Diabetes Mellitus

Front 1

What are the types of symmetric neuropathies of DM?

Back 1

1) Distal, primary sensory polyneuropathy (can be either mainly marge fibers, small fibers or mixed)
2) Autonomic neuropathy
3) chronic evolving proximal motor neuropathy


often caused by osmotic pressure on then nerves from the hyperglycemia / sorbitol / polyol damage

ex1: foot with cocked toes due to loss of motor fc in the extensors > flexors --> ulcer under foot due to no sensation = most common from is this mixed kind;

ex2: autonomic destruction leads to the sudden death in DM because the warning signs of an MI are missing - also no sensation of the angina...

Front 2

What are the types of asymmetric neuropathies of DM?

Back 2

1) Acute or subacute proximal motor neuropathy
2) cranial mononeuropathy
3) Truncal neuropathy
4) Entrapment neuropathy in the limbs

mechanism is mostly ischemic damage due to blockage of vasa vasorum, so there is often PAIN first and then dysfct:

ex1: wrist drop after falling asleep on arm: radial nerve damage = mononeuritis simplex

ex2: CN3 palsy causing double vision and unability to look up; but the pupils REACT, because that's regulated by parasympathetic - which runs on the inside of then nerve closest to the blood vessel - is it's affected last = mononeuritis simplex

ex3: atrophy of all the hamstring muscles = Amyotrophy - diabetic myopathy - misnomer bc it's the nerve, not the muscle; this is Mononeuritis multiplex

Front 3

Sulfonylurea

Back 3

long acting Secretagogue
for basal glucose control

blocking the K+ channel causes depolarization --> Ca channel opening --> inceased Ca in cell causes release of Insulin

SE: problem is: Hypoglycemia (you have to eat because you're constantly emitting insulin)

SE: weight gain, SIADH

depends on the presence of b-cells

Front 4

Repaglinide, Nateglinide

Back 4

short acting secretagoges
for post-prandial control of glucose

blocking the K+ channel causes depolarization --> Ca channel opening --> inceased Ca in cell causes release of Insulin

SE: problem is: Hypoglycemia (you have to eat because you're constantly emitting insulin)

SE: weight gain, SIADH

Front 5

Biguanide

Back 5

Metformin

activation of AMP-Kinase --> signals that we have apparently "low energy" so we get increased fatty acid oxidation and hepatic glucose production as well as decreased glycolysis and more muscle uptake.


SE: problem is: Patients with heart conditions or chronic liver disease, or lung disease --> increased risk of lactic acidosis

SE: Lactic acidosis, weight loss, Diarrhea

Front 6

Thiazolidinediones

Back 6

TZD's = insulin sensitizers

Rosiglitazone, Pioglitazone

nuclear receptor PPAR-y activation -- more gene activation for insulin production

act primarily on adipose cells and secondarily sensitize muscle cells to insulin. (Lipodystrophy study moved fat from the wrong places = inside the organs, to the right places)

Side effect: Heart failure!, weight gain

Front 7

a-glucosidase inhibitors

Back 7

Acarbose, Mitigol
inhibit the absorption of carbohydrates by inhibiting the breakdown to glucose --> malabsorption

for post-prandial hyperglycemia

SE: some weight loss, but flatulence

Front 8

intensive DM therapy

Back 8

must be multifactorial - treating all risk factors such as high LDL, HTN, body fat (provides 50% increased risk reduction)

The A1c control eventually reaches the same lvl as the conventional and the slope of increase is the same too - due to loss of beta cells

BUT at least we can prevent to microvascular complications (not necessarily what they die from)

BUT even after 10yrs later, we still have benefit from the tight glucose control: still have less mortality from CV

Front 9

Diabetes diet

Back 9

calories from
30% fat - better saturated
50% carbs - better complex ones
15% protein
low salt

type II DM is same, just also includes calorie reduction overall

Front 10

before we do pharmacotherapy with DM, what do we order

Back 10

Exercise and Weight loss

Front 11

GLP-1 analog

Back 11

GLP-1 analog: the spit from the dragon gives us Exanatide® which is an incretin. These are substances secreted in the anticipation of getting a meal – act on pancreas to secrete insulin

DM have blunting of GLP-1

Front 12

Amylin

Back 12

Pramlintide (tradename)

synergizes with insulin

Front 13

types of insulin

Back 13

Lispro/Aspart = fast acting (fish insulin - only 2 aa different from human, but faster action)

