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Endocrinology Flashcards

1
Q

Where does the thyroid diverticulum arise from?

A

The floor of primitive pharynx and descents into the neck

connected to the tongue by thyroglossal duct which normally disappears.

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2
Q

pt presents with a anterior midline neck mass that moves with swallowing and protrusion of the tongue.

A

thyroglossal duct that persists as cysts or the pyramidal lobe of the thyroid

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3
Q

What is the most common ectopic thyroid tissue site?

A

tongue (lingual thyroid)

removal can result in hypothyroidism if its the only thyroid tissue present

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4
Q

What is the normal remnant of the thyroglossal duct?

A

foramen cecum

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5
Q

Follicular cells are derived from? Parafollicular cells like C cells that product calcitonin are derived from?

A

1) endoderm

2) neural crest

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6
Q

Adrenal cortex is derived from? medulla?

A

1) mesoderm

2) neural crest

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7
Q

Layers of the adrenal cortex?

A

Zona Glomerulosa –> Zona Fasciculata –> Zona Reticularis

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8
Q

Layers of the adrenal cortex and what they produce? How are they regulated?

A

think GFR, the deeper you go the sweeter it gets

G-glomerulosa –> salt (mineralocorticoids) –> aldosterone regulated by angiotensin II
F-Fasciculata –> sugar (glucocorticoids) –> cortisol regulated by ACTH,CRH
R-Reticularis –> Sex (androgens) –> DHEA regulated by
ACTH, CRH

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9
Q

What are the cells of the medulla (core of adrenal cortex) made of? What do they make? How is it regulated?

A

medulla is made of chromaffin cells which make catecholamines like epinephrine and NE. Regulated by preganglionic sympathetic fibers

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10
Q

What is the anterior pit (adenohypophysis) derived from? What is the posterior pit (neurohypophysis) derived from?

A
  • oral ectoderm (Rathke pouch)

- neuroectoderm

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11
Q

What does the anterior pituitary secrete?

A

FASH,LH,ACTH, TSH,prolactin, GH, beta endorphin, melanotropin (MSH is from intermediate lobe of pit)

alpha subunit - hormone subunit common to TSH,LH,FSH,hCG

Beta subunit-determines hormone specificity

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12
Q

Pit hormones that are acidophils? Basophils?

A

B-FLAT : basophils are FSH,LH, ACTH, TH

acidophils are GH and PRL

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13
Q

What does the posterior pituitary do?

A

Hypothalamus makes vasopressin (ADH/antidiuretic hormone) and oxytocin via the supraoptic and paraventricular nuclei –> transported via neurophysins carrier proteins –>the posterior pituitary stores and releases

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14
Q

Islets of langerhans arise from? cells in them? what they produce?

A

Islet of langerhans arise from pancreatic buds

They have alpha, beta, and delta cells

alpha - glucagon (peripheral)
beta-insulin (Central)
delta - somatostatin (interspersed)

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15
Q

Insulin synthesis

A

1) preproinsulin is made by RER
2) Cleavage of presignal form proinsulin which is stored in secretory granules
3) cleavage of prosinulin
4) exocytosis of insulin and c peptide equally

note: insulin receptors have tyrosine kinase activity
note: insulin cannot pass the placenta

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16
Q

Pt with an insulinoma or sulfonylurea use will have ____ c peptide and ____ insulin levels

A

increased both

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17
Q

Pt taking exogenous insulin will have ____ c peptide and ____ insulin levels

A

increased insulin

low c peptide because exogenous insulin lacks c peptide

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18
Q

GLUT4

A

adipose tissues and striated muscles

insulin dependent

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19
Q

GLUT1

A

insulin independent transporter

RBCs, brain, cornea, placenta

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20
Q

GLUT2

A

insulin independent transporter

transports glucose, fructose, galactose to blood

bidirectional, beta islet cells, liver, kidney, small intestine

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21
Q

GLUT3

A

insulin independent transporter

brain placenta

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22
Q

GLUT5

A

insulin independent transporter

fructose is taken up by fascillitated diffusion

spermatocytes, GI tract

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23
Q

SGLT1/SGLT2

A

insulin independent transporter for glucose and galactose

Na-glucose cotransporters in kidney and small intestine

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24
Q

What does the brain use for metabolism when in starvation mode?

A

normally it is glucose but during starvation it is ketone bodies

note: RBCs cant use ketone bodies because lack mitochondria for aerobic metabolism

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25
Q

How does glucose cause in increase in insulin response?

