NR 283 / NR283: Pathophysiology Exam 3 Review (Latest 2021 / 2022) Chamberlain College, Study Guides, Projects, Research of Nursing

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NR283 IPathophysiology IExam I 3 IReview

Chapter I 19 I Alterations Iof IHormonal I Regulation

- Addison’s Idisease I – I (A drenal I Insufficiency)-

- - I I A uto immune I diso rder I w here I body I creat es I antigens It hat I att ack I the I adrenal I glands

- - Idecrease I in I ho rmones Iin I adrenal I co rtex I such I as I co rtico stero id I and

I mineralo co rt icoid Isynthesis I and Ielevated I levels I of IA CTH I (loss I of Inegat ive I feedback).

- -Mo re I t hen I 90% I o f I adreno co rt ical I t issue I is I dest ro yed I causing I clinical I manifest atio ns.

- - I No I adrenal I glands I wo rking I resulting I in I hypo co rtiso lism I (lo w I levels Iof I co rt iso l)

I andIhypo aldost eronism

- - I Clinical I M anifest at io ns: I Weakness, I fatigue I hypo tensio n, I hyperkalemia I (^K),

I hypo glycemia,Ielevated IA CTH, Iskin Ichanges I(hyperpigment ation I and I vit iligo) I may Ioccur

- Cushings ISyndrome- I caused I by Ichro nic Iexpo sure It o Iexcess Ico rtiso l I (t oo I much I st eroid).

- Co rtical I hyperfunctio n I (hyperco rt iso lism) I – IDOES I NOT I invo lve I the I pit uit ary I gland.

- Hypo kale mia I(decrease IK), Iincrease Iin INa+ Iresulting Iin I^BP, Ihyperglyce mia,

Imet abo licIa lka lo sis I (decrease I H+)

- Weight I gain I is I the I mo st I co mmo n I feature I and I result s I fro m I the I accumulation I o f I adipose

Itissue I in It he It runk, Ifacial, I and I cervical I areas I (t runcal I obesit y, I moon I face, I and I buffalo Ihump)

- Glucose I int o lerance I o ccurs I because I o f I co rtiso l-induced I insulin I resist ance I and

I increasedIgluco neo genesis Iand Iglyco gen Ist o rage I by It he Iliver.

- caused I by

Ieither

Iexcessive

Icortiso l-

likeImedicat

ionIsuch

as

Ipredniso ne Io r

a Itumo r It hat

Ieither

Ipro duces Io r

Iresults I in

Ithe Iproductio

n IofIexcessive

Ico rtiso l Iby

Ithe I adrenal

Iglands.

- Cases I due It o I a I pituit ary I adeno ma I are I kno wn I as I Cushing's Idisease.

Acromegaly- I Hypersecretion I of I Growth I Hormone-

o A I d isord er Iin I ad u lts I in I wh ich Ithe I p itu it ary Igland Ipro duces Itoo I much Igr owth Ihor mon e

- Resu lts I fro m Icon tinuous Ie xpo sure Ito Ih igh Ile ve ls Io f I gro wth Ihor mon e I (GH) I and Iinsu lin -like I gro wth I factor

I 1 I (IGF-1); Iit Ial mo st Ialways Iis Ic au se d Ib y Ia IGH Isec re t in g Ip itu it ar y Iad e no ma.

-

Pheochromocytoma I- IChromaffin Icell ITumors

- A Ihor mone - secret ing I tu mor I (ben ign) I th at Ican Ioccur I in I the I adren al I glands I (neuro endocr ine Itu mo r

I of Ith e I medu lla Io f Ith e Iadren al I glands).

- adr en al I gland I r ele ases I hor mone s I th at I cau se I per siste nt I or I ep iso dic I high I b loo d I pre ssur e,

I head ache s, Id iap horesis, Ip alp it atio ns

- Symp at het ic I p ar aganglio mas I cau se I e xcessive I p roduct ion I of I nore pineph rine I and I e pinephr in e.

- Tu mor I re le ases I catecho lamine I (Ep i I & I N E) I e pisod ically I so I sympto ms I occur I in I paro xysmal I (co me I and I go )

- Catecho lamine Ib re akdo wn It o I met ab olit es I th at I ar e Itested I in Iur in e:

- VM A I & IHVA Ithe I VM A I wit h I be Iincreased.

