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My step 1 mnemonics > Endocrine > Flashcards

Endocrine Flashcards

1
Q

InsuIin-independent transporters - GLUT1

A

RBCs, brain, cornea, placenta

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2
Q

InsuIin-independent transporters - GLUT2

A

(bidirectional): beta islet cells, liver, kidney, GI

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3
Q

InsuIin-independent transporters - GLUT3

A

brain, placenta

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4
Q

InsuIin-independent transporters - GLUT5

A

(Fructose): spermatocytes, GI tract

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5
Q

InsuIin-independent transporters - SGLTl/SGLT2

A

(Na+-glucose cotransporters):

kidney, small intestine

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6
Q

Anabolic effects of insulin: (7)

A

Anabolic effects of insulin:
• Inc. glucose transport in skeletal muscle and adipose tissue
• Inc. glycogen synthesis and storage
• Inc. triglyceride synthesis
• Inc. Na+ retention (kidneys)
• Inc. protein synthesis (muscles)
• Inc. cellular uptake of K+ and amino acids
• Dec. glucagon release
• Dec. lipolysis in adipose tissue
Unlike glucose, insulin does not cross the placenta.

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7
Q

insulin receptors - tyrosine kinase - activate two pathways:

A

Phosphoinositide-3 kinase pathway ->glicogen/lipid\protien synthesis + vesicles (GLUT 4)

RAS/MAP kinase pathway -> Cell growth and DNA synthesis

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8
Q

Insulin regulation:

A

alfa 2 dec.

beta 2 inc.

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9
Q

GHRH Analog

A

Tesamorelin - used to treat HIV-associated lipodystrophy.

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10
Q

Oxytocin Modulates

A

fear, anxiety, social bonding, mood, and depression

MD SAFe

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11
Q

TRH increases…

A

TSH

Prolactin

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12
Q

Dopamine decreases…

A

TSH

Prolactin

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13
Q

Somatostatin decreases…

A

TSH

GH

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14
Q

Prolactin increases____ and decreases____.

A

increases dopamine and decreases GnRH.

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15
Q

____,____,____ increases Prolactin

A

TRH
Estrogen (pregnancy)
Renal failure
(“RET”)

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16
Q

GHRH induced by

A 
P-  Puberty
E - Exercise
G - hypoGlycemia
S - deep Sleep
S - Stress
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17
Q

GHRH inhibited by

A 
AGO:
Aging
Obesity
Glucose
Somatostatin
Somatomedin
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18
Q

other names for GH and IGF-1

A

GH - somatotropin

IGF-1 - somatomedin C

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19
Q

GH metabolic effects:

A

dec. glucose uptake and Inc. lipolysis in FAT CELLS

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20
Q

IGF-1 metabolic effects in the BONE:

A 
BONE:
Inc. amino acid uptake
Inc. Protein synthesis 
Inc. DNA and RNA synthesis
Inc. Chondroitin sulfate
Inc. Collagen
Inc. Cell size and number
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21
Q

IGF-1 metabolic effects in the Muscle

A

Inc. amino acid uptake

Inc. Protein synthesis

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22
Q

Cortisol function in general:

A

Cortisol is A BIG FIB.

Appetite increased

Blood pressure
Insulin resistance (diabetogenic)
Gluconeogenesis, lipolysis, and proteolysis all increase (dec. glucose utilization)

Fibroblast activity decreased (poor wound healing, dec. collagen synthesis - striae)
Inflammatory and Immune responses decreased
Bone formation decreased (dec. osteoblast activity)

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23
Q

Cortisol function - blood pressure mechanisms

A
  • Upregulates alfa 1 - receptors on arterioles - inc. sensitivity to norepinephrine and epinephrine (permissive action)
  • At high concentrations can bind to mineralocorticoid (aldosterone) receptors
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24
Q

Cortisol function - Inflammatory and Immune responses mechanisms

A

just CHILL:
C - Cells: Eosinopenia, lymphopenia
H - Histamin: Blocks histamine release from mast cells
I - IL-2: Blocks IL-2 production
L - leukotrienes and prostaglandins: Inhibits production of leukotrienes and prostaglandins
L - Loose WBC: Inhibits WBC adhesion -> neutrophilia

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25
Q

Calcium homeostasis: Plasma Ca2+ exists in three forms:

A

Plasma Ca2+ exists in three forms:
• Ionized/free (45%, active form)
• Bound to albumin (40%)
• Bound to anions (15%)

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26
Q

Calcium homeostasis: Regulation of PTH (pH/albumin/Ca2+)

A

Ionized/free Ca2+ is 1° regulator of PTH

changes in pH alter PTH secretion

changes in albumin concentration do not.