A

via incretins like glucagon-like peptide 1 (GLP1) and glucose-dependent insulinotropic polypeptide (GIP)

they are released after meals and increase beta cell sensitivity to glucose

Release is decreased by alpha2 and increased by beta 2

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26
Q

How does glucose result in increased insulin RELEASE?

A

1) glucose enters beta cells
2) glucose used to make ATP
3) increased ATP closes K channels
4) Results in depolarized beta cell membrane
5) voltage gated Ca channels open
6) Calcium influx
7) stimulation of insulin exocytosis

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27
Q

Glucagon

A

released in response to hypoglycemia due to alpha cells

inhibited by insulin, hyperglycemia, somatostatin

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28
Q

What hormone increases water permeability of distal convoluted tubule and collecting duct cells in kidney in response to increased plasma osmolality? What is the exception?

A

ADH

exception: SIADH (Syndrome of inappropriate antidiuretic hormone secretion) where ADH is inappropriately elevated despite decrease plasma osmolality

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29
Q

Corticotropin-releasing hormone (CRH)

A

increases ACTH, MSH, beta endorphin

CRH decreases in exogenous steroid use

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30
Q

Dopamine function

A

function to decrease prolactin and TSH

inhibits prolactin via the tuberoinfundibular pathway of the hypothalamus. (prolactin inhibits its own secretion by increasing dopamine from hypothalamus)

dopamine antagonists can cause galactorrhea due to hyperprolactinemia

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31
Q

GHRH (growth hormone releasing hormone)

A

Increases GH

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32
Q

GnRH (Gonadotropin-releasing hormone)

A

Increases FSH and LH

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33
Q

MSH (Melanocyte-stimulating hormone)

A

Increases melanogenesis by melanocytes

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34
Q

Why do cushings patients also suffer from hyperpigmentation?

A

Due to MSH which shares the same precursor molecule as ACTH - proopiomelanocortin

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35
Q

What hormone is important for the suckling reflex and uterine contractions?

A

Oxytocin

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36
Q

Prolactin

A

Causes a drop in GnRH which is important for FSH and LH synthesis.

stimulates milk production
inhibits ovulation and spermatogenesis
Decreased libido

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37
Q

The analog of what hormone is used to treat acromegaly?

A

Somatostatin because it decreases GH and TSH

“somatostatin keeps your growth STATIC”

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38
Q

Thyrotropin-releasing hormone (TRH)

A

Increase TSH and prolactin

excess will cause increased prolactin which will result in galactorrhea

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39
Q

Pt presents with amenorrhea, osteoporosis, hypogonadism, galactorrhea, decreased libido. Patient has low GnRH levels, FSH, an LH. What is causing these labs and symptoms?

A

Pituitary prolactinoma

can treat with a dopamine agonist

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40
Q

What is estrogens effect on prolactin?

A

stimulates prolactin release

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41
Q

What hormone stimulates linear growth and muscle mass through IGF-1 (somatomedin C) secreted by the liver?

A

Growth hormone (somatotropin)

“somatoMEDIN MEDIATES your growth”

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42
Q

How does GH impact diabetes?

A

Secretion increase during hypoglycemia. Secretion inhibited by glucose and somatostatin.

Increases insulin resistance therefore it is diabetogenic

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43
Q

What hormone has an orexigenic effect? What is its impact on GH?

A

Ghrelin increases GH release (makes you hungry and grow)

Increases with sleep deprivation and prader willi syndrome

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44
Q

What hormone is important for Satiety? where is it produced?

A

Leptin “leptin keeps you thin” produced by adipose tissue

Decrease with sleep deprivation
Mutation causes congenital obesity

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45
Q

Leptin acts on the _______ area of the _____ to decrease appetite?

A

Acts via the ventromedial area of hypothalamus to decrease appetite

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46
Q

Ghrelin acts on the _____ area of the ______ to increase hunger

A

Acts via the lateral are of hypothalamus to increase appetite

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47
Q

Endocannabinoids act on the _____ in the ________ and ___________, two key brain areas for the homeostatic and hedonic control of food intake. Increases appetite

A

cannabinoid receptors in the hypothalamus and nucleus accumbens

exogenous cannabinoids cause the munchies

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48
Q

Where is ADH/Vasopressin synthesized?

A

hypothalamus at supraoptic and paraventricular nuclei then stored and secreted by the posterior pituitary. Ultimately increases aquaporin channel insertion in principal cells of renal collecting duct

regulates serum osmolality with V2 receptors and blood pressure with V1 receptors

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49
Q

What are ADH levels in central DI? nephrogenic DI?

