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STEP 1 ENDOCRINE > ENDOCRINE > Flashcards

ENDOCRINE Flashcards

1
Q

THYROID FOLICULAR CELLS (EMBIOLOGY)

A

DERIVED FROM ENDODERM

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2
Q

PARAFOLICULAR CELLS
(EMBRIOLOGY)

A

ARISE FROM 4TH POUCH

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2
Q

PARATHYROID GLANDS

A

FORMED BY 3RD AND 4TH PHARYNGERAL POUCH

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3
Q

INFERIOR THYROID ARTERY COMES FROM

A

LEFT SUBCLAVIAN ARTERY

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4
Q

SUPERIOR THYROID ARTERY COMES FROM

A

EXTERNAL CAROTID ARTERY

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4
Q

ADENOHYPOPHYSIS CONTAINS BLOOD BRAIN BARRIER?

A

NO!

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5
Q

ADENOHYPOPHYSIS
DERIVED FROM

A

ORAL ECTODERM
(RATHKE POUCH)

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5
Q

ADENOHYPOPHYSIS SECRETS

A

FSH
LH
TSH
ACTH
GH
MHS
PROLACTIN
BETA ENDORPHIN

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5
Q

NEUROHYPOPHYSIS
DERIVED FROM:

A

NEUROECTODERM

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5
Q

ADRENAL CORTEX COMES FROM:

A

MESODERM

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5
Q

ZONA FASCICULATA PRODUCED:

A

CORTISOL
(GLUCOCORTICOIDS)

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6
Q

WHERE ADH AND OXYTOCIN ARE PRODUCED?

A

HYPOTHALAMUS: SUPRAOPTIC AND PARAVENTRICULAR NUCLEI

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6
Q

ADRENAL MEDULA COMES FROM:

A

NEURAL CREST

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6
Q

ZONA GLOMERULOSA PRODUCE

A

ALDOSTERONE
(MINERALCORTICOIDS)

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6
Q

ZONA GLOMERULOSA IS REGULATED BY

A

ANGIOTENSIN II

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7
Q

ZONA FASCICULATA IS REGULATED BY

A

ACTH AND CRH

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8
Q

OCREOTIDE

A

SOMATOSTATINE ANALOGE
REDUCES GH, IGF-1 AND ADENOMA SIZE

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9
Q

PEGVISOMANT

A

COMPETITIVE INHIBITOR OF GH BLOCKS THE BINDING RECEPTOR OF GH, REDUCES IGF-1, NOT REDUCES ADENOMA AND GH.

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10
Q

SGLT-2 INHIBITOR
NA-GLUCOSE TRANSPORTER
DRUGS

A

CANAGLIFLOZIN
DAPAGLIFLOZIN
EMPAGLIFLOZIN
´´GLUCOSE FLOWS IN URINE´´

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11
Q

NA - GLUCOSE CO-TRANSPORTER 2 INHIBITORS MECANISM

A

BLOCK ABSORTION OF GLUCOSE IN PROXIMAL CONVOLUTED TUBULE

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12
Q

NA-GLUCOSE CO-TRANSPORTER 2 INDICATION

A

*DECRESE BLOOD PRESURE
*REDUCE MORTALITY FOR HF
*SLOW DABETIC NEPHROPATHY

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13
Q

NA-GLU CO -TRANSPORTER 2 SIDE EFECTS

A

REDUCE BONE DENSITY
CANDIDIASIS
ORTHOSTATIC HIPOTENSION

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14
Q

GLP1 ANALOGS

A

EXENATIDE
LIRAGLUTIDE
SEMAGLUTIDE

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15
Q

GLP1 ANALOGS MECANISM

A

REDUCE : GLUCAGON RELEASE AND GASTRIC EMPTYING.
INCREASE GLUCOSE-DEPENDENT INSULIN RELEASE

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16
Q

CONGENITAL HYPOTIRODISM

A

POOR FEDING
PROLONGED JAUNDICE
UMBILICAL HERNIA
ENLARGEMENT OF THE ANTERIOR FONTANELA
MACROGLOSSIA

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16
Q

GALACTOSEMIA

A

PROLONGED JAUNDICE
VOMITING
HEPATOMEGALY
LETHARGY

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17
Q

PHENYLKETONURIA

A

DEVELOMENTAL DELAY
LIGHT PIGMENTATION
MUSTY BODY ODOR

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18
Q

ALDOSTERONE FUNTION

A

ABSORVERS SODIUM AND RELEASE POTASSIUM.