Alterations IinIAdrenal IFunction

Thyroid I Dysfunction- I Hypothyroidism- I Underactive I Thyroid I Gland

- deficient Ipro duction Io f ITH Ib y Ithe Ith yro id I gland

- DX I w/ I b lood It est I loo ks Iat IT3, IT4, I an d ITSH ILe ve ls

- T3 Ior I T4 Ibo th Io f I wh ich Ire gu late I me t abo lism.

o thyroid^ Ig land^ I^ predominant ly^ Isecretes^ Ithyroxine^ I^ (T 4 ),^ Iwhich^ Iis^ Iconverted^ I^ into^ Itriiodothyronine^ I^ (T 3 )^ I^ in

Iother Iorgans Iby Ithe Iselenium-dependent I enzy me Iiodothyronine Ideiodinase.

o Triiodothyronine Ibinds Ito Ithe Ithyroid I hor mone Ireceptor Iin Ithe Inuc leus Iof Ic ells , I where Iit Istimulates Ithe

Iturning Ion I of I particular Igenes Iand Ithe Iproduction Iof Ispecific Iproteins

- too I litt le I iod in e I in I the I diet I is Ithe I most Ico mmo n Ic ause Io f I hyp oth yroid ism

- Primary I H ypothyroidis m I – I Autoimmune I T hyroiditis - I loss I of I thyroid I function I leads I to

I decreas eIproduction Iof I TH I and Iincreas ed Is ecretion I of ITS H I (thyroid-s timulating I hormone) I and

ITR H.

o Common I reas on I is I loss I of I thyroid I tiss ue Iafter Is urgical I or Iradioactiv e Itreatment.

- Secondary I H ypothyroidis m - I pituitary I failure I to I s ynthesize I adequate I amounts I of I TS H I or I lack

I ofIT R H

o surgical Iremov al Iof I the I thyroid, I and I radiation Itreatment

Parathyroid I Dysfunction- I Hyperparathyroidism I – I Excessive I Secretion I of

I ParathyroidIHormone I(PTH) Iby Iparathyroid Igland

- Hyperkalemia I^Ca+ I and IHypophosphatemia

- Prim ary- I Problem I with I parathyroid Igland

o Noncancerous Igrowth I“Adenoma” I(most Icommon Icause)

o Hyperplasia I of I gland

o Cancer Igrowth

- Secondary I– IDisease Icausing Iparathyroid Ito Imess Iup

o Chronic Irenal Ifailure; I over I working Iof I parathyroid Igland I(m ost I comm on)

o Hyperkalem ia; I low I levels Iover I work Ithat I parathyroid

o Vitam in I D I Deficiency

Diabetes IMellitus I(DM)- I a Igroup Iof Imetabolic Idisease Icharacterized Iby IhyperglycemiaIresulting

Ifrom Idefects Iin Iinsulin Isecretion, Iinsulin Iaction, Ior Iboth.

- Body I cannot I properly I use I insulin I leading I to I hyperglycem ia

Type I I I Diabetes: I beta- I cell I destruction, I usually I leading I to I absolute I insulin I deficiency I (insulin-

Idependent I diabetes)

- Most Icommon Ipediatric Ichronic Idisease

- Ketones Iin Iurine

Type III IDiabetes: I I ranging Ifrom I predom inantly I insulin Iresistance I with Irelative I insulin I deficiencyIto

Ipredom inantly Ian I insulin Isecretory I defect I with I insulin Iresistance. I Cells I stop I responding I to I insulin

I “insulin I resistant” I glucose I hangs I in I the I body, I pancreas I thinks I you I need I insulin I to I m akes Im ore,

Iover I secretion I of Iinsulin I(hyperinsulem ia)

- Related Ito I lifestyle I(poor I diet, Iover Iweight, Isedentary,

Igenetics) INorm al I Feedback ILoop:

Diabetes IMellitus- IAssessment Ifindings Iin Ihypoglycemia- I reduction Iin Iplasma Iglucose

Iconcentration Ito Ia Ilevel Ithat Imay Iinduce Isymptoms Ior Isigns Isuch Ias Ialtered Imental Istatus

Iand/orIsympathetic Inervous Isystem Istimulation.

Diabetic Iketoacidosis I– I A Iserious Idiabetes Icomplication Iwhere Ithe Ibody Iproduces Iexcess

IbloodIacids I(ketones)-

- acute, I major, I life-threatening I com plication I of I diabetes I that I mainly I occurs I in

I patientsIwith I type I 1 I diabetes, I but I it I is I not I uncommon I in I some I patients I with I type I 2

I diabetes Iwith Isever Iillness.

- disordered I metabolic I state I characterized I by I hyperglycemia, I ketoacidosis,

I andIketonuria.

- comm on I early I sym ptom s I of I DKA I are I the I insidious I increase I in I polydipsia I and I polyuria

o Po lydipsia I – Icell I dehydrat ion - Ifrequent Idrinking I fro m I feeling Io f Ithirst

o I Po lyuria I– Io smo tic Idiuresis Ito o Imuch Iglucose Ifo r Ikidneys Ito Ireabso rbed It o

Ifrequent Iurinat io n.

- Malaise, I generalized I weakness, I and I fatigability

- tachycardia

- Altered Iconsciousness

- Kussmal IBreathing I– Irespiratory Isystem Itrying Ito Icompensate Imetabolic Iacidosis