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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
Tx for acromegaly
Try to resect | If not cured then octreotide (somatostatin analog) or pegvisomant (GH receptor antagonist)
26
Differentiate DI based on water restriction test
Central DI will show > 50% increase in urine osmolarity Nephrogenic DI while show no change in urine osmolarity
27
Tx for central DI
Intranasal DDAVP & hydration
28
Tx for nephrogenic DI
HCTZ, indomethacin, amiloride; | Hydration
29
What are secondary causes of Nephrogenic DI?
hypercalcemia; lithium, demeclocycline (ADH antagonist that is former antibiotic rarely used)
30
What can cause SIADH?
Ectopic ADH from small cell lung CA; CNS d/o or head trauma; Pulmonary disease; Drugs => cyclophosphamide
31
Tx for SIADH?
fluid restrict; IV hypertonic saline; | Conivaptan, tolvaptan, demeclocycline
32
Tx for hypopituitarism
HRT => corticosteroids, thryoxine, sex steroids, GH
33
What 2 blood disorders can occur due to hyperthyroidism?
hypocholesterolemia => increased LDL receptor expression | hyperglycemia => gluconeogenesis & glycogenolysis
34
What are the labs associated w/ the most common cause of hyperthyroidism?
Graves disease increased total & free T4; decreased TSH; hypocholesterolemia (increased LDL expression) increased serum glucose
35
Tx for Graves disease
Beta-blockers Thioamide (blocks peroxidase) Radioiodine ablation
36
Patient comes w/ elevated catecholamines after birth with arrhythmia, hyperthermia, vomiting & hypovolemic shock. What is the treatment?
Thyroid storm Give PTU, beta-blockers, steroids
37
What is the association of the most common type of hypothyroidism?
Hashimoto thyroiditis => AI destruction of thyroid gland assoc w/ HLA-DR5
38
What AI Ab are present in Hashimoto thyroiditis?
Antithyroglobulin & antimicrosomal Ab => markers that damage has occurred
39
What are the labs assoc with Hashimoto thyroiditis?
decreased T4 => controls # of TRH receptors which controls amount of TSH produced => always opposite increased TSH
40
What type of cancer is assoc w/ hashimoto thyroiditis?
B cell lymphoma => marginal cell lymphoma
41
Young woman comes in with tender thyroid after viral infection. What is Dx & Px?
Subacute (deQuervain) Granulomatous thyroiditis self limited transient hyperthyroidism w/ NO progression to hypothyroidism
42
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?
Reidel fibrosing thyroiditis => fibrosis may extend to local structures such as airway anaplastic thyroid
43
increased I radioactive up results in what Dx? decreased?
increased in Graves or nodular goiter decreased in adenoma & carcinoma (do FNA Bx)
44
What are the 4 types of thyroid carcinoma?
papillary, follicular, medullary, anaplastic
45
What is the MC thyroid CA? What is a major risk factor?
papillary Ca => ionizing radiation in childhood (severe acne)
46
What typically defines papillary CA of the thyroid?
nuclear features of orphan-annie eyes, psammoma bodies, nuclear grooves
47
What is oncogenes are mutated in papillary CA of thyroid?
RET & BRAF
48
Px of papillary CA after lymph node spread?
excellent
49
Tx for thyroid cancer? complications of treatment?
remove the thyroid Hoarseness (recurrent laryngeal nerve damage); hypocalcemia (removal of parathyroid glands); transection of inferior thyroid artery
50
Hallmark of follicular CA of thyroid
malignant proliferation of follicles w/ invasion through the capsule
51
Why cannot FNA Bx distinguish between follicular adenoma & follicular CA?
needle insertion will only see follicular proliferation as seen in both invasion through the capsule distinguishes them & not seen on FNA
52
How does follicular CA of thyroid spread?
hematogenously
53
What are the CA that like to spread via blood?
Renal cell CA; follicular CA of thyroid hepatocellular CA; ChorioCA
54
FNA Bx done and see malignant cells in amyloid stroma
medullary CA => malignant proliferation of C cells
55
What are the Sx related to of medullary CA?
high levels of calcitonin produced by tumor lead to hypocalcemia Calcitonin often deposits w/in tumor as amyloid
56
what are the familial cases of medullary CA of thyroid associated w/?
MEN 2A & 2B => mutations in RET oncogene
57
Mutation in RET oncogene warrants what procedure?
prophylactic thryoidectomy
58
Older person presents w/ dysphagia & respiratory compromise w/ swollen neck. what is Dx & Px?
anaplastic CA of thyroid => undifferentiated malignant tumor Poor Px
59
What is MCC of primary hyperparathyroidism?
parathyroid adenoma => benign neoplasm
60
What are the results of primary hyperparathyroidism?
``` Stones, bones, groans, psych overtones nephrolithiasis; nephrocalcinosis; CNS disturbances; Constipation, PUD, acute pancreatitis; Osteitis fibrosa cystica ```
61
Define osteitis fibrosa cystica
cystic bone spaces w/ brown fibrous tissue => bone pain
62
Labs of primary hyperparathyroidism
increased serum PTH, Ca+, alk phos (due to osteoblast turned on) decreased serum phosphate increased urinary cAMP (PTH stimulates Gs receptor)
63
What is MCC of secondary hyperparathyroidism?
chronic renal failure => excess PTH extrinsic to parathyroid gland
64
Labs of secondary hyperparathyroidism
increased PTH, phosphate, alk phos | decreased serum Ca+
65
What are causes of hypoparathyroidism?