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19
Q

ESPIRONOLACTONA MECANISM

A

BLOCKS ALDOSTERONE FUNTION.
INCREASED EXCRETION OF NA AND WATER AND DECREASED LEVEL OF K IN THE SERUM

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20
Q

ADISSON DISEASE CLINIC

A

ABDOMINAL PAIN
WEIGHT LOSS
SALT CRAVING
ORTHOSTASIS (HYPOVOLEMIA - ADH)
ELECTROLYTE DISTURBANCE - HYPONATREMIA AND HYPERKALEMIA - ALDOSTERONE;CORTISOL; ADH)

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21
Q

REDUCED CORTISOL INCRESE

A

NOREPINEPHRINE

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22
Q
A
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23
Q

REDUCED CORTISOL DECREASE

A

EPINEPHRINE

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24
Q

PRIMARY ADRENAL INSUFFICIENCY (PAI)

A

ADDISON DISEASE

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25
Q

REDUCESD CORTISOL CAN CAUSE:

A

HYPOGLYCEMIA
NORMOCYTIC ANEMIA
EOSINOPHILIA

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26
Q

LOW CORTISOL INCREASED OU DECREASED ADH?

A

INCREASE

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27
Q

POSTPARTUM THYROIDITIS

A

AUTOIMMUNE DESTRUCTION OF THYROID FOLLICLES
FIRST HYPERTHYROID ANN TRANSIENT TO HYPOTHYROID PHASE.

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28
Q

POSTPARTUM THYROIDITIS
(HYSTOLOGIC INSPECTION)

A

LYMPHOCYTIC INFILTRATION, SOMETIMES FORMATION OF GERMINAL CENTERS

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29
Q

POST PARTUM DIAGNOSE

A

ELEVETED THYROGLOBULIN
ELEVETED RADIOIODINE UPTAKE
US: DIFFUSE THYROID ENLARGEMENT WITH REDUCED BLOOD FLOW.

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30
Q

THINNING OF THE LATERAL EYEBROWS

A

HYPOTHYRODISM

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31
Q

24 HOUR URINARY CORTISOL ASSAY AND DEXAMETHASONE SUPRESSION

A

SCREEN FOR CUSHING SYNDROME

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32
Q

HEREDITARY HEMOCROMATOSIS INCITIAL EVALUATION

A

SERUM IRON
FERRITIN
TRANSFERRIN SATURATION

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33
Q

CLINIC FROM HEMOCHROMATOSIS

A

ARTHRITIS
DM
SKIN PIGMENTATION
HEPATOMEGALY

34
Q

THE MOST SENSITIVE TEST FOR PRIMARY HYPOTHYROIDISM

A

TSH

35
Q

GH PROMOTES GROWTH BY

A

GH MOLECULE BINDS TO JAK -STAT RECEPTOR IN THE SURFACE OF THE HEPATIC CELL THAN INDUCES GENE TRANSCRIPTION OF IGF-1.

36
Q

JAK-STAT PATHWHAY MOLECULES THAT USE

A

HEMATOPOIETIC GROW FACTORS (G-CSF, ERYTHROPOIETIN)
CYTOKINES (INTERFERON)

37
Q

CYCLIC AMP-PROTEIN KINASE A PATHWAY MECANISM

A

ACTIVATED ADNYLYL CYCLASE AFTER BINDING G PROTEIN-COUPLED RC TO CONVERTS ATP TO CYCLIC AMP AND ACTIVATED PROTEIN KINASE A

38
Q

HORMONS WHO USES CYCLIC AMP-PROTEIN KINASE A PATHWAY

A

´´FLAT ChAMPs CHuGG´´

FHS ; LH ; ACTH; TSH; CRH; hCG; ADH; MSH; PTH; Calcitonin; Histamine; Glucagon; Ghrh

39
Q

ADRENAL CORTICAL HYPERPLASIA CLINIC

A

PREMATURE PUBARCHE/HIRSUTISM
RAPID GOWTH
BODY ODOR
ACNE

40
Q

ADRENAL CORTICAL HYPERPLASIA LABS

A

HIGH CONCENTRATIONS OF:
17-HYDROXYPROGESTERONE AND TESTOSTERONE

41
Q

21-HYDROXYLASE DEFICIENCY CLINICAL SYNDROMES

A

*CLASSIC- SALT WASTING
*CLASSIC NON-SALT WASTING
*NONCLASSIC - LAT ONSET

42
Q

ADRENAL MEDULLARY HYPERPLASIA CLINIC

A

HYPERTENSION
TACHYCARDIA
SWEATING

43
Q

SEMINOMA DERIVED FROM

A

SEMINIFERUS TUBULES, NOT ELEVATED TESTOSTERONE

44
Q

TREATMENT OF CONGENITAL ADRENAL HYPERPLASIA DUE TO 21-HYDROXYLASE

A

LOW DOSES OF EXOGENOUS CORTICOSTEROIDS TO SUPRESS EXCESS ACTH

45
Q

21-HYDROXYLASE DEFICIENCY BLOCKS PRODUCTION OF

A

ALDOSTERONE AND CORTISOL

46
Q

21-HYDROXYLASE DEFICIENCY INCREASED:

A

ANDROSTENEDIONE AND DEHYDROEPIANDROSTERONE.
AND ACTH BECAUSE THE CORTISOL LEVEL IS LOW.

