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Flashcards in 3/8 endo Deck (129):
1

How does excess cortisol lead to HTN?

-up-regulates alpha-1 receptors on arterioles.
-has slight mineralocorticoid ability.

2

Dexamethasone suppression test
-low dose suppresses ACTH =
-high dose (8mg) suppresses ACTH =
-no suppression w/high dose (8mg) =

-low dose suppresses ACTH = normal
-high dose suppresses ACTH = pituitary adenoma
-no suppression w/high dose = ectopic ACTH prod.

3

How does excess cortisol lead to osteoporosis?

-cortisol dec. osteoblastic activity

4

CRH stimulation test

-differentiate btwn a pituitary adenoma and ectopic source.
-an ectopic source will not increase cortisol production in response to CRH b/c the pituitary is super suppressed by all the negative feedback of the ectopic ACTH.
-the pituitary adenoma will make even more ACTH and thus cortisol in response to CRH b/c its negative feedback mechanism is obviously fucked up which is a key property thats allowing it to pump out all of this ACTH in the first place.

5

Inoperable Cushings
-Tx:

Ketoconazole

6

Primary or secondary hyperaldo
-Tx:

-surgery (primary) or spironolactone

7

Which bug has been known to destroy the adrenals?

TB

8

Waterhouse-Friderichsen syndrome
-potential causes?

-Neisseria meningitidis septicemia, DIC, and endotoxic shock

9

Resting tone on vasculature?

-sympathetic
-hence neurogenic shock - you lose that sympathetic tone.

10

Neuroblastoma
-originates from what tissue?
-presentation?

-Neural crest cells
-abdominal distension and a firm, irregular mass B that can cross the midline (vs. Wilms tumor, which is smooth and unilateral).
*it does not cause HTN like pheo does.

11

Neuroblastoma
-what is increased in urine?
-associated w/which oncogene?

-Homovanillic acid (HVA) = breakdown product of dopamine.
-N-myc

12

Homovanillic acid (HVA)
-inc urinary levels in what disease?
-HVA is breakdown product of what?

-neuroblastoma
-breakdown product of dopamine.

*dopamine = precursor to catecholamines.

13

Neuroblastoma
-bombesin + or -
-what do you see on histology?

-bombesin + (tumor marker)
-rosettes & classic small, round, blue/purple nuclei.

14

pheochromocytoma
-arise from what cells?
-what color is it usually?

chromaffin cells
-neural crest cells
-brown - the adrenal medulla is usually brown.

15

pheochromocytoma
-rule of 10s

Rule of 10’s:
10% malignant
10% bilateral
10% extra-adrenal
10% calcify
10% kids

*More than 70% of cases of pheochromocytomas
are bilateral when familial.

16

pheochromocytoma
-associated w/which diseases?

-Associated with von Hippel-Lindau disease, MEN 2A and 2B.

17

pheochromocytoma
-Tx:

Irreversible α-antagonists (phenoxybenzamine) and β-blockers followed by tumor resection.
-α-blockade must be achieved before giving
-β-blockers to avoid a hypertensive crisis.

18

Hyperthyroidism
-diarrhea or constipation?
-inc or dec reflexes?

-diarrhea
-inc. reflexes

19

hyperthyroidism
-whats the skin & hair like?
-hypo or hypercholesterolemia?

-Warm, moist skin; fine hair
-Hypocholesterolemia (due to inc. LDL receptor expression). *you're basically burning more fuel.

20

hyperthyroidism
-calcium level?
-blood glucose?

-hypercalcemia (inc. burn resorption).
-hyperglycemia (gluconeo & glycogenolysis going on).

21

dyspnea on exertion
-Sx of hypo or hyperthyroidism

hypothyroidism

22

large fontanels & macroglossia in children.
-hypo or hyperthyroidism?

hypothyroidism

23

Whats the most common cause of myopathy?

hypothyroidism
-myoedema will be present (edema of muscle s/p percussion), inc. creatine kinase, + other hypothyroid Sxs like weight gain, fatigue, etc.
-will present w/myalgia, proximal muscle weakness, & cramping.