AI damage, surgical excision, DiGeorge syndrome
66
Presentation of hypoparathyroidism?
numbness/tingling & muscle spasms (tetany) => Trousseau's sign (BP cuff), Chavsofic sign (tap on jaw)
67
Labs for hypoparathyroidism
low PTH & low serum Ca+
68
What is the cause of pseudohypoparathyroidism?
organs not responding to PTH so hypocalcemia w/ elevated PTH
69
The end organ resistance of pseudohypoparathyroidism is due to what?
AD mutation in Gs protein assoc w/ short stature & short 4th & 5th digits
70
What causes type I DM? What is it associated with?
autoimmune destruction of Beta cells of T lymphocytes => Ab against insulin leading to inflammation of islets Assoc w/ HLA-DR3 & DR4
71
What are the clinical features of a type I DM patient in DKA?
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
Tx of DKA
fluids, insulin replacement of electrolytes w/ K+
73
What is the mechanism of insulin resistance in type II DM?
decreased numbers of insulin receptors on skeletal muscle & adipose tissue
74
How does insulin concentration change during the course of type II DM?
rises due to resistance then very decreased bc of Beta cell exhaustion amyloid deposits
75
Tx of type II DM
weight loss (1st always); Rx to counter insulin resistance; end stage is insulin dependent
76
What is a risk for uncontrolled type II DM? How does it present?
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
Vascular complications of DM?
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
What cells/structures are at risk for osmotic damage due to high sugar?
Schwann cells => basis of neuropathy in diabetics Pericytes in retina blood vessels => aneurysm causing rupture to blindness lens
79
Pancreatic endocrine tumors are associated with what?
MEN 1 => parathyroid hyperplasia & pituitary adenoma
80
How does an insulinoma present? what relieves Sx? What are the labs?
episodic hypoglycemia w/ mental changes relieved by glucose low glucose; high insulin & C peptide
81
Patient w/ Treatment resistant PUD. what is Dx?
Gastrinoma => ZE syndrome can be multiple & extend into jejunum
82
Patient w/ low stomach pH along with gallstones & steatorrhea. Dx? Why the Sx?
Somatostatinoma inhibits gastrin so achlorhydria inhibits CCK => cholelithiasis & steatorrhea
83
Patient w/ watery diarrhea, hypokalemia, achlorhydria. Dx?
VIPoma
84
How does cortisol raise the blood sugar? What are the effects of the elevated blood glucose?
breakdown muscle causing weakness w/ thin extremities; insulin is released to store fat on face, back, trunk
85
What is the mechanism of abdominal striae in Cushings?
ruptured blood vessels due to collagen damage
86
How does stress or any increase in cortisol raise HTN?
upregulate alpha-1 receptors on arterioles thus increasing effect of catecholamines (esp NE)
87
What are the 3 mechanisms by which cortisol leads to immune suppression?
1) inhibits phospholipase A2 => cannot produce arachidonic acid metabolites 2) inhibits IL-2 3) inhibits histamine release from mast cells
88
What are the 4 major causes of cushing syndrome?
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
Prolonged exogenous corticosteroids will result in what grossly?
atrophy of both adrenals
90
How would ATCH pituitary adenoma be differentiated from paraneoplastic ACTH secretion?
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
What is the MCC of primary hyperaldosteronism? how is it characterized?
MCC is adrenal adenoma high aldosterone & low renin (high flow)
92
What is the cause of secondary hyperaldosteronism? how is it characterized?
activation of RAAS => high aldosterone & high renin due to sensing less flow
93
Define congenital adrenal hyperplasia
excess sex steroids w/ hyperplasia of both adrenal glands
94
What is the mechanism of pathology in 21 hydroxylase deficiency?
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
Differentiate 11 vs 21 hydroxylase deficiency
There will not be salt wasting in 11 deficiency
96
What is the findings in 17 deficiency?
excess mineralocorticoids; no sex hormones so look like opposite of genotype; excess ACTH
97
What is the acute cause of adrenal insufficiency?
waterhouse-friderichsen syndrome => N. meningitides after DIC then massive hypoTN Look for sack of blood of adrenals
98
Define chronic adrenal insufficiency and give 3 MCC
progessive destruction of adrenal glands AI destruction of adrenals; TB; metastatic CA
99
What cancer loves the adrenal?
lung
100
Why is hyper pigmentation assoc w/ adrenal insufficiency or any increase in ACTH?
ACTH is derived from POMC which makes melanocyte stimulating hormone
101
Where do the chrommafin cells of adrenals come from embryologically?
neural crest cells
102
How does a pheochromocytoma present grossly?
brown tumor due to chrommafin cells in adrenal medulla being brown
103
How is pheochromocytoma diagnosed?
increased serum metanephrines & 24 hr urine metanephrines & VMA
104
For the 10% of pheochromocytomas that are not in the adrenal medulla, where is the MC location? how will it present?
bladder wall => pt urinates causing HTNive episode
105
What are the genetic association of pheochromocytomas?
MEN 2A & B; VHL disease; NF type 1

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