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27
Q

Calcium homeostasis: Inc. pH?

A

Inc. pH (less H+) -> albumin binds more Ca2l+ -> dec. ionized Ca2+ (eg, cramps, pain, paresthesias, carpopedal spasm) -> Inc. PTH.

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28
Q

Calcium homeostasis: Dec. pH?

A

Dec. pH (more H+) -> albumin binds less Ca2+ -> Inc. ionized Ca2+ -> dec. PTH.

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29
Q

PTH secretion induced by:

A

Dec. Ca2+
Dec. Mg2+
Dec. 1,25(OH) D3
Inc. PO4-

CaMPeD

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30
Q

PTH secretion inhibited by:

A

Very low Mg2+

Inc. 1,25(OH) D3

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31
Q

Dec. Mg2+ caused by:

A 
Diarrhea
Aminoglycosides
Diuretics
Alcohol abuse.
DADA!
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32
Q

25 (OH) D3 -> 1,25 (OH) D3 conversion induced by?

A

High PTH
Low PO4-
“induced by a high and a low P”

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33
Q

Functions of thyroid peroxidase include:

A

Oxidation
Organification of iodide
Cupling of monoiodotyrosine (MIT) and diiodotyrosine (DIT).

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34
Q

Wolff-Chaikoff effect-

A

Excess iodine temporarily turns off thyroid peroxidase - dec. T3 & T4 production (protective autoregulatory effect).

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35
Q

T3 functions in general:

A

“Energy for work and growing”

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36
Q

T3 functions - Energy:

A
  • Blood sugar (Inc glycogenolysis, gluconeogenesis)

* Break down lipids (inc. lipolysis)

37
Q

T3 functions - Work:

A

Beta-adrenergic effects. Inc. beta 1 receptors in the heart -> t CO, HR, SV, contractility
(beta-blockers alleviate adrenergic symptoms in thyrotoxicosis)

Basal metabolic rate Inc. (via Na+/K+ ATPase activity -> Inc. O2 consumption, RR, body temperature)

38
Q

T3 functions - Growing:

A
  • Brain maturation

* Bone growth (synergism with GH)

39
Q

Thyroid hormones negative feedback

A

Negative feedback primarily by free T3/4:
• Anterior pituitary -dec sensitivity to TRH
• Hypothalamus - dec TRH secretion
All about the TRH

40
Q

Thyroxine-binding globulin (TBG) increased and decreased by:

A

Increased: TBG in pregnancy, OCP use (estrogen)
Decreased: hepatic failure, steroid use, nephrotic syndrome

41
Q

Signaling pathways of endocrine hormones - cAMP

A

“5 CAMPS”:

  1. FLAT - FSH, LH, ACTH, TSH
  2. “2” ADH (V2-receptor), histamine (H2-receptor).
  3. “Ca2+” - PTH, calcitonin
  4. “weird” - CRH, GHRH
  5. Sweet Black Baby - glucagon, MSH, hCG
42
Q

Signaling pathways of endocrine hormones - cGMP

A

BNP, ANP, EDRF (NO)

43
Q

Signaling pathways of endocrine hormones - IP3

A

G - GnRH
O - Oxytocin
A - ADH (V1-receptor)
T - TRH

H - Histamine (H1-receptor)
A - Angiotensin ll
G - Gastrin

44
Q

Signaling pathways of endocrine hormones -

Intracellular receptor

A

Adrenals Progesterone, Estrogen, Testosterone, Cortisol, Aldosterone, Thyroid and vitamin D.

45
Q

Signaling pathways of endocrine hormones - Receptor tyrosine kinase

A

Insulin, IGF-1, FGF, PDGF, EGF

MAP kinase pathway

46
Q

Signaling pathways of endocrine hormones - Nonreceptor tyrosine kinase

A

JAK/STAT pathway

G - G-CSF
E - Erythropoietin
T - Thrombopoietin

a

P - Prolactin
I - immunomodulators (eg, cytokines IL-2, IL-6, IFN)
G - GH

47
Q

Neuroendocrine tumors contain a special type of enzyme.

A

Cells contain amine precursor uptake decarboxylase (APUD).