24

Abs found in hashimotos thyroiditis

-anti-thyroid peroxidase
-antithyroglobulin antibodies
-anti-microsome

*they do not cause the disease, they are byproducts of the disease.

25

hashimotos
-HLA association?

HLA-DR5
*Pernicious anemia also associated w/HLA-DR5

26

hashimotos
-inc risk of what cancer?

non-Hodgkin lymphoma
-chronic inflammatory states like hashimotos (or sjogrens or h.pylori gastritis) inc. risk of developing a marginal zone lymphoma.

27

Hürthle cells
-which disease?

hashimotos thyroiditis

28

Which hypothyroid states can present w/initial transient hyperthyroid state?

-hashimotos
-Subacute thyroiditis (de Quervain)

29

Long standing hashimoto pt that suddenly has an progressively enlarging thyroid, think what?

B-cell lymphoma

30

Congenital hypothyroidism (cretinism)
-Sxs:

The 6 P’s
Pot-bellied
Pale
Puffy-faced child
Protruding umbilicus
Protuberant tongue
Poor brain development

31

Subacute thyroiditis (de Quervain)
-What type of inflammation?
-Tx?

-granulomatous inflammation (released colloid acts as a foreign body)
-aspirin for pain.

32

Reidel thyroiditis
-manifestation of what?

-Considered a manifestation of IgG4 -related
systemic disease.

33

Wolff-Chaikoff:

-Reduction in thyroid hormone levels caused by
ingestion of a large amount of iodine.

34

Histo look of goiter:

enlarged follicles and flattened epithelial cells

35

Toxic multinodular goiter

-Focal patches of hyperfunctioning follicular cells working independently of TSH due to mutation in TSH receptor.
-inc. T4 & T3

*Hot nodules are rarely malignant.

36

Jod-Basedow phenomenon

-Thyrotoxicosis if a patient with iodine deficiency goiter is made iodine replete.

37

Thyroid storm
-most common cause of death?
-ALP level? why?

-tachyarrythmia
-Inc. ALP due to  bone turnover.

38

"scalloping" of the colloid
-which disease?

Graves

39

Are thyroid cancers usually functional?

-no
-and remember, "hot" (functional) nodules are rarely malignant.

40

Thyroid adenomas & carcinomas
-inc or dec iodine uptake?

-dec.

41

“Orphan Annie” eyes & psammoma bodies
-which disease?

papillary carcinoma of thyroid.
-Orphan annie eyes = white clearing in the center of the nucleus

-also see "nuclear grooves" which are dark lines in middle of nucleus.

42

Papillary carcinoma of thyroid
-inc. risk w/mutations in which genes?
-inc. risk w/exposure to what?

-RET and BRAF mutations.
-childhood exposure to radiation.

*-RET - receptor tyrosine kinase encoding gene.

43

Orphan Annie eyes
-aka?

ground glass nuclei

44

Follicular carcinoma vs follicular adenoma

Follicular carcinoma invades thru the capsule.

45

Medullary carcinoma
-which cells?
-produce what?
-histo appearance?

-From parafollicular “C cells”; produces calcitonin.
-sheets of cells in an amyloid stroma.

46

Medullary carcinoma
-associated w/which mutations/diseases?

-Associated with MEN 2A and 2B (RET mutations).

47

osteoclast-like multinucleated giant cells found
-which thyroid cancer?

anaplastic

48

hyperparathyroidism
-urinary cAMP levels?
-ALP levels?

-high urinary cAMP = PTH works through Gs pathway
-inc ALP

49

hyperparathyroidism & acute pancreatitis
-connection?

-hypercalcemia due to PTH can cause acute pancreatitis.

*high calcium always = chance of metastatic calcification. ie. nephrocalcinosis.