A

central it is low (give analog Desmopressin)

nephrogenic it is normal or hgh but mutation in V2 receptor

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50
Q

17 alpha hydroxylase pathway and deficiency

A

Important in using pregnenolone and progesterone (in zona glomerulosa) to form 17 hydroxypregnenolone and progesterone (zona fasiculata). 17 alpha hydroxylase further takes these and forms DHEA and androstenedione, respectively. These are important for testosterone synthesis.

Because it cant make testoterone. The pathway is shunted within the zona glomerulosa to form more aldosterone.

results: Increased mineralocorticoids, increase BP, decreased sex hormones, decreased K, decreased androstenedione

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51
Q

17 alpha hydroxylase in men vs women

A

In men: ambiguous genitalia, undescended testes

women: lacks secondary sexual development

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52
Q

21- hydroxylase pathway and deficiency

A

important for taking progesterone in zona glomerulosa to form 11-deoxycorticosterone –> –> aldosterone

Also important for taking 17 hydroxyprogesterone in the zona fasiculata to form 11 deoxycortisol –> cortisone

Deficiency prevents formation of aldosterone and cortisone. Shunted down the 17 alpha hydroxylase pathway to make testosterone.

results: decreased mineralocorticoids, cortisol, BP. Increased sex hormones, K+, renin activity

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53
Q

21 hydroxylase deficiency presentation

A

presents in infancy as salt wasting or childhood as precocious puberty

girls are virilized

most common deficiency

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54
Q

11 beta hydroxylase pathway and deficiency

A

similar to 21 hydroxylase deficiency, blocks the pathways to form aldosterone and cortisone. Difference is that there is still accumulation of 11-deoxycorticosterone in zona glomerulosa. This causes rise in BP eventhough aldosterone is low. Rest shunted towards testosterone pathway

results: low aldosterone, high 11 deoxy, low cortisol, low K+, low renin activity,increased sex hormones, increased BP

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55
Q

11 beta hydroxylase deficiency presentation

A

XX: virilization

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56
Q

11 beta hydroxylase
21 hydroxylase
17 alpha hydroxylase

memory tool

A

if starts with a 1: hypertension
if ends with a 1: virilization

note: any congentital adrenal enzyme deficiency are characterized by skin hyperpigmentation due to increased MSH production which is coproduced with ACTH

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57
Q

Why do exogenous corticosteroids cause the reactivation of TB and candidiasis?

A

blocks IL2 production

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58
Q

Cortisol effects on appetite? BP? insuline resistance? glucose utilization? fibroblast activity? inflammatory an immune response? bone?

A
  • increases appetite
  • Increases BP via upregulation of alpha 1 receptors and at high concentrations also mineralocorticoid (aldosterone) receptors
  • increases insulin resistance
  • increases gluconeogenesis, lipolysis, and proteolysis (decreased glucose utilization)
  • decreased fibroblast activity causes poor wound healing
  • decreased inflammatory and immune responses
  • decreased bone formation
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59
Q

Effect of pH on calcium homeostasis

A

increase in pH will increase albumins affinity for Ca which results in hypocalcemia

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60
Q

What is the primary regulatory of PTH?

A

ionized/free Ca

NOT albumin bound

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61
Q

PTH pathway

A

PTH secreted by the chief cells of the four parathyroid glands where they go to the renal tubular cells and have the follow effects:

1) renal effects
Increases 1,25 (OH)2D3 synthesis
Increases reabsorption of Ca and decreases PO4
Urine is low Ca high PO4

2) Bone
(low PO4 and) PTH + stimulate 1alpha hydroxylase to convert 25 OH D3 to 1,25 OH2 D3 –> Increases Ca and PO4 release from bones

3) Intestine
(Low PO4 and) PTH + stimulate 1alpha hydroxylase to convert 25 OH D3 to 1,25 OH2 D3 –> increased absorption of Ca and PO4

OVERALL: increase serum Ca and decrease serum PO4

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62
Q

How does PTH cause increase bone resporption?

A

it increases RANK-L secreted by osteoblasts and osteocytes.

Binds RANK receptor on osteoclasts

increase bone resorption

note: intermittent PTH release can also stimulate boen formation

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63
Q

Parafollicular cells (C cells) of the thyroid secrete?

