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FA: random > Random Organ systems - endo > Flashcards

Random Organ systems - endo Flashcards

1
Q

What is the function of CRH of HPA? clinical notes?

A

increase ACTH, MSH, Beta-endorphin

CRH is decreased in chronic exogenous steroid use

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2
Q

What is the function of Dopamine of HPA? clinical notes?

A

decrease prolactin

Dopamine antagonists (antipsychotics) can cause galactorrhea

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3
Q

What is the function of GnRH of HPA? clinical notes?

A

increase FSH & LH

regulated by prolactin;
Tonic GnRH suppresses HPA axis
Pulsatile GnRH leads to puberty & fertility

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4
Q

What is the function of Prolactin of HPA? clinical notes?

A

decreases GnRH

Pituitary prolactinoma leads to amenorrhea & osteoporosis

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5
Q

What is the function of somatostatin of HPA? clinical notes?

A

decrease GH & TSH

Analogs used to treat acromegaly

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6
Q

What is the function of TRH of HPA?

A

increase TSH & prolactin

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7
Q

Name the neuroendocrine glands controlled by the medulla

A

Posterior pituitary => ADH & OT
Adrenal medulla => catecholamines
Hypothalamus => releasing hormones

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8
Q

What increases or decreases cholesterol desmolase action to convert cholesterol to pregnenolone?

A

increases => ACTH

decreases => ketoconzale

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9
Q

WRT calcium homeostasis, an increase in pH will cause what Sx?

A

increase in pH leads to increase affinity of albumin (neg charge) to bind to Ca+ causing hypocalcemia symptoms of cramps, pain, paresthesias, carpopedal spasm

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10
Q

What endocrine signaling pathways use cAMP?

A

FLAT ChAMP
FSH; LH, ACTH, TSH
CRH, hCG, ADH (V2 receptor), MSH, PTH
calcitonin, GHRH, glucagon

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11
Q

What endocrine signaling pathways use cGMP?

A

ANP & NO (EDRF) => think vasodilators

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12
Q

What endocrine signaling pathways use IP3?

A

GOAT HAG
GnRH, Oxytocin, ADH (V1 receptor), TRH;
Histamine (H1-receptor), AT-II, Gastrin

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13
Q

What endocrine signaling pathways use steroid receptor (intracellular action)?

A

VETTT CAP
Vit D, Estrogen, Testosterone, T3/T4;
Cortisol, Aldosterone, Progesterone

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14
Q

What endocrine signaling pathways use intrinsic tyrosine kinase?

A

MAP kinase pathway => think growth factors

Insulin, IGF-1, FGF, PDGF, EGF

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15
Q

What endocrine signaling pathways use receptor associated tyrosine kinase?

A

JAK/STAT pathway => think acidophiles & cytokines
PIG

Prolactin, Immunomodulators, GH

IL-2, IL-6, IL-8, IFN

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16
Q

Steroid hormones are lipophilic & bound to SHBG. Describe the increase & decrease in SHBG in men & women

A

men=> increase SHBG lowers free testosterone causing gynecomastia

women=> increase SHBG is found in OCPs & pregnancy but free estrogen is unchanged;
decreased SHBG raises free testosterone leading to hirsutism

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17
Q

What does T3/T4 do to the heart?

A

increases B1 receptors leading to increased CO, HR, SV, contractility

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18
Q

What does T3/T4 do to the BMR?

A

increases BMR via increase in Na/K ATPase activity causing more O2 consumption, increased RR & body temp

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19
Q

What causes a decrease in TBG? increase in TBG?

A

hepatic failure;

pregnancy or OCP use along w/ estrogen

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20
Q

What converts T4 to T3 in the periphery?

A

5’-deiodinase

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21
Q

What is the role peroxidase of thyroid hormones?

A

Peroxidase responsible for oxidation & organification of iodide; couples MIT & DIT

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22
Q

What is the Wolff chaikoff effect?

A

excess iodine temporarily inhibits thyroid peroxidase leading to decreased T3/T4 production

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23
Q

Differentiate the Rx used for hyperthyroidism

A

Propylthiourcil inhibits both peroxidase & 5’-deiodinase

Methimazole inhibits peroxidase only

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24
Q

Treatment for prolactinoma

A

DA agonists => bromocriptine or cabergoline

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25
Q

Tx for acromegaly

A

Try to resect

If not cured then octreotide (somatostatin analog) or pegvisomant (GH receptor antagonist)

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26
Q

Differentiate DI based on water restriction test

A

Central DI will show > 50% increase in urine osmolarity

Nephrogenic DI while show no change in urine osmolarity

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27
Q

Tx for central DI

A

Intranasal DDAVP & hydration

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28
Q

Tx for nephrogenic DI

A

HCTZ, indomethacin, amiloride;

Hydration

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29
Q

What are secondary causes of Nephrogenic DI?