50

hyperparathyroidism
-mnemonic for Sxs

“Stones, bones, groans, and psychiatric overtones.”
-stones = calcium oxalate renal stones
-bones = osteitis fibrosa cystica
-groans = constipation
-depression

51

Tertiary hyperparathyroidism

-Refractory (autonomous) hyperparathyroidism resulting from chronic renal disease.
-very high PTH, high calcium

52

Chvostek sign:
-what is it?
-sign of what?

-Tapping of facial nerve (tap the Cheek) => contraction of facial muscles.
-hypocalcemia

53

Pseudohypoparathyroidism (Albright hereditary osteodystrophy):
-inheritance pattern:
-what is it?
-Sxs:

-autosomal dominant
-unresponsiveness of kidney to PTH.
-Hypocalcemia, shortened 4th/5th digits, short
stature.

*defective Gs receptors, b/c PTH acts via Gs receptors.

54

Pseudohypoparathyroidism (Albright hereditary osteodystrophy):
-inheritance pattern:
-what is it?
-Sxs:

-autosomal dominant
-unresponsiveness of kidney to PTH.
-Hypocalcemia, shortened 4th/5th digits, short
stature.

55

cabergoline

dopamine agonist
-like bromocriptine

56

Link btwn GH secreting tumor & DM2

GH causes insulin resistance and hyperglycemia.

57

pegvisomant

-growth hormone receptor antagonist

58

demeclocycline

-ADH antagonist

59

Nephrogenic DI
-Tx:

-HCTZ, indomethacin, amiloride, Hydration

60

complete central DI vs partial central DI

-follow water deprivation & subsequent DDAVP admin.
-In pts w/complete central DI, urine osmolarity should rise >50%! So less than 50 would be partial central DI.

61

Does cortisol inc or dec glycogen synthesis in the liver?

-inc. glycogen synthesis!
-seems counter intuitive!

62

Why do glucocorticoids cause muscle weakness?

Proteolysis

63

Which organ actually has increased protein synthesis in response to glucocorticoids?

Liver
-upregulated proteins (enzymes) involved w/gluconeo & glycogenesis (glycogen synthesis!)

*cortisol increases glycogen synthesis, NOT breakdown!

64

Why does BUN increase w/glucocorticoid administration?

Proteolysis!

65

Miglitol

alpha glucosidase inhibitors

66

canagliflozin, dapagliflozin
-mechanism
-side effects

SGLT-2 inhibitors: oral DM drugs.
-prevent glucose resorption at PCT.
-causes urinary excretion of glucose.

-may cause urinary tract & genital mycotic infections due to glucosuria.

*assess renal fcn before starting this drug.

67

Age range for DM1?

68

Fasting blood sugar of _____ of ____ separate occasions is diagnostic of DM.

> 126mg/dl, two.

69

PTH level & magnesium

-Hypoparathyroidism may be caused by severe hypomagnesemia which can be seen in prolonged diarrhea.

70

Serum chemistry in pseudohypoparathyroidism
-Ca
-phosphate
-PTH

-low Ca
-high phosphate
-high PTH

71

Suprasellar mass w/3 components (solid, liquid, calcification) is suggestive of what?

craniopharyngioma

72

Renal failure - serum levels of:
-Ca
-PTH

-Ca = low
-PTH = high

73

Why is hypernatremia rarely observed in mineralocorticoid excess?

Aldosterone escape w/ANP.
-also, inc. Na and water retention will increase renal blood flow and GFR => inc rate of sodium excretion.
-ADH also kicks in to keep Na conc. in check.

74

Why do you get profound muscle weakness w/too much Aldo?
-how about parasthesias?

-Hypokalemia leads to muscle weakness.
-hypokalemia & met. alkalosis can cause parasthesias.

75

Stimulation tests are used in times of hormone excess or insufficiency?

insufficiency

76

Whats the most common cell type in the ant. pituitary?

