Endocrine Flashcards
Endocrine organs
Hypothalamus and pit.
Thyroid
Parathyroid =Phosphate and Ca2+ metabolism
Adrenal gland
Endocrine dis.
Hypotha./pith. -DI -SIADH -Sheehan synd. Adrenal gland -addison dis. -cushing synd. -pheochromocytoma Thyroid -Goiter -Thyroiditis -graves dis. Parathyroid -osteomalacia -HyperCa2+emia
Ant. and Post. pituitary
Neurohyophysis=post. pit. (N.) -Diabetes insipid. -SIADH Adenohypophysis=ant. pit. (hormones) -adenomas -sheehand synd.
Neurohypophysis-DI
HypoADH=INCRE. H2O secretion
-hyperNa+emia and incre. osmo.
Caused by head trauma, tumors, inflamm. of hypoth. pit.
2 types
-central DI=insuff. ADH
-Nephrogenic DI=ADH insensitivity (kid. not respond to norm. ADH level)
Neurohypophysis-central DI
S/S -incre. urination and thrist (b/c incre. Na+) -cause life threatening dehydration Tx -mild=drink more H2O -severe=exogenous ADH(vasopressin)
Neurohypophysis-synd. of inappropriate ADH secretion (SIADH)
Caused by -ADH secreting tumor (small cell lung carcinoma) -drugs -CNS dis. Incre. ADH -incre. H2O -Dilute blood=hypoNaemia Clinical -HypoNatrimia -ceberal edema -Neuro dysfunction (~ H2O intoxication) Tx -inhib. drug -tx tumor -depend on CNS issue tx cuase
Adenohypophysis=sheehan synd.
Ant. pit. hypertrophy w/o angiogen.=minor anoxia–>ischemic necrosis of adenhypohysis
Incre. sensitivity of cells to low BP
-hypovolemic shock due to hem. from delivery
:during prego. ant. hypergrophic b/c incre. FSH and LH
-infarct in ant. pit.
-necrosis–>fibrosis
Adenohypophysis=sheehan synd. s/s
Ischemic tissue replaced by fibrotic nodule=postpartum hypopituitarism -->decre. adenoph. function Lack of horm. -FSH/LH=amenorrhea/infertile -prolactin=no lactation -TSH=hypothyroid -MAS/POMC=pale
during prego.=hypertrophic ant. pit. b/c of which horm.
Incr. FS, LH and PRL
Need incre. horm. to support prego.
-HCG + product of horm.
-Progesteron is produced by corpus luteum
-inhib. of additional follicle
LH and prolactiin
-Support copus luteum function
-PRL inhib. GnRH=decre. LH
:Prog. and estrogen inhib. it until parturtion
-PRL release stim. by estrogen but activated when estrogen decr.
why is adrenal gland sim. to hypoth/pit.
N. and glandular tissue(horm.)
Adrenal gland and horm.
Cortex=steroid hom.
-adrenocorticotropic/tropic horm. form adenohypot.
Medulla=catacholamines/peptide homr. (N. epi/epi)
-release by N. sig.
Adrenal gland dis.
Addison dis.=1mry chronic adrenocortical insufficiency Cushing synd. -AKA hypercortisolims -Exogenous and endogenous causes Pheochromocytoma -Medullary tumor
Addison Dis. is caused by
Autoimmune adrenalitis(MC) Infection=TB/fungal AIDS metastatic cancer
Addison dis. -autoimmune adrenalitis
Auto-antBD to steriod synth. enzymes
-immune syst. distroys steriod producing cells in adrenal cortex
Assoc. w/ autoimmune polyendocrine synd. (APS)
-dis. destroying multiple endocrine tissue/organs
-MC=APS1
:AutoantBD to IL-17 and 22(produced by THC)
:Chromo 22 single gene mutation
*gene product= AIRE so the thymus prot. expression to remove autoreactive T cells to adrenal cortex antGN
Addison Dis.-gross appearance of gland
Varies
Autoimmune=shrunk
infection=inflam. rxn
Cancer=enlarged w/ tumor
Addison dis. Histo.
extensive mononuclear infiltrate nd lost most of cortical cell
Addison Dis. S/S
Notice when 90% is lost 1st=prog. wk w/ easily fatigue GIT b/c decre. cortisol=inhib. brk dwn fat, carb, and prot. -anorexia, nausea, vomit and wt loss, diarrhea Skin hyperpig. (~sheehan) -no cortisol=anti. pit. need ACTH -incre. POMC brkdwn to incre. ACTH -POMC=MSH frag. Decre. aldosterone (cortex)=decre. Na while incre. K+ -Decre. vol. and hypoTN Decre. glucocorticoids leads to hypoglycemia and lack of gluconeogenesis -Cortisol incre. gluconeogenesis -Stress=adrenal crisis :No cortisol=no gluconeogenesis :fatal :Cont' vomit :abdo. pain :hypoTN :vascular collapse :coma
What can glucocorticoids produce
Hyperglycemia
Glucosuria
2ndry diabetes
decre. immune
Aldosterone usual responsible
incre. Na reab .
incre. K+ and H+ secretion
How can cortisol cause vasconstruction
catecholamines
Cushing synd.