47
Q

G PROTEIN-COUPLED RECEPTORS ON PANCREATIC BETA CELLS

A

MUSCRININC
GLUCAGON
B2 ADRENERGIC
GLUCAGON-LIKE PEPTIDE-1
ALFA 2 ADRENERGIC
SOMATOSTATIN 2

48
Q

G PROTEIN-COUPLED RECEPTORS ON PANCREATIC BETA CELLS WHO INCREADES INSULIN SECRETION

A

MUSCARINIC
GLUCAGON
B2 ADRENERGC
GLUCAGON-LIKE PEPTIDE

49
Q

G PROTEIN-COUPLED RECEPTORS ON PANCREATIC BETA CELLS WHO DECREASED INSULIN SECRETION

A

ALFA 2 ADRENERGIC
SOMATOSTATIN 2

50
Q

HYPOGONADISM SINTOMS

A

FATIGUE
LOSS MUSCLE MASS
DECREASED BONE DENSITY
LOS LIBIDO

51
Q

CLUMSINESS

A

TORPEZA

52
Q

MEN 1

A

PRIMARY HYPERPARATHYROIDISM
PITUIRATY TUMORS (PROLACTIN)
PANCREATIC TUMORS (GASTRINOMAS)

53
Q

MEN 2A

A

MEDULLAR THYROID CANCER
PHEOCHROMOCYTOMA
PRIMARY HYPERPARATHYROIDISM

54
Q

MEN 2 B

A

MEDULLARY THYROID CANCER
PHEOCHROMOCYTOMA
MUCOSAL NEUROMAS/MARFANOID HABITUS

55
Q

POTASSIUM IODINE GIVEN WHEN

A

WE HAVE A NUCLERAR ACCIDENT

56
Q

POTASSIUM IODINE FUNTION

A

INHIBITS THYROID UPTAKE OF RADIOCTIVE IODINE ISOTOPES

57
Q

GLUCAGOMA CLINIC

A

HYPERGLYCEMIA
WEIGTH LOSS
ANEMIA
NECROLYTIC MIGRATORY ERYTHEMA

58
Q

SOMATOSTINOMA

A

HYPERGLYCEMIA
WEIGHT LOSS
ABDOMINAL PAIN
STEATORREHEA
CHOLELITHIASIS
HYPOCHLORHYDRIA

59
Q

SOMATOSTATIN INDUCED INHIBITION OF

A

INSULIN
GASTRIN
SECRETIN
CHOLECYSTOKININ SECRETION

60
Q

VIPOMAS

A

DIARREHEA
HYPOKALEMIA
IMPAIRED GASTRIC ACID SECRETION

61
Q

EXOGENUS ANDROGENS SUPPRESS

A

GnRH / LH/ FSH

62
Q

EXOGENUS ANDROGENS CAUSE

A

ACNE
NEUROPSYCHIATRIC CHANGES (AGGRESSION, IRRITABILITY AND ANXIETY)
GYNECOMASTIA
TESTICULAR ATROPHY
IMPAIRED SPERMATOGENESIS
PREMATURE EPIPHYSEAL CLOSURE = SHORT STATURE

63
Q

AUTOIMMUNE DESEASES ASSOCIATED WITH HYPOTHYROIDISM:

A

CELIAC DISEASE
PERNICIOUS ANEMIA

64
Q

LEUPROLIDE

A

GnRH analogue used to treatmente of prostate cancer to suppress testorene levels

65
Q

NOREPINEPHRINE CONVERTED TO EPINEPHRINE BY WHICH ENZYME?

A

PHENYLETHANOLAMINE-N-METHYLTRANSFERASE WHO IS ACTIVATED BY CORTISOL

66
Q

CATECHOL-O-METHYLTRANSFERASE (COMT) AND MONOAMINE OXIDASE (MAO) INATIVATED:

A

CATECHOLAMINES

67
Q

MAN WITH 1 TESTIS

A

ERECTILE FUNCTION: OK
SPERM COUNT: DECREASED

68
Q

SEVELAMER

A

DECREASES ABSORPTION OF PHOSPHATE IN GI TRACT, AND IS USED TO TRAT HYPERPHOSPHATEMIA IN PATIENTS ON DYALYSIS.