A

Calcitonin which decreases bone resorption of Ca due to high serum Ca

opposes PTH which increases resorption

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64
Q

Source of thyroid hormones (and enzyme)

A

follicles of thyroid

5’-deiodinase converts T4 to T3 in peripheral tissues

this is inhibited by glucocorticoids, beta blockers, propylthiouracil (PTU)

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65
Q

Function of thyroid perioxidase

A

oxidation, organification, and coupling

DIT + DIT = T4

DIT + MIT = T3

note: only free thyroid hormone is active

66
Q

Wolff chaikoff effect

A

excess iodine temporarily inhibits thyroid peroxidase which decreases T3 and T4

by prevent DIT + DIT = T4
MIT +DIT = T3

67
Q

Which thyroid hormone binds nuclear receptors with greater affinity? What are its effects?

A

T3 binds nuclear receptors with greater affinity than T4

6 Bs?
Brain maturation, Bone growth, Beta adrenergic effects, Basal metabolic rate, Blood sugar (increase gluconeogenesis and glycogenolysis), break down lipids

68
Q

How is T3/T4 regulated? What protein binds them?

A

Hypothalamus –> TRH —> stimulate Ant. pit –> TSH –> stimulate thyroid follicular cells –> T3/T4

bound by thyroxine-binding globulin (TBG)

69
Q

Sex hormone-binding globulin

A

in men : can get gynecomastia if increases SHBG because there will be less free active testosterone

In women: can get hirsutism because decrease in SHBG raises free testosterone

OCP and pregnancy cause an increase in SHBG

70
Q

What three things can cause the increase in cortisol thats seen in cushing syndrome?

A

1) exogenous corticosteroids –> drop in ACTH –> adrenal atrophy
2) primary adrenal adenoma, hyperplasia, or carcinoma –> drop in ACTH –> adrenal atrophy
3) MOST COMMON: Cushings DISEASE or ACTH-secreting pituitary adenoma

71
Q

Characteristic findings in cushings?

A
  • Moon facies
  • abdominal striae
  • truncal obesity
  • buffalo hump
  • can have pseudohyperaldosteronism

other: HTN, hirsutismm, osteoporosis, hyperglycemia, amenorrhea, immunosuppression

72
Q

How do you screen for Cushings syndrome?

A

Increase free cortisol on 24 hr analysis
increase midnight salivary cortisol
no suppression with overnight low dose dexamethasone test

Cushings syndrome!

Then measure ACTH: if low then suspect arenal tumor or exogenous glucocorticoids. If high then think ACTH dependent cushings syndrome

If adequate suppression on high dose dexamethasone test or increase ACTH and cortisol on CRH stimulation test–> cushings

If no suppression and no increase in ACTH and cortisol then —> ectopic ACTH secretion

73
Q

Patient presents with high ACTH and low cortisol?

A

primary adrenal insufficiency - loss of gland function causes deficiency in cortisol and aldosterone

classic triad: Hypotension due to hyponatremia, hyperkalemia, metabolis acidosis

skin pigmentation due to MSH production as ACTH is produced (same precursor of proopiomelanocortin)

74
Q

Patient presents with low ACTH and low cortisol

A

secondary or tertiary adrenal insufficiency

75
Q

metyrapone stimulation test for adrenal insufficiency

A

metyrapone blocks last step of cortisol synthesis (11-deoxycortisol to cortisol)

normal: decrease cortisol but increase ACTH
primary: ACTH high and 11-deoxycortisol stays low
secondary/tertiary: both low

76
Q

A type of primary adrenal insufficiency, chronic, hypotension, hyponatremia, hyperkalemia, metabolic acidosis.

Autoimmune destruction of adrenal gland

A

Addisons disease

A=autoimmune

77
Q

A type of primary adrenal insufficiency, chronic, hypotension, hyponatremia, hyperkalemia, metabolic acidosis.

Adrenal hemmorrhage due to septicemia

A

Waterhouse friderichsen syndrome

waterhouse=hemorraging fills the house with liquid

78
Q

Adrenal insufficiency due to drop in pituitary ACTH production that spares the skin/mucosa

A

secondary

no skin/mucosa
no hyperkalemia because intact renin angiotensin aldosterone axis

79
Q

Adrenal insufficiency due to chronic exogenous steroid use that is abruptly stopped

A

tertiary

aldosterone synthesis unaffected

80
Q

Triad for hyperaldosteronism

A

HTN
decreased or normal K
metabolic alkalosis

81
Q

High aldosterone
Low renin
Causes resistent hypertension
does not directly cause edema

A

primary hyperaldosteronism due to adrenal adenoma (conn syndrome) or bilateral adrenal hyperplasia

Has aldosterone escape mechanism and therefore does not directly cause edema

82
Q

Seen in patients with renovascular HTN
Juxtaglomerular cell tumors that produce renin
edema due to HF etc.

