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Internal Medicine EOR > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Acromegaly etiology

A

Parotid gland producing too much GH

Gigantism: before closure of epiphyses (kiddos)

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2
Q

Acromegaly manifestations

A

Excessive growth of hands, feet, jaw, internal organs
Almost always a pituitary adenoma

Amanorrhea, HTN, HA, visual field loss, weakness

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3
Q

Acromegaly Dx

A

elevated serum IGF-1 (confirmed by GTT (glucose not suppressed following oral glucose

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4
Q

Acromegaly tx

A

Pituitary transsphenoidal microsurgery TOC

Meds: dopamine agonists, somatostatin analogs, tamoxifen

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5
Q

Primary Adrenal Insufficiency etiology

A

Decreased cortisol, increased ACTH

Can lead to hyponatremia, hyperkalemia, hypovolemia, hypotension

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6
Q

Primary adrenal insufficiency manifestations

A

Disorientation, weakness, fatigue, body aches, n/v, hyperpigmentation

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7
Q

Primary adrenal insufficiency Dx

A

Testing AM cortisol levels (6-8am)

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8
Q

Primary Adrenal Insufficiency Tx

A

Acute crisis: IV corticosteroids/rehydration. Transfer to steroids when stable

Long term: prednisone +/- mineraocorticoids

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9
Q

Addisons disease etiology

A

Autoimmune adrenal insufficiency d/t infiltration/destruction of adrenals from: TB, amyloidosis, hemochromatosis, bilateral adrenal CA, infections

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10
Q

Addisons sx/tx

A

exactly like primary adrenal insufficiency

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11
Q

Cushing’s Syndrome etiology

A

Syndrome: sx of excess cortisol
Disease: cushings syndrome SPECIFICALLY caused by pituitary increased ACTH secretion

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12
Q

Cushing’s Syndrome Manifestations

A

Redistribution of fat: central trunk obesity, moon face, buffalo hump

Wasting of extremities, skin atrophy

HTN, weight gain, hypokalemia, acanthosis nigricans

Hirtuism, oily skin, acne, virilization

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13
Q

Cushing’s Dx

A

Low dose Dexameth suppression test: a normal test is cortical suppression

24 hours urinary free cortisol level

Salivary Cortisol levels

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14
Q

Cushing’s Tx

A

Transsphenoidal surgery, steroid taper

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15
Q

DM insipidus etiology

A

ADH (vasopressin) deficiency or insensitivity

Central DI: decreased ADH production (MC)
Nephrogenic DI: partial or complete insensitivity to ADH (D/T drugs usually)

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16
Q

DM Insipidus manifestations

A

Polyuria, polydipsia, nocturia

Hypernatremia if severe or decreased water intake

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17
Q

DM insipisdus Dx

A

Fluid deprivation: establishes Dx –> continued production of dilute urine

Desmopressin Stim test

  • Central: reduced urine output
  • Nephro: continued production of dilute urine (no response)
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18
Q

DM insipidus Tx

A

Central: demopression/ DDVAP / Carbamezapine

Nephro: Na/protein restriction

If +sx: hypotonic solution, D5W, 1/2NS

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19
Q

DM etiology

A

Type I: pancreatic cell destruction, no insulin
- patient usually in DKA

Type II: insulin resistance and impraired secretion
- genetic or obesity/lack of activity MC>40yo

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20
Q

Gestational DM

A

Prego. Complications:

Neuropathy: decreased DTR, paresthesias

Autonomic: orthostatic hypotension, gastroparesis

Retinopathy: painless detrioration of small retinal vessels

Nephropathy: microalbuminuria

HYPOGLYCEMIA

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21
Q

Sx of hypoglycemia

A

Sweating, tremors, palpitations, nervousness, tachycardia

Dx: BS<70

Tx: mild: give sugar
severe<40 IV bolus of D50

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22
Q

Dawn Phenomenon

A

normal glucose until rise in serum glucose level between 2am and 8am

tx: injection of intermediate acting insulin before bed

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23
Q

Somogyi effect

A

nocturnal hypoglycemia followed by rebound hyperglycemia

tx: eat snack before bed

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24
Q

DM Dx

A

Fasting BG >126
A1C >6.5
Random Glucose >200

2/3 to dx
SCREEN ANY 40-70 year old that is overweight, check q 3 years

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25
Q

DM Tx

A

Lifestyle mods first
Insulin therapy for Type I
Oral Antihyperglycemic for Type II

