endocrine Flashcards

1
Q

thyroid hormone fxn

A

T4 = 90%, T3 = 10% of production, also calcitoninaffects almost all body tissuesmaintains metab stability by regulating O2 reqs & metabprotein synthesis & catabolism (if x hormone)temp regimpacts CHO metab: enhances epi to stim glycogenolysis & gluconeogenesisaffects lipid metabolism (accelerates degradation of LDL)↑s AV node depol to ↑ HR↑s resp drive, mental alertness, GI motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

when hypothalamus releases TRH x2

A

in resp to ↓ circulating T3 & T4cerebral cortex resp to ↓ body T or cold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

TRH & TSH impact

A
  • TRH: anterior pituitary → release TSH * TSH stimulates thyroid to release T3 & T4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

thyroid hormones: secreted most vs active hormone

A

T4 secreted 90%unbound T3 is most active (90% from T4 deiodination)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

hormone ↑ in primary hypothyroidism

A

TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

hormone ↓ in primary hyperthyroidism

A

aka Graves DiseaseTSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

hormone ↑ in primary hyperthyroidism

A

FT4 (false if on heparin)T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

hormone ↓ in primary hypothyroidism

A

FT4T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

palpable thyroid nodules: mgmt

A

1. thyroid fxn tests (TSH, FT4, thyroid antibodies)#2. imaging – US (assess if more than 1 nodule, if it is a cyst or solid)#3. Fine Needle Aspiration bx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

thinning of outer third of eyebrows sign of

A

hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

primary vs secondary hypothyroidism

A

primary: gland dysfxnsecondary: pituitary or hypothalamus dysfxn (normal or ↓TSH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

most common cause of hypothyroidism

A

Hashimoto’s (autoimmune)- evidence of ab to thyroid ags

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Hashimoto’s Thyroiditis

A

transient hyperthyroidism w/ an ↑in antibodies fol↓ed by hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Graves Disease

A

autoimmune disease w enlarged thyroid goiterthyroid eye disease (opthalmoptosis)↓TSH↑ T4 or Ft4↑ antithyroglobulin ab, alk phos, thyroid radioactive iodine uptake)hypercalcemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

hypothyroidism tx

A

Levothyroxine (Synthroid, Levoxyl)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Graves Disease tx

A
  • inderal (Propranolol)- thiourea drugs: PTU, methimazole (Tapazole)- radioactive I- surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

thiourea drugs

A

block synthesis of T3 & T4PTU, methimazole (Tapazole)call NP: fever, infection, agranulocytosis (abs neut count lt 500)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

hypothyroidism: monitor & goal

A

TSH (barometer vs T4 for dx)maintenance dosage levothyroxine 100 - 200 ug/d

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

if thyroid replacement too rapid

A

↑HR, dyspnea, orthopnea, angina, palpitations, nervousness, insomnia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

thyroid crises + s/s

A

myxedema or thyroid stormAMS, altered thermal reg, precipitating event/illness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q
  • myxedema *
A

Severe HYPOTHYROIDISM- ↓ thyroid fxn + subsequent ↓T3 & T4 → alteration F/E - ↑ capillary permeability, fluid retention- non-pitting edema hands/feet- 50-80% mortality rate d/t hypercapnia & hypoventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q
  • myxedema presenting s/s *
A
  • resp depression, hypotension *stupor, coma, hypothermia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

thyroid storm

A

Extreme form of HYPERTHYROIDISMMay be brought on by stressful illness or trauma, radioactive iodine, or thyroid surgery↑ mortality rate

24
Q
  • thyroid storm s/s *
A
  • CV collapse *↑ feverSevere agitationConfusionResp distress if thyroid enlargedVomiting & Diarrhea
25
Q

thyroid storm tx

A

Inderal (monitor carefully: HF)Thiourea Drugs (PTU, Tapazole)HydrocortisoneSodium Iodine (radioactive I) - 1 hr after Thiourea- goal: destroy thyroid parenchyma

26
Q

adrenal layers - what secretes what?

A

outer: aldosteroneinner: cortisol

27
Q

cortisol

A

major glucocorticoid, counters insulin → inhibits insulin secretion, ↑ hepatic gluconeogenesis

28
Q
  • ↑ skin pigmentation cardinal sign of *
A

Addison’s disease

29
Q

Addison’s dx

A

Cosynthropin Stimulation Test → give ACTH (corticotropin) & check serum cortisol levels in 30 & 60 minutes,eval for plasmas cortisol rise, in Addison’s level ↓

30
Q

Cosynthropin Stimulation Test

A

Addison’s dx test

31
Q

Addison’s tx

A

replacement tx: mineralocorticoidsglucocorticoids- hydrocortisone- prednisone (alternate)- fludrocortisone

32
Q

fludrocortisone

A

for insufficient salt retention during Addison’s, stimulates renal tubules to reabsorb Na/excrete K

33
Q

adrenal crisis

A

acute adrenal insufficiencyresult of insufficient cortisol either from insufficient intake or ↑d need

34
Q
  • adrenal crisis s/s *
A
  • hypotension s/t ↓ vascular tone (shock-like state), hyperpigmentation *HA, confusion, coma, n/v/d, abd pain, fever, dehydration
35
Q

addison’s + infections

A

must be tx immediately & vigorously: ↑ hydrocortisone - w major stresses, surgery, trauma, ↑ dose, MediAlert bracelet!

