ENDOCRINE Flashcards
1
Q
THYROID FOLICULAR CELLS (EMBIOLOGY)
A
DERIVED FROM ENDODERM
2
Q
PARAFOLICULAR CELLS
(EMBRIOLOGY)
A
ARISE FROM 4TH POUCH
2
Q
PARATHYROID GLANDS
A
FORMED BY 3RD AND 4TH PHARYNGERAL POUCH
3
Q
INFERIOR THYROID ARTERY COMES FROM
A
LEFT SUBCLAVIAN ARTERY
4
Q
SUPERIOR THYROID ARTERY COMES FROM
A
EXTERNAL CAROTID ARTERY
4
Q
ADENOHYPOPHYSIS CONTAINS BLOOD BRAIN BARRIER?
A
NO!
5
Q
ADENOHYPOPHYSIS
DERIVED FROM
A
ORAL ECTODERM
(RATHKE POUCH)
5
Q
ADENOHYPOPHYSIS SECRETS
A
FSH
LH
TSH
ACTH
GH
MHS
PROLACTIN
BETA ENDORPHIN
5
Q
NEUROHYPOPHYSIS
DERIVED FROM:
A
NEUROECTODERM
5
Q
ADRENAL CORTEX COMES FROM:
A
MESODERM
5
Q
ZONA FASCICULATA PRODUCED:
A
CORTISOL
(GLUCOCORTICOIDS)
6
Q
WHERE ADH AND OXYTOCIN ARE PRODUCED?
A
HYPOTHALAMUS: SUPRAOPTIC AND PARAVENTRICULAR NUCLEI
6
Q
ADRENAL MEDULA COMES FROM:
A
NEURAL CREST
6
Q
ZONA GLOMERULOSA PRODUCE
A
ALDOSTERONE
(MINERALCORTICOIDS)
6
Q
ZONA GLOMERULOSA IS REGULATED BY
A
ANGIOTENSIN II
7
Q
ZONA FASCICULATA IS REGULATED BY
A
ACTH AND CRH
8
Q
OCREOTIDE
A
SOMATOSTATINE ANALOGE
REDUCES GH, IGF-1 AND ADENOMA SIZE
9
Q
PEGVISOMANT
A
COMPETITIVE INHIBITOR OF GH BLOCKS THE BINDING RECEPTOR OF GH, REDUCES IGF-1, NOT REDUCES ADENOMA AND GH.
10
Q
SGLT-2 INHIBITOR
NA-GLUCOSE TRANSPORTER
DRUGS
A
CANAGLIFLOZIN
DAPAGLIFLOZIN
EMPAGLIFLOZIN
´´GLUCOSE FLOWS IN URINE´´
11
Q
NA - GLUCOSE CO-TRANSPORTER 2 INHIBITORS MECANISM
A
BLOCK ABSORTION OF GLUCOSE IN PROXIMAL CONVOLUTED TUBULE
12
Q
NA-GLUCOSE CO-TRANSPORTER 2 INDICATION
A
*DECRESE BLOOD PRESURE
*REDUCE MORTALITY FOR HF
*SLOW DABETIC NEPHROPATHY
13
Q
NA-GLU CO -TRANSPORTER 2 SIDE EFECTS
A
REDUCE BONE DENSITY
CANDIDIASIS
ORTHOSTATIC HIPOTENSION
14
Q
GLP1 ANALOGS
A
EXENATIDE
LIRAGLUTIDE
SEMAGLUTIDE
15
Q
GLP1 ANALOGS MECANISM
A
REDUCE : GLUCAGON RELEASE AND GASTRIC EMPTYING.
INCREASE GLUCOSE-DEPENDENT INSULIN RELEASE
16
CONGENITAL HYPOTIRODISM
POOR FEDING
PROLONGED JAUNDICE
UMBILICAL HERNIA
ENLARGEMENT OF THE ANTERIOR FONTANELA
MACROGLOSSIA
16
GALACTOSEMIA
PROLONGED JAUNDICE
VOMITING
HEPATOMEGALY
LETHARGY
17
PHENYLKETONURIA
DEVELOMENTAL DELAY
LIGHT PIGMENTATION
MUSTY BODY ODOR
18
ALDOSTERONE FUNTION
ABSORVERS SODIUM AND RELEASE POTASSIUM.
19
ESPIRONOLACTONA MECANISM
BLOCKS ALDOSTERONE FUNTION.