48
Q

Neuroblastoma lab findings:(4)

A

Bombesin positive.
NSE positive.
Homer-Wright rosettes.
HVA and VMA (catecholamine metabolites) in the urine.

49
Q

Neuroblastoma clinical findings: (4)

A

Children, usually< 4 years old.
Abdominal distension and a firm, irregular mass that can cross the midline.
Normotensive.
Opsoclonus-myoclonus syndrome (“dancing eyes-dancing feet”).

50
Q

Neuroblastoma pathology findings:

A

Originates from Neural crest cells.
N-myc oncogene.
Classified as an APUD tumor.

51
Q

Carcinoid syndrome rules of 1/3 and 3’s:

A

Rule of 1/3 and 3’s:
1/3 metastasize
1/3 present with 2nd malignancy
1/3 are multiple
Telotristat (telo-3-stat) and octreotide.
Dec. B3 (used for serotonin synthesis)
Tricuspid regurgitation, pulmonic stenosis

52
Q

Pheochromocytoma Rule of 10’s:

A 
10% malignant
10% bilateral
10% extra-adrenal (eg, bladder wall, the organ of Zuckerkandl)
10% calcify
10% of kids
53
Q

Pheochromocytoma (5 P’s):

A 
Episodic hyperadrenergic symptoms (5 P's):
Pressure (inc BP)
Pain (headache)
Perspiration
Palpitations (tachycardia)
Pallor
54
Q

Pheochromocytoma May be associated with germline mutations eg:

A

NF-1
VHL
RET (MEN 2A, 2B)

55
Q

insulinoma - Whipple triad:

A

Low blood glucose
Symptoms of hypoglycemia (eg, lethargy, syncope, diplopia)
Resolution of symptoms after normalization of glucose levels.

56
Q

Glucagonoma 5D’s:

A 
Dermatitis (necrolytic migratory erythema)
Diabetes (hyperglycemia)
DVT
Declining weight
Depression
57
Q

Somatostatinoma -> Dec. secretion of:

A

Dec. secretion of: SIC G’s

S -secretin
I - insulin
C - cholecystokinin

G - glucagon
G - gastrin
G - gastric inhibitory peptide (GIP).

58
Q

Somatostatinoma - May present with:

A 
D (cell) - GAS
diabetes/glucose intolerance
steatorrhea
gallstones
achlorhydria.
59
Q

Zollinger-Ellison syndrome - Positive secretin stimulation test:

A

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

60
Q

Hypothyroidism - electrolytic changes:

A

hyponatremia (dec. free water clearance)

61
Q

Hypothyroidism vs hyperthyroidism - Both present:

A

Periorbital edema (Hypothyroidism- myoedema)
Myopathy (Hypothyroidis- inc CK and myoedema, hyperthyroidism -osteoporosis)
Sex - Abnormal uterine bleeding, dec libido, infertility (hyperthyroidism -gynecomastia)
Myxedema (hyperthyroidism -pretibial myxedema)

62
Q

Congenital hypothyroidism (cretinism) 6 P’s:

A 
Pot-bellied
Pale
Puffy-faced child 
Protruding umbilicus
Protuberant tongue
Poor brain development.
63
Q

Hashimoto thyroiditis risk and histology?

A

Risk of non-Hodgkin lymphoma (typically of B-cell origin)

Hurthle cells, lymphoid aggregates with germinal centers.

64
Q

Riedel thyroiditis findings

A

Fibrosis may extend to local structures (eg, trachea, esophagus - mimicking anaplastic carcinoma. 1/3 are hypothyroid.

65
Q

Riedel thyroiditis considered a manifestation of

A

Considered a manifestation of lgG4 - related systemic disease (eg, autoimmune pancreatitis, retroperitoneal fibrosis, noninfectious aortitis).

66
Q

Graves disease - activation of…

A

Activation of T-cells - lymphocytic infiltration of retroorbital space -> inc cytokines (eg, TNF-alfa, IFN-gamma ) -> inc fibroblast secretion of hydrophilic GAGs -> inc osmotic muscle swelling, muscle inflammation, and adipocyte count -> exophthalmos.

67
Q

Jod-Basedow phenomenon

A

Iodine-induced hyperthyroidism. This occurs when a patient with iodine deficiency and partially autonomous thyroid tissue (eg, autonomous nodule) is made iodine replete. It can happen after iodine IV contrast or amiodarone use. Opposite to the Wolff-Chaikoff effect.

