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First Aid Endocrine Flashcards

1
Q

In addition to congenital cause, name 3 causes of nephrogenic diabetes

A

MC congenital (mutation in ADH receptor rendering it nonresponsive)

Others

  • Lithium toxicity
  • hypercalcemia (chronic Ca over 11)
  • demeclocycline: abx that reduces responsiveness of collecting tubules to ADH (used in the tx of SIADH)
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2
Q

Key feature to distinguish primary hyperparathyroidism and familial hypocalciureic hypercalcemia

A

FHH = defect in calcium sensor in the parathyroid glad => PTH levels are normal despite hypercalcemia

In FHH urine calcium is low, while hypercalciuria in primary hyperPTH

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3
Q

What are the anterior vs. posterior pituitary derived from?

A

Anterior pituitary derived from oral ectoderm (Rathke pouch)

Posterior pituitary derived from neuroectoderm (connected to hypothalamus by neurophysis)

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4
Q

Describe vitamin D’s impact on serum Ca+2 and PO4-3

A

Vit D increases intestinal absorption of both Ca and phosphorus

Vit D also stimulates bone breakdown => increases both Ca and PO in serum

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5
Q

Desmopressin

(a) What is it
(b) Indication

A

Desmopressin = ADH analog

(a) Vasopressin/ADH analog
(b) Used to tx diabetes insipidus

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6
Q

How may IgG4 related disease present w/ thyroid manifestation?

A

Ridel Thyroiditis = chronic thyroiditis that can be a manifestation of IgG4-related systemic disease

Causes normal thyroid tissue to be replaced by fibrous tissue => dense, fixed thyroid gland (painless goiter)

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7
Q

MC hormone deficiency in congenital adrenal hyperplasia

A

21 hydroxylase

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8
Q

Analogs of what hypothalamic hormone can be used to treat acromegaly

A

Somatostatin analog b/c somatostatin inhibits GH and TSH secretion

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9
Q

Clinical presentation of glucagonoma

A

Very high glucagon: 4 D’s

  • dermatitis (necrolytic migratory erythema)
  • diabetes (hyperglycemia)
  • DVT
  • depression
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10
Q

MC cause of acromegaly

(a) Serum marker

A

Acromegaly = effect of elevated growth hormone in adults, MC 2/2 pituitary adenoma

(a) Elevated IGF-1 (insulin growth factor 1) whose release is stimulated by GH

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11
Q

How does pH affect serum calcium levels

(a) Basic or acidic environment cause muscle cramps/paresthesias?

A

40% of serum calcium exists bound to albumin, pH can change conformation/affinity of albumin

(a) Increased pH (basic) makes albumin more negative (fewer H+ around) => albumin has higher affinity for Ca2+ => less free (unbound) serum calcium => symptoms of hypocalcemia such as muscle pain, cramps, and paresthesias

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12
Q

Name 4 genetic syndromes w/ pheochromocytomas

A

Pheo found in

  • MEN2A
  • MEN2B
  • von Hippel Lindau (pheo, b/l renal cell carcinoma, retinal and intracranial hemangioblastoma
  • NF1
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13
Q

Name the d/o of vit D deficiency in

(a) Children
(b) Adults

A

Vit D deficiency in

(a) Children = Rickets
(b) Adults = osteomalacia

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14
Q

Which GLUT receptor is insulin sensitive?

(a) Where are they located?

A

GLUT4 is insulin sensitive

(a) Insulin sensitive tissues = striated muscle, adipocytes, cardiomyocytes

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15
Q

Clinical features of cretinism (congenital hypothyroidism)

A

Either thyroid agenesis or iodine deficiency =>

Severe MR (poor brain development)
Large protruding tongue
Protruding umbilicus (ventral hernia)
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16
Q

MC adrenal tumor in

(a) Adults
(b) Children

A

MC adrenal tumor in

(a) Adults = pheochoromocytoma (nonmalignant tumor of adrenal medulla)
- p/w episodic HTN
(b) Children = neuroblastoma (malignant tumor of neural crest cells anywhere along sympathetic chain)

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17
Q

Presentation of nonfunctional pituitary adenoma

A

Mass effect => bitemporal hemianopsia (visual field deficits), headache, symptoms of hypopituitarism

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18
Q

Adrenal medulla

(a) Type of cells
(b) Secretory product
(c) Control system

A

Adrenal medulla

(a) Cromaffin cells
(b) Secrete catecholamines: epi and norepi
(c) Controlled by sympathetic fibers

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19
Q

Function of the posterior pituitary

A

Posterior pituitary stores ADH and oxytocin produced by hypothalamus

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20
Q

Name the 3 complications of thyroidectomy surgery

A

Thyroidectomy complications

  1. Hoarseness 2/2 damage to recurrent larygneal nerve
  2. Hypocalcemia 2/2 accidental removal of parathryoid glands
  3. Airway compromise of b/l transection of superior laryngeal nerve
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21
Q

What type of hypersensitivity is Hashimoto’s thyroiditis?