INCREASED EXCRETION OF NA AND WATER AND DECREASED LEVEL OF K IN THE SERUM
20
ADISSON DISEASE CLINIC
ABDOMINAL PAIN
WEIGHT LOSS
SALT CRAVING
ORTHOSTASIS (HYPOVOLEMIA - ADH)
ELECTROLYTE DISTURBANCE - HYPONATREMIA AND HYPERKALEMIA - ALDOSTERONE;CORTISOL; ADH)
21
REDUCED CORTISOL INCRESE
NOREPINEPHRINE
22
23
REDUCED CORTISOL DECREASE
EPINEPHRINE
24
PRIMARY ADRENAL INSUFFICIENCY (PAI)
ADDISON DISEASE
25
REDUCESD CORTISOL CAN CAUSE:
HYPOGLYCEMIA
NORMOCYTIC ANEMIA
EOSINOPHILIA
26
LOW CORTISOL INCREASED OU DECREASED ADH?
INCREASE
27
POSTPARTUM THYROIDITIS
AUTOIMMUNE DESTRUCTION OF THYROID FOLLICLES
FIRST HYPERTHYROID ANN TRANSIENT TO HYPOTHYROID PHASE.
28
POSTPARTUM THYROIDITIS
(HYSTOLOGIC INSPECTION)
LYMPHOCYTIC INFILTRATION, SOMETIMES FORMATION OF GERMINAL CENTERS
29
POST PARTUM DIAGNOSE
ELEVETED THYROGLOBULIN
ELEVETED RADIOIODINE UPTAKE
US: DIFFUSE THYROID ENLARGEMENT WITH REDUCED BLOOD FLOW.
30
THINNING OF THE LATERAL EYEBROWS
HYPOTHYRODISM
31
24 HOUR URINARY CORTISOL ASSAY AND DEXAMETHASONE SUPRESSION
SCREEN FOR CUSHING SYNDROME
32
HEREDITARY HEMOCROMATOSIS INCITIAL EVALUATION
SERUM IRON
FERRITIN
TRANSFERRIN SATURATION
33
CLINIC FROM HEMOCHROMATOSIS
ARTHRITIS
DM
SKIN PIGMENTATION
HEPATOMEGALY
34
THE MOST SENSITIVE TEST FOR PRIMARY HYPOTHYROIDISM
TSH
35
GH PROMOTES GROWTH BY
GH MOLECULE BINDS TO JAK -STAT RECEPTOR IN THE SURFACE OF THE HEPATIC CELL THAN INDUCES GENE TRANSCRIPTION OF IGF-1.
36
JAK-STAT PATHWHAY MOLECULES THAT USE
HEMATOPOIETIC GROW FACTORS (G-CSF, ERYTHROPOIETIN)
CYTOKINES (INTERFERON)
37
CYCLIC AMP-PROTEIN KINASE A PATHWAY MECANISM
ACTIVATED ADNYLYL CYCLASE AFTER BINDING G PROTEIN-COUPLED RC TO CONVERTS ATP TO CYCLIC AMP AND ACTIVATED PROTEIN KINASE A
38
HORMONS WHO USES CYCLIC AMP-PROTEIN KINASE A PATHWAY
´´FLAT ChAMPs CHuGG´´
FHS ; LH ; ACTH; TSH; CRH; hCG; ADH; MSH; PTH; Calcitonin; Histamine; Glucagon; Ghrh
39
ADRENAL CORTICAL HYPERPLASIA CLINIC
PREMATURE PUBARCHE/HIRSUTISM
RAPID GOWTH
BODY ODOR
ACNE
40
ADRENAL CORTICAL HYPERPLASIA LABS
HIGH CONCENTRATIONS OF:
17-HYDROXYPROGESTERONE AND TESTOSTERONE
41
21-HYDROXYLASE DEFICIENCY CLINICAL SYNDROMES
*CLASSIC- SALT WASTING
*CLASSIC NON-SALT WASTING
*NONCLASSIC - LAT ONSET
42
ADRENAL MEDULLARY HYPERPLASIA CLINIC
HYPERTENSION
TACHYCARDIA
SWEATING
43
SEMINOMA DERIVED FROM
SEMINIFERUS TUBULES, NOT ELEVATED TESTOSTERONE
44
TREATMENT OF CONGENITAL ADRENAL HYPERPLASIA DUE TO 21-HYDROXYLASE
LOW DOSES OF EXOGENOUS CORTICOSTEROIDS TO SUPRESS EXCESS ACTH
45
21-HYDROXYLASE DEFICIENCY BLOCKS PRODUCTION OF
ALDOSTERONE AND CORTISOL
46
21-HYDROXYLASE DEFICIENCY INCREASED:
ANDROSTENEDIONE AND DEHYDROEPIANDROSTERONE.