Neuropathy: gabapentin
Retinopathy: eye screening yearly
Nephropathy: ACEi

METFORMIN 1st line PO

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26
Q

DM Goals

A

A1C <7%
Preprandial glucose 80-130
Postprandial glucose <180

Lipid control LDL <100, HDL>40, TG <150

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27
Q

Hypercalcemia sx/ tx

A

lethargy, hypoereflexia, kidney stones

tx: NS, lasixs, dialysis

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28
Q

Hypocalcemia sx/tx

A

Perioral tingle, hyperreflexia, CHVOSTEK SIGN, prolonged QT

Tx: IV calcium gluconate

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29
Q

Hypernatremia sx/tx

A

Restlessness, ataxia, seizures, lethargy, AMS

Tx: FWD = TBW x (Serum Na - 140)/140

Do not correct more than 10mEq/day or 0.5mEq/hr

30
Q

Hypovolemic hypernatremia sx/tx

A

Total body sodium deficit + free water deficit

tx: Isotonic Crystalloid (NS/LR), minimiz Na containing fluids

D5W @ 1.35 ml/hr /kg

31
Q

Hyponatremia sx/tx

A

Mild: anorexia, nausea, lethargy
Mod: disoriented, agitated, AMS
Sev: seizures, coma, death

Tx: water restriction for mild, hypertonic saline for severe but dont correct more than HALF the deficit in the first 24 hours

32
Q

Hyperparathyroidism etiology

A

Primary: increased PTH (MC type)

