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Endocrine Flashcards

1
Q

high renin, high aldosterone

A 
secondary hyperaldosteronism (renin-secreting tumor, renovascular disease, malignant HTN)
sx: hypertension, hypokalemia, mm weakness
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2
Q

low renin, low aldosterone, HTN

A

secondary hypertension due to pituitary tumor
ACTH-secreting adenoma causing cushing’s disease
CAH
exogenous mineralocorticoids

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3
Q

low renin, high aldosterone

A 
primary hyperaldosteronism
(aldosterone-producing tumor, bilateral adrenal hyperplasia)
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4
Q

Male fetus, external genitalia feminized, internal normal

A

5 alpha-reductase def (testosterone cannot be converted to dihydrotestosterone)
No fusion of labial folds

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5
Q

Excess androgens and virilization in female fetus. Salt retention (dec aldo, dec renin). HYPERTENSION.

A

11-beta-hydroxylase def (2nd MC CAH)

labs: dec cortisol, dec renin, dec aldosterone (due to elevated BP)

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6
Q

XX virilization. Inc renin, inc ACTH, inc 17 hydroxyprogesterone. Hyperkalemia, salt wasting

A

21-hydroxylase def

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7
Q

Female normal. Male fetuses feminized. HTN, hypokalemia, low renin

A

17-alpha-hydroxylase def
Lack androgens
Inc mineralocorticoids

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8
Q

What syndrome is characterized by:
Hyperpigmentation, inc ACTH, GI sx, orthostatic hypotension, hyponatremia, hyperkalemia, hyperchloremia, and NAG met acidosis

A

Addison’s disease
Causes
- autoimmune destruction of all layers of the adrenal cortex
- Tb, tumor mets, sarcoidosis, fungal granulomas
Hyperpigmentation d/t ACTH conversion to a-melanocyte-stimulating hormone.

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9
Q

What syndrome is characterized by:

Hypertension, hypernatremia, hypokalemia (hyperaldosteronism)

A

Conn syndrome

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10
Q

What syndrome is characterized by:

Extreme hyperpigmentation

A

Nelson’s syndrome (hx of adrenalectomy to tx Cushing disease). D/t excess secretion of ACTH from a pituitary adenoma.

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11
Q

How can TNF-a, catecholamines, glucocorticoids, and glucagon lead to insulin resistance?

A

They phosphorylate serine and threonine residues of insulin receptors and insulin receptor substrate by serine kinase. This inhibits tyrosine phosphorylation

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12
Q

Prolactinomas do what to GnRH, LH and testosterone?

A

Elevated prolactin –> suppress GnRH –> dec LH secretion –> impaired testosterone production in males
Also causes galactorrhea, amenorrhea

Note: prolactin secretion is inhibited by dopamine (antipsychotics cause inc prolactin)

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13
Q

Patients with PCOS who desire fertility can be treated with what? MOA?

A

Clomiphene
Estrogen receptor modulator - dec neg feedback inhibition on hypothalamus by circulating estrogen –> inc gonadotropin production

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14
Q

2 mech for development of diabetic neuropathy

A
  1. non-enzymatic glycosylation of proteins –> hyalinization of artery walls –> ischemic nerve damage
  2. glucose accum –> sorbitol and fructose –> inc cell osmolarity –> osmotic damage to axons and Schwann cells
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15
Q

How do you treat congenital adrenal hyperplasia?

A

Low dose exogenous corticosteroids to suppress excess ACTH secretion and reduce stimulation of the adrenal cortex.

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16
Q

What 2 hormones have incretin effects (ie stim pancreatic insulin secretion in response to sugar-containing meals)?

A

Glucagon-like peptide (GLP-1)

Gastric inhibitory peptide (GIP)

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17
Q

What causes bronze diabetes (skin hyperpigmentation, DM, pigment cirrhosis with hepatomegaly)?

A

Late-stage hemochromatosis - AR

Fe overload in heart, pancreas, and liver.

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18
Q

How does diabetes cause CN III mononeuropathy? (down and out)

A

Central ISCHEMIA (involves core of CN III with sparing of the peripheral part). The somatic component of CN III that innervates EOM is located centrally, but the autonomic part that constricts the pupil and helps with accommodation is located peripherally.

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19
Q

Inherited hyperlipoproteinemia: Recurrent acute pancreatitis, lipemia retinalis, skin xanthomas, hepatosplenomegaly
Dx? Defect? Elevation?

A

Familial chylomicronemia syndrome
Defect: Lipoprotein lipase; ApoC-II
Elevated chylomicrons

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20
Q

Inherited hyperlipoproteinemia: Premature coronary artery disease, corneal arcus, tendon xanthomas
Dx? Defect? Elevation?