Chronic exposure to high blood glucocorticoid levels
MC causes=incre. ACTH secretion by adenohypophysis
Types
-Iatrogenic
-Endogenous (non-iatrogenic)
Cushing synd.-Iatrogenic
Medical admin. of glucocorticoids to tx non-endocrine disorder Immiune suppression for atutoimmune, transplant pt.
Cushing synd.-endogenous type
ACTH depend
ACT. indip.
Cushing synd.-endogenous ACTH DEP.
Cushing dis.=ACTH secreting pt. adenoma
-incre. ACTH=incre. cortisol (bilat. adrenal hyperplasia)
-monoclonal microadenomas
-incre. cortisol cuases
:decre. CRH (hypoth.)
:decre. ACTH (directly and b/c decr. CRH to pit.)
:inhib. GH, TSH gonadotropin release
:directly affect insulin prod. and gluconeogen in liver
Ectopic ACTH syn.
-spont.
-MC=paraneoplastic cushing synd.
:tumor outside adrenal cortex=small cell lung carcinoma/bronchial carcinoid tumor
-incre. ACTH=incre. cortisol (adrenal hyperplasia)
Cushing synd.-endogenous ACTH INID.
Adrenal cortical tumor=ACTH or ACTH like peptide
-w/in adrenal cortex=cn be tumor or nodular hyperplasia
Cushing synd. and adrenal gland changes
Depend on cuases Iatrogenic=cortical atrophy -exogenous GC decre. ACTH -no sitm.=atrophy Cushing dis.=diffuse hyperplasia ACTH indi.=nodular hyperplasia Adenoma/carcinoma=causative
Cushings synd. and pit. changes
Dnt depend on cuase
Corticotorpic basophils=paler, fill w/ keratin filaments (crooke hyaline change)
Cushing synd.-his.
pig. micronodules
Lipofuscin-containing cells=pig. nodules
Cushing synd.-S/S
HTN
WT gain
-centralized (trunk/post neck)
Selective atrophy of fast-twitch fiber atrophy=proximal limb. wk
Glucocorticoid
-hyperglycemia, glucosuria and 2ndry diabetes
incre. gluconeogen and decre. gluc uptake/immune
Cushing synd.-catabolism
Inhib. fibroblast funciton w/ collagen -Fragile skin w/ poor wound healing -stria skin (esp. on abdo.,) -central obesity -~ stretch marks Bone=osteoporosis
Pheochromocytoma-basic
Benign tumor in chromaffin cells in adrenal medulla
-affect adrenorecp, for N. epi.
Pheochromocytoma-S/S
Tachycardia=pound heart
-@ B1 recp.=incre. HR/contractaility
Cold hand/feet
-@a1 recp. w/ vasoconstriciton=decre. BF
Hot feeling b/c no dissipate heat
Throbbing headache
-sever HTN and incre. HR, contrast and vasoconstriction
Nausea/vomit b/c decre. BF and sm. muscle relax
Visual disrupt. @B recp.
-alpha1 Recp.=dialte pupile
Thyroid dis,.
Goiter=enlarged thyroid gland
Thyroiditis=inflammation
Graves dis.=MC cause of persisitent hyperthyroidism
-MC in women
Goiter
Impaired synth. of thyroid horm. -MC iodine insuff. Decre. T3/4 -induce TRH and TSH release -Incre TSH=thyroid hypertrophy
Thyroid horm. pord.
Thyroglobulin -produce in RER -glycosylated -exocytose into follicular lumen Iodide from blood -transported by symptorter -in lumen=oxidation Throglobulin brk dwn=T3/4 w/ iodine
2 types of goiter
Simple=diffuse and not toxic -endemic :More than 10% of population :Usually related to diet -sporadic :MC in women @/after puberty :not really explained Multinodular =repeated hypertorphy episode
Goiter-dietary causes
Insuf. Iodine
-MC in mountain regeions b/c decre. seaH2O
-decre. supplementation
Goitrogenic food intake
-certain vegies
:cruciferous(cabbage, cauliflower, cassava root-pastacio)
-cassava root has thiocyanate that inhib. iodine transport
Goiter consequences
Compressive synd.
