
Stored in posterior pituitary
Allows renal collecting ducts to become more permeable to water

A

Antidiuretic Hormone (ADH)

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11
Q

ADH

A

⬇️ Diuretic
Water conservation
Urine concentration
⬇️ UO

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12
Q

What increases ADH secretion?

A
Osmoreceptors in hypothalamus respond to changes in serum osmolality
N/V
Stress
Morphine
Nicotine
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13
Q

Blood glucose

A

Acute hypoglycemia

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14
Q

Three causes of acute hypoglycemia

A

Endogenous - within body
Exogenous - diabetic agent
Functional - use all of insulin - status epilepticus

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15
Q

Hypoglycemia causes stimulation of counterregulatory hormones:

E G G G

A

Epinephrine
Glucagon
Glucocorticoids
Growth hormones

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16
Q

Acute hyperglycemia with acidosis cause by not enough insulin, stress trauma or infection

Hypovolemia due to hypotonic fluid loss

Ketonemia

Anion gap > 14

A

Diabetic ketoacidosis

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17
Q

Normal anion gap and formula

A

Normal: 8

Formula: (Na+K) - (HCO3 + Cl)

18
Q

Pathophysiology of DKA

A

⬆️ blood glucose ➡️ No insulin is released ➡️ without insulin, glucose just not enter cells and accumulates in the blood ➡️ hyperglycemia

19
Q

Why is acidosis present in DKA?

A

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

20
Q

Increased at first due to acidosis and decreased perfusion

Decreased after insulin is replaced

21
Q

Increase due to sodium chloride infusions and sodium loss

Consider K phosphate or K acetate for replacement fluids

22
Q

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

23
Q

Decreased due to osmotic diuresis

A

Phosphate and Magnesium

24
Q

Decreased if phosphate replacement was high

Inverse relationship with phosphate

25
Manifestations of DKA
Serum glucose > 300 | pH
26
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
27
Managing DKA
Volume replacement ➡️ NS or LR (if Cl is ⬆️) ➡️ If Na > 145 = 0.45% NS ➡️ If Na
28
Dilute urine Not enough ADH Not able to concentrate urine
Diabetes insipidus (DI)
29
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
30
Manifestations of DI
``` Dehydration ⬆️ SERUM osmolality > 295 ⬆️ SERUM Na > 145 ⬆️ BUN and Cr ⬇️ URINE osmolality ```
31
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
32
Too much ADH Excessive reabsorption of water ⬆️ volume ⬇️ Na
Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
33
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
34
Manifestations of SIADH
``` ⬇️ SERUM osmolality 300 ⬆️ URINE Na > 20 ⬆️ URINE specific gravity > 1.025 Hypertension Dyspnea on exertion Wt gain without edema ```
35
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
36
``` 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
37
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
38
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 ```
39
Management of inborn errors of metabolism
Amino acids or enzyme cofactors for metabolic deficiencies ➡️ arginine Dietary modification
40
What is the purpose of endocrine system?
``` Maintain body's internal environment Growth Reproduction metabolism Fluid and electrolyte balance Coordination body's stress response ```