A

Hashimoto’s thyroidism = combined type II and type IV hypersensitivity reaction

Type II = 2/2 preformed antibodies (anti-TSH receptor antibodies)
Type IV = direct destruction of thyroid tissue by CD8 (cytotoxic killer T cells) and by CD4-attracted macrophages

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22
Q

Waterhouse-Friderichsen

(a) What is it?
(b) Classic cause
(c) Physical exam

A

Waterhouse-Friderichsens

(a) Acute adrenal insufficiency 2/2 b/l adrenal hemorrhage/infarct
(b) Classically caused by neisseria meningitides septicemia 2/2 endotoxicemia and DIC
(c) Meningitis and petechiae

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23
Q

Tx of DKA

A

DKA tx

-IV fluids (b/c pt is wildly dehydrated and hyperosmolar)
-IV insulin (need to get that glucose into the cells!! cells are starving)
-give glucose as well b/c the amount of insulin you’ll need to give, need to prevent hypoglycemia
-K+ b/c as you give insulin this will push K+ into cells and pt will get hypokalemic
-

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24
Q

Distinguish MEN1, MEN2A, MEN2A

A

MEN 1 (3 P’s): parathyroid carcinoma, pancreatic adenoma (gastrinoma => Zollinger-Ellison), pituitary adenoma (prolactinoma)

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25
Q

Is serum CK elevated in hypo or hyperthyroidism?

A

Hypothyroidism myopathy
-about 80% of pts w/ chronic hypothyroidism have some muscle/weakness complaint

Elevated CK seen in hypothyroidism

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26
Q

DKA

(a) Triggers
(b) Explain where the ketones come from

A

DKA

(a) Increased insulin requirement in times of stress: such as infection, MI, drugs, also med noncompliance or undiagnosed
(b) Lipolysis reved up to make more substrate, producing ketones (mostly beta-hydroxybutyrate)

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27
Q

Describe the effect of thyroid hormone on serum cholesterol?

(a) Hypercholesterolemia seen in hyper or hypothryoidism?

A

Thyroid hormone induces LDL receptor expression => increased cholesterol uptake by cells

(a) So hypercholesterolemia (more chol left in blood) 2/2 reduced LDL receptor expression seen in hypothyroidism

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28
Q

Hyperaldosteronism

(a) Clinical features
(b) pH abnormality
(c) Tx

A

Hyperaldo: high aldo causes retention of Na+ while dumping up K+

(a) Hypokalemia (=> weakness, tetany), sometimes HTN 2/2 hypernatremia, but often pt is normonatremic 2/2 compensatory diuresis
(b) Metabolic alkalosis
(c) Tx = Spironolactone = aldo receptor antagonist

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29
Q

What part of the hypothalamus produces

(a) ADH
(b) Oxytocin

A

Hypothalamic nuclei

(a) Supraoptic nuclei contains osmoreceptors that secrete ADH in response to low osmolality
(b) Oxytocin produced in paraventricular nuclei

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30
Q

How does 21-hydroxylase deficiency present in

(a) infancy
(b) childhood

A

21-hydroxylase (congenital adrenal hyplerplasia): low aldo, low cortisol, high androgens

(a) Infancy presents w/ salt wasting (2/2 low aldo)- extreme thirst and salt cravings, polyuria, hypotension => syncope or orthostatic symptoms
(b) presents w/ precocious puberty in childhood 2/2 high androgens

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31
Q

Can the following agents be used w/o any islet cell function?

(a) Metformin
(b) Glyburide
(c) Exenatide
(d) Sitagliptin

A

Islet cell function

(a) Metformin can be used in pts w/o islet function b/c it increases glucose uptake peripherally (improves insulin sensitivity)
(b) Glyburide (sulfonylurea) works to stimulate endogenous release of insulin => requires some islet fxn (useless in type 1)

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32
Q

Differentiate primary and secondary adrenal insufficiency

(a) Cause
(b) Clinical presentation

A

Primary adrenal insufficiency

(a) Due to adrenal damage (ex: Addison’s disease) where adrenal gland isn’t producing cortisol
(b) Presents w/ skin hyperpigmentation (2/2 elevated melanocyte secreting hormone as byproduct of ACTH), hypotension 2/2 hyponatremic volume contraction (b/c low aldo), hyperkalemia (b/c low aldo), metabolic acidosis

Secondary adrenal insufficiency

(a) pituitary reduced release of ACTH (so the adrenal gland itself is fine)
(b) No hyperpigmentation (b/c ACTH is reduced not elevated) and no hyperkalemia/hypotension (b/c aldo secretion is normal since controlled by RAS system)
- so just the symptoms of hypocortisol = fatigue, weakness, GI symptoms, wt loss

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33
Q

DKA ketones

(a) Ketone produced in the highest amount
(b) How ketones are measured

A

DKA ketones: 3 are produced- acetoacetate, beta-hydroxybutyric acid, and acetone

(a) Beta-hydroxybutyrate is produced in the highest amount
- accounts of the anion gap
(b) First start w/ urine dipstick that uses nitroprusside tablet just to see if there are ketones present, if positive can then do direct beta-hydroxybutyrate serum test to quantify

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34
Q

Diabetes drugs: wt loss of wt gain?

