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FA17 Endocrine > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

Type I DM pathophys

A

type 1A - immune mediated

type 1B - idiopathic (no apparent cause)

beta cell destruction causes levels of insulin to drop, until 80-90% gone and intake of food causes no response from pancreas

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2
Q

immune mediated T1Dm

A

vigorous autoimmune response to infectious or toxic insult

circulating Abs to islet cells tag and destroy them

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3
Q

Type I DM epidemiology

A

occurs MC in juveniles with greatest peak of early adolescence (13-14)

highest rates are in Scandinavian descent

type I DM affects about 1/400-600, more common in males, HLA subtypes

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4
Q

pathophysiology of Type II DM

A

state of hyperglycemia and hyperinsulinemia

deficient B cell response to hyperglycemia and tissue insensitivity to endogenous insulin

mechanisms are further aggravated by resultant hyperglycemia

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5
Q

deficient B cell response to hyperglycemia

A
  1. at first, B-cell hyperplasia and increased insulin production
  2. overdriving of pancreas will compensate for some time
  3. progressive amyloid deposition leads to B cell insufficiency and failure
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6
Q

how does T2DM cause vascular disease

A

hyperinsulinemia, hyperglycemia, and increased free fatty acid production causes endothelial cell dysfunction, inflammation (which causes increased insulin resistance)

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7
Q

when should you consider testing diabetes patients for autoantibodies

A

2 of following:

age of onset <50 y/o

acute symptoms

BMI <25

personal family history of autoimmune disease

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8
Q

LADA

A

adult onset of T1DM

no rapid decline of beta cells like in normal T1DM

may find high GAD Abs

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9
Q

MODY

A

T2DM in young patients

no antibodies

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10
Q

symptoms of T1DM

A
  1. weight loss/polyphagia (first due to loss of water weight, then depletion of H2O)
  2. Polyuria (increased urination)
  3. Polydipsia (thirst)
  4. Blurred Vision
  5. Postural Hypotension
  6. Paresthesias
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11
Q

diagnostic testing for type I DM

A

C Peptide levels (low C Peptide levels - T1DM)

Autoantibody tests (specific to insulin, GAD, Zinc transporter)

Autoabs to beta cells

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12
Q

C Peptide Function

A

produced by pancreas when proinsulin is cleaved to insulin

lasts 3-4x longer in serum than insulin

T1DM have LOW
T2DM have HIGH

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13
Q

T1DM screening in children

A

annual screening for children of T1DM before 10, then once again in adolescence

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14
Q

treatment of T1DM

A

multispecialty team

dietician to control diet, exercise

life long insulin therapy (7.5% HgbA1c goal)

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15
Q

T2DM risk factors

A
  1. obesity (central)
  2. ethnicity
  3. life style choices
  4. genetics
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16
Q

symptoms of T2DM

A

typically asymptomatic (4-7 yrs before diagnosis)

recurrent/chronic vaginal candidiasis 
OB complications 
balantitis 
UTI 
acanthus nigrans 
unintentional weight loss
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17
Q

lab analysis of T2DM

A

fasting plasma glycose

finger stick (not diagnostic)

glycated HgB

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18
Q

T2DM treatment

diet

A

very rare if they stick to it

limit hyperglycemia, lower LDL, lower hypertriglyceridemia

increase fiber intake and artificial sweeteners

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19
Q

initial DM treatment

A1c > 7 but < 9%

A

metformin + lifestyle modification

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20
Q

initial DM treatment

A1c > 9%

A

dual drug therapy + insulin

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21
Q

initial DM treatment

A1c > 10%

A

insulin immediately

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22
Q

commonly used drugs

A 
metformin
sulfonylureas 
GLP-1 agonists
DDP-4 inhibitors 
SGLT-2 
insulin
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23
Q

Metformin (Glucogphage)

works by

A

decreasing hepatic production of glucose and increasing muscle uptake of glucose from serum

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24
Q

advantages of Metformin (Glucophage)

A

absence of CI

reduces A1C by 1.5-2%

modest weight reduction or stabilization

monotherapy- doesn’t cause hypoglycemia

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25
Q

disadvantages of Metformin

A

GI side effects
metabolized in kidney (avoided in CKD)
use with caution in those with IV contrast, hypotension, lactic acidosis)