69
Q

POSTOPERATIVE HYPOPARATHYROIDISM SUPPLEMENTATION:

A

ORAL CALCIUM AND VITAMIN D

70
Q

KETOCONAZOLE AND TESTOSTERONE

A

DECREASES TESTOSTERONE SYNTHESIS

71
Q

SPIRONOLACTONE AND TESTOSTERONE

A

DECREASES TESTOSTERONE SYNTHESIS

72
Q

SYNDROME OF INAPPROPITE ANTIDIURETIC HORMONE SECRETION
(SIADH) CAUSED BY DRUGS

A

CARBAMAZEPINE
CTCLOPHOSPHAMIDE
SSRI eg. Sertralina

73
Q

CHERRY RED MACULA

A

NIEMANN PICK DISEASE

74
Q

EXOGENOUS THYROXICOSIS (CAUSES)

A
  • THYROID REPLACEMENT DOSING ERROR
    *LEVOTHYROXINE SUPPESSION OF THYROID CANCER
  • NONPRESCRIBED THYROID HORMONE USE (FACTITIOUS DISORDER, WEIGH LOSS SUPPLEMENTS)
75
Q

EXOGENOUS THYROTOXICOSIS LABS

A

ELEVATED T4 AN THYROXINE LEVELS
(SUPPLEMENT ELEVATED T3 ONLY)
SUPPRESSED TSH
LOW SERUM THYROGLOBULIN
LOW RADIOIODINE UPTAKE

76
Q

PACIENTS WITH THYROID CANCER NEED TO RECIVE LECOTHYROXINE HIGHER DOSIS, WHY?

A

BECAUSE TSH VAN PROMOTE GOWTH OF THE RESIDUAL MALIGNANT CELLS

77
Q

SPHUNGOLIPIDOSES (7)

A

*FABRY DISEASE (XLR = X - LINKED RECESSIVE)
*TAY-SACHS DISEASE (AR)
*GAUCHER DISEASE (AR)
*NIEMANN- PICK DESEASE (AR)
*KRABBE DISEASE (AR)
*METACHROMATICC *LEUKODYSTROPHY (AR)

78
Q

FABRY DISEASE DEFICIENCY

A

ALFA GALACTOSIDASE A

79
Q

FABRY DISEASE ACUMMULATED SUBSTRATE

A

GLOBOTRIAOSYLCERAMIDE

80
Q

FABRY DISEASE CLINC

A

ANGIOKATOMAS
PERIPHERAL NEUROPATHY
GLOMERULOPATHY

81
Q

TAY-SACHS DISEASE DEFICIENCY

A

BETA- HEXOSAMINIDASE A

82
Q

TAY-SACHS DISEASE ACCUMULATED SUBSTRATE

A

GM2 (GANGLIOSIDE)

83
Q

TAY-SACHS DISEASE CLINIC

A

MACULAR CHERRY RED SPOT
PROGRESSIVE NEURODEGENERATION

84
Q

GAUCHER DISEASE DEFICIENCY

A

BETA GLUCOCEREBROSIDASE

85
Q

GAUCHER DISEASE ACUMULATED SUSTRATE

A

GLUCOCEREBROSIDE

86
Q

GAUCHER DISEASE CLINIC

A

HEPATOSPLENOMEGALY
PANCYTOPENIA
BONE PAIN/OSTEOPENIA

87
Q

NIEMANN PICK DISEASE DEFICIENCY

A

SPHINGOMYELINASE

88
Q

NIEMAN PICK ACUMULATED SUBSTRATE

A

SPHINGOMYELIN

89
Q

NIEMANN PICK DISEASE CLINIC

A

MACULAR CHERRY-RED SPOT
PROGRESSIVE NEURODEGENERATION
HEPATOSPLENOMEGALY

90
Q

KRABBE DISEASE DEFICIENCY

A

GALACTOCEREBROSIDASE

91
Q

KRABBE DISEASE ACCUMULATED SUBSTRATE

A

GALACTOCEREBROSIDE AND PSYCHOSINE

92
Q

KRABBE DISEASE

A

PROGRESSIVE NEURODEGENERATION
PERIPHERAL NEUROPATHY
OPTIC ATROPHY

93
Q

METACHROMATIC LEUKODYSTROPHY DEFICIENCY

A

ARYLSULFATASE A

94
Q

METACHROMATIC LEUKODYSTROPHY SUBSTANCE ACUMULATED

A

CEREBROSIDE SULFATE

95
Q

METACHROMATIC LEUKODYSTROPHY CLINIC

A

PROGRESSIVE NEURODEGENERATION
PERIPHERAL NEUROPATHY

96
Q

MACULAR CHERRY-RED SPOT, WHAT´S DISEASE CAUSED THIS?

A

NIEMANN-PICK AND TAY-SACHS

97
Q
A

STEP 1 ENDOCRINE (1 decks)

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