(a) metformin
(b) pioglitazone

A

(a) Metformin causes modest wt loss
(b) Pioglitazone (PPAR-alpha agonist) can cause wt gain
- also hepatotoxic

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35
Q

What is a craniopharyngioma?

(a) Presenting feature

A

Craniopharyngioma = Rathke pouch tumor arising from the pituitary stalk

(a) Presenting feature of bitemporal hemianopsia from mass effect causing compression of the optic nerve

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36
Q

What are Hurthle cells?

(a) 2 associated conditions

A

Hurthle cells = type of thyroid cell

(a) Associated w/ Hashimoto’s thyroiditis (autoimmune hypothyroidism) and follicular thyroid carcinoma

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37
Q

Hashimoto’s thyroiditis

(a) Symptoms- early vs. late in disease course
(b) Physical exam of thyroid
(c) Tx
(d) Increased risk of what malignancy?

A

Hashimoto’s thyroiditis

(a) In beginning may have hyperthryoid as follicular cells rupture and release contents, then hypothyroid as cells die off and are no longer producing hormone
(b) Moderately enlarged, non-tender gland
(c) Tx = thyroid hormone supplementation
(d) Increased risk of thyroid lymphoma, particularly B-cell non-Hodgkin’s lymphoma

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38
Q

GLUT2 receptors

(a) Function
(b) Location

A

GLUT2 receptors are low affinity

(a) Fxn to safe glucose for more vital tissues during fasting (so places like adipocytes and hepatocytes don’t uptake glucose during starvation)
- Also fxns to mediate glucose storage in hepatocytes during surplus
- Stimulate insulin release from beta-islet cells

(b) Hepatocytes, kidney, small intestines, beta-islet cells

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39
Q

What cells produce

(a) PTH
(b) Calcitonin

A

(a) PTH produced by chief cells of the parathyroid gland

(b) Calcitonin produced by parafollicular (C-cells) cells of the thyroid gland

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40
Q

Hormone reduced in congenital obesity

A

Congenital obesity: decreased levels of leptin

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41
Q

Clinical features of Cushing’s syndrome

(a) Main features
(b) Changes in appearance

A

Cushing’s syndrome = clinical findings of high cortisol levels

(a) HTN, Flushing, palpitations, wt gain, depression, weakness (2/2 catabolism of muscle for gluconeogenesis)
(b) Buffalo hump, striae, moon facies, truncal obesity, hirsuitism, easy bruising and thin skin (2/2 weakened collagen)

Also: immunosuppression, osteoporosis, hyperglycemia, amenorrhea

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42
Q

Causes of SIADH

A

Causes of SIADH

  • head trauma, CNS disorder
  • Ectopic ADH secretion (ex: small cell lung cancer)
  • pulmonary disease
  • drugs (ex: cyclophosphamide)
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43
Q

Name 3 clinical features of hypocalcemia

A
  1. tetancy
  2. ‘C’hvostek’s sign = ‘c’ontraction of facial muscles when tapped rapidly
  3. ‘T’rousseau’s sign = carpal sapsm following occlusion of brachial artery (‘t’ricep) w/ BP cuff
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44
Q

MC cause of secondary hyperparathyroidism

A

Chronic renal failure

-kidneys can’t reabsorb Ca2+ => hypocalcemia causes high PTH secretion

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45
Q

Which hypothalamic hormone secretion is regulated by prolactin

A

Prolactin regulates GnRH secretion from hypothalamus

-therefore prolactin regulates FSH/LH release (so ovulation/puberty etc)

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46
Q

How to treat pheochromocytoma

A

Pheo- imperative to first give alpha blockage, then give beta-block prior to tumor resection

-if give beta-block first then unopposed alpha-action can cause hypertensive crisis

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47
Q

How does calcium travel in serum?

A

Calcium travels
45% ionized (active form)
40% bond to albumin
15% bound to anions

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48
Q

Describe how demeclocycline can help in the tx of SIADH

A

Demeclocycline (tetracycline abx) works as an ADH antagonist => helps in SIADH

-but if not used in SIADH, can cause nephrogenic DI

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49
Q

Name congenital d/o w/ increased ghrelin production

A

Ghrelin production pathologically increased in Prader-Willi (paternal chromosome 15 microdeletion)

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50
Q

SIADH

(a) How is euvolemia maintained?
(b) Na+ status

A

SIADH = too much ADH produced => can’t get rid of excess water and pee out too much salt

End up with euvolemic (b) hyponatremic state
(a) Euvolemia b/c aldo secretion decreased in response to hyponatremia, maintaining a rather euvolemic state

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51
Q

Name 2 malignancies associated w/ hypercalcemia

A
  1. Small cell lung cancer- PTHrP secretion
  2. Multiple myeloma
    - CRAB (calcium, renal insufficiency, anemia, bone breakdown)
    - IL-1 production activates osteoclast-driven bone resoprtion
52
Q

Differentiate etiologies of primary and secondary hyperaldosteronism

A

Primary hyperaldo = adrenal cortex overproducing aldo
-adrenal adenoma = Conn’s

Secondary hyperaldo = overstimulation by overactive RAS system (aka too much renin) 2/2 renal artery stenosis or CHF
-chronically high renin b/c kidneys seeing low flow despite normal/high flow elsewhere

53
Q

What is a pituitary apoplexy?