AND ACTH BECAUSE THE CORTISOL LEVEL IS LOW.
47
G PROTEIN-COUPLED RECEPTORS ON PANCREATIC BETA CELLS
MUSCRININC
GLUCAGON
B2 ADRENERGIC
GLUCAGON-LIKE PEPTIDE-1
ALFA 2 ADRENERGIC
SOMATOSTATIN 2
48
G PROTEIN-COUPLED RECEPTORS ON PANCREATIC BETA CELLS WHO INCREADES INSULIN SECRETION
MUSCARINIC
GLUCAGON
B2 ADRENERGC
GLUCAGON-LIKE PEPTIDE
49
G PROTEIN-COUPLED RECEPTORS ON PANCREATIC BETA CELLS WHO DECREASED INSULIN SECRETION
ALFA 2 ADRENERGIC
SOMATOSTATIN 2
50
HYPOGONADISM SINTOMS
FATIGUE
LOSS MUSCLE MASS
DECREASED BONE DENSITY
LOS LIBIDO
51
CLUMSINESS
TORPEZA
52
MEN 1
PRIMARY HYPERPARATHYROIDISM
PITUIRATY TUMORS (PROLACTIN)
PANCREATIC TUMORS (GASTRINOMAS)
53
MEN 2A
MEDULLAR THYROID CANCER
PHEOCHROMOCYTOMA
PRIMARY HYPERPARATHYROIDISM
54
MEN 2 B
MEDULLARY THYROID CANCER
PHEOCHROMOCYTOMA
MUCOSAL NEUROMAS/MARFANOID HABITUS
55
POTASSIUM IODINE GIVEN WHEN
WE HAVE A NUCLERAR ACCIDENT
56
POTASSIUM IODINE FUNTION
INHIBITS THYROID UPTAKE OF RADIOCTIVE IODINE ISOTOPES
57
GLUCAGOMA CLINIC
HYPERGLYCEMIA
WEIGTH LOSS
ANEMIA
NECROLYTIC MIGRATORY ERYTHEMA
58
SOMATOSTINOMA
HYPERGLYCEMIA
WEIGHT LOSS
ABDOMINAL PAIN
STEATORREHEA
CHOLELITHIASIS
HYPOCHLORHYDRIA
59
SOMATOSTATIN INDUCED INHIBITION OF
INSULIN
GASTRIN
SECRETIN
CHOLECYSTOKININ SECRETION
60
VIPOMAS
DIARREHEA
HYPOKALEMIA
IMPAIRED GASTRIC ACID SECRETION
61
EXOGENUS ANDROGENS SUPPRESS
GnRH / LH/ FSH
62
EXOGENUS ANDROGENS CAUSE
ACNE
NEUROPSYCHIATRIC CHANGES (AGGRESSION, IRRITABILITY AND ANXIETY)
GYNECOMASTIA
TESTICULAR ATROPHY
IMPAIRED SPERMATOGENESIS
PREMATURE EPIPHYSEAL CLOSURE = SHORT STATURE
63
AUTOIMMUNE DESEASES ASSOCIATED WITH HYPOTHYROIDISM:
CELIAC DISEASE
PERNICIOUS ANEMIA
64
LEUPROLIDE
GnRH analogue used to treatmente of prostate cancer to suppress testorene levels
65
NOREPINEPHRINE CONVERTED TO EPINEPHRINE BY WHICH ENZYME?
PHENYLETHANOLAMINE-N-METHYLTRANSFERASE WHO IS ACTIVATED BY CORTISOL
66
CATECHOL-O-METHYLTRANSFERASE (COMT) AND MONOAMINE OXIDASE (MAO) INATIVATED:
CATECHOLAMINES
67
MAN WITH 1 TESTIS
ERECTILE FUNCTION: OK
SPERM COUNT: DECREASED
68
SEVELAMER
DECREASES ABSORPTION OF PHOSPHATE IN GI TRACT, AND IS USED TO TRAT HYPERPHOSPHATEMIA IN PATIENTS ON DYALYSIS.