68
Q

Thyroid cancer - Complications of surgery include:

A

Hypocalcemia (due to the removal of parathyroid glands).

Transection of the recurrent laryngeal nerve - during ligation of the inferior thyroid artery.

Injury to the external branch of the superior laryngeal nerve - during ligation of superior thyroid vascular pedicle (noticeable in professional voice users).

69
Q

Papillary carcinoma mutation(s):

A

RET/PTC rearrangements and BRAF mutations

70
Q

Follicular carcinoma mutation(s):

A

RAS mutation and PAX8-PPAR-gamma translocations.

71
Q

Medullary carcinoma mutation(s):

A

MEN 2A and 2B (RET mutations).

72
Q

Anaplastic carcinoma mutation(s):

A

TP53 mutation.

73
Q

Albright hereditary osteodystrophy:

A

shortened 4th/5th digits
short stature
obesity,
developmental delay.

74
Q

Pseudohypoparathyroidism type 1A pathophysiology:

A

Autosomal dominant.

Due to inactive Gs protein alfa-subunit causing end-organ (kidney and bone) resistance to PTH.

hypocalcemia despite inc PTH levels.

Albright hereditary osteodystrophy

The defect must be inherited from the mother due to imprinting.

75
Q

Pseudopseudohypoparathyroidism

A

Autosomal dominant.

Albright hereditary osteodystrophy

Without end-organ PTH resistance - PTH level normal and normal calcium levels.

Gs protein alfa-subunit inherited from the father - maternal a llele maintains responsiveness.

76
Q

Familial hypocalciuric hypercalcemia

A

Excessive renal Ca2+ reabsorption -> mild hypercalcemia and hypocalciuria with normal to inc PTH levels.

Defective G-coupled Ca2+- sensing receptors in multiple tissues

Higher than normal Ca2+ levels required to suppress PTH.

77
Q

Hypopituitarism (causes for) :

A 
R - Radiation
A - apoplexy
 I - injury to the brain
N - Nonsecreting pituitary adenoma, craniopharyngioma
E - Empty sella syndrome
S - Sheehan syndrome
78
Q

pegvisomant

A

GH receptor antagonist

79
Q

Laron syndrome

A

Autosomal recessive.

Defective GH receptors:
dec linear growth
inc GH,
dec IGF-1.

Clinical features: short stature (dwarfism), small head circumference, characteristic facies with saddle nose and prominent forehead, delayed skeletal maturation, small genitalia.

80
Q

SIADH causes include:

A 
L - Lung disease
A - ADH (Ectopic - small cell lung cancer)
C - CNS disorders/head trauma
e - empty.
D - Drugs (eg, cyclophosphamide)
81
Q

Drugs affecting ADH:

A

Analog: Desmopressin
antagonist: conivaptan, tolvaptan, demeclocycline

82
Q

MEN2B

A

Medullary thyroid carcinoma

Pheochromocytoma

MucosaI neuromas (oral/intestinal ganglioneuromatosis)

Associated with marfanoid habitus; mutation in RET gene

83
Q

MEN syndromes

A

MEN1 = 3 P’s: Pituitary, Parathyroid, and Pancreas

MEN2A = 2 P’s: Parathyroid and Pheochromocytoma, Medullary thyroid carcinoma

MEN2B = 1 P: Pheochromocytoma, Medullary thyroid carcinoma, MucosaI neuromas

84
Q

Demeclocycline USE AND ADVERSE EFFECTS

A

USE: SIADH

ADVERSE EFFECTS: Nephrogenic DI, photosensitivity, abnormalities of bone and teeth.

85
Q

Fludrocortisone
MECHANISM
USE
ADVERSE EFFECTS

A

MECHANISM: Synthetic analog of aldosterone wi th little glucocorticoid effects.

USE: Mineralocorticoid replacement in primary adrenal insufficiency

ADVERSE EFFECTS: Similar to glucocorticoids; also edema, exacerbation of heart failure, hyperpigmentation. (black heart)

86
Q

Somatostatin (octreotide) USE

A

A - Acromegaly
C - Carcinoid syndrome
E - Esophageal varices

Gs’ - gastrinoma, glucagonoma

87
Q

GH USE

A

GH deficiency, Turner syndrome.

88
Q

Desmopressin USE

A

Central DI, von Willebrand disease, sleep enuresis, hemophilia A.

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