(a) Presentation

A

Pituitary apoplexy = bleeding into an abnormal blood supply of the pituitary region, usually 2/2 underlying pituitary adenoma (often not previously diagnosed)

(a) Presents w/ sudden onset headache and visual symptoms

54
Q

Location of both steps of vitamin D activation

A

Vit D –> 25-OH, Vit D in liver

Then activated into 1,25(OH)2, Vit D in kidney

55
Q

Metformin

(a) Activity
(b) Contraindication

A

Metformin = first line oral diabetes agent

(a) Exact mechanism unknown, but increases insulin sensitivity
- decreases gluconeogenesis, increases glycolysis and peripheral glucose uptake

(b) Contraindicated in renal insufficiency b/c can cause lactic acidosis

56
Q

Graves disease treatment

(a) First line meds
(b) Monitor what on these meds
(c) Definitive management
(d) Meds for extra-thyroid manifestation
(f) Which during pregnancy

A

Treating Graves’ disease (autoimmune hyperthyroid)

(a) Propranolol (beta-blocker) + thionamide (PTU, methimazole) to decrease hormone synthesis
(b) Beware of agranulocytosis w/ PTU
(c) Definitive management = radioactive iodine ablation in general, or thyroidectomy in extreme cases (pregnancy)
(d) Steroids for exophthalmus
(f) Use PTU during pregnancy
- methimazole is a possible teratogen

57
Q

MC pituitary adenoma

(a) Tx

A

Prolactinoma

a) Bromocriptine = dopamine agonist (b/c DA inhibits prolactin release
- also transphenoidal resection of pituitary

58
Q

Features of malignant thyroid nodule

A

Cold (low 131-I uptake indicating low T3/T4 production)

Bad prognostic factors: men and children (women more likely to have benign cysts or follicular adenoma)

59
Q

Name 2 things that

(a) Stimulate growth hormone release
(b) Inhibit growth hormone release

A

(a) GH release stimulated by exercise and sleep

(b) GH inhibited by glucose and somatostatin

60
Q

What is Addison’s disease?

(a) Name other causes besides AI
(b) Clinical features
(c) Lab findings

A

Addison’s disease = autoimmune destruction of adrenal cortex => low aldo, cortisol, and androgens

(a) 80% autoimmune, can also be congenital or caused by Tb/AIDS
(b) Clinically:
-low cortisol => weakness, fatigue,
-low aldo => 2/2 hyponatremic volume contraction
-high MSH => hyperpigmentation (MC seen in mouth)
-low androgens => amenorrhea
(c) Labs
Low cortisol => hypoglycemia, eosinophilia/leukocytosis (b/c usually are suppressed)
Low aldo => hyperkalemia, hyponatremia
Metabolic acidosis 2/2 bicarbonate

61
Q

Sheehan’s syndrome

(a) What happens?
(b) MC initial symptom

A

Sheehan’s syndrome

(a) Ischemic infarct of the pituitary gland 2/2 hypovolemia/blood loss during childbirth
(b) Failure (or trouble w/) to lactate
- then amenorrhea
- cold intolerance

62
Q

Effect of glucagon on

(a) Gluconeogenesis
(b) Lipolysis
(c) Ketone production

A

Glucagon (catabolic hormone) release stimulated by hypoglycemia

(a) Stimulates gluconeogenesis
(b) Stimulates lipolysis (lipid break down)
(c) Stimulates ketone production

63
Q

What is osteitis fibrosa cystica?

(a) Etiology

A

Osteitis fibrosa cystica = skeletal d/o caused by (a) primary hyperparathyroidism

  • chronically high PTH stimulates osteoclast bone resorption, so calcified supporting structure of bone gets replaced w/ brown fibrous tissue
  • see cyst-like brown ‘tumors’ in and around bone
64
Q

Clinical features of carcinoid syndrome

(a) MC
(b) pulm
(c) cards

A

Carcinoid syndrome clinically

(a) Diarrhea (2/2 bowel motility) and flushing
(b) Asthmatic wheezing 2/2 bronchospasm
(c) Right sided heart murmurs- ‘TIPS’
Tricuspid insufficiency, pulmonary stenosis

65
Q

Graves disease

(a) What type of hypersensitivity?
(b) Exact antibodies
(c) Physical exam finding

A

Graves disease

(a) Type II hypersensitivity due to pre-formed antibodies
(b) Antibodies that stimulate TSH-receptor (TSH stimulating antibodies)
(c) Non-tender, symmetrically and diffusely enlarged thyroid

66
Q

Which two types of GLUT receptors are present in the brain?