NPH = neutral protamine hagedorn = intermediate acting

Lente and Ultralente = long acting

Glargine = ultra-long acting; peak-LESS insulin, prevents DKA

Front 14

autonomic neuropathy in DM examples

Back 14

Cardiovascular: orthostatic hypotension, tachycardia, sudden death

Gastroparesis (devestating, can't dose insulin well)

Erectile dysfunction

Cystopathy (large post-void residual - ifections)

Sudomotor disorders

Hypoglycemia unawareness (sweats and others are missing)

Front 15

erectile dysfunction in DM

Back 15

not purely neuropathic, it's a marker for CV disease

Front 16

Sildenafil

Back 16

PDE-5 inhibitor --> constant cGMP increase --> dialate blood vessels in penis

least effective in DM because they don't have a pure neuropathy or a pure vasculopathy

(if it were pure n or v, sildenafil might be able to overcome the it)

but still 1/3 are helped

Front 17

valsalva with DM?

Back 17

deep breath, strain
breath normal

test finds the changes in the puls and respiration --> changes in sympathetic and parasympathetic

normally you should get sinus arrhyhmia with HR changes

DM loose this: they'll have a relatively constant pulse

do this bc: autonomic NS loss causes sudden cardiac death in DM!

Front 18

skin findings in DM

Back 18

1) 50-60% will get diabetic dermopathy
past - bad control of DM

2) Necrobiosis lipodica diabeticor - infarction of the fat under the skin

Front 19

strategies to reduce microvascular complications

why?
how?

Back 19

prevention is proven to work by intervetion on:
hyperglycemia
hypertension

treatments proven by intervention trials:
-ACE inhibitiors for neuropathy
-Laser photocoagulation for retinopathy

Front 20

what are the macrovascular complications of DM

Back 20

Angina, exercise intolerance (if ANS neuropathy - silent) ---> CAD (2-3x higher; 4x higher risk of dying during MI; 2x higher risk of dying post-MI, also higher risks in Impaired Fasting Glucose pt)

Claudication ---> PVD

TIA's, strokes --> CVA

Renal artery sclerosis ---> renal failure

Front 21

Risk of MI in people with DM and without

Back 21

risk of MI in DM if you've never had an MI = same as risk of non-DM who's had an MI

same in several ethnic populations

Front 22

what causes the increased CVD in DM?

Back 22

hyperclycemia: as it increases, the risk increases

even before HA1c is before 6 it increaes the risk - so even though in the nl population without DM

Front 23

pattern of DM dyslipidemia

Back 23

increased fraction of small, dense LDL-cholesterol (without increase in total quantitiy of LDL-C) - more atherogenic

high TG (independent strong risk factor proven only for DM)

low HDL

Postprandial lipemia (free FA are high in DM persistently)

Front 24

pathophys of macro-vasc dz in DM

Back 24

"AGE" of endothelial proteins

HTN

accelerated artheroscleros

Dyslipidemia (peculiar type)

Front 25

prevention of macrovascular complications

Back 25

Consider:

HTN
Hyperglycemia
Obesity
Cigarrette smoking
Dyslipidemia
Altered coagulation, platelet fct, fibrinosis,
Nephropathy
Insulin resistance

Front 26

early and aggressive tx to reduce macrovascular complications

Back 26

dyslipidemia
HTN
anti-platelet

(not proven yet - thrombolysis, endothelial disorders)

Front 27

skin finding from severe dyslipidemia

Back 27

Eruptive Xanthomas - look like red bumps = blobs of VLDL

Front 28

normally, how do we break TG

changes with insulin type I?

Back 28

hormone sensitive lipase(HSL) turns the TG into FFA and ships it to the liver --> makes more ApoB, VLDL, TG --> VLDL is released and transported to fat cells and LPL turns it into fat; (LPL prevents the conversion of VLDL into IDL -- LDL)


Changes in DM I:

1) Insulin stops HSL and activates LPL
--> greater influx of FFA to liver
---> more VLDL
also the VLDL is not taken up by the fat cells
--------> shunting to IDL and LDL

2) CETP = cholesterol transporter protein is increased in DM:
a)it moves cholesterol from LDL into VLDL and it and moves TG from VLDL into LDL --> we get a small LDL
b) moves cholesterol from HDL to VLDL, and TG from VLDL to HDL

---> depletes VLDL of TG and depletes HDL/LDL of cholesterol

THIS is the reason for "low HDL" "nl LDL" because they measure the cholersterol in there - however these modified lipid particles are more artherogenic