A

Familial hypercholesterolemia
Defect: LDL receptor; ApoB-100
Elevated LDL

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21
Q

Inherited hyperlipoproteinemia: Premature coronary artery disease, peripheral vascular disease, tuboeruptive and palmar xanthomas

A

Familial dysbetalipoproteinemia
Defect: ApoE
Elevated Chylomicrons and VLDL remnants

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22
Q

Inherited hyperlipoproteinemia: Obesity, insulin resistance, inc pancreatitis risk

A

Familial hypertriglyceridemia
Defect: ApoA-V
Elevated VLDL
Inc Triglycerides –> inc free FA conc, exceeding binding capacity of albumin –> direct injury to pancreatic acinar cells.

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23
Q

What side effect of antithyroid drugs (eg methimazole, PTU) present with sudden onset of fever and sore throat?

A

Agranulocytosis

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24
Q

What can be used to dissolve cholesterol gallstones?

A

Bile acid supplements (eg ursodeoxycholic acid)

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25
Q

Small cell carcinoma of the lung secretes what 2 things?

A

ACTH and/or vasopressin

ACTH –> hypercortisolism (cushings) - paraneoplastic synd

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26
Q

Squamous cell lung carcinoma can be assoc with secretion of what?

A

PTHrP –> hypercalcemia

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27
Q

How does sarcoidosis cause hypercalcemia?

A

parathyroid hormone-INDEPENDENT formation of 1,25-dihydroxyvit D by activated MACROPHAGES.

Increased intestinal calcium absorption induced by high serum calcitriol concentrations (1,25-dihydroxyvitamin D, the most active metabolite of vitamin D) is the primary abnormality, although a calcitriol-induced increase in bone resorption may also contribute [5-8].

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28
Q

Patients with chronic T2DM treated with insulin will have (high, med, low) endogenous fasting serum insulin concentration?

A

low

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29
Q

Treatment of thyroid storm

A

4P’s

bb - propranolol, PTU, corticosteroids - prednisolone, potassium iodide

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30
Q

Which Vit D? from exposure of skin to sun

A

D3 (24,25 (OH)2 D3) - inactive form

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31
Q

Which Vit D? from ingestion of plants

A

D2

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32
Q

Where is D2 and D3 converted? and to what?

A

Liver

25-OH

33
Q

Which Vit D? Active form. And where is it converted?

A

1,25 (OH)2

in kidney

34
Q

Which of the following sx of Graves disease cannot be managed with beta blockers and why?
Mood swings, palpitations, tremor, fatigue, exophthalmos

A

exophthalmos - due to inc soft tissue mass and not related to adrenergic receptors.

35
Q

What is a contraindication for metformin? What should be used to treat T2DM as second line to metformin?

A

renal dysfunction

Sulfonylureas, DDP-4 inhibitors, GLP-1 agonists or glitazones

36
Q

What is a contraindication for sulfonylureas?

A

Hepatic dysfunction

37
Q

How do you treat acute adrenal crisis?

A

Aggressive fluid resuscitation and immediate glucocorticoid supplementation

38
Q

In primary hyperaldosteronism, why is there not an elevated level of serum sodium? What are other lab findings?

A

Aldosterone escape - inc intravascular volume –> inc renal blood flow –> release of ANP (natriuresis), limiting net Na retention and vol overload.
Dec renin, hypoK, inc bicarb (in response to inc H+ excretion)

39
Q

How does deficient T4 cause yellow dry skin?

A

Dec conversion of carotene to vit A –> inc serum carotene -> yellow skin
Deficiency of T4 also causes bradycardia (dec sensitivity to catecholamines)

40
Q

Signs of hypothyroidism + breast discharge and decreased TSH indicates what? Labs?

A

Secondary hypothyroidism - eg at pituitary level
Increased TRH from hypothalamus
Secondary hypothyroidism ca also be due to insufficient TRH, but no breast discharge would be seen

41
Q

Primary hyperparathyroidism presents with what signs and symptoms?

A 
CNS effects (lethargy, depression)
Hypercalcemia
Ocular - band keratopathy
CV - HTN, shortened QT interval
GI - constipation, peptic ulcer, pancreatitis
42
Q

How do steroids result in infertility?

A

Inc androgen –> dec GnRH –> Reduces LH and FSH. –> dec LH causes dec endogenous testosterone –> testicular atrophy

43
Q

How does hemochromatosis cause erectile dysfunction?