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26
Q

sulfonylureas

A

stimulating pancreatic beta cells to secrete more insulin

regardless of blood glucose - hypoglycemia

effectiveness decreases over time, causes weight gain, increase mortality

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27
Q

incretin therapy

A

hormones released from gut with meal to promote insulin secretion

proliferation and growth of beta cells and prevent apoptosis

GLP-agonists and DDP-4 inhibitors

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28
Q

GLP-1 analogs

MOA

A

glucose dependent insulin release

reduce glucagon secretion

slow gastric emptying

may also stimulate beta cell recovery

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29
Q

disadvantages of GLP-1 analogs

A

administration is Sub Q

can cause hypoglycemia and pancreatitis

can be used in CKD up to stage 3B

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30
Q

DPP-IV

A

inhibits breakdown of endogenous GLP-1

weight neutral and less effective than GLP-1 RA bc rely on body to work normally

lower A1c by 0.5-0.7%

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31
Q

DPP-IV negatives

A

associated with pancreatitis

increase in URI’s

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32
Q

SGLT2-Inhibitors

A

Inhibits transporter that is responsible for reabsorbing glucose from proximal renal tubule

decrease the renal glucose threshold and increasing urinary glucose excretion

lower A1c by 0.5-1%

33
Q

benefits and negatives of SGLT-2 inhibitors

A

weight neutral and may predispose patient to weight loss

increased risk of genitourinary infection and some bone loss

must be dose adjusted in mild CKD (GFR <45)

risk of hypoglycemia

34
Q

thiazolidinoediones

A

lower blood glucose concentration by increasing glucose uptake in muscle and fatty tissues

decrease hepatic glucose production

do not cause hypoglycemia in mono therapy

lower A1c by 0.5-1%

weight gain and fluid retention

35
Q

risks of thiazolidinediones

A

contraindicated in patients with NYHA class III or IV heart failure

can be associated with bladder cancer

higher risk of fracture

36
Q

types of insulin

A

rapid acting

regular insulin

NPH

long acting insulin

ultra long acting insulin

37
Q

rapid acting insulin

A

absorbed more quickly than regular insulin

38
Q

regular insulin

A

same insulin your pancreas produces

39
Q

when are rapid acting and regular insulin typically used

A

mealtimes to provide coverage of prandial hyperglycemia

40
Q

basal insulins

A

give 1-2 injections daily to maintain all day control of blood sugar

NPH insulin
Insulin glargine and deter
Insulin degludec

41
Q

NPH insulin

A

inexpensive

req. two daily injections

42
Q

Insulin glargine and deter

A

require 1 (or 2) injections

nearly peak less

expensive

43
Q

Insulin degludec

A

daily injections provide steady state

lasts almost 2 days in the body

44
Q

how is insulin therapy given in type II patient

A

long acting basal bolus + rapid acting insulin to get best results

must have multiple injections

45
Q

complications of insulin therapy

A

insulin allergy
lipodystrophy
hypoglycemic reactions

46
Q

lipodystrophy

two types

A

complication of insulin therapy

atrophy (SC fatty tissue from immune run, loss of tissue)

Lipohypertrophy (SC of fatty tissue from repeated injection of insulin at same site)

47
Q

hypoglycemic reactions

A

most common in older diabetics, those on insulin pimp, pts with pumps nc

more likely to forget to eat or take meds

improper management of pump

48
Q

slow development of hypoglycemia symptoms

A

confusion, seizures

neuroglycopenic

49
Q

rapid development of hypoglycemia symptoms

A

catecholemine reactions

Epinephrine

50
Q

blunting of sympathetic system

A

body doesn’t have typical reactions to hypoglycemia

blunting of sympathetic system by age, beta blocker therapy, repeated hypoglycemia

increases risk of complications

51
Q

goals of T2DM treatment

A

obtain level of glucose control for individual pt without causing fq. hypoglycemia

52
Q

glycemic targets

HgB A1c 6.5%

A

for otherwise healthy patients with DM of short duration, w/o CVD, long line expectancy

53
Q

glycemic targets

HgB A1c 7% or less

A

pts with longer duration DM, those with significant CVD

54
Q

glycemic targets

HgB A1c 8% or Less

A

pts with severe comorbidities, limited life expectancy those with freq. hypoglycemia