Somatotrophs
-make GH
-50% of normal pituitary

77

Oxytocin
-made in which nucleus?

paraventricular nucleus of hypothalamus

78

SIADH
-serum Na?
-volume status?

Euvolemic hyponatremia.
-ADH leads to excess water.
-Body responds w/dec. aldo.
-Dec. aldo = losing sodium and water.

79

What happens if you correct SIADH pt's sodium too quickly?

Central pontine myelinolysis
-neuron dysfunction due to destruction myelin covering neurons in the middle of the brainstem (pons).
-AKA osmotic demyelination syndrome.

80

Which drugs can cause SIADH?
-mnemonic?

Can’t Concentrate Serum Sodium
-Carbamazepine
-Cyclophosphamide
-SSRIs

81

SIADH
-first step in management?
-tx:

-1st step = water restriction
-demeclocycline = ADH antagonist
-lithium
-conivaptan, tolvaptan = ADH antagonists

82

conivaptan, tolvaptan =

-ADH antagonists
-Tx for SIADH

83

Losing pubic hair after pregnancy

Sheehan
-need LH for pubic hair.

84

Empty sella syndrome
-what is it?
-common in who?

-atrophy or compression of pituitary, often idiopathic, common in obese women.
-could be due to trauma/congenital reasons.

85

Severe hypoglycemia
-Tx?

glucagon injection

86

Most common cause of death in DM?

MI

87

DM1
-HSR, which type?

-type 4 HSR

88

DM1
-HLA association? if so, which ones?

-HLA-DR3 and 4
-Sxs may be preceded by a viral infection.

89

What does glucose intolerance mean?

Unable to take up insulin into cells.
-no insulin.

90

Maturity-onset diabetes of the young (MODY)
associated w/mutation in what?

-Glucokinase mutation.

91

Genetic predisposition in DM1 or 2?

DM2
-90% concordance in idential twins
*(DM1 has 50% concordance in identical twins).

92

What triggers DKA?

-inc. insulin req due to inc. stress (ie. infection).
-stress triggers symp. nervous system = catecholamines & glucagon.

93

Name some Sxs of DKA.

-Abdominal pain
-delirium
-kussmaul respiration
-fruity breath
-N/V
-dehydration

94

DKA
-total body K?
-serum K?

-depleted intracellular K = low total body K
-normal/high serum K

95

Why do you get dehydrated in DKA?

-glucosuria causes osmotic diuresis.
-can lead to pre-renal azotemia & elevated BUN.

96

Whipple triad of episodic CNS symptoms:
-what is it?
-whats it seen in?

-lethargy, syncope, and diplopia
-insulinoma

97

Episodic hypoglycemia w/mental status changes that
are relieved by glucose.

insulinoma

98

Neuroendocrine tumors are positive for what?

chromagranin

99

carcinoid tumor can lead to what vitamin deficiency?

niacin deficiency
-tryptophan required to make niacin, but your bodys stores are being used to make serotonin instead.

100

carcinoid heart disease
-mnemonic:

TIPS: tricuspid insufficiency, pulmonary stenosis.

101

Zollinger Ellison
-mechanism behind steattorhea / malabsorption

-too much acid = pancreatic enzymes wont work. They need alkaline environment to operate!

102

Rapid acting insulin
-mnemonic?
-use?

There is no LAG w/rapid acting insulin.
Lispro
Aspart
Glulisine
-postprandial glucose control.

103

Long acting insulin

Glargine
Detemir

104

Biguanides
-aka?
-mech:
-major side effects?

-Metformin
-dec. gluconeo, inc. glycolysis, inc. glucose sensitivty.
-GI upset, lactic acidosis.
*contraindicated in renal failure

105

Sulfonylureas
-1st gen:
-2nd gen:

First generation:
Tolbutamide
Chlorpropamide

Second generation:
Glyburide
Glimepiride
Glipizide

106

OSUs (sulfonylureas)
-used in DM1 or DM2?

