Diabetes Mellitus Flashcards
1
Q
diabetes mellitus
A
- wide-spread metabolic disease
- hypoactivity of insulin (secretion or action of insulin defective)
- impacts almost every cell and area of body (CV, renal, ocular, NS)
- cmplx will develop, with Tx, it can be delated
- life-threatening if not controlled
2
Q
absolute deficiency
A
absence of insulin or very little amount
3
Q
relative deficiency
A
insulin present, but not very effective
4
Q
classifications of DM
A
- type 1
- type 2
- LADA
- MODY
- gestational diabetes
- drug-induced diabetes
5
Q
type 1 DM
A
- absolute insulin deficiency –> beta cells producing insulin are absent or damaged by autoimmunity
- 2 subgroups
6
Q
type 1A DM
A
- immune mediated
- 90-95%
- autoimmune destruction of beta cells
7
Q
type 1B DM
A
- not autoimmune –> idiopathic destruction of beta cells
8
Q
type 2 DM
A
- less severe
- beta cells can still produce insulin
- receptors do not respond to insulin
- 90%
9
Q
latent autoimmune diabetes of the adult (LADA)
A
- type 1 DM developing gradually and appearing later in life
10
Q
maturity onset diabetes in the young (MODY)
A
- type 2 DM developing in early life d/t poor lifestyle
11
Q
gestational diabetes
A
- hyperglycemia during pregnancy, but normoglycemic postpartumu
12
Q
drug-induced diabetes
A
- ex. steroids
13
Q
etiology for both types of DM
A
- complex trait (polygenic - requiring multiple defective genes, & environmental factors such as viral infection)
14
Q
type 1 etiology
A
- MHC genes on Chr 6 (40% have defective MHC genes)
- insulin gene on Chr 11 (10% have defective I gene)
- T cell hypersensitivity to Beta cell antigen
- familial risk (10x) increased –> if your sibling has type 1 DM, you are 10x more likely to develop it
15
Q
MHC genes of Chr 6 (type 1 etiology)
A
- codes for proteins that sit on the surface of cells to show them pathogens (so that defense cells can recognize pathogens)
- MHC = major histocompatibility complex –> the cell surface proteins used in the acquired (non-innate) immune system to recognize foreign molecules
- MHC binds to peptide fragments of pathogens and display them on the cell surface for recognition of T cells
- MHC II on antigen presenting cells and presents extracellular peptides
- MHC I holds self antigens identifying the cell
- some viruses reduce the amount of MHC I so they can “hide” from defense cells and not be detected as foreign. In response to his, NK cells destroy all cells with reduced MHC I
16
Q
insulin gene on Chr 11 (type 1 etiology)
A
- codes for a protein that regulates division and Fx of beta cells
- impacts insulin production
17
Q
type 2 etiology
A
- strong, unclear genetic component
- MODY = type 2 DM developing in early life d/t poor lifestyle
- in 50% of cases, it is the glucokinase gene on Chr 7 that is affected
18
Q
glucokinase gene on Chr 7 (type 2 etiology)
A
- this gene codes for a protein (ex. glucokinase Es)
- glucose w/ the addition of phosphate is said to be phosphorylated, which allows glucose to be converted into glycogen and stored
- phosphorylation is brought on by glucokinase, but if the gene coding for this liver Es is defective then phosphorylation cannot occur. Insulin will take in glucose, but it will go right back into the bloodstream, resulting in hyperglycemia
19
Q
prediabetes
A
- a warning sign for DM
20
Q
prediabetes metabolic changes
A
- impaired fasting glucose (IFG) = 6.1-6.9mmol/L
- glucose tolerance test (GTT)
- increased HbA1C (6-6.4% is prediabetes, 6.5%+ is diabetes)
21
Q
impaired fasting glucose (IFG)
A
- after an overnight fast, BG is measured; fasting is a more precise estimation of glucose uptake, needed to Dx DM
- 3.5-5.5mmol/L is normal fasting glucose
22
Q
glucose tolerance test (GTT)
A
- 2hr OGTT = oral glucose tolerance test (ingest glucose and monitor plasma levels for 2 hrs)
23
Q
increased HbA1C
A
- A1C is a subclass of HbA (adult Hgb)
- measurement of glucose binding to Hgb (the higher the levels of glucose, the more that will bind to HbA1C)
24
Q
metabolic syndrome
A
- predisposes individual to cardiovascular disease & Type 2 DM
- 70% of ppl w/ T2 DM have metabolic syndrome (if you have metabolic syndrome, but do not have T2 DM, you will develop it eventually)
25
Q
metabolic syndrome features
A
- abd obesity
- HTN
- hyperlipidemia
- IFG
- IGT
- insulin resistance
26
Q
type 1 characteristics
A
- early age onset (exception: LADA)
- progressive autoimmune destruction of beta cells (up to 90% destruction –> overt DM) = absolute insulin deficiency
- insulin autoantibody production –> target beta cell antigens
- islet cell autoantibody production –> target islets of Langerhans antigens (not just beta cells)
- insulitis = swollen/edematous islets of Langerhans d/t infiltration of lymphocytes
27
Q
type 2 characteristics
A
- adult onset (exception: MODY)
- beta cells intact (# is not diminished, no autoimmunity)
- insulin is either not being produced at the right time, not enough is being produced or the insulin
is not effective at the target cells = relative insulin deficiency - insulin resistance = in hyperglycemic states, the presence of insulin does not induce a hypoglycemic response
- delayed secretion of insulin