55
Q

importance of early DM control

A

intensity glycemic control at diagnosis have continued benefits and prevention of complications

56
Q

treatment guidelines for T2DM HgB A1c

less than 7.5% @ diagnosis

A

lifestyle changes + metformin

57
Q

alternatives to metformin

less than 7.5%

A 
GLP-1 RA 
SLGT2-I 
DPP4
TZDs
Alpha glycosides inhibitors 
sulfonylureas
58
Q

treatment guidelines for T2DM HgB A1c

> or = to

A

lifestyle changes and dual therapy with metformin and another agent

59
Q

if pt on monotherapy does not achieve goal A1c in 3 months

A

dual therapy

GLP-1 RA
SGLT2 
DPP4-I 
TZDs 
Basal Insulin, alpha glucosidase, sulfonylureas
60
Q

if dual therapy with metformin and another agent are initiated and the patient does not achieve goal A1c in 3 months

A

triple therapy is indicated

61
Q

what is triple therapy

A

metformin

another first line agent

plus:

GLP RA, SGLT2, TZD (caution), Basal insulin, DPP4, alpha glucosidade inhibitors, sulfonylureas

62
Q

if triple therapy does not achieve goal of A1c in 3 months

A

insulin is added or intensified until goal is achieved

63
Q

patient has A1c > 9%

A

dual therapy is immediately initiated if patient is asymptomatic

Insulin +/- other agents

64
Q

surgical treatment for diabetes

A

pats with obesity (BMI > 30) should be considered

can be curative

lap band and roux-en-y gastric bypass

65
Q

lap band

A

band is surgically implanted around the stomach and restricted to limit gastric size, procedure is reversible, performed laparoscopically

66
Q

drawbacks of weight loss surgery

A

protein/calorie malnutrition

surgical complications

anastomotic leak (decreased protein and decreased healing)

67
Q

somogyi effect

A

notctural hypoglycemia leads to a surge of counter regulatory hormones hyperglycemia by 7am

glucose drops overnight then rises so hyperglycemic by 7 AM

68
Q

how do we fix somogyi

A

eliminate dinnertime intermediate insulin and give it back at a lower dose at bedtime

alternative give a snack at bedtime

69
Q

dawn phenomenon

A

secretion of GH overnight or cortisol surge causes increased insulin resistance and morning hyperglycemia

70
Q

health care management of diabetic (10)

A

PCP visit 3-6 months

exam of feet

screen for albuminuria, CAD/lipids

asses glycemic control

smoking cessation

ASA, BP control

routine cancer screenings

dental disease

vaccination

contraception and pre-preg

71
Q

diabetics and surgery outcomes

A

hyperglycemia is significant cause of M & M B/c:

all infectious issues are worse, poor healing of

typically go for < 180

72
Q

T2DM and glucose control

minor procedures or non-general anesthesia

A

meds up to day of surgery

on day of hold meds and resume after procedure

73
Q

T2DM and glucose control

general anesthesia

A

have their oral and non-insulin injectable meds held on day of surgery and added back as diet is advanced

sliding scale insulin in mean time

74
Q

T1DM/insulin dependent T2 and glucose control

surgery

A

reduced dose of usual insulin on morning of surgery

75
Q

T2DM and glucose control

long surgery

A

performed if long/ocmplex

simultaneous insulin got with dextrose containing IV solutions to avoid starvation ketosis

76
Q

gestational diabetes

A

pregnancy and hormones associated with it causes increased tissue resistance to insulin

screening b/t 24th and 28th week of pregnancy

increased risk of developing frank DM in 10-15 years

77
Q

diabetes and pregnancy

pre pregnancy

A

counseling and eval of HgbA1c

asses baseline renal, ocular, and CV disease

try to get HgB A1c to 6%

78
Q

first trimester and diabetes

A

congenital abnormalities

result from hyperglycemia during organogenesis in first 4-8 weeks

principal cause of perinatal fetal death (miscarriage)

79
Q

third trimester and diabetes

A

fluctuations in blood glucose grow worse

regular antepartum fetal testing is indicated to see how much longer the pregnancy can go

true to deliver b/t 38-39 weeks

FA17 Endocrine (10 decks)

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