DM2
-requires some islet function, so useless in DM1.
-closes the K channel (so it mimics normal action of ATP)

107

sulfonylureas
-side effects
-1st gen:
-2nd gen:

Risk of hypoglycemia inc. in renal failure.
-First generation: disulfiram-like effects.
-Second generation: hypoglycemia.

*-can cause weight gain b/c anything that inc. insulin inc. TG storage in adipocytes.

108

Diazoxide and minoxidil mechanism
-opposite of which drugs?

-exactly the opposite as sulfonylureas, which is how they can cause drug induced diabetes (prevent insulin release from beta-cells).
-potassium channel openers, causing hyperpolarization of cell membranes.

109

Glitazones
-aka?
-mech?
-inc levels of what?

-thiazolidinediones (TZDs)
-inc. insulin sensitivity in peripheral tissue. Binds to PPAR-γ nuclear transcription regulator.
-increase levels of adiponectin (inc. insulin sensitivity).

110

Glitazones/TZDs
-side effects?

-Weight gain, edema, Hepatotoxicity, heart failure (CHF).

111

Amylin analogs
-name?
-mech?

-Pramlintide
-dec. gastric emptying, dec. glucagon.
-amylin deposits in islets seen in DM2.

112

GLP-1 analogs
-name them:
-mech:
-notable tox:

-Exenatide, Liraglutide
-inc. insulin release
-pancreatitis

*An incretin. Its a small peptide released from small intestine whenever you eat.

113

Which DM drug can lead to pancreatitis?

GLP-1 analogs (incretins)
-exenatide, liraglutide.

114

DPP-4 inhibitors ("liptins")
-name them
-mech
-tox

-Linagliptin, Saxagliptin, Sitagliptin
-DPP-4 = enzyme that breaks down GLP-1. So by inhibiting DPP-4 you inc. GLP-1.
-indirectly inc. insulin release.

-tox: Mild urinary or respiratory infections.

115

Propanolol
-addition effect thats useful in thyrotoxicosis besides bocking beta receptors?

-also inhibits 5′-deiodinase

116

Propylthiouracil, methimazole
-which one used in pregnancy?
-toxicities?

-PTU used in pregnancy, highly protein bound.
-Skin rash, agranulocytosis (rare), aplastic anemia, hepatotoxicity (propylthiouracil).
-Methimazole is a possible teratogen (can cause aplasia cutis).

117

Demeclocycline
-side effects

-Nephrogenic DI, photosensitivity, abnormalities of bone and teeth.

*member of the tetracycline family. hence the s/e profile.

118

Do glucocorticoids inhibit or stimulate txn factors like
NF-κB?

-Inhibit transcription factors such as NF-κB.

*NF-kB: transcription factor that stimulates cytokine production in the immune response to infectious pathogens.
-needed for inflammation.

119

Glucocorticoids & peptic ulcers
-how?

-phospholipase A2 inhibitor
-so same mech as NSAID ulcer.

120

Spondyloarthropathies
-HLA association?
-HLA association of RA?

-spondylos = HLA-B27
-RA = HLA-DR4

121

Crest Abs =
Systemic sclerosis Abs =

-CREST=anti-centromere
-SS=anti-DNA topoisomerase 1

122

Anti-histone Abs

Drug induced lupus
-no renal or CNS involvement

123

Antiphospholipid ab syndrome
-Sxs
-PTT time

-hypercoag state, frequent miscarriages
-PTT increased (paradoxically)

124

chronic anemia affect on cardiac output.

-chronic anemia inc. CO.

125

Sup. gluteal nerve.
-if you give an injection in which quadrant will you likely damage this nerve?

Supero-medial quadrant.

126

PTH
-which pathway

inc. cAMP.

127

ankylosing spondylitis
-which murmur can it lead to?

-aortic regurg.

128

Probenacid

-inhibits resorption of uric acid in PCT
-also inhibits secretion of penicillin.

*dont give if possible uric acid stones.

129

febuxostat

xanthine oxidase inhibitor
-like allopurinol