A

GLUT1 and GLUT3 are in the brain (both are high affinity uptake)

GLUT1 is high-affinity for glucose => saturated at normal levels of serum glucose

GLUT3 only in brain and neurons, high affinity uptake

67
Q

Insulin’s effect on

(a) TG synthesis
(b) Renal sodium
(c) K+

A

Insulin

(a) Stimulates TG synthesis
(b) Increases renal sodium excretion
(c) Increases cellular uptake of K+
- hence why giving insulin in hyperkalemia pushes K+ intracellularly

68
Q

Explain the extra-thyroid manifestations of Graves’ disease

A

Anti-TSH antibodies also stimulate

(a) Retro-orbital fibroblasts => exopthlamus
(b) Dermal fibroblasts => pretibial myxedema

69
Q

Embryologic origin of the pyramidal lobe of the thyroid

A

Pyramidal lobe of the thyroid is persistent from the thyroid’s descent (it’s a remnant of the thyroglossal duct which connects the thyroid’s original and final location)

70
Q

PTH’s effect on

(a) Bone
(b) Renal Ca2+
(c) Renal PO4-3
(d) Vit D

A

PTH

(a) Stimulates bone resorption => releases Ca and PO4 into serum
(b) PTH stimulates Ca2+ reabsorption in distal convoluted tubule
(c) PTH inhibits PO4 reabsorption in proximal convoluted tubule
- ‘PTH as phosphate trashing hormone’
(d) PTH stimulates 1-alpha hydroxylase in the kidney to activate more vitamin D

71
Q

How does MEN1 present?

A

MEN1 presents w/

  • gastric ulcers from gastrinoma (pancreatic islet cell cancer)
  • kidney stones from chronic hypercalcemia from PTH (parathyroid cancer)
72
Q

Tx options for SIADH

A

SIADH tx

  • fluid restriction, IV hypertonic saline
  • ADH receptor antagonists = conivaptan, tolvaptan
  • deemeclocycline
73
Q

Explain how deficiency in an enzyme to make cortisol causes bilateral adrenal enlargement

A

Low cortisol gives negative feedback to ACTH, high ACTH secretion further stimulates both adrenal glands (hyperplasia)

74
Q

Tx for Addison’s disease

A

Addison’s = autoimmune destruction of adrenal cortex => low aldo, cortisol, and androgens

Tx by replacing mineralocorticoid and glucocorticoid (and sex hormones as needed), and by providing stress-dose steroids when needed (ex: severe illness, surgery)

75
Q

How to differentiate primary and secondary hyperparathyroidism

A

Primary hyperparathyroidism (parathyroid adenoma or hyperplasia) = high PTH, high Ca, low PO4

Secondary hyperparathyroidism (chronic renal disease) = low Ca2+ and high PO4 causes high PTH

76
Q

What differentiates toxic multinodular goiter from iodine deficiency thyroid hyperplasia?

A

Toxic multinodular goiter is when the TSH receptors mutate (increased risk from iodine-deficiency induced hyperplasia) to be constitutively active => TSH receptors no longer depend on signal => hyperthyroidism

77
Q

What is Cushing’s disease?

(a) Name two other causes of Cushing’s syndrome

A

Cushing’s disease is specifically hypercortisol 2/2 ACTH secreting pituitary adenoma

(a) While the constellation of symptoms caused by high cortisol can also be induced by
- exogenous corticosteroids (MC)
- primary adrenal adenoma/hyperplasia/carcinoma

78
Q

Explain how high cortisol levels can lead to a reactivation of Tb

A

Cortisol inhibits the inflammatory and immune response by inhibiting leukotriene, prostaglandin, and IL-2 production

Inhibited immune response = more susceptible to Tb and candidiasis reactivation

79
Q

Function of ADH

A

ADH upregulates aquaporin channels on principle cells of renal collecting duct => increase water reabsorption by the kidneys

Released in response to hypothalamus sensing high serum osmolality

80
Q

Name the 6 hormones secreted by the anterior pituitary

A 
Anterior pituitary 'FLAT PiG'
FSH
LH
ACTH
TSH
Prolactin
Growth hormone
81
Q

Are the following found in hyper or hypo- thyroidism?

(a) Constipation
(b) Wt loss
(c) Hyperreflexia
(d) Diarrhea
(e) Facial/peri-orbital myxedema
(f) Pretibial myxedema
(g) Osteoporosis
(h) HTN
(i) Cold, dry skin
(j) CP/palpitations

A

(a) Constipation = hypothyroid
(b) Wt loss = hyper
(c) Hyperreflexia = hyper
(d) Diarrea = hyper
(e) Facial/peri-orbital myxedema = hypo
(f) Pretibial = hyper
(g) Osteoporosis = hyper
(h) HTN in both
- diastolic HTN in hypo, systolic HTN is hyper
(i) Cold dry skin in hypo
- vs warm moist skin in hyper
(j) CP/palpitations in hyper

