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Internal Medicine EOR > Endocrine > Flashcards

Endocrine Flashcards

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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
DM Tx
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
26
DM Goals
A1C <7% Preprandial glucose 80-130 Postprandial glucose <180 Lipid control LDL <100, HDL>40, TG <150
27
Hypercalcemia sx/ tx
lethargy, hypoereflexia, kidney stones tx: NS, lasixs, dialysis
28
Hypocalcemia sx/tx
Perioral tingle, hyperreflexia, CHVOSTEK SIGN, prolonged QT Tx: IV calcium gluconate
29
Hypernatremia sx/tx
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
Hypovolemic hypernatremia sx/tx
Total body sodium deficit + free water deficit tx: Isotonic Crystalloid (NS/LR), minimiz Na containing fluids D5W @ 1.35 ml/hr /kg
31
Hyponatremia sx/tx
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
Hyperparathyroidism etiology
Primary: increased PTH (MC type) Secondary: increased PTH d/t hypocalcemia or Vit D Tertiary: prolonged PTH stimulation from secondary
33
Primary Hyperparathyroidism
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
Secondary hyperparathyroidism
increased PTH d/t hypocalcemia or Vit D deficiency - Parathyroid cland is compensating - Chronic Kidney failure MC cause
35
Tertiary Hyperparathyroidism
prolonged PTH stim after secondary --> autonomous PTH secretion Often in post transplant patients
36
Hyperparathyroidism manifestations
Stones Bones Grones Overtones Decreased DTRs
37
Hyperparathyroidism Dx or primary
Tirad: hypercalcemia, increased intact PTH, decreased phosphate 24 urine calcium secretion, increased vit D, osteopenia on bone scan
38
Hyperparathyroidism management
Surgery Fit D/Ca supps if secondary Tx hypercalcemia if sx: IV fluids, furosemide
39
Hypoparathyroidism etiology
RARE, either low PTH or insensitivity to its action
40
Hypoparathyroidism etiologies
2 MC causes: postsurgical or autoimmune
41
Hypoparathyroidism sx
sx: carpopedal spasms, trousseaus, chvostek, increased DTRS
42
Hypoparathyroidism dx/tx
dx: Triad of hypocalcemia, decreased PTH and increased phosphate Tx: calcium supplementation and Vit D
43
Grave's etiology
Autoimmune | Increased thyroid hormone synthesis, worse with stress/prego/illness
44
Grave's sx
Thyroid bruits, enlarged thyroid, ophthalmopathy Pretibial myxedema: nonpitting, edematous, pink to brown plaques, on shin
45
Grave's Dx
+thyroid stimulating immunoglobulins Hyperthyroid TFTs: increased T4, decreased TSH Raiu: increased diffuse uptake or radioactive iodine
46
Grave's sx
Radioactive iodine MC therapy Methimazole or PTU Thyroidectomy
47
Toxic Multinodular Goiter
Plummer's Disease | Autonomous functioning nodules
48
Toxic adenoma
One autonomous functioning nodule
49
Sx of both TMG and TA
Clinical hyperthyroidism, no skin changes, palpable nodules Compressive symptoms: dyspnea, dysphagia, stridor, hoarseness
50
Dx of Grave's
Increased T4 Decreased TSH RAIU: patcy
51
Grave's management
Radioactive iodine MC therapy Surgery Methimazole, PTU
52
TSH secreting pituitary adenoma etiology / sx
autonomous TSH secretion by pituitary adenoma Sx: Bitemporal Demianopsia, enlarged thyroid, amenorrhea, galactorrhea, HA
53
TSH secreting pituitary adenoma Dx/Tx
Increased T4 Increased TSH Sellar Turcica Mass RAIU: diffuse uptake Tx: surgery
54
Thyroid storm etiology
Potentially life threatening complication of untreated thyrotoxicosis usually after precipitating event RARE AF
55
Thyroid storm PE/Dx
Hypermetabolic state: palpitations, tachycardic, Afib, fever, nausea, tremors Dx: Primary hyperthroid TFT: increased T4 decreased TSH
56
Thyroid Storm Tx
Anti-thyroid meds: IV PTU or methimazole Beta Blockers IV Glucocorticoids
57
Pheochromocytoma etiology
catecholamine secreting adrenal tumor (CHROMAFFIN CELLS) Secretes norepi and epi autonomously and intermittently 90% are benign
58
Pheochromocytoma sx
HTN | PHE palpitations, HAs, excessive sweating
59
Pheochromocytomam Dx
Plasma fractionated metanephrines Increased 24 hours urinary catecholamines MRI/CT visualizes adrenal tumor
60
Pheochromocytoma Tx
complete adrenalectomy Phenoxybenzamine first then beta blocker
61
Hypothyroidism etiology
MC: hashimoto's thyroiditis
62
Hypothyroidism PE
Generalized weakness, fatigue, facial swelling, constipation, cold intolerance, weight gain, periorbital edema, dry skin, coarse brittle hair
63
Hypothyroidism Labs
High TSH | Low T4
64
Hypothyroidism Tx
LEVO: takes about 6 weeks to see effects
65
Myxedema Crisis etiology
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
Myxedema Crisis Manifestations
bradycardia, obtunded, hypothermia decreased mental status hypothermia
67
Myxedema Crisis Dx
Serum Studies - increased TSH - decreased T4
68
Myxedema Crisis Tx
IV LEVO, supportive
69
Paget Disease etiology
Abnormal bone remodeling and disorganized osteoid formation
70
Paget Disease Sx
Asx MC, found incidentally on imaging Bone pain, skull involvement
71
Paget Dx
labs: increased Alk Phos, normal Ca and Phos Imaging: XR: blade of grass, flame shaped, cotton wool on skull imaging
72
Paget Tx
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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