Front 29

management of Dyslipidemia

Back 29

ATP III diet for metabolic syndrome

Hyper-TG / low HDL-C: Niacin (blocks release of FA), Fibrates(activates the oxidization of FA)

LDL-C: statins

Combinations (beware of rhabdomyolysis -- renal disease)

Front 30

what type of obesity is worse?

fat location

Back 30

apple shaped - MALE pattern of putting on fat is worse
= the central fat is more toxic
(means more visceral obesity ---> higher TG, higher cholesterol, lower HDL, more insulin resistance)


pear shaped - women is better

Front 31

management of AMI in DM

Back 31

b-blockers
ASA
ACE inhib

Angiopasty vs bypass ?? angioplasty might be worse for DM

Glucose control even in hospital:
-continuous intravenous insulin
-followed by intensive glucose control

Front 32

"HONK"

Back 32

HHNS

extreme hyperglycemia
-poorly treated/undetected DM
-renal insufficiency
-age/mental obtundation -> decreased oral fluids

absence of ketosis
-insulin is not totally deficient

severe dehydration and volume depletion

coexisting chronic illnesses

high mortality

Front 33

what should you calculate with HONK presentation

Back 33

effective osmolariy


2(Na) + glucose/18 + BUN/2.8

if it's over 300 --> person is hyperosmolar (must be there if you want to diagnose HONK)

important bc > 330 greatly increases the risk for seizures and increased mental obtundation

Front 34

HHNS treatment

Back 34

Isotonic and hypotonic fluids (unlike DKA, where the main problem is isotonic loss with some degree of free water loss, in HONK it's a mix of both - with tremendous hypovolemia + tremendous dehydration)
(first enough volume, till pressure is restored - and then start giving water to correct the Na)
MONITOR
electrolyte replacement
Insulin (no longer on top)
Treatment

Front 35

difference btw dehydration and hypovolemia

Back 35

loss of salt and water in nl proportion = hypovolemia; no good blood tests - Na is variable;
(BP, skin turgur, urine output)

loss of water alone = dehydration; plasma Na is high

Front 36

Lactic acidosis

why is DM more prone?
causes?
type?

Back 36

normal healthy persion will have LA <1
well controlled DM has higher baseline >1
DM more prone, also bc tendency of vascular disease and also bc drugs for DM can cause this


CAUSES (2)
Lack of Oxygen or a Toxin that prevents the pyruvate dehydrogenase shunt to the krebs cycle:

Types (2)

with hypoxemia/shock(type A)
without hypoxemia/shock (typeB)
-illnesses
-toxins
-hereditary
-miscellaneous

Front 37

what contributes to lactic acidosis in DM?

Back 37

Hypotension (acute GI hemorrhage, sepsis, pancreatits)

Arterial oxygen desaturation

Decreased Cardiac output

Regional hypoperfusion

Drugs (Metformin)

Front 38

biochemical basis of lactic acidosis

Back 38

Glycolysis supplies ATP but requires NAD

Pyruvate to Lactate sustains the cycle because it yields fresh NAD

self-sustaining

Front 39

treatment of lactic acidosis

Back 39

1) correct hypoxia

2) remove toxins

bicarbonate (caution because more CO2 --> pH more acidic if you can't blow it off)

dichloroacetate (for one condition in children - shunts more oxygen down )

Front 40

serious complications of DM

Back 40

retinopathy
nephropathy (leading cause of ESRD)
neuropathy (feet hurt like hell, ED, paresthesias..)
stroke
CVD

Front 41

Retinopathy

causes

Back 41

can be traced to a glucose alone phenomenon - more than the others

increased polyol accumulation --> deminishes myo-inositol

formation of AGE's - becomes a problem if glucose sticks to a protein that makes up the BM of a vessel -- makes blidness

increased oxygen stress

increased protein kinase C - beta activity = leakage of vessel

Front 42

Polypol pathway

Back 42

D-glucose -- sorbitol -- fructose

more sorbitol = it's more poorely metabolized and so it sits there and causes osmosis --> swelling

Front 43

AGE's

where from?
Shiff base...