A

Secondary hyperaldosteronism

impaired aldosterone escape mechanism and therefore does cause edema

83
Q

Pt is a 4 yo child that presents with abdominal distension and a firm irregular mass that crosses the midline. Pt is normotensive

A

Neuroblastoma-Most common tumor of the adrenal medulla in children

can also present with opsoclonus-myoclonus syndrome or dancing eyes dancing feet

84
Q

This tumor originates from neural crest cells and can occur anywhere along the sympathetic chain

A

Neuroblastoma

associated with overexpression of n-myc gene and is classified as an APUC tumor (neuroendocrine tumor cells contain amine precursor uptake decarboxylase)

elevated HVA and VMA which are catecholamine metabolites in urine

histology: see homer wright rosettes, Bombesin and NSE +

85
Q

This tumor of the adrenal medulla causes episodic hypertension and polycythemia

A

Pheochromocytoma - most common tumor of the adrenal medulla in adults and is derived from chromaffin cells (neural crest)

secretes EPI, NOREPI, Dopamine (increases catecholamines and metabolites)

86
Q

Rule of 10 in pheochromocytoma

A 
10% malignant
10% bilateral
10% extraadrenal
10% calcify
10% kids
87
Q

Episodic hypertension

A

spells that relapse and remit

Pressure due to increase BP
Pain due to headache
Perspiration
Palpitations due to tachy
Pallor
88
Q

Treatment for pheochromocytoma

A

tx: irreversible alpha antagonist followed by beta blockers prior to tumor resection. alpha antagonist prevents hypertensive crisis

Phenoxybenzamine

89
Q

Patient presents with watery diarrhea, hypokalemia, achlorhydria (absence of hydrochloric acid in the gastric secretions)

A

VIPoma

secretes vasoactive intestinal peptide (VIP)

usually in pancreas and associated with MEN1

90
Q

In what thyroid disorder do you see proximal mm weakness with increased CK and myoedema

A

hypothyroid myopathy

also see carpal tunnel syndrome

note :myoedema is having a small lump rise on the surface of a mm when struck with a hammer

91
Q

In what thyroid disease do you see proximal mm wekaness with normal CK and an increased risk of osteoporosis

A

hyperthyroid

thyrotoxic myopathy

increased risk of fracture due to high T3 and T4

92
Q

Which thyroid disease causes increased reflexes? which causes decreased?

A

hypo is decreased reflex

hyper is increased reflex

93
Q

In which thyroid disease do you see hypercholesterolemia due to a drop in LDL receptor expression? In which do you see a decrease in LDL, HDL, and total cholesterol?

A

1) hypothyroid

2) hyperthyroid

94
Q

Thyroid disease with increased number and sensitivity of beta adrenergic receptors, increased expression of cardiac sarcolemmal ATPase, and decrease expression of phospholamban

A

hyperthyroid

95
Q

Hashimotos thyroiditis

A 
hypothyroid
antithyroid peroxidase (antimicrosomal)
antithyroglobulin antibodies
HLA DR3
Increased risk of non hodgkins lymphoma
Histo: hurthle cells, lymphoid aggregates with germinal centers
large nontender thyroid
96
Q

Pregnant women present with this thyroid disorder 1 year after delivery

A

postpartum thyroiditis

transient

97
Q

Baby is pot bellied, pale, ouffy faced, protruding umbilicus, protuberant tongue, poor brain development

A

Congential hypothyroidism (cretinism)

severe fetal hypothyroid due to antibody mediated maternal hypothyroidism, thyroid agenesis, thyroid dysgenesis (most common in us), iodine deficiency, dyshormonogenetic goiter

98
Q

pt was sick with the flu and now presents with jaw pain and severely tender thyroid

A

subacute granulomatous thyroiditis aka de quervain “pain”

self limiting

histology shows granulomatous inflammation

high ESR

99
Q

Patient prevents with a fixed hard rock like painless goiter

A

Riedel thyroiditis

thyroid is replaced by fibrous tissue with inflammatory infiltrate. fibrosis extends to local tissues and resembles anaplastic carcinoma.

