L15 DM 2 Flashcards

1
Q

LO2: main diffs T1 and 2. both hyperg.

A

T1:
- cant prod insulin as beta cell fail. autoimm/non. prog loss all/most beta.
- most comm type in yng, but can occ any age.
-rap fatal w/o tx. need insulin tx.
T2:
- insulin prod adeq but resis prev func. not work at R.
-effs LOT peop, us older.
-slow prog loss beta along with disords of insulin sec and tiss resis to insulin.
-may be present long time bef symp and diag.
-may not init req insulin tx but us event do.

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2
Q

LO3: desc and expl typ patt present T1 and 2

A

-hyperg symps:
polyuria and polydipsea- osmot duiresis as over 10mM filt out gluc to kidney.
blurr vis, alt refrac index, gluc into vitreous fluid.
UG infec- thrush as gluc in urine.
-symps of inadeq energ util- tired, weak, lethergy, weight loss as fat breakd.
symp sev deps on rate incr BG and absol lev.

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3
Q

LO3: but specif diag

A

-diag lab test:
fasting BG. oral gluc tol 2hr blood. HbA1c % sat RBCs gluc att, show BG while cell in circ, T2 only!
need symp+1 abn test OR asymp +2.
-T1- can present with HLA markers and auto Ab w/o insulin or gluc abn. subseq dev imp gluc tol then DM then insulin dep.
T2 - can present insulin resis then decr prod=imp gluc tol then DM init diet and tab contr then insulni dep.
-diag criteria- fasting ven PG over 7mM. or
rand ven PG over 11.1mM (esp for T1 as rap symp onset) or
elev HbA1c over 6.5%, T2 only. or
oral gluc tol- fasting ven PG over 7 and/or 2hr ven PG over 11.1. rarely used excep preg.
-levs picked as sudd incr in % pt with complics.

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4
Q

T1

A

-diff rates btw countries. poss genet predisp interac with env. eg enterovir eg coxsackie. water nitrates. not breast fed etc.
-killer lymphocs and mac att and destr beta var rate. presence of Ab- ag iselt cell, GAD65 beta prot.
-genet predisp assoc with genet markers HLA DR3 and DR4.
-strng seas var sugg vir/infec link as trigg to rap deterior.
-classic yng person recent hx vir infec. triad of symps:
polyuria- healthy nephron all gluc filt from blood reabs at end proxim sec tobule- isosmotic. in DM lot gluc in blood filt by kidn not all reabs. =osmot load on nephron= less water reabs to maint isosmot char. excret.
thirst- as excess water loss and osmot effs of gluc on thirst centres.
weight loss- fat and prot metab as insulin absent.
rap onset symps. imm supp if BG high long. often v ill.
-90% diag under 30 but can occ any age.
-lack insulin= decr upt gluc to adip and skel musc, decr stor in liv and musc. and incr glycog breakd and gluconeogen in liv. prom lipolysis and prev clear FA. glycosuria. prog to ketoacidosis. prev aa into cell. incr prot catab.
-diag- v high ven PG. ketones in urine by strip over 1mM.
-tx- exog insulin immed. subcut injec ev day. amnt req var. pump. fast death if untx. ideal shuld mimic norm chars- peak foll meal. injec bef/after eat. intrmed/rap act. req educ. need incr dose eg infec/trauma or risk acidosis. soc and psych impact. diet managemn and exerc. monit BG reg. know symps hypo. educ fam.

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5
Q

LO4: expl seq events lead to ketoacidosis in uncontr diabetic.

A

insulin lack proms lipolysis= incr FFA. prod ketone bods high amnts overcome buff capac= acidosis.
high beta oxid in liv coup with low insulin/anti insulin ratio= prod lot ket bods eg acetoacetate, acetone and beta hb. smell acetone breath. H+ assoc with ketones prod ketoacidosis- hypervent, naus, vom, dehyd, abdo pain. test ketones in urine.