Back 43

Shiff base still reversible, but then Amadori product --- further products

if Hg is glycosylated it's that way for ever- till the RBC dies - A1c is that
- so it's used to measure

Front 44

eye disease in DM

frequency
stages
3causes of blindness in DM

Back 44

1/2 of all DM
incidence is not parallel to nephropathy - it flattens out after 25y

Stages
-Background - microaneurisms, dot-blot hemorhage, hard exudates(white)

-pre-prolif: soft exudates, IRMA, large hemorrhage

-Proliferative - hypoxia causes Neovascularization (= key for prevention of blindness)
[increased endothelial cells and less pericytes cause leaky vessels and hypoxia --> VEGF/PKC --> angiogenesis , vitreal and retinal]

circinate exudates = warning of impending macular edema [ other cause of blindness besides neovascularization and bleeding ] - before they get angio

pre-retinal hemorrhage - serous complication of proliferative retinop

chronic complications of neovasc after bleed-- vitreus pulls on retina -

Front 45

laser ablation of which vessels?
photo-coagulation

Back 45

pan-retinal laser destroys the vessels on the periphery and leaves the center of the macula; central area is clean

this is supposed to shunt the blood to the right areas, preventing blindnes

Front 46

Rubeosis iridis

Back 46

neovascularization of the IRIS

Front 47

glycemic control and retinopathy

DCCT

Back 47

trial convinced us that
intensive glucose Rx reduced development of

retinopathy

- the microvascular complications at least
with the glucose control + eye doctor

Front 48

kidney disease in DM

Back 48

very high morbidity and mortality type 1 > type 2

distinct susceptibility genes
-Na/H pump overexpression
-ethnic differences
-simpling pair analysis

Front 49

natural Hx of kidney disease

MEMORIZE THIS

Back 49

larger kidney - GFR higher
(increased pressure is actually bad)
creatinine is great in the silent period
but if you dont' do anything, the'll get proteinuria, azotemia and then ESRD


3yrs prior to onset of DM:
-GFR 120, creat 1, ureaN 15

onset of DM
-GFR 150, creat 0.8, ureaN 10

3yrs post onset: Diabetic Glomerulosclerosis
-GFR 150, creat 0.8, ureaN 10

MICROALBUMINURIA
(earliest sign - seen in the silent period - test: must be able to find low lvl of albumin - here we can still slow it down)

-15yrs post onset of DN: time of silent period is over: onset of proteinuria
-GFR 120, creat 1, ureaN 15


20yrs post onsetDM: Azotemia
-GFR 60, creat >2, ureaN >30


23yrs post onset DM: ESRD
-GFR <10, creat >10, ureaN >110

Front 50

renal changes in DM

Back 50

1) renal hyperfiltration
2) renal lesions without clinical signs
(microalbuminuria)
3) Nephropathy (microalbuminuria)
Kippel-wilson
4) ESRD


Focal glomerulosclerosis

Front 51

hemodialysis

Back 51

only prolongs life by another 5-6yrs

Front 52

Albuminuria

Back 52

normal <20
Microaluminuria 30mg - 300 / 24h
Macroalbuminuria >300
- increased risk for renal disease and macrovascular disease

so microalbumin is almost as impotant as a signal as high LDL for risk of MI

Front 53

why ACE - I?

cant give to?

Back 53

in addition to glycemic control, for nephrotic prevention:

ACE-I because the pressure must be dropped by releasing the efferent constriction

BUT we can't give it to sb who already has afferent disease because they won't have enough flow to the kidney at all

Front 54

proximal/afferent vascular disease?

Back 54

put them on a small dose of the ACE-I

if the creatinine goes up - you know you can't use up because they already have afferent arterioal disese

Front 55

most common chronic complication of DM

pathology?

Back 55

nervous system dysfunction
ex: ED

sensory, motor, cranial, autonomic


Types:
Symmetric is most common
Asymmetric
Radiculopathy
Autonomic




Pathology:
distal, multiple neuropathies -- usually polyol pathway

proximal, mononeuropathies usually vascular

Front 56

Parent or Sibling with DM what's worse?

for DM type I ?
and for DM type 2?

Back 56

For DM I it's higher risk if sibling had it

For DM II it's higher if parents had it (45% if they both had onset <50; identical twin 60%)

Front 57

MODY

type of defect?

Back 57

maturity onset diabetes of youth

type II DM

the genes associated with each of the MODY syndromes is mostly to do with the insulin secretion rather than insulin action; so they're b-cell defects

startling, because the whole time we thought that DM type II was a problem of insulin action - not a destruction of the b-cells ( = type I);

but apparently the MODY's are type II because they don't need that much insulin

Front 58

Calpain-10, TCF7-L2

Back 58

genes that are part of the group that cause the common DM type II
polygenetic - common forms of DMII

are still functions of the b-cell!!

Front 59

Glucokinase

mutation?