- airway obstruction b/c thyroid infront of neck
- compression of large blood vs.
- difficult y swallowing (dysphagia)
Goiter-tx
surgery to remove excess tissue
Thyroiditis-types
Hashimoto
Granulomatous
Subacute lymphocytic
Hashimoto thyroiditis
Autoimmune disorder/genectic omp. -antBD against thyroglobulin and thyroid peroxidase (prod. of iodinated thryoglobulin) Unknown exact cease -abnormal Tcell -thyroid antGN exposure Histo. -monoculear infiltrate -atrophic follices -huerthle cells=DX for stressed follicular cells (eosin)
is hashimoto thyroidits=hypoth.
Yes Inflammation=enlarge thyroid -diffuse or nodular(cancer) Destroy parenchyma=decre. T3/4 (~1ry hypothyroid) -@ 1st ~s/s as depression (vague) :fatigue :apathy :mental sluggish -slower metab. -cold intol. -decre. symp. N. activity(constipation/decre. sweating) -decre. BF=pale/cool skin -decre. CO=SOB, decre. exercise capability -ECM accum. in skin (hylornic acid) :Non pitting edema :enlarg tongue :deep voice Nonspecific s/s=serum dx -serum TSH INCRE. (import.) -serm T4 DECER.
Graves dis.=hyper thyroid
yes
Graves dis.
Autoimmune
-genetic susceptibility linked to mutation in immune function
-antBD + thyroid
:dnt recog. thyroid as self antGN @ TSH Recp.
:MC antBD
*IgG agonist for TSH Recp.
#+follicular cell to incre. horm.
*thyroid growth +IgG
#follicular cell hyperplasia
*TSH-binding inhib. IgG
#decre. activity and no hyperthryo.
TRH–>TSH =thyorid stim. horm. (thyrotropin)
-TRH inhib. by T3/4
Graves dis.-clinical
Thyroid hypertorphy=tx destroy excess tissue (diffused)
Extra-thyroidal (beta-adrenergic effects)
-generalized lympohid hyperplasia
-cardiac hypertrophy iscehmia
-exophthalmos-edema in tissue around eye
:also fibrosis, lympohcyte infiltrates
-dermal thickening –>lymphocyte infiltrate
Localized infiltrate demopathy (skin)
Graves dis.-clinical
Thyroid hypertrophy=tx destryo excess tissue (diffused)
Extra thyroidal (beta Adrenergic effects)
-Generalized lymphoid hyperplasia
-cardiac hypertrophy/ischemia
-exophthalmos=edema in tissue around eye
:also fibrosis, lymphocyte infiltrates
-dermal thickening=lympohcyte infiltrate
localized infiltrate demopathy (skin)
Parathyroid-release PTH
PTH release by cheif cells -Ca2+ recep. located :GPCR messages that enough Ca2+=no PTH -low Ca2+=release PTH :bind to + osteoclast to incre. Ca2+ and incre. Phosphat. in kid.
Parathyroid dis. types
Osteomalacia=sk. dis. assoc. w/ vit. D def.
Hypercalcemia=clinically apparent is most often due to malignancy
-Asymp. is assoc. w/ hyperparathyroidism
Parathyroid-osteomalacia
Excess persistent osteoid -osteoblast dnt have Vit. D NO mineralization -Vit. D def. :no sun :freq. prego w/ children followed by lactation (not enough of Ca2+) -HypoCa2+emia :Renal disorder :malabsorp Ca2+ def.
Parathyroid-osteomalacia clinical
Soft bone=incre. brk
~osteoporosis
Children w/ rickets
Tx=Vit D supplement (ie milk)
Parathyroid-Hypercalcemia
1ry hyperparathyroidism -95%=solitary parathyroid adenoma -incre. PTH production incre. blood Ca2+ by promoting resorption from bone :cnt crontral chem. of Ca2+ recpt. 2ndry hyperparathyroidism -MC w/ chronic renal failure :Vit D. conversion :re-absorption -any hypocalcemia will cause 2ndry hyperparathyrodisim
Parathyroid-hyperparathyroidism and morphologic changes
Bone -incre. osteoclast :Erode Bone matrix=mobilize Ca2+salts -~ osteoporosis=thinner trabeculae) -Advanced dis. :thin bone cortex :marrow contains fibrosis and clumps of irregular cells that mimic neoplasms Kidney -Formation of kidney stones -Calcification of instertitium and tubules