69
POSTOPERATIVE HYPOPARATHYROIDISM SUPPLEMENTATION:
ORAL CALCIUM AND VITAMIN D
70
KETOCONAZOLE AND TESTOSTERONE
DECREASES TESTOSTERONE SYNTHESIS
71
SPIRONOLACTONE AND TESTOSTERONE
DECREASES TESTOSTERONE SYNTHESIS
72
SYNDROME OF INAPPROPITE ANTIDIURETIC HORMONE SECRETION
(SIADH) CAUSED BY DRUGS
CARBAMAZEPINE
CTCLOPHOSPHAMIDE
SSRI eg. Sertralina
73
CHERRY RED MACULA
NIEMANN PICK DISEASE
74
EXOGENOUS THYROXICOSIS (CAUSES)
* THYROID REPLACEMENT DOSING ERROR
*LEVOTHYROXINE SUPPESSION OF THYROID CANCER
* NONPRESCRIBED THYROID HORMONE USE (FACTITIOUS DISORDER, WEIGH LOSS SUPPLEMENTS)
75
EXOGENOUS THYROTOXICOSIS LABS
ELEVATED T4 AN THYROXINE LEVELS
(SUPPLEMENT ELEVATED T3 ONLY)
SUPPRESSED TSH
LOW SERUM THYROGLOBULIN
LOW RADIOIODINE UPTAKE
76
PACIENTS WITH THYROID CANCER NEED TO RECIVE LECOTHYROXINE HIGHER DOSIS, WHY?
BECAUSE TSH VAN PROMOTE GOWTH OF THE RESIDUAL MALIGNANT CELLS
77
SPHUNGOLIPIDOSES (7)
*FABRY DISEASE (XLR = X - LINKED RECESSIVE)
*TAY-SACHS DISEASE (AR)
*GAUCHER DISEASE (AR)
*NIEMANN- PICK DESEASE (AR)
*KRABBE DISEASE (AR)
*METACHROMATICC *LEUKODYSTROPHY (AR)
78
FABRY DISEASE DEFICIENCY
ALFA GALACTOSIDASE A
79
FABRY DISEASE ACUMMULATED SUBSTRATE
GLOBOTRIAOSYLCERAMIDE
80
FABRY DISEASE CLINC
ANGIOKATOMAS
PERIPHERAL NEUROPATHY
GLOMERULOPATHY
81
TAY-SACHS DISEASE DEFICIENCY
BETA- HEXOSAMINIDASE A
82
TAY-SACHS DISEASE ACCUMULATED SUBSTRATE
GM2 (GANGLIOSIDE)
83
TAY-SACHS DISEASE CLINIC
MACULAR CHERRY RED SPOT
PROGRESSIVE NEURODEGENERATION
84
GAUCHER DISEASE DEFICIENCY
BETA GLUCOCEREBROSIDASE
85
GAUCHER DISEASE ACUMULATED SUSTRATE
GLUCOCEREBROSIDE
86
GAUCHER DISEASE CLINIC
HEPATOSPLENOMEGALY
PANCYTOPENIA
BONE PAIN/OSTEOPENIA
87
NIEMANN PICK DISEASE DEFICIENCY
SPHINGOMYELINASE
88
NIEMAN PICK ACUMULATED SUBSTRATE
SPHINGOMYELIN
89
NIEMANN PICK DISEASE CLINIC
MACULAR CHERRY-RED SPOT
PROGRESSIVE NEURODEGENERATION
HEPATOSPLENOMEGALY
90
KRABBE DISEASE DEFICIENCY
GALACTOCEREBROSIDASE
91
KRABBE DISEASE ACCUMULATED SUBSTRATE
GALACTOCEREBROSIDE AND PSYCHOSINE
92
KRABBE DISEASE
PROGRESSIVE NEURODEGENERATION
PERIPHERAL NEUROPATHY
OPTIC ATROPHY
93
METACHROMATIC LEUKODYSTROPHY DEFICIENCY
ARYLSULFATASE A
94
METACHROMATIC LEUKODYSTROPHY SUBSTANCE ACUMULATED
CEREBROSIDE SULFATE
95
METACHROMATIC LEUKODYSTROPHY CLINIC
PROGRESSIVE NEURODEGENERATION
PERIPHERAL NEUROPATHY
96
MACULAR CHERRY-RED SPOT, WHAT´S DISEASE CAUSED THIS?
NIEMANN-PICK AND TAY-SACHS
97
