Endocrine Disorders (Part 2) - Unit 3 Flashcards

1
Q

What increases ADH Secretion?

A

osmoreceptors in hypothalamus respond to changes in serum osmolality

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2
Q

What is diabetes insipidus?

A

NOT ENOUGH ADH

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3
Q

DI - kidney’s cannot reabsorb water, cannot concentrate urine, and they have concentrated blood. T/F?

A

True

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4
Q

What are the 3 types of DI?

A

central (not enough ADH) and nephrogenic (lack of renal response to adh), dipsogenic (oral intake of large amounts of water suppresses release of ADH)

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5
Q

Central DI - what causes it?

A

head injury, neurosurgery, tumor, hypoxic injuries, infection (meningitis, encephalitis), congenital CNS defects

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6
Q

What causes nephrogenic DI?

A

drug toxicity (amphotericin, gentamicin, lasix), electrolyte disturbances, sickle cell disease, renal disease

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7
Q

Dipsogenic - more than likely psych T/F?

A

TRUE

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8
Q

Dipsogenic - might also be because we fead an infant what?

A

Water. do not do that until they’re about 6 months old / can hold a sippy cup.

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9
Q

What are some manifestations of DI?

A

dehydration, increased plasma osmolality >295, hypernatremia, decreased urine osmolality, decreased urine Na5ml/kg/hr, SG

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10
Q

What is hypernatremia and what does it indicate?

A

serum sodium greater than 145, indicates dehydration

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11
Q

What are some signs of dehydration?

A

Dry mucus membranes, irritability, lethargy, headache, seizures

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12
Q

How do we manage central DI?

A

Rapid volume expansion with isotonic fluids if in shock, slowly decrease Na by 1-2 mew/hr over 24 hours, hypotonic fluid replacement, DDAVP (spray in nose), vasopressin, NS/LR

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13
Q

What are the goals of UO and SG in managing central DI?

A

UO = 1.010

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14
Q

what is SIADH?

A

Syndrome of inappropriate antidiuretic hormone secretion - aka, TOO MUCH ADH

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15
Q

SIADH - excessive reabsorption of water, hypervolemia, hyponatremia, etc. T/F?

A

True

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16
Q

What are some causes of SIADH?

A

Pulmonary conditions (infection, asthma, pneumothorax, positive pressure ventilation — increased pressure), CNS conditions (infections, trauma and hypoxic injuries, hydrocephalus, vascular abnormalities), medications (vasopessin, antidepressants antianxiety, antipsychotic, seizure meds, DDAVP, narcotics, chemo, barbituates), post-operative patients

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17
Q

SIADH - may have increased vasopressin for 3-4 days post-op. T/F?

A

True

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18
Q

What are some manifestations of SIADH?

A

Decreased urine output 20, low serum osmolality

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19
Q

What are some manifestations of hyponatremia?

A

headache, nausea/vomiting, confusion, seizures, muscle twitching, cerebral edema

20
Q

How do we treat SIADH?

A

eliminate excess water, increase serum osmolality, fluid restriction (30-75% of maintenance!!), hypertonic saline for SEVERE cases, loop diuretics

21
Q

For treating SIADH, what’s the initial goal for severe cases?

A

Initial goal 125-230 then Na should rise by 0.5 meq/l every hour - - risk of cerebral demyelination.

22
Q

Fill in the info!

23
Q

How many children in the US have DM Type 1 + 2?

A

216,000, with AA’s and Hispanics at greater risk.

24
Q

When’s the typical age of onset for Type 1? (Hint, 2 sets!)

25
Type 1 Dm - info?
Insulin-producing cells in the pancreas are destroyed, cells starve to death so glucose in unable to enter the cell and remains in the bloodstream.
26
Dm Type 1 tends to affect males more than females - T/F?
True
27
How do we diagnose DM Type 1?
may mimic severe case of flu, ketosis, weight loss, vomiting, polydipsia, polyuria, polyphagia, malaise, coma, random plasma glucose \>126, 2 hr pplasma glucose \>200 during an OGTT
28
how do we manage Type 1?
insulin therapy, glucose monitoring (goal range 80-120), lab measurement of AIC, urine testing for ketones
29
do we always test for ketones?
No - tested every 3 hours during illness and whenever glucose is \>240 when illness not present.
30
Hypoglycemia - symptoms?
Cold and clammy, needs some candy! Hunger, shakiness, weakness, paleness, blurry vision, sleepiness, sweating, anxiety, dilated pupils, dazed appearance, restlessness, seizures, etc.
31
severe hypoglycemia episodes may result in permanent cognitive development, especially under age 5. T/F?
True
32
How do we treat hypoglycemia?
15 grams of carbs - like apple juice, orange juce.. THEN cheese, etc.
33
What is glucagon used for?
Emergency injection for unconscious person - stimulates liver to releasea stored glucose. However, it's icky and makes people feel nasty as fuck!
34
What are some mild symptoms of hyperglycemia? Moderate? Severe?
Mild = lack of concentration, thirst, frequent urination, sweet/fruity breath, thirst. Mod = vomiting, nausea, dry mouth, stomach cramps, Severe = labored breathing (metabolic acidosis), confused, very weak, unconscious. High and dry, my sugar is high!
35
Know this!
Here we go!
36
Insulin pump - needle and catheter changed every 48-72 hours. T/f?
True
37
What's the glucose tragets (premeal) for toddlers/preschool? BS, A1C
BS 100-180, A1C 7.5-8.5
38
What's the glucose tragets (premeal, BS & A1C) for school age kids?
BS 90-180, A1C goal \<8
39
What's the glucose tragets (premeal, BS & A1C) for adolescents?
BS 90-130, A1C goal \<7.5
40
What is ketoacidosis?
Results from progressive deterioration with dehydration, electrolyte imbalance, acidosi, coma..and can cause death!
41
Ketones in blood are strong acids that lower serum pH and produce ketoacidosis - T/F?
True
42
When glucose isn't available, what does the body break down?
Other shit!
43
How do we manage ketoacidosis?
Insulin 0.1u/kg/hr, goal is to decrease glucose by 50-100 mg/dl/hr, dehydration correction with IV fluids
44
We want to get glucose down as quickly as possible. T/F? Dextrose is added once glucose falls to \_\_\_.
FALSE - slowly. 300
45
DM Type 2 - ages? Things about it?
Insulin resistance, ages 10-19, obestiy, heredity, diet, sedentray lifestyle, acanthosis nigricans!!!!!!!!! (dark line around neck)
46
What are some long-term complications of DM type 2?
microvascular complications, especially nephropathy and retinopathy, macrovascular disease, neuropathy
47