A

Inc Fe in testes –> hypogonadism and dec testosterone production
note: also presents with bronze diabetes bc Fe deposits in pancreas

44
Q

How do thiazides decrease urine flow rate in patients with nephrogenic DI?

A

Decrease urine flow rate by increasing reabsorption of solutes and water from the proximal tubule (note: patient first loses Na and Cl in DCT –> inc urine out –> dec plasma volume –> inc overall reabsorption of solute and H2o in PCT –> net dec in urine flow rate)

45
Q

How can acute pancreatitis cause hypocalcemia?

A

Ca is sequestered by saponification with fatty acids produced in the retroperitoneum by pancreatic lipases.
Commonly seen with pancreatic necrosis
Note: nonspecific finding. Can be due to any type of pancreatitis

46
Q

Hypoparathyroidism can cause hypocalcemia s/p thyroidectomy. What causes the hypocalcemia?

A

Dec 1,25-dihydroxyvitamin D

PTH acts on the kidney to induce synthesis of 1,25-dihydroxyvitamin D.

47
Q

HTN, hypoK, metabolic alkalosis, normal to low aldosterone is suggestive of what?

A

Pseudo Hyperaldosteronism
Liddle syndrome: constitutive reabsorption of Na+ and secretion of K+ and H+ in the collecting duct –> suppressed secretion of renin and aldosterone by the volume expansion to maintain electroneutrality. Treat with amiloride (K sparing diuretic that blocks ENac).

48
Q

What would IGF-1 levels be in a kid with stunted growth?

A

IGF-1 would be low - GH normally stimulates IGF-1 and IGFBP3 secretion by the liver.

49
Q

GI symptoms (chronic diarrhea) in chronic pancreatitis is due to what pancreatic cell type ?

A

Acinar cells - produce enzymes needed to digest fat and protein –> steatorrhea

50
Q

Pancreatic cell function?

  1. alpha cell
  2. beta cell
  3. delta cell
  4. F cell
A
  1. alpha cell - glucagon
  2. beta cell - insulin
  3. delta cell - somatostatin
  4. F cell - pancreatic polypeptide that stimulates gastric chief cells and inhibits intestinal motility
51
Q

Hypercortisolism during pregnancy is due to what, and what can be used to treat it postpartum?

A

high hCG from pregnancy bind LH receptors on adrenal cortical cells, increasing cortisol release. OCP postpartum suppress LH release

52
Q

Consider what endocrine organ dysfunction in an elderly patient’s inability to handle pneumonia?

A

Thyroid gland - hypothyroidism undiagnosed can impair tolerance to infections and ability to heal after injury or surgery

53
Q

What is a specific lab finding for alcohol-related pancreatitis aside from >2AST:ALT and absence of gallstones?

A

Macrocytosis - poor nutrition (folate deficiency)

Note: hypocalcemia is nonspecific and can occur in pancreatitis of any etiology

54
Q

What converts androstenedione to estrone and testosterone to estradiol? Deficiency causes clitoromegaly in newborn females and maternal virilization during pregnancy.

A

Aromatase

Aromatase deficiency

55
Q

Tumor that causes necrolytic migratory erythema (central clearing of bronze-colored induration), hyperglycemia.

A

Glucagonoma - arises from alpha cells of pancreatic islets of Langerhans

56
Q

What hormone in pregnancy increases maternal insulin resistance during the second and third trimester –> gestational diabetes?

A

Human placental lactogen (peptide hormone secreted by the syncytiotrophoblast)
Also increases maternal lipolysis

57
Q

Why is it common to see elevated CK in patients with hypothyroidism?

A

hypothyroid myopathy - myalgia, proximal mm weakness and cramping.

58
Q

What is one factor that might be responsible for beta cell dysfunction in type 2 DM?

A

Pancreatic islet amyloid deposition

59
Q

What is associated with T1DM?

A

HLA class II
pancreatic islet infiltration with leukocytes (insulitis)
Ab against islet antigens

60
Q

Prolactin is under inhibitory control by what NT?

How does sarcoidosis cause hypercalcemia and a hyperprolactinemia?

A
  1. Dopamine
  2. Sarcoidosis can produce excess calcitriol —> hypercalcemia. An infiltrating sarcoid lesion in the pituitary stalk – >loss of inhibitory control of prolactin
61
Q

Most sensitive screening test for hypothyroidism

A

serum TSH

Note: T4 can be WNL in pt w/subclinical hypothyroidism. SH levels rise bf T4 fall below nl. T3 is last to decline

62
Q

Admin of metyrapone tests for what?

A

hypothalamic-pituitary-adrenal axis
Blocks 11-B-hydroxylase
Normal: Reactive ACTH inc, 11-deoxycortisol and urine 17-hydroxycorticosteroid inc.