82
Q

How does thyroid hormone increase metabolic rate

A

Thyroid hormones stimulate activity of Na/K ATPase => increasing metabolic rate

83
Q

Diabetes insipidus

(a) Main clinical features
(b) Treatment: central vs. nephrogenic

A

DI

(a) Polyuria and polydipsia
(b) Tx
- central = hydration and desmopressin (ADH analog)
- nephrogenic = HCTZ, amiloride (K+ sparing diuretic), hydration, indomethacin

84
Q

Pt p/w enlarged and tender neck w/ fever, malaise, and myalgia 1 week s/p URI

(a) Dx
(b) Tx

A

(a) Subacute thyroiditis (de Quervain’s thyroiditis) = painful acute enlargement of thyroid gland s/p viral infection
(b) Tx = just pain management (NSAID)
- self limited and rarely recurs => don’t need to treat the thyroid symptoms (early hyperthyroidism, late hypothyroid)

85
Q

42 yo obese F p/w diastolic HTN and menstrual irregularities

  • On exam: full, plethoric face w/ facial hair, truncal obesity, and purple stria around the abdomen
  • Labs: Hb 18, WBC 18k
  • Normal CXR

(a) Dx?
(b) MC cause

A 
Dx = Cushing's syndrome 
2/2 hypercortisolism
-wt gain
-leukocytosis 2/2 marginalization by cortisol 
-striae 2/2 weakening of collagen

(a) MC cause = pituitary adenoma secreting ACTH (Cushing’s disease)
- but can be 2/2 exogenous steroids, ectopic ACTH production (ex: small cell lung cancer), adrenal hyperplasia/carcinoma

86
Q

Why is DKA so dangerous?

aka what are the serious complications

A

Complications of DKA

  • mucormycosis (rhizopus) infection: thrive in ketoacidotic state
  • cerebral edema
  • arrhythmias 2/2 electrolyte abnormalities
  • HF due to hypovolemia
87
Q

Neuroblastoma

(a) Presentation
(b) Clinical hallmark
(c) Associated genetic issue
(d) UA finding
(e) Tx

A

Neuroblastoma = malignant adrenal tumor in kids

(a) Unilateral, off-centered irregular abdominal mass in children under 4 yoa
- while Wilm’s tumor is smooth and midline)
(b) Opsoclonus-myoclonus = dancing eyes, dancing feet
(d) Elevated HVA (DA breakdown product) and VMA (epi and norepi breakdown product) in urine
(e) Tx = surgical removal

88
Q

What are the adrenal cortex and adrenal medulla derived from?

A

Adrenal cortex derived from mesoderm

Adrenal medulla derived from neural crest cells (forms neuroblastoma in children, secretes epi and norepi)

89
Q

2 consequences of persistent thyroid gland tissue

A
  1. pyramidal lobe of the thyroid

2. thyroid duct cyst

90
Q

Exact mechanism of sulfonylureas

A

Sulfonyulreas (glyburide, glimepiride) close K+ channels on beta-islet cell membranes => depolarizing the cell (causing Ca2+ influx) => induces insulin release

Useless in type 1 b/c needs functional beta-islet cells, only acting to stimulate endogenously produced insulin (doesn’t work peripherally to improve sensitivity)

91
Q

Explain iatrogenic adrenal insufficiency

A

Tertiary/iatrogen adrenal insufficiency: abrupt withdrawal from exogenous steroids

This is why you need to taper prednisone- exogenous corticoids suppress ACTH release => adrenal gland isn’t being stimulated to make any

92
Q

Fxn of calcitonin

A

Calcitonin works to counteract PTH, doesn’t have much of a function in overall Ca2+ homeostasis
-inhibits bone resorption

93
Q

What is thyroid storm?

a) Clinical presentation
(b) Tx (3 Ps

A

Thyroid storm = large release of thyroid hormone that causes systemic effect

(a) Hyperpyrexia (like over 104F, 40C, super high), tachyarrhythmia, N/V, coma, hypotension
- what can be fatal is the arrhythmias
(b) Tx:
- Propranolol (beta-blocker) for HR
- PTU to decrease hormone synthesis
- Prednisone: decreases peripheral conversion of P4 to P3
- Anti-pyretic, fluids, supportive measures (cooling blanket)

94
Q

Name 3 electrolytes whose levels can stimulate PTH secretion

A

PTH release stimulated by

  • hyperphosphatemia (high PO4)
  • hypocalcemia (low Ca)
  • hypomagnesemia (low Mg)
95
Q

Compare tonic and pulsatile GnRH

A

Tonic GnRH suppresses the HPA axis

While pulsatile GnRH (yay) leads to puberty and fertility (by correct secretion of FSH/LH)

96
Q

Primary energy source and source during starvation

(a) RBC
(b) Brain

A

(a) RBC don’t have mitochondria => can’t do aerobic glycosis so only can use glucose for energy (even in starvation)
(b) Brain primarily uses glucose, can use ketones during starvation

97
Q

Differentiate central from nephrogenic diabetes insipidus

(a) ADH level
(b) Urine specific gravity
(c) Serum osmolality
(d) Test used to differentiate

A

Central DI = brain (hypothalamus) not making ADH. Nephrogenic DI when sufficient ADH is produced by kidneys are not responsive to it (ex: mutated receptor)

(a) ADH low is central, ADH normal in nephrogenic
(b) Urine SG low in both b/c peeing out all water (SG under 1.006)
(c) Serum osmolality high in both (over 290) b/c can’t retain water
(d) Give ADH analog (desmopressin acetate) and see if urine osmolality increases
- Uosm increases = central, Uosm nonresponsive (doesn’t increase) = nephrogenic

98
Q

Is it the glucose or the insulin that is harmful to the fetus in maternal diabetes?