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6
Q

T2

A
  • rel comm n all affluent pops. us older and fat. often present long bef diag. good ev for genet predisp but rec ev imm inv. at diag pt have 50% beta cells, often decr to none= incr BG.
  • may present with triad but more likely var symp eg lack energ, persis infec esp thrush or feet, slow heal, vis imp.
  • dual pathol- insulin resis and rel insulin lack, event beta fail. both necess. obes biggest cause insulin resis. fat= inflamm in organ. genet and env facs. env not genet, eat less kcal but also less exerc.
  • obes= insulin resis first.= more insulin sec. panc exhaust then hyperg. first pahse sec lost then basal insulin sec. amyloid type prot deposits in islet cells=beta fail.
  • 7 day fasting BG norm in T2 w/o weigth loss. mass fall liiv fat cont and return norm insulin sensit. over 8wk first pahse insulin rel and max rel after meal norm. decr panc fat. so poten reversib metab disord precip by chronic intraorgan fat.

low kcal decr fastin ggluc, HGP, liv TG and panc TG. and incr insulin resp.
post bariatric surg same effs. sudd decr fat to store= fat mobil from liv and other ectopic sites first bef visc or subcut. norm heapt insul sensit.
-var present. can be triad. poss asymp. routine screen. incr in yng. lot obese.
-diag- no ketones in urine as beta still make some insulin. able to supp lipolysis not contr gluc.
-if untx grad worsen symps. hyperg, inadeq energ use. complics eg infec, BV.
-tx- oral hypoglycaemics eg sulphonylureas incr rel from beta, or reduce resis partic metformin reduces gluconeogen. diet and exerc.
some orals incr sensit. sod gluc transp inhibs block reabs gluc in kidn so out in urine. glycation light peps stim insulin rel and make feel full, slow gastric emp, decr weight. exerc impr sensit w/o weight loss. lot pt dont take as prescribed.

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7
Q

LO1: desc cond of DM

A

-diab= when BG too high and over yrs= dam small and large (brain, heart, lower limb) BV= premat death from CVD.
incr prob. 3.9m UK, 90% T2. lot undiag, mostly T2.
due to insulin defic, resis, or both.

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8
Q

LO5: expl conseqs and causes hyper and hypog.

A

-persis hyperg abn gluc metab can harm cells. upt of gluc into periph nerves, eye and kidn not req insulin and is determ by ocnc. so in hyperg intracell conc incr and gluc metab by alodse reductase forms sorbitol. depeletes NADPH, incr S-S form. sorbitol cause osmot dam.
incr non enz glycation of plasma prots eg lipop. gluc reac with free amino grps form cov bonds. extent deps on gluc conc and t1/2 of prot. alts net charge of 3d prot.
glyctaed HbA1c. gluc reac with termin val of Hb. % indics contr. av conc over past 2-3mnth. norm 4-6%.

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9
Q

LO6: desc outl princips of managem DM.

A

-

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10
Q

LO7: expl princip and prac of using Hb glycosylat as index of BG contr.

A
  • monit well being, capill BG with targs, other vasc RFs eg BP, lips, smok, exerc, sruv chronic complics.
  • glycated Hb reliable indic of contr.
  • more impact if reduce from vv high than small reuc from lower.
  • retinop screen ev yr. neurop screen and educ. nephrop check urine prot and kidn func.
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11
Q

LO8: list comm LT s/e of DM incl CV probs, diab eye dis, and kidn dis, diab neuropathy, diab foot.

A

-macrovasc- stroke risk, MI risk, poor periph circ eg feet.
MICROVASC:
-diab eye dis- change lens due to osmot effs=glaucoma, poss cataracts. more imp is retinopathy- dam to BV in retine can blind. vess leak and form prot exudates in retina, or can rupt and bleed eye. prolif retinop when new vess form, are weak and bleed eas.
-diab kidn dis- nephropathy. dam glomeruli, poor blood supp as aff vess, or UTI dam. early sign is microalbuminuria.
-diab neuropath- dam periph nerves= eg loss sensat, alt func ANS.
-diab feet- poor blood supp, nerve dam and incr risk infec.

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