Back 59

Glucose is converted to Glucose-6P
this is the beginning of the glucose breakdown to ATP which eventually tells the cells that they need to make insulin; it's sometimes called the insulin sensor because of that

MODY-2 has a mutation in this
they have a higher "set point" because they're not effectively sensing the glucose --> they'll have a mild stable hyperglycemia
- they have an altered setpoint

Front 60

2 principles of type 2 DM

2 starting points --- >>>

Back 60

Insulin resistance + b-cell dysfunction
(+ environment)
I I
I I
Inpaired Glucose TOlerance
I
Type II DM

from this further Gluco-/Lipo- Toxicity leads to more insulin resistance and more b-cell dysfunction


often not detected till it's type 2 and it's already in the vicious cycle

Front 61

stages of type II DM

path to the development of DM

Back 61

Peripheral insulin resistance (high insulin) / b-cell dysfunction ---> Impaired glucose tolerance ---> early b-cell damage --> early DM --> late bcell damage --> late DM

Front 62

5 acute complications of DM

Back 62

Insulin-induced hypoglycemia
DKA
Hyperosmolar hyperglycemic nonketotic state (HONK)
Lactic acidosis

Front 63

Hypoglycemic reactions

2 types

Back 63

Neurogenic: (Sympathetic and parasympathetic activation)
-sweating
-hungry
-tingling
-shaky
-heart pounding
-nervous/anxious

neuroglycopenic (CNS symptoms):
-warm
-weak
-difficulty in thinking
-tired / drowsy
-faint
-dizzy
-difficulty speaking
-blurred vision


these are to be considered separately because they have different thresholds - usually you get the autonomic sx first; however, DM pt with neurpathic damage might loose the neurogenic signs and the first presentation is the seizure

Front 64

insulin injection

Back 64

release of Epi (very high) and Ne fast

little bit later glucagon
cortisol
GH

Front 65

DKAhave to have all 3:

Back 65

hyperglycemia: osmotic diuresis, volume depletion, dehydration

ketoacidosis: anion-gap acidosis

other metablic changes

Front 66

how do we get DKA

K:
the ketones

Back 66

adipocyte release FFA
the controls is via insulin/glucagon ratio

Liver turns the FFA into Ketone bodies or TG; The production into Ketone is also under control of: insulin/glucagon ratio

high insulin and low glucagon prevent the DKA - so the DM pt has a perfect set up:
decreased insulin --> lipolysis --> FFA to liver

+

increased glucagon --> increased hepatic carnitine content/decreased malonyl CoA : so now the FFA can get into the mitochondria--> activation of CAT

--> accelerated ketones

both together cause the ketones

Front 67

reason for tipping to DKA

Back 67

historical: they're type I and something that tipped it over:

-alcohol, drugs, infection , MI/stroke, trauma, pregnancy, didn't take their insulin

but now we know:
Blacks and Hispanics have almost equal chance of being type I or type II phenotype when they are found w/ DKA; so now we consider:

"Ketosis - prone - DM" KPD

Front 68

DKA: D: hyperglycemia

cause:

effects:

Back 68

hyperglycemia
cause: insulin deficiency, leading to increased hepatic glucose production
decreased peripheral glucose utilization


effect:
-osmotic effect: water pulled from ICF to ECF, osmotic diuresis
-ECF volume:
-Renal loss of water > electrolytes
volume depletion
some degree of dehydration

Front 69

DKA: A: metabolic acidosis
cause:

effects:

Back 69

cause:
-xs acetoacetic acid and b-OH butyric acid production
-deminished renal excretion of H+

effect:
-H+ HCO- ---- H2CO3 -- CO2 H2O
ultimate correction of H+ xs depends on:
oxidation of AAA + bOHB, renal excretion of H+
-exchange of H+ for Na
-anemia --> ammonium
loss of electrolytes in urine

Front 70

water and electrolyte imbalance in DKA

Back 70

cause:
-osmotic diuresis
-vomiting
-increased aldo
-ICF - ECF shift (K+ PO4)

effect:
-10% body weight loss as fluid!!
50% extracell, 50% intra
-loss of:
K+, Na+, PO4-

Front 71

symptons of DKA

Back 71

N/V
polyuria/polydipsia
abdominal pains
mental changes (leathery to near-coma)

signs:
-fruity breath (due to acetone)
-Kussmaul respirations (rapid, deep breaths pH7.2 or less)
-signs of volume depletion (tachycardia, orthostatic hypoTN)
-sings related to precipitating factors (infection , MI, trauma)