A

Glucose can cross the placenta while insulin can’t. Problem is that high maternal glucose causes the fetus to overproduce its own insulin

99
Q

Growth hormone

(a) Intermediate molecule
(b) Effect on diabetes
(c) Frequency of release

A

Growth hormone

(a) GH stimulates linear growth and muscle mass thru IGF-1 (somatomedin)
(b) Growth hormone is diabetogenic, it stimulates insulin resistance
(c) GH released in pulses in response to GHRH

100
Q

What differentiates toxic vs. nontoxic thyroid goiter?

A

Nontoxic goiter meaning the tissue is dependent on TSH stimulation, hyperplasia is 2/2 T3/T4 deficiency
-compensatory hyperplasia from low thyroid hormone levels systemically

While toxic goiter is when the hyperplasia becomes independent of TSH

101
Q

DKA clinically

(a) Symptoms
(b) Signs
(c) Odor of breath

A

Clinical picture of DKA

(a) Abdominal pain, N/V
(b) Physical exam signs
- Kussmal respirations 2/2 metabolic acidosis
- delirium
- dehydration (2/2 polyuria and high serum osmolality from hyperglycemia), coma
(c) Fruity breath odor 2/2 exhaled acetone (one of three ketone bodies that accumulate)

102
Q

Explain how cortisol can cause an increase in BP

A

Cortisol upregulates alpha1 receptors on arterioles to increase their sensitivity to epi and norepi

103
Q

Give examples of each type of insulin

(a) Rapid acting
(b) Short acting
(c) Intermediate acting
(d) Long acting

A

Insulinnnn

(a) Rapid acting = aspart (Novolog), glulisine, lispro (Humalog): work in like 15 mins
(b) Short acting = regular insulin (Humulin, novolin)
(c) Intermediate acting = NPH: works in 1-2 hrs
(d) Long acting = glargine (Lantus) and detemir (Levemir)

104
Q

Describe how the following impact prolactin release

(a) bromocriptine
(b) hypothyroidism

A

Prolactin release

(a) Bromocriptine is a dopamine agonist, dopamine inhibits prolactin release => use bromocriptine to treat prolactinoma medically
(b) TRH increases prolactin secretion, so hypothyroid => high TSH => galactorrhea/amenorrhea

105
Q

Changes in thyroid hormone levels w/

(a) OCP use
(b) hepatic failure
(c) PTU

A

Thyroid hormone: free levels decrease it TBG (thyroid binding globulin) concentration increases

(a) OCPs/estrogen increase TBG synthesis => hypothyroid (b/c less free thyroid hormone since more is bound)
(b) Estrogen breakdown occurs in the liver => during hepatic failure estrogen levels rise => increased TBG (hypothyroid)
(c) PTU inhibits peroxidase (oxidizes I- –> I2) and enzyme that combines MIT and DIT to form T3/T4 in lumen => PTU decreases thyroid hormone synthesis
- used in Graves

106
Q

Explain the lab findings in DKA

(a) CBC abnormality
(b) pH abnormality
(c) Explain K+ levels

A

DKA lab abnormalities

(a) Leukocytosis 2/2 stress-induced cortisol release
(b) Metabolic acidosis 2/2 accumulate of ketones and lactate
(c) Need insulin to push K+ into cells, also K+ exchanged out for extra H+ to get into cells => serum hyperkalemia but intracellular K+ deficit

107
Q

Clinical features of hyperparathyroidism

A

High PTH => hypercalcemia, hypercalciura, hypophosphatemia

Symptoms of hypercalcemia: “stones, bones, groans, psychiatric overtones”

  • kidney stones 2/2 hypercalciuria
  • bone weakening due to loss of calcified supporting structures
  • constipation
  • depression
108
Q

Pt p/w diarrhea and facial flushing, murmur of tricuspid regurg: describe how you would screen for carcinoid syndrome

A

Carcinoid syndrome

  • first can screen urine for 5-HIAA (breakdown product of 5-HT)
  • then CT scan abdomen for tumor
109
Q

Pharmacologic tx of hyperparathyroidism

A

Treating hypercalcemia: give tons of fluids

  • furosemide to increase renal Ca excretion
  • bisphosphonates
  • Cinacalcet sensitizes the CaSR (calcium sensing receptor) in the parathyroid gland => works to make parathyroid cells more sensitive to high serum calcium and decrease PTH production
110
Q