- defective target cell response
- hepatic glucogenesis
- insulin levels in body in T2 can be normal, dec or in –> insulin cannot b used to make a Dx as can in T1
- results from altered gened
28
Q
hepatic glucogenesis
A
- formation of glucose (breakdown of glycogen in liver) b/c glucose not effective at site of cells are deprived of glucose, so liver releases more glucose (furthering hyperglycemia)
29
Q
patho of type 1 and type 2
A
- some type of insulin deficiency (absolute or relative)
- insulin deficiency –> impaired glucose utilization and hepatic glucogenesis (liver releases more glucose, which is compensatory but is not beneficial) –> hyperglycemia (11-67mmol/L) –> renal threshold of glucose exceeded –> glucosuria (excess sugar in urine) –> inc osmotic pressure in filtrate –> fluid enters filtrate –> polyuria (abn large amounts of urine) –> dehydration –> polydipsia (excess thirst
- glucose is filtered in the glomerulus of the kidney. Excess glucose is filtered out into the urine, which inc osmotic pressure of the filtrate. This causes more fluid to be pulled in, inc vol of filtrate (polyuria)
- there is usually no glucose in the urine
- problem = body only has so many glucose carriers, if the amount of glucose exceeds the quantity of these carriers, it must be excreted
- impaired glucose utilization by cells –> inc mobilization and use of proteins and lipids as fuel source –> inc lipid and protein metabolites in blood (ex. ketones) –> accum of ketones –> filtered by glomeruls and enter the urine –> ketouria -> enhances polyuria (can lead to ketoacidodis)
30
Q
mnfts
A
- type 1 –> abrupt onset / weight loss
- type 2 –> insidious (subtle) onset / obesity
S&S of hyperglycemia: - polyuria (& frequency) = inc voiding
- polydipsia (excessive thirst d/t loss of fluid and dehydration)
- polyphagia (inc appetite)
31
Q
acute cmplx
A
1) hypoglycemia
2) DKA
3) HHS
32
Q
hypoglycemia
A
- occurs when pt receives too much insulin, does not eat enough food, or overexerts themselves
- Tx: 15g or CHO PO
- hypoglycemic coma
33
Q
hypoglycemic coma (+ Tx)
A
- loss of consciousness d/t inadequate glucose supply to neurons
- Tx: glucagon breaks down glycogen and releases glucose
- admin 1mg glucagon SC or IM
- 20-50ML 50% glucose IV
34
Q
DKA
A
- byproduct of lipid metb is ketones
- usualy in type 1 DM
3 requirements: - must be hyperglycemic
- requires ketosis
- metabolic acidosis
35
Q
DKA patho
A
- begins w/ hyperglycemia from an I deficiency and glucagon in excess
- lipids and proteins broken down
- gluconeogenesis –> hyperglycemia
- excess glucose excreted in urine, along with water causing dehydration and effecting cardiac Fx
- mobilization of FFA (free fatty acids) from triglycerides stores in adipose tissue –> inc ketone production and acidosis
36
Q
HHS (hyperosmolar hyperglycemic state)
A
- usually in T2 and elderly
- can occur from other causes (ex. infection)
- caused by excessive CHO intake, insulin resistance
- hyperosmolarity and dehydration
- ketoacidosis DOES NOT occur b/c I present in T2 (lipolysis does not occur –> no excess of ketones)
- severe hyperglycemia –> hyperosmolarity –> cellular efflux –> polyuria and glucosuria –> fluid loss –> dehydration
37
Q
HHS patho
A
- severe hyperglycemia –> hyperosmolarity –> cellular efflux –> polyuria and glucosuria –> fluid loss –> dehydration
38
Q
chronic cmplx
A
- cannot be reversed, these cmplx will continue to persist
- gradual onset
- cannot prevent cmplx, but can delay them
- metabolic changes –> vascular damage (root cause of cmplx)
- cmplx: microvascular, macrovascular, infections
39
Q
vascular damage
A
- if capillaries damaged = microvascular
- if arteries damaged = macrovascular
- d/t: altered metb, glycosylated proteins, poor healing d/t damaged vessels, anaerobic bacteria
40
Q
microvascular cmplx
A
- retinopathy
- nephropathy
- neuropathy
41
Q
retinopathy
A
- capillary damage in retina –> aneurysms –> rupture –> visual impairment
- cataracts (clouding of lens)
- glaucoma (damage to optic nerve d/t inc intraocular pressure from buildup of fluid in eye)
42
Q
nephropathy
A
- glomerular damage –> dec renal fx –> renal failure –> death
43
Q
neuropathy
A
- damage to neurons
- neural ischemia
- demyelination of neurons –> “neural deficit” or poor conduction
- foor care important
44
Q
macrovascular cmplx
A
- CAD –> hyperlipidemia d/t altered metb –> atherosclerosis –> MI
- CVA –>hyperlipidemia –> atherosclerosis –> CVA
- PVD –> damaged vessel in limb
45
Q
infections
A
- high prevalence in DM
- foot infections and UTIs common
- difficult to manage b/d vascular insufficiencies, impaired lymphocyte Fx, pt doesn’t notice infection symptoms d/t neuropathies
46
Q
UTI
A
- microbes move up urethra and normally fought off
- in uncontrolled DM, glycosuria (glucose in urine) provides microbes w/ resources to metb and proliferate
47
Q
Dx of DM
A
- Hx (polyuria, polydipsia, polyphagia, unexplained weight loss)
- blood glucose levels (RBG = >11mmol/L; fasting glucose = >7mmol/L)
- HbA1C > 6.5%
48
Q
Tx of DM
A
- modify lifestyle (ex. improved diet, weight loss, activity)
- glycemic control with drugs (oral hypoglycemics - Metformin)
- I given injection to those w/ type 1
