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!

A

Bingo

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!)

A

4-6

10-14

25
Q

Type 1 Dm - info?

A

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
Q

Dm Type 1 tends to affect males more than females - T/F?

A

True

27
Q

How do we diagnose DM Type 1?

A

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
Q

how do we manage Type 1?

A

insulin therapy, glucose monitoring (goal range 80-120), lab measurement of AIC, urine testing for ketones

29
Q

do we always test for ketones?

A

No - tested every 3 hours during illness and whenever glucose is >240 when illness not present.

30
Q

Hypoglycemia - symptoms?

A

Cold and clammy, needs some candy! Hunger, shakiness, weakness, paleness, blurry vision, sleepiness, sweating, anxiety, dilated pupils, dazed appearance, restlessness, seizures, etc.

31
Q

severe hypoglycemia episodes may result in permanent cognitive development, especially under age 5. T/F?

A

True

32
Q

How do we treat hypoglycemia?

A

15 grams of carbs - like apple juice, orange juce.. THEN cheese, etc.

33
Q

What is glucagon used for?

A

Emergency injection for unconscious person - stimulates liver to releasea stored glucose. However, it’s icky and makes people feel nasty as fuck!

34
Q

What are some mild symptoms of hyperglycemia?

Moderate?

Severe?

A

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
Q

Know this!

A

Here we go!

36
Q

Insulin pump - needle and catheter changed every 48-72 hours. T/f?

A

True

37
Q

What’s the glucose tragets (premeal) for toddlers/preschool?

BS, A1C

A

BS 100-180, A1C 7.5-8.5

38
Q

What’s the glucose tragets (premeal, BS & A1C) for school age kids?

A

BS 90-180, A1C goal <8

39
Q

What’s the glucose tragets (premeal, BS & A1C) for adolescents?

A

BS 90-130, A1C goal <7.5

40
Q

What is ketoacidosis?

A

Results from progressive deterioration with dehydration, electrolyte imbalance, acidosi, coma..and can cause death!

41
Q

Ketones in blood are strong acids that lower serum pH and produce ketoacidosis - T/F?

A

True

42
Q

When glucose isn’t available, what does the body break down?

A

Other shit!

43
Q

How do we manage ketoacidosis?

A

Insulin 0.1u/kg/hr, goal is to decrease glucose by 50-100 mg/dl/hr, dehydration correction with IV fluids

44
Q

We want to get glucose down as quickly as possible. T/F?

Dextrose is added once glucose falls to ___.

A

FALSE - slowly.

300

45
Q

DM Type 2 - ages? Things about it?

A

Insulin resistance, ages 10-19, obestiy, heredity, diet, sedentray lifestyle, acanthosis nigricans!!!!!!!!! (dark line around neck)

46
Q

What are some long-term complications of DM type 2?

A

microvascular complications, especially nephropathy and retinopathy, macrovascular disease, neuropathy

47
Q
A