Chapter 20- Endocrine Flashcards

1
Q

S/S type 1 DM

A
  1. polydipsia
    (intracell dehydration, hypothalamus increases thirst)
  2. polyuria
    (high BS= osmotic diuretic; glucose in urine)
  3. polyphagia
    (cell starvation)
  4. weight loss
    (protein/fat energy, osmotic diuresis/fluid loss)
  5. fatigue
    (metabolic change, poor use food)
  6. recurrent infection
    (high sugar, ischemia, neuropathy)
  7. prolonged wound healing
    (impaired blood supply)
  8. genital pruritus
    (fungal growth high BS)
  9. visual changes
    (water balance r/t high BS, microvascular)
  10. paresthesia
    (neuropathy)
  11. cardiovascular sx
    (chest pain, extremity pain, neuro deficit d/t
    atherosclerotic plaques)
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2
Q

Clinical findings DM 1 & 2

A
  1. HbA1c > 6.5%
  2. FPG > 126
  3. 2hr plasma > 200 oral glucose test
  4. Sx and random glucose > 200
  5. glucose in urine
  6. low C peptide in DM1 sometimes 2 (means low insulin)
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3
Q

Patho of DM1

A
  1. autoimmune- destroys beta cells
  2. lack of insulin
  3. decreased amylin
  4. excessive glucagon
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4
Q

Antibody type 1 DM

A

ZnT8Ab
Genetic disease

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5
Q

Risk factors DM2

A
  1. > 40 y/o
  2. african american/native american
  3. obesity
  4. HTN
  5. poor diet
  6. poor exercise
  7. genetics
  8. insulin resistance
  9. dyslipidemia
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6
Q

Patho DM 2

A
  1. obesity > hyperinsulunemia > insulin resistance
  2. low amylin, high glucagon
  3. low ghrelin (GI)
  4. low incretins (GI)
  5. renal absorption glucose (block to treat)
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7
Q

S/S DM 2

A
  1. nonspecific
  2. fatigue
  3. pruritus
  4. recurrent infection
  5. vision change
  6. neuropathy
  7. maybe polydipsia & polyuria
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8
Q

S/S metabolic syndrome (risk DM)

A
  1. increased weight circumference/central obesity
  2. triglycerides > 150
  3. HDL < 40 (men) < 50 (women)
  4. SPB >130 DBP > 85
  5. FPG > 100
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9
Q

Quick facts gestational DM

A
  1. 2nd/3rd trimester
  2. no previous h/o DM
  3. monitored postpartum Q3yrs
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10
Q

Maturity-onset diabetes of youth (MODY)

A
  1. < 25 y/o
  2. genetic
  3. neonatal DM
  4. atypical presentation
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11
Q

Acute complications of DM

A
  1. hypoglycemia (more risk DM1 d/t insulin tx)
  2. DKA (DM1)
  3. Hyperosmolar hyperglycemic nonketotic syndrome (DM2)
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12
Q

Sx HYPOglycemia

A
  1. pallor
  2. tremor
  3. anxiety
  4. tachycardia
  5. palpitations
  6. diaphoresis
  7. HA
  8. dizzy
  9. irritable
  10. fatigue
  11. poor judgement, confusion
  12. visual disturb
  13. hunger
  14. seizures/coma
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13
Q

Patho/clinical DKA

A

*Low insulin= breaking down fat too quickly > fatty acid increase to liver > stimulates:
1. low insulin, high catecholamines, cortisol, glucagon
2. HYPERglycemia
3. ketonuria
4. metabolic acidosis
5. hyperkalemia

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14
Q

S/S DKA

A
  1. Kussmaul respirations (hypervent)
  2. postural dizzy
  3. CNS depression
  4. ketonuria
  5. anorexia/weight loss
  6. n/v
  7. abdominal pain
  8. thirst
  9. dry mouth
  10. fruity/acetone breath
  11. HA
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15
Q

S/S hyperglycemic nonketotic syndromes

A

High glucose WITHOUT metabolic acidosis
1. polyuria
2. polydipsia
3. hypovolemia/dehydration (turgor, lips)
4. hypotension
5. tachycardia
6. n/v/abdominal pain
7. weakness
8. hypothermia
9. stupor/coma/seizure

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16
Q

3 Microvascular diseases DM

A
  1. diabetic retinopathy
    (leading cause blindness) & macular edema (blurry/loss
    vision)
  2. diabetic nephropathy
    (DM most common CKD/ESRD; glomerular damage)
  3. Diabetic neuropathy
    (most common; ischemia & demyelination)
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17
Q

3 Macrovascular diseases DM

A
  1. cardiovascular disease
    (CAD, CHF)
  2. stroke
  3. PVD
18
Q

Why is DM infection risk? (5 reasons)

A
  1. impaired senses
  2. hypoxia
  3. pathogens like glucose
  4. decreased blood supply
  5. suppressed immune response
19
Q