A

hypercalcemia; lithium, demeclocycline (ADH antagonist that is former antibiotic rarely used)

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30
Q

What can cause SIADH?

A

Ectopic ADH from small cell lung CA;
CNS d/o or head trauma;
Pulmonary disease;
Drugs => cyclophosphamide

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31
Q

Tx for SIADH?

A

fluid restrict; IV hypertonic saline;

Conivaptan, tolvaptan, demeclocycline

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32
Q

Tx for hypopituitarism

A

HRT => corticosteroids, thryoxine, sex steroids, GH

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33
Q

What 2 blood disorders can occur due to hyperthyroidism?

A

hypocholesterolemia => increased LDL receptor expression

hyperglycemia => gluconeogenesis & glycogenolysis

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34
Q

What are the labs associated w/ the most common cause of hyperthyroidism?

A

Graves disease

increased total & free T4;
decreased TSH;
hypocholesterolemia (increased LDL expression)
increased serum glucose

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35
Q

Tx for Graves disease

A

Beta-blockers
Thioamide (blocks peroxidase)
Radioiodine ablation

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36
Q

Patient comes w/ elevated catecholamines after birth with arrhythmia, hyperthermia, vomiting & hypovolemic shock. What is the treatment?

A

Thyroid storm

Give PTU, beta-blockers, steroids

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37
Q

What is the association of the most common type of hypothyroidism?

A

Hashimoto thyroiditis => AI destruction of thyroid gland assoc w/ HLA-DR5

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38
Q

What AI Ab are present in Hashimoto thyroiditis?

A

Antithyroglobulin & antimicrosomal Ab => markers that damage has occurred

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39
Q

What are the labs assoc with Hashimoto thyroiditis?

A

decreased T4 => controls # of TRH receptors which controls amount of TSH produced => always opposite
increased TSH

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40
Q

What type of cancer is assoc w/ hashimoto thyroiditis?

A

B cell lymphoma => marginal cell lymphoma

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41
Q

Young woman comes in with tender thyroid after viral infection. What is Dx & Px?

A

Subacute (deQuervain) Granulomatous thyroiditis

self limited transient hyperthyroidism w/ NO progression to hypothyroidism

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42
Q

young female patient presents w/ nontender, hard thyroid w/ hypothyroidism. What is Dx & what is at risk? What would be the Dx if the patient was older?

A

Reidel fibrosing thyroiditis => fibrosis may extend to local structures such as airway

anaplastic thyroid

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43
Q

increased I radioactive up results in what Dx? decreased?

A

increased in Graves or nodular goiter

decreased in adenoma & carcinoma (do FNA Bx)

44
Q

What are the 4 types of thyroid carcinoma?

A

papillary, follicular, medullary, anaplastic

45
Q

What is the MC thyroid CA? What is a major risk factor?

A

papillary Ca => ionizing radiation in childhood (severe acne)

46
Q

What typically defines papillary CA of the thyroid?

A

nuclear features of orphan-annie eyes, psammoma bodies, nuclear grooves

47
Q

What is oncogenes are mutated in papillary CA of thyroid?

A

RET & BRAF

48
Q

Px of papillary CA after lymph node spread?

A

excellent

49
Q

Tx for thyroid cancer? complications of treatment?

A

remove the thyroid

Hoarseness (recurrent laryngeal nerve damage);
hypocalcemia (removal of parathyroid glands);
transection of inferior thyroid artery

50
Q

Hallmark of follicular CA of thyroid

A

malignant proliferation of follicles w/ invasion through the capsule

51
Q

Why cannot FNA Bx distinguish between follicular adenoma & follicular CA?

A

needle insertion will only see follicular proliferation as seen in both

invasion through the capsule distinguishes them & not seen on FNA

52
Q

How does follicular CA of thyroid spread?

A

hematogenously

53
Q

What are the CA that like to spread via blood?