63
Q

CKD does what to phosphate, PTH and calcitriol?

A

CKD –> metabolic bone disease
CKD dec GFR –> dec filtered phosphate –> dec serum free ca
Inc phosphate
Inc PTH
Dec calcitriol - dec intestinal ca and phosphate absorption

64
Q

Most characteristic skeletal manifestation of primary hyperparathyrodism?

A

Osteitis fibrosa cystica
Bone pain, subperiosteal erosions affecting phalanges of hands
Histo: subperiosteal resorption with cystic degeneration
Salt and pepper skull

65
Q

GLUT transporters are what type of transporters?

A

Carrier-mediated transport

Stereoselective and have preference for D-glucose

66
Q

Admin of T3 in a patient with hypothyroidism does what to TSH, T3, Reverse T3, and T4?

A

TSH - decrease (under neg feedback by T3)
T3 - increase
Reverse T3 (inactive form) - decrease
T4 - decrease

67
Q

What drug is used to supplement ca after parathyroidectomy?

A

calcitriol (active form of vit D)
note: cinacalcet is a calcimimetic that activates ca sensing receptor in the parathyroid, decreasing PTH release. Used for secondary hyperparathyroidism in dialysis patients

68
Q

How does exercise affect insulin-treated diabetics?

A

Skeletal mm contraction –> inc glucose uptake by mm –> insulin levels not regulated –> impaired endogenous glucose production and persistently high mm glucose uptake –> risk of hypoglycemia

69
Q

Why is a stress dose of glucocorticoids needed for surgery if patient has hx of chronic glucocorticoid use?

A

Glucocorticoids maintain normal vascular tone by inc NE, renin and AT vasoconstrictive activity. Deficiency can precipitate hypotension/shock in high stress situations such as surgery.

70
Q

How does potassium iodide work to treat iodine toxicity from nuclear accidents or to prevent radiation-induced thyroid carcinoma?

A

Competitively inhibits thyroid uptake of radioactive iodine isotopes

71
Q

MCC of T1DM?

A

Autoimmune insulitis with progressive beta cell loss
Islet leukocytic infiltration
Cell-mediated immuity

72
Q

Glucagon induces metabolic changes by increasing what and where?

A

Glycogenolysis and gluconeogenesis in the LIVER
Increase blood glucose
When blood sugar is low, glucagon signals the adipocytes to activate HORMONE-SENSITIVE LIPASE, and to convert triglycerides into free fatty acids

73
Q

An increase in estrogen activity (eg preg or post-menopausal estrogen replacement) increases levels of what thyroid substance?

A

Thyroxine-binding globulin (binds circulating thyroid hormone)–> inc total T4 pool.
Note: feedback control maintains normal levels of free (biologically active) thyroid hormone

74
Q

What’s the cause of hyperglycemia in a T1DM?

A

type 1 = no insulin
given insulin [dependent on dose] - > decrease cAMP - > PFK2 activated [storage]

hyperglycemia - > leads to glyogen synthesis in NORMAL conditions***

since diabetic no insulin - > glucagon is present again after “few hours” + Epinephrine - > increase cAMP - > glycogen phosphorylase activation - > HYPERGLYCEMIA

75
Q

How is hypothyroidism assoc with paresthesias of the hands?

A

Although the association between hypothyroidism and peripheral neuropathy isn’t fully understood, it’s known that hypothyroidism can cause fluid retention resulting in swollen tissues that exert pressure on peripheral nerves.

76
Q

Stones, bones, groan, thrones, psychiatric overtones if a mneumonic for what?

A

Hypercalcemia

- hyperparathyroidism, hypercalcemia of malignancy (eg SCC –> Parathyroid related protein)

77
Q

What are serum levels of B-hydroxybutyrate, osmolaltiy, and anion gap in DKA?

A

B- hydroxybutyrate: increased
Osmolality: increased (loss of water via osmotic diuresis from high glucose spilling into urine)
Anion gap: increased

78
Q

damage to the pituitary stalk may result in increased secretion of what pituitary hormone?

A

Prolactin
With an intact hypothalamus-pituitary axis, prolactin is normally inhibited (by dopamine) while the rest of the hormones are normally stimulated. Damage to the stalk leads to loss of inhibition on prolactin (stimulation) and loss of stimulation on all other hormones (resulting in inhibition)

79
Q

What is the etiology of Addison’s disease (primary adrenal insufficiency)

A

Autoimmune - most often due to damage by the body’s own immune system in the developed world
D/t tuberculosis in the developing world.

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