Tx for carcinoid syndrome if tumor is non-resectable

A

Octreotide = somatostatin analog

-somatostatin decreases 5-HT production

111
Q

Appetite regulation

(a) Which hormone stimulates appetite
(b) Which hormones reduces appetite

A

Appetite regulation

(a) Appetite stimulated by ghrelin
(b) Appetite suppressed by leptin

112
Q

Pheochromocytoma

a) What is it?
(b) Clinical features (5 P’s
(c) Rule of 10s

A

Pheo

(a) Nonmalignant tumor of adrenal medulla that secretes epi, norepi, and dopamine
(b) Episodic symptoms:
Pressure (HTN)
Palpitations
Pain (headache)
Perspiration
Pallor
(c) 10% malignant, 10% bilateral, 10% extra-adrenal (bladder, organ of Zuckerkandl), 10% calcify, 10% in children (MC 40-50yoa)

113
Q

2 functions of prolactin

(a) Use this to explain the clinical presentation of prolactinoma

A

Prolactin

  • stimulates lactation
  • inhibits GnRH release to inhibit ovulation and spermatogenesis

(a) Galactorrhea and loss of libido

114
Q

Explain why a well controlled schizophrenic pt may exhibit galactorrhea

A

Many antipsychotics are dopamine antagonists, dopamine is needed to inhibit prolactin so w/o DA there is hyperprolactinemia => galactorrhea

115
Q

Classic cause of Waterhouse-Friederichsen

A

Neisseria meningitides septicemia causing endotoxic shock and DIC => b/l adrenal hemorrhage and infarct

116
Q

MC malignancy of the small intestines

A

Carcinoid tumor (neuroendocrine cells)

117
Q

If MEN2A and MEN2B have different clinical features, why aren’t they separated into MEN2 and MEN3…?

A

B/c both caused by (or associated with) RET proto-oncogene
-therefore both have medullary thyroid carcinoma and pheo

MEN2A: + parathyroid cancer
MEN2B: + marfanoid body habitus, mucosal neuromas

118
Q

Causes of hypoparathyroidism

(a) Genetic
(b) Iatrogenic
(c) Electrolyte abnormality

A

Hypoparathyroidism

(a) DiGeorge syndrome- congenital absence of parathyroid glands
(b) Accidental surgical removal during thyroidectomy
(c) Hypomagnesmia

119
Q

Test used to differentiate Cushing’s disease vs. ectopic ACTH production

A

High dose dexa test

  • if cortisol suppressed w/ high-dose dexa = Cushing’s disease = Cushing disease (ACTH secreting pituitary adenoma)
  • if cortisol not suppressed by high-dose dexa = Ectopic ACTH production (ex: small cell lung cancer): ACTH source is resistant to negative feedback by dexa
120
Q

Lab findings of pt w/ insulinoma

A

Elevated C-peptide, hypoglycemia

121
Q

Does type 1 or 2 diabetes have a stronger genetic predisposition?

A

Type 2 has relatively strong (90% concordance in identical twins), while type 1’s genetic association is relatively weak (50% concordance in identical twins)

122
Q

Possible toxicity of levothyroxine

A

Levothyroxine (T4) which is then converted to T3 (active form) can cause tachycardia, heat intolerance, tremors, arrhythmias

123
Q

4 lesions in von-Hippel-Lindau syndromef

A

Von-Hippel Lindau

  • b/l renal cell carcinoma
  • pheochromocytoma
  • retinal hemangioblastoma
  • intracranial hemangioblastoma
124
Q

Name two negative consequences of high cortisol levels

A

Cortisol causes decreased bone formation, increased insulin resistance (diabetogenic)

-also can be immunosuppressing (but sometimes this is what we use it for…)

125
Q

Carcinoid syndrome

(a) Cause
(b) How does location of carcinoid tumor determine if pt gets syndrome or not

A

Carcinoid syndrome- clinical features of high serotonin 2/2

(a) Carcinoid tumor = neuroendocrine cell tumor that secretes tons of 5-HT
(b) Location, location, location
- carcinoid tumors only in the GI tract (w/o mets) don’t cause carcinoid syndrome b/c all the 5-HT they secrete gets metabolized during first pass metabolism thru the liver
- therefore causes carcinoid syndrome if blood drainage doesn’t go thru portal system => liver mets or extra-GI carcinoid tumors

126
Q

Screening test used for Cushing’s syndrome

(a) Next step if screening test is positive

A

Screening test = low dose dexa test- this should suppress cortisol levels

Positive if low-dose dexa doesn’t suppress cortisol levels (aka the synthetic cortisol doesn’t inhibit ACTH or ACTH isn’t controlling cortisol production)

(a) If positive, measure serum ACTH
- Low serum ACTH = adrenal tumor
- High serum ACTH: use high-dose dexa test to differentiate Cushing disease (ACTH secreting pituitary adenoma) from ectopic ACTH production

Boards - Step 1 (26 decks)

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