36
Q

adrenal crisis mgmt

A

hydrocortisone IV STAT3L bolus NS or D5NS over 2-3 hrtx precipitating factors & hypoglycemiaone resolved, determine degree of insufficiency - cosynthropin stimulation test

37
Q

Cushing’s Sydrome causes x3

A

exces intake glucocorticoids (Prednisone)if spontaneous (rare):- excess ACTH by pituitary (70%)- lung cancer (SCLC = ectopic source, 15%)- adrenal tumor (15%)

38
Q

Cushing’s tests x3

A

screening: 1mg dexamethasone (Decadron) @ 2300 + check serum cortisol @ 080024 hr urine test (cortisol & creatinine; cort/cr gt 95mcg = hypercort)suppression test (further testing)- give decadron, collect urine day 2- urine free cortisol gt 20 = Cushing’s

39
Q
  • the key to Cushing’s mgmt *
A

DETERMINE CAUSE/SOURCE- ACTH normal or ↓: ot pituitary- ACTH ↑ = Cushing’s

40
Q

Cushing’s tx

A

treat the causetransphenoidal resection if pituitary tumor +/- radunilateral adrenalectomy + hydrocort replacement tx until remaining gland recovers

41
Q

ADH

A

works in tubules: ↑ H2O reabsorptionreleased: serum Na ↑(hyperosmolar) or hypovolemiaunder influence of neural input (CNS) & baroreceptors in the chest

42
Q

diabetes insipidus causes

A

familialpituitary or hypothalamus damagenephrogenic DI (inability of kidney to respond to vasopressin)

43
Q
  • DI dx *
A
  • 24 hour urine ** vasopressin challenge: desmopressin (IN) = measure UOP & intake *clinical s/sMRI: pituitary tumor
44
Q

DI tx

A

desmopressin (IN, PO, IV)mild: adeq fluid intake

45
Q

SIADH s/s

A
  • euvolemic & not osmolality dependent- hyponatremia- serum osm lt 280 mOsm/kg + inappropriate ↑ urine osm gt 900mOsm/kg- no cardiac, liver, lung dz- urine Na gt 20mEq/L- no edema or HTN bc ↑ H2O evenly distributed
46
Q

SIADH causes

A

CNS structural (basilar skull fx) or metabolic disorderSCLC (ectopic source)drug induced: antidepressants (amitriptyline), carbamazepine, haloperidol, chlorproamide

47
Q

SIADH tx

A

drug induced? dcmild-mod H2O intox? restrict fluid 800-1000 mL/daysevere hypoNa + neuro changes: 250 - 500 mL 3% NaCl over 2-4 hr and Lasix- avoid rapid correction d/t risk of demyelination of pons!

48
Q

somogyi phenomenon + mgmt

A

morning REBOUND hyperglycemia & ketouria responding to NOCTURAL HYPOGLYCEMIA (stims counter-reg hormones)monitor: 3AM glucoses (expect ↓)tx: ↓ insulin qH 10% or + ↑ CHO @ qHS

49
Q

dawn phenomenon + mgmt

A

AM fasting hyperglycemia, no sx nocturnal hypoglycemia Normal or ↑BG @ qHS blood glucose checkd/t circadian rhythm & release of growth hormone → ↑ BG btw 5 & 8AMtx: ↑qHS insulin 2-3 units

50
Q

non-ketotic hyperglycemic hyperosmolar coma: serum osm 310 manifestation

A

lethargy & confusion

51
Q

non-ketotic hyperglycemic hyperosmolar coma: serum osm 320 - 330 manifestation

A

coma

52
Q

non-ketotic hyperglycemic hyperosmolar coma: dx

A

hyperglycemia 600+serum osm 310+pH 7.3+HCO3 15+anion gap lt 14

53
Q

non-ketotic hyperglycemic hyperosmolar coma

A

partial/relative insulin insufficiency triggering gluconeogenesis but NOT ACIDOSIS= profound volume depletion (6-10 L) resulting in RENAL INSUFFIENCY = ↓ glucose excretion & contrib to ↑BGpoorly recognized until profound volume depletion

54
Q
  • cornerstone of non-ketotic hyperglycemic hyperosmolar coma therapy *
A
  • FLUID REPLACEMENT! *- hypotn: NS 1-2L first hr- normotn: 0.45% NS 4-6L in 1st 8 hrs- glucose @~250 = D5W or D1/2NSgoals- glucose: 250-300 (↓ risk cerebral edema)- UOP 50cc +monitor for HF esp elderly
55
Q

critically ill: target glucose

A

140 - 180monitor q 30 w 2 hr IV infusions

56
Q

non-critically ill: target glucose

A

fasting lt 140random checks lt 180preferred insulin: scheduled SQ + basal, nutritional, correction components

57
Q

basal insulin requirement

A

0.01 u/kg/hr