IgG4 related systemic dz

100
Q

wolf chaikoff effect

A

thyroid gland downregulation in response to increased iodide

101
Q

Graves disease pathway

A

thyroid stimulating immunoglobulin (IgG type II hypersensitivity) stimulates TSH receptors on thyroid and dermal fibroblasts (pretibial myxedema)

HLA DR3 and HLA B8

histology: tall crowded follicular epithelial cells, scalloped colloid

102
Q

Graves disease - exophthalmos disease pathway

A

Infiltration of retroorbital space by activated T cells causes an increase in cytokines (TNF alpha and IFN gamma etc.) which increase fibroblast secretion of hydrophilic GAGs and increase osmotic swelling, mm inflammation, and adipocyte count

103
Q

What causes lid lag in graves disease

A

increased sympathetic stimulation of the levator palpebrae superioris

104
Q

Toxic multinodular goiter

A

focal patches of hyperfunctioning follicular cells distended with colloid and working independently of TSH

hot nodules are rarely malignant

105
Q

Patient presents with agitation, delirium, fever, diarrhea, coma, tachyarrhythmia post thyroid surgery. how do you tx this patient?

A

thyroid storm. tachyarrhythmias are the main cause of death

tx with a beta blocker, propylthiouracil, corticosteroids, potassium iodide

106
Q

Jod-Basedow phenomenon

A

thyrotoxicosis

iodine deficient and partially autonomous thyroid tissue is suddenly made iodine replete

can happen after iodine iv contrast

opposite of wolf chaikoff effect

think “job well done”

107
Q

Causes of smooth goiter/diffuse

A

graves disease
hashimoto thyroiditis
iodine deficiency
TSH-secreting pituitary adenoma

108
Q

Thyroid adenoma

A

nonfunctional/cold
mostly follicular
absence of capsular or vascular invasion

109
Q

Thyroid cancer complications: hoarseness

A

recurrent laryngeal nerve damage

110
Q

Thyroid cancer complications: dysphagia and dysphonia

A

transection of recurrent and superior laryngeal nerves during ligation of inferior thyroid artery and superior laryngeal artery

111
Q

Papillary carcinoma

A

Most common thyroid cancer
Orphan annie eyes
psammoma bodies

RET/PTC rearrangements and BRAF mutations or childhood irradiation

112
Q

Follicular carcinoma

A

invades thyroid capsule and vasculature
uniform follicles
hematogenous spread is common

RAS mutation and PAX8-PPARgamma

113
Q

Medullary carcinoma

A

parafollicular c cells
produce calcitonin
sheets of cells in an amyloid stroma (congo red stain)

MEN2A and 2B (RET mutations)

114
Q

undifferentiated/anaplastic carcinoma

A

older patients
invades local structures
very poor prognosis

115
Q

Hypoparathyroidism lab findings?

A

Low Ca
high PO4
tetany

116
Q

Sign that involves tapping of facial nerve (tap the cheek) that causes contraction of facial mm

A

Chvostek sign for hypoparathyroidism

Ch=Cheek

117
Q

Sign that involves the occlusion of brachial artery with BP cuff (cuff the triceps) –> carpal spasm

A

Trousseau sign for hypoparathyroidism

T=Triceps

118
Q

Pseudohypoparathyroidism type 1A

A

unresponsiveness of kidney to PTH. Defective Gs protein alpha subunit causing end organ resistance to PTH

albright hereditary osteodystrophy - shortened 4th/5th digits, short stature, obesity, developmental delay

aut. dominant - defect inherited from MOTHER

119
Q

Pseudopseudohypoparathyroidism

A

features of albright hereditary osteodystrophy

no end organ PTH resistance (PTH level normal)

defective Gs protein alpha subunit is inherited from FATHER

120
Q

Primary hyperparathyroidism

A

Parathyroid adenoma or hyperplasia

Hypercalcemia, hypercalciuria (renal stones), polyuria (thrones), hypophosphatemia, increased PTH, increased ALP, increase cAMP in urine

pt has constipation, neuropsychiatric disturbances

classically you see osteitis fibrosa cystica

121
Q

cystic bone spaces filled with brown fibrous tissue (brown tumor) consisting of osteoclasts and deposited hemosiderin for hemorrhages, causes bone pain

A

osteitis fibrosa cystica

classically seen in primary hyperparathyroidism

122
Q

Secondary hyperparathyroidism

A

decreased calcium absorption and or increase PO4

chronic renal disease (low vit D and high PO4 –> low Ca)

hypocalcemia, hyperphosphatemia (chronic renal failure), increase ALP, increase PTH