Front 72

Labs of DKA

Back 72

elevated blood glucose
pH < 7.35
low HCO3-
high anion gap
positive serum ketones

Front 73

calculation of corrected Na concentration

Back 73

you expect them to be hypernatremic bc. so much water loss, but the pt is often "hyponatremic" when you see them : artificially bc glucose is sucking water in the blood;

tells you what the pt would have been without the glucose

Na + 1.6 (glucose - 100) / 100

Front 74

Anion Gap

Back 74

Na - (Cl + HCO3) = 8-12 (+/-2 )

if it's 14, it's already enough

check if it's complex or simple

Front 75

DKA treatment

order

Back 75

Isotonic fluids
Insulin
potassium
Monitor
treat precipitating cause

Front 76

who get's HONK

Back 76

older folks who don't have
typical type I DM

not a complete lack of insulin

it's like DKA without ketones

the glucose will be like 900!!!
they have other things that prevent them from drinking...

Front 77

Besides type I or II what other conditions could you classify the diabetic as?

Back 77

Cushings disease - pituitary adenoma
Obesity
Addisons (autoimmune disorder, as is DM I, also check thyroiditis pt for this)

Drug or chemical induced

Turners
Klinefelters

X-linked insulin receptor mutation

Gestational DM

Front 78

Gestational DM

Back 78

induces insulin resistance

2-13% of pregnant women get DM (higher in AA < asian ) , usually 2nd - 3rd trimester

GDM is associated with increased fetal and materal morbidity

xs morbidity can be reased by maintaining normoglycemia:

increase in insulin production to compensate for the insulin resistance; you can also give her insulin

diagnostic criteria by OGTT; very strict - lower than non-preg;

after delivery, risk of type II is 30-40% in 10yrs

Front 79

risk of getting type I DM

a) no Fhx
b) father with type I
c) mother with type I; <25yo @ child birth
d) mother with type I > 25yo
e) sibling

Back 79

a) 1%

b) 6%
c) 4%
d) 1%

sibling 5-10%

2 relatives 20%
identical twin 25-50%

Front 80

autoimmune type I DM

genes

Back 80

HLA DQA1, B1, B1 ((chromosome 6)

cytokines

T-cell

b-cell: insulin

Front 81

environmental triggers of autoimmune DM

Back 81

coxackie,
milk

Front 82

markers for type I DM

Back 82

GAD antibodies - glutamic acid decraboxylase antibodies

antibodies against IA-2 (b-cell phosphatase)

antibodies against ZnT8

antibodies against Insulin


serum from the pt looking for Igs fluorescence

the titers rise years before the onset of DM (is this the incubation period?)

Front 83

progression of DM type I

Back 83

genetic predisposition

immunologic abnomalities

progressive impairment in insulin release

presentation at doctor


80% loss of b-cells

give insulin --> honeymoon period

but then overt DM

Front 84

Risks for type II DM

Back 84

Native american > mexican > african americans > caucasians

obesity

metabolic syndrome (IGT/IFG)[low HDL, high LDL, HTN, waist cicrumference]

environment (sedentary, fast food)

Front 85

factors progressing IGT to type 2 DM

Back 85

insulin resistance / hyperinsulenmia
central obesity
hyerTG
HDL <35
HTN
family x
Hx of gestational DM

Front 86

inputs into/causing: Insulin resistance


outputs?

Back 86

Aging, medications (steroids, b-blockers), Fat cell defects, obesity and inactivity, genetic abnormalities, type 2 DM

----> hypertension, Dyslipidemia, Atherosclerosis, PCOS

as long as the b-cell is ok, this will still not give you DM - but if it starts dying...

Front 87

changes in insulin secretion, glucose disposal and blood glucose

Back 87

normal person has high normal insulin with high glucose excretion

obese pt has higher insulin and lower glucose excretion

IGT pt has peak insulin and lowest glucose excretion

"here the pancreas is still trying to compensate for the insulin resistance by making more insulin, but then it gives up: ..."

early diabetic has low insulin and still lowest glucose excretion

late DM - insulin down and so is gluc excretion

pancreas is failed

at the very end, the type II DM becomes a type I DM

Front 88

DM skin

Back 88

acanthosis nigircans

Front 89

diagnostic criteria for diabetes

Back 89

symptoms + random plasma glucose >200

or

FG >125 (= 126 or higher)

or

OGTT > 200

Front 90

diagnostic criteria for impaired glucose tolerance

Back 90

FG: >100 - 125

OGTT 140 - 200