Secondary: increased PTH d/t hypocalcemia or Vit D

Tertiary: prolonged PTH stimulation from secondary

33
Q

Primary Hyperparathyroidism

A

MC cause: Adenoma
Occurs in 20% of people using Lithium

MEN-1: P’s: parathyroid, pancreas tumors, pituitary tumors

MEN-2A: hyperparathyroidism, pheochromocytoma, medullary thyroid carcinoma

34
Q

Secondary hyperparathyroidism

A

increased PTH d/t hypocalcemia or Vit D deficiency

  • Parathyroid cland is compensating
  • Chronic Kidney failure MC cause
35
Q

Tertiary Hyperparathyroidism

A

prolonged PTH stim after secondary –> autonomous PTH secretion

Often in post transplant patients

36
Q

Hyperparathyroidism manifestations

A

Stones
Bones
Grones
Overtones

Decreased DTRs

37
Q

Hyperparathyroidism Dx or primary

A

Tirad: hypercalcemia, increased intact PTH, decreased phosphate

24 urine calcium secretion, increased vit D, osteopenia on bone scan

38
Q

Hyperparathyroidism management

A

Surgery

Fit D/Ca supps if secondary

Tx hypercalcemia if sx: IV fluids, furosemide

39
Q

Hypoparathyroidism etiology

A

RARE, either low PTH or insensitivity to its action

40
Q

Hypoparathyroidism etiologies

A

2 MC causes: postsurgical or autoimmune

41
Q

Hypoparathyroidism sx

A

sx: carpopedal spasms, trousseaus, chvostek, increased DTRS

42
Q

Hypoparathyroidism dx/tx

A

dx: Triad of hypocalcemia, decreased PTH and increased phosphate

Tx: calcium supplementation and Vit D

43
Q

Grave’s etiology

A

Autoimmune

Increased thyroid hormone synthesis, worse with stress/prego/illness

44
Q

Grave’s sx

A

Thyroid bruits, enlarged thyroid, ophthalmopathy

Pretibial myxedema: nonpitting, edematous, pink to brown plaques, on shin

45
Q

Grave’s Dx

A

+thyroid stimulating immunoglobulins

Hyperthyroid TFTs: increased T4, decreased TSH

Raiu: increased diffuse uptake or radioactive iodine

46
Q

Grave’s sx

A

Radioactive iodine MC therapy
Methimazole or PTU
Thyroidectomy

47
Q

Toxic Multinodular Goiter

A

Plummer’s Disease

Autonomous functioning nodules

48
Q

Toxic adenoma

A

One autonomous functioning nodule

49
Q

Sx of both TMG and TA

A

Clinical hyperthyroidism, no skin changes, palpable nodules

Compressive symptoms: dyspnea, dysphagia, stridor, hoarseness

50
Q

Dx of Grave’s

A

Increased T4
Decreased TSH
RAIU: patcy

51
Q

Grave’s management

A

Radioactive iodine MC therapy
Surgery
Methimazole, PTU

52
Q

TSH secreting pituitary adenoma etiology / sx

A

autonomous TSH secretion by pituitary adenoma

Sx: Bitemporal Demianopsia, enlarged thyroid, amenorrhea, galactorrhea, HA

53
Q

TSH secreting pituitary adenoma Dx/Tx

A

Increased T4
Increased TSH
Sellar Turcica Mass
RAIU: diffuse uptake

Tx: surgery

54
Q

Thyroid storm etiology

A

Potentially life threatening complication of untreated thyrotoxicosis usually after precipitating event
RARE AF

55
Q

Thyroid storm PE/Dx

A

Hypermetabolic state: palpitations, tachycardic, Afib, fever, nausea, tremors

Dx: Primary hyperthroid TFT: increased T4 decreased TSH

56
Q

Thyroid Storm Tx

A

Anti-thyroid meds: IV PTU or methimazole
Beta Blockers
IV Glucocorticoids

57
Q

Pheochromocytoma etiology

A

catecholamine secreting adrenal tumor (CHROMAFFIN CELLS)

Secretes norepi and epi autonomously and intermittently
90% are benign

58
Q

Pheochromocytoma sx

A

HTN

PHE palpitations, HAs, excessive sweating

59
Q

Pheochromocytomam Dx

A

Plasma fractionated metanephrines
Increased 24 hours urinary catecholamines
MRI/CT visualizes adrenal tumor

60
Q

Pheochromocytoma Tx

A

complete adrenalectomy

Phenoxybenzamine first then beta blocker

61
Q

Hypothyroidism etiology

A

MC: hashimoto’s thyroiditis

62
Q

Hypothyroidism PE

A

Generalized weakness, fatigue, facial swelling, constipation, cold intolerance, weight gain, periorbital edema, dry skin, coarse brittle hair

63
Q

Hypothyroidism Labs

A

High TSH

Low T4

64
Q

Hypothyroidism Tx

A

LEVO: takes about 6 weeks to see effects

65
Q

Myxedema Crisis etiology

A

extreme form of hypothyroidism associated with high mortality rate

Usually d/t underlying factor w/

  • longstanding undiagnosed hypothyroidism
  • d/c noncompliance of taking levo
  • failure to start levo after radioactive ablation of thyroid
66
Q

Myxedema Crisis Manifestations

A

bradycardia, obtunded, hypothermia
decreased mental status
hypothermia

67
Q

Myxedema Crisis Dx

A

Serum Studies

  • increased TSH
  • decreased T4
68
Q

Myxedema Crisis Tx

A

IV LEVO, supportive

69
Q

Paget Disease etiology

A

Abnormal bone remodeling and disorganized osteoid formation

70
Q

Paget Disease Sx

A

Asx MC, found incidentally on imaging

Bone pain, skull involvement

71
Q

Paget Dx

A

labs: increased Alk Phos, normal Ca and Phos

Imaging: XR: blade of grass, flame shaped, cotton wool on skull imaging

72
Q

Paget Tx

A

Bisphosphonates: TOC (alendronate)

  • High incidence of esophagitis: take with glass of water
  • Black Box warning: atypical femur fracture and jaw osteonecrosis

Internal Medicine EOR (8 decks)

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