123
Q

_________ is renal disease in secondary and tertiary hyperparathyroidism that leads to bone lesions

A

Renal osteodystophy

124
Q

Tertiary hyperparathyroidism

A

Refractory (autonomous)hyperparathyroidism resulting from chronic renal disease

increase in PTH and increase in Ca

Renal osteodystrophy

125
Q

Familial hypocalciuric hypercalcemia

A

defective G coupled Ca sensing receptors that are less sensitive to Ca levels

more Ca is requried to suppress PTH

therefore there is excessive renal Ca reuptake –> mild hypercalcemia and hypocalciuria with normal to high PTH levels

126
Q

Patient had a bilateral adrenalectomy and now suffers from hyperpigmentation, headaches, and bitemporal hemianopia (blindness over half of vision)

A

Nelsons syndrome- enlargement of existing ACTH secreting pit adenoma after bilateral adrenalectomy for refractory cushing disease. This is due to removal of cortisol feedback

127
Q

Excess GH in adults due to a pituitary adenoma can cause __? in Children? how is it diagnosed? how to tx?

A

Acromegaly in adults
Gigantism in children

HF is most common cause of death

dx: increased serum IGF-1, failure to suppress serum GH following oral glucose tolerance test, pituitary mass seen on brain MRI
tx: pit adenoma resection. If not cured then give octreotide (somatostatin analog) or pegvisomany (growth hormone receptor antagonist), dopamine agonist

128
Q

Acromegaly findings

A 
large tongue
frontal bossing
coarsening of facial features with aging
insulin resistance
large hands and feet
129
Q

pt presents with short height, small head circumference, saddle nose, and prominent forehead, delayed skeletal maturation, and small genitalia

A

Dwarfism/Laron syndrome- defective GH receptors cause a decrease in linear growth

causes a upreg of GH and down reg of IGF-1

130
Q

Pt presents with intense thirst and polyuria with inability to concentrate urine

A

Diabetes insipidus

lack of ADH (Central) or failure of response to circulating ADH (nephrogenic)

131
Q

Low ADH levels with increased urine osmolality only after administration of ADH analog (desmopressin)

A

Central Diabetes insipidus

ADH analog only given if serum osm between 295-300, plasma Na >= 145, or urine osm does not rise despire a rising plasma osm

132
Q

Normal or high ADH levels with minimal change in urine osmolality even after adminisration of ADH analog

A

Nephrogenic DI

133
Q

Syndrome of inappropriate ADH secretion

A
  • excessive free water retention
  • euvolemic hyponatremia with continued urinary Na excretion
  • urine osm >serum osm

very low Na levels can lead to cerebral edema and seizures. Correct slowly to prevent osmotic demyelination syndrome

134
Q

First line treatment for syndrome of inappripriate ADH secretion?

A

fluid restriction

135
Q

What causes the euvolemic hyponatremia seen in syndrome of inappropriate ADH secretion?

A

Body responds to water retention with decreased aldosterone and increased ANP and BNP

this results in increased urinary Na secretion –> normalization of extracellular fluid volume

136
Q

Pt suffered from significant postpartum bleeding and now has failure to lactate, absent menstruation, and cold intolerance. What syndrome are we worried about?

A

Sheehan syndrome-ischemic infarct of pituitary following postpartum bleeding

postpartum pituitary gland necrosis

“she hamaraged”

137
Q

Empty sella syndrome

A

atrophy or compression of pituitary which lies in the sella turcica

common in obese women

idiopathic intracranial HTN

138
Q

Pt presents with a sudden onset severe headache, visual impairment (bitemporal hemianopia, diplopia due to CN III plasy), and features of hypopituitarism

A

pituitary apoplexy

sudden pit hemorrhage often in presence of existing adenoma

139
Q

Examples of small vessel diseases seen in DM?

A

retinopathy, glaucome, neuropathy, nephropathy (ACEi are renoprotective, arteriolosclerosis –> HTN

nephropathy: nodular glomerulosclerosis aka Kimmelstiel Wilson nodules which result initially in microalbuminuria and then progressive proteinuria

140
Q

What is the most common cause of death in a diabetic patient?

A

MI

141
Q

Osmotic damage in DM?

A

sorbitol accumulation in organs with aldose reductase and decrease or absent sorbitol dehydrogenase

results in neuropathy and cataracts

142
Q

Diagnostic cut offs for DM?
HbA1c?
Fasting plasma glucose?
2 hr oral glucose tolerance test?