What is Grave’s Disease

A

Autoimmune HYPERthyroidism
Type II hypersensitivity

20
Q

Grave’s patho/lab findings

A
  1. autoantibodies against TSH receptor
  2. Goiter (large thyroid)
  3. increased TH (T3/T4) especially T3
  4. low TSH
21
Q

Grave’s clinical manifestations

A

EYES: protruding eyeball, periorbital edema, double
vision; ophthamopathy (large ocular muscles or lag
of globe upward gaze and of upper lid downward
gaze)

DERMOPATHY (SMALL # have pretibial myxedema; SQ
swell anterior legs, indurated/erythematous skin)

22
Q

S/S Grave’s

A

Think hyperactive/fast

Exophthalmos (bulging swollen eyes)
Thin hair
Goiter (warm, nodular)
Tachycardia
Diarrhea
Warm skin, sweaty palms
Hyperreflexia
Weight loss
Pretibial edema

23
Q

What’s thyrotoxic crisis (thyroid storm)

A
  • undiagnosed/tx Grave’s
  • TH levels rise dramatically, death within 48 hrs w/o tx
  • response to physiologic stress (esp. thyroid surgery)
24
Q

Thyroid storm sx

A
  1. hyperthermia
  2. tachycardia/tachydysrhythmias
  3. HF
  4. agitation/delirium
  5. n/v/d
25
Q

What’s cushing’s syndrome

A

s/s from chronic exposure to excess cortisol regardless of cause

26
Q

What’s cushing’s disease

A

excess endogenous secretion Adrenocorticotropic hormone (ACTH)

27
Q

What’s cushing-like syndrome

A

SE long-term glucocorticoids

28
Q

S/S cushing’s

A
  1. high cortisol
  2. weight gain: trunk, face, cervical region
    “moon face”, “truncal obesity”, “buffalo hump”
  3. glucose intolerance (cortisol insulin resist)
  4. polyuria & glycouria
  5. muscle wasting/weakness (thin extremities)
  6. osteoporosis w/ patho fx
  7. acne
  8. thin scalp hair
  9. emotional instability
  10. facial hair
  11. cardiac hypertrophy, HTN
  12. striae of skin (stretch marks)
  13. easy bruising
  14. DM
  15. disturbed sleep
  16. memory loss, difficulty concentrating
29
Q

Lab values Cushing

A
  1. hyperglycemia
  2. glycosuria
  3. hypokalemia
  4. metabolic alkalosis
  5. high cortisol
  6. low ACTH (d/t neg feedback)
30
Q

What is Addison’s and who does it affect

A

primary adrenal insufficiency, rare, age 30-60, can be autoimmune

31
Q

Addison’s patho

A

Low corticosteroid and mineral corticoid synthesis, elevated ACTH

32
Q

What other diseases associated w/ Addison’s

A

When organ-specific autoimmune, associated with Hashimoto thyroiditis, pernicious anemia, idiopathic hypoparathyroidism

33
Q

Labs in Addison’s

A
  1. low cortisol
  2. low aldosterone
  3. high ACTH
  4. low glucose
  5. BUN high d/t dehydration
  6. high eosinophils & lymphocytes
  7. ***Hyperkalemia (cause mild alkalosis)
34
Q

S/S Addison’s

A
  1. personality change
  2. anorexia, n/v/d, abdominal pain
  3. hyperpigmentation & vitiligo
  4. HYPOtension (cardiac insufficiency)
  5. adrenal atrophy
  6. muscle weakness
  7. fatigue
35
Q

Biggest concern in Addison’s

A

Adrenal or Addisonian crisis
Hypotension > complete vascular collapse > shock

36
Q

What’s Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

A

High ADH increases water reabsorption by kidneys. High extracellular fluid volume, low sodium, hypoosomolarity. usually d/t tumors, lungs, CNS, meds, surgery

37
Q

S/S SIADH

A

Sx of hyponatremia, overhydrated. “Soggy Sid”. High ADH.
1. thirst
2. impaired taste
3. anorexia
4. dyspnea on exert
5. fatigue
6. GI
7. weight gain from retention w/o edema
8. confusion, lethargy, muscle twitch
9. low u/o
10. high urine osmolality and SG, low serum osmolality

38
Q

What’s diabetes insipidus (DI) and 2 types

A

Insufficient (low) ADH= too much free water fluid loss into urine. Partial/total inability concentrate urine
1. Neurogenic= insufficient secretion ADH
2. Nephrogenic= renal tubules don’t respond to ADH
(pyelonephritis, amyloidosis, uropathies, polycystic
kidney disease)

39
Q

S/S diabetes insipidus

A
  1. polyuria/nocturia/LG volumes dilute urine (increased
    plasma osmolality)
  2. Polydipsia
  3. Dehydration
  4. Hypernatremia
  5. lg bladder capacity & hydronephrosis
  6. low urine osmolality and SG, high serum osmolality
40
Q

U/o with DI

A

8-12 L/day

41
Q

What are pheochromocytomas

A

Chromasffin cell tumors of the adrenal medulla that cause HYPERfunction of adrenal medulla

42
Q

S/S phe

A