A

Renal cell CA;
follicular CA of thyroid
hepatocellular CA;
ChorioCA

54
Q

FNA Bx done and see malignant cells in amyloid stroma

A

medullary CA => malignant proliferation of C cells

55
Q

What are the Sx related to of medullary CA?

A

high levels of calcitonin produced by tumor lead to hypocalcemia

Calcitonin often deposits w/in tumor as amyloid

56
Q

what are the familial cases of medullary CA of thyroid associated w/?

A

MEN 2A & 2B => mutations in RET oncogene

57
Q

Mutation in RET oncogene warrants what procedure?

A

prophylactic thryoidectomy

58
Q

Older person presents w/ dysphagia & respiratory compromise w/ swollen neck. what is Dx & Px?

A

anaplastic CA of thyroid => undifferentiated malignant tumor

Poor Px

59
Q

What is MCC of primary hyperparathyroidism?

A

parathyroid adenoma => benign neoplasm

60
Q

What are the results of primary hyperparathyroidism?

A 
Stones, bones, groans, psych overtones
nephrolithiasis;
nephrocalcinosis;
CNS disturbances;
Constipation, PUD, acute pancreatitis;
Osteitis fibrosa cystica
61
Q

Define osteitis fibrosa cystica

A

cystic bone spaces w/ brown fibrous tissue => bone pain

62
Q

Labs of primary hyperparathyroidism

A

increased serum PTH, Ca+, alk phos (due to osteoblast turned on)
decreased serum phosphate

increased urinary cAMP (PTH stimulates Gs receptor)

63
Q

What is MCC of secondary hyperparathyroidism?

A

chronic renal failure => excess PTH extrinsic to parathyroid gland

64
Q

Labs of secondary hyperparathyroidism

A

increased PTH, phosphate, alk phos

decreased serum Ca+

65
Q

What are causes of hypoparathyroidism?

A

AI damage, surgical excision, DiGeorge syndrome

66
Q

Presentation of hypoparathyroidism?

A

numbness/tingling & muscle spasms (tetany) => Trousseau’s sign (BP cuff), Chavsofic sign (tap on jaw)

67
Q

Labs for hypoparathyroidism

A

low PTH & low serum Ca+

68
Q

What is the cause of pseudohypoparathyroidism?

A

organs not responding to PTH so hypocalcemia w/ elevated PTH

69
Q

The end organ resistance of pseudohypoparathyroidism is due to what?

A

AD mutation in Gs protein assoc w/ short stature & short 4th & 5th digits

70
Q

What causes type I DM? What is it associated with?

A

autoimmune destruction of Beta cells of T lymphocytes => Ab against insulin leading to inflammation of islets

Assoc w/ HLA-DR3 & DR4

71
Q

What are the clinical features of a type I DM patient in DKA?

A

hyperglycemia (>300)
anion gap metabolic acidosis due to ketoacids in blood
hyperkalemia but getting losses in urine so ends in low body potassium bc it is not in cells
Kussmaul respirations, mental change, fruity breath

72
Q

Tx of DKA

A

fluids,
insulin
replacement of electrolytes w/ K+

73
Q

What is the mechanism of insulin resistance in type II DM?

A

decreased numbers of insulin receptors on skeletal muscle & adipose tissue

74
Q

How does insulin concentration change during the course of type II DM?

A

rises due to resistance then very decreased bc of Beta cell exhaustion

amyloid deposits

75
Q

Tx of type II DM

A

weight loss (1st always);
Rx to counter insulin resistance;
end stage is insulin dependent

76
Q

What is a risk for uncontrolled type II DM? How does it present?

A

hyperosmolar non-ketotic coma => very very high glucose leading to life threatening diuresis causing hypoTN & coma w/ absent ketones (small amounts of insulin counteracts glucagon)

77
Q

Vascular complications of DM?

A

NEG of vascular BM =>

NEG of large/medium vessels leads to atherosclerosis;
NEG of small vessels leads to hyaline arteriosclerosis;
NEG of Hgb leads to HbA1c (marker of glycemic control)

78
Q

What cells/structures are at risk for osmotic damage due to high sugar?

A

Schwann cells => basis of neuropathy in diabetics
Pericytes in retina blood vessels => aneurysm causing rupture to blindness
lens

79
Q

Pancreatic endocrine tumors are associated with what?

A

MEN 1 => parathyroid hyperplasia & pituitary adenoma

80
Q

How does an insulinoma present? what relieves Sx? What are the labs?