A

> = 6.5%
= 126
=200

143
Q

Type 1 diabetes characteristics

A

autoimmune destruction of beta cells

  • weak genetic predisposition
  • HLADR4 and HLADR3 (4-3=1)
  • Severe glucose intolerance
  • Insulin sensitivity high
  • Keto acidosis common
  • histology shows islet leukocytic infiltrate
144
Q

Type 2 diabetes characteristics

A

Hyperosmolar hyperglycemic state
Increased resistance to insulin, progressive pancreatic beta cell failure
Strong genetic predisposition
Low insulin sensitivity
histology shows islet amyloid polypeptide (IAPP) deposits

145
Q

Diabetic ketoacidosis is usually due to

A

insulin noncompliance or increased insulin requirement form stress in a pt with type I DM

ketone bodies: beta-hydroxybutyrate > acetoacetate

146
Q

DKA symptoms and tx

A 
Delirium/psychosis
Kussmall respirations (rapid deep breathing)
ab pain nausea and vomiting
dehydration
fruity breathe due to exhaled acetone

tx: IV fluid, IV insulin, K+ to replenish intracellular stores, glucose to prevent hypoglycemia

147
Q

DKA labs

A

High H+
Low bicarb (increase anion gap metabolic acidosis)
leukocytosis
hyperkalemia (intracellular depleted)
osmotic diuresis results in increased K in urine and thus total body K+ depletion

148
Q

Complications of DKA

A

life threatening mucormycosis (rhizopus infection)
cerebral edema
cardiac arrhythmias
HF

149
Q

Hyperosmolar hyperglycemic state

A

state of profound hyperglycemia induced dehydration and increased serum osmolality

labs: hyperglycemia >600,serum osm >320,no acidosis,

150
Q

tumor of pancreatic alpha cell that causes hyperglycemia

A

glucagonoma

overproduced glucagon –> increase glycogen breakdown into glucose

dermatitis- necrolytic migratory erythema
diabetes
DVT

151
Q

tumor of pancreatic beta cells that cause hypoglycemia

A

Insulinoma

whipple triad: low blood glucose, sx of hypoglycemia, resolution of sx after normalization of glucose levels

10% associated with MEN1 syndrome

152
Q

Tumor of pancreatic delta cells that cause diabetes/glucose intolerance, steatorrhea, gallstones, achlorhydria

A

somatostatinoma

increase somatostatin causes a drop in secretin, CCK, glucagon, insulin, gastrin, GIP

153
Q

Carcinoid syndrome

A

syndrome caused by carcinoid tumor (neuroendocrine cells) which secrete high levels of serotonin (5HT).

use neuroendocrine tumor markers chromagranin A and synaptophysin

not seen if tumor is limited to GI tract because 5HT undergoes first pass metabolism in the lvier

154
Q

Rule of 1/3 for carcinoid syndrome

A

1/3 metastasize
1/3 present with second malignancy
1/3 are multiple

155
Q

what is the most common malignancy in the small intestine?

A

carcinoid tumours

156
Q

pt presents with recurrent diarrhea, cutaneous flushing, ashtmatic wheezing, right sided valvular heart disease

A

carcinoid syndrome

R sided valvular disease is due to lung MAO-A enzymatic breakdown of 5HT before left heart return

increase in 5 hydroxyindoleactic acid (5-HIAA) in urine

niacin deficiency –> pellagra

157
Q

Zollinger-Ellison syndrome

A

Gastrin secreting tumor (gastrinoma) of pancreas or duodenum

acid hypersecretion causes recurrent ulcers in duodenum and jejunum

positive secretin stimulation test : gastrin levels remain elevated after administration of secretin, which normally inhibits gastrin release

158
Q

MEN syndromes

A

multiple endocrine neoplasias

all are autosomal dominant

MEN are DOMINANT

159
Q

MEN1

A

3 Ps

pituitary tumors
pancreatic tumors
parathryoid adenoma

mutation in MEN1 (menin, a tumor suppressor, chromosome 11)

160
Q

MEN2

A

2 Ps

Parathyroid hyperplasia
Medullary thyroid carcinoma
Pheochromocytoma

mutation in RET (codes for tyrosine kinase receptor) in cells of neural crest origin

161
Q

MEN3

A

1 Ps

Medullary thyroid carcinoma
Pheochomocytoma
mucosal neuromas

associated with marfanoid habitus. mutation in RET gene

162
Q

Medullary thyroid cancer

A

parafollicular calcitonin secreting c cells

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