A

episodic hypoglycemia w/ mental changes relieved by glucose

low glucose;
high insulin & C peptide

81
Q

Patient w/ Treatment resistant PUD. what is Dx?

A

Gastrinoma => ZE syndrome

can be multiple & extend into jejunum

82
Q

Patient w/ low stomach pH along with gallstones & steatorrhea. Dx? Why the Sx?

A

Somatostatinoma
inhibits gastrin so achlorhydria
inhibits CCK => cholelithiasis & steatorrhea

83
Q

Patient w/ watery diarrhea, hypokalemia, achlorhydria. Dx?

A

VIPoma

84
Q

How does cortisol raise the blood sugar? What are the effects of the elevated blood glucose?

A

breakdown muscle causing weakness w/ thin extremities;

insulin is released to store fat on face, back, trunk

85
Q

What is the mechanism of abdominal striae in Cushings?

A

ruptured blood vessels due to collagen damage

86
Q

How does stress or any increase in cortisol raise HTN?

A

upregulate alpha-1 receptors on arterioles thus increasing effect of catecholamines (esp NE)

87
Q

What are the 3 mechanisms by which cortisol leads to immune suppression?

A

1) inhibits phospholipase A2 => cannot produce arachidonic acid metabolites
2) inhibits IL-2
3) inhibits histamine release from mast cells

88
Q

What are the 4 major causes of cushing syndrome?

A

MCC=> exogenous corticosteroids;
Primary adrenal adenoma, hyperplasia, or CA (one large & one atrophic adrenal gland)
ACTH secreting pituitary adenoma (hyperplastic adrenals);
paraneoplsatic ACTH secretion (bilateral hyperplastic adrenals)

89
Q

Prolonged exogenous corticosteroids will result in what grossly?

A

atrophy of both adrenals

90
Q

How would ATCH pituitary adenoma be differentiated from paraneoplastic ACTH secretion?

A

High dose dexamethasone (cortisol analog) then measure cortisol levels

If ACTH is suppressed then pituitary adenoma;

If no ACTH suppression then small cell lung CA

91
Q

What is the MCC of primary hyperaldosteronism? how is it characterized?

A

MCC is adrenal adenoma

high aldosterone & low renin (high flow)

92
Q

What is the cause of secondary hyperaldosteronism? how is it characterized?

A

activation of RAAS => high aldosterone & high renin due to sensing less flow

93
Q

Define congenital adrenal hyperplasia

A

excess sex steroids w/ hyperplasia of both adrenal glands

94
Q

What is the mechanism of pathology in 21 hydroxylase deficiency?

A

knock out mineral & gluco-corticoids leading to shunting to sex steroids (F: clit enlarge; M: precocious pub)
lack of cortisol will have life threatening hypoTN & excess ACTH (lack of inhibition) leading to hyperplasia of both adrenals;
Salt wasting & hyperkalemia & hypovolemic

95
Q

Differentiate 11 vs 21 hydroxylase deficiency

A

There will not be salt wasting in 11 deficiency

96
Q

What is the findings in 17 deficiency?

A

excess mineralocorticoids;
no sex hormones so look like opposite of genotype;
excess ACTH

97
Q

What is the acute cause of adrenal insufficiency?

A

waterhouse-friderichsen syndrome => N. meningitides after DIC then massive hypoTN

Look for sack of blood of adrenals

98
Q

Define chronic adrenal insufficiency and give 3 MCC

A

progessive destruction of adrenal glands

AI destruction of adrenals;
TB;
metastatic CA

99
Q

What cancer loves the adrenal?

A

lung

100
Q

Why is hyper pigmentation assoc w/ adrenal insufficiency or any increase in ACTH?

A

ACTH is derived from POMC which makes melanocyte stimulating hormone

101
Q

Where do the chrommafin cells of adrenals come from embryologically?

A

neural crest cells

102
Q

How does a pheochromocytoma present grossly?

A

brown tumor due to chrommafin cells in adrenal medulla being brown

103
Q

How is pheochromocytoma diagnosed?

A

increased serum metanephrines & 24 hr urine metanephrines & VMA

104
Q

For the 10% of pheochromocytomas that are not in the adrenal medulla, where is the MC location? how will it present?

A

bladder wall => pt urinates causing HTNive episode

105
Q

What are the genetic association of pheochromocytomas?

A

MEN 2A & B;
VHL disease;
NF type 1

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