Diabetes

Question 1

Insulin effects:
Decreases 2
Increases 6

Answer 1

Dec: appetite and glucagon
Inc: glucose uptake by muscle and fat, glycolysis, glycogen synthesis, tg synthesis, aa uptake, protein synthesis

Question 2

Lack of insulin/glucagon presence effects
Decrease 1
Increase 8

Answer 2

Dec glucose uptake by muscle and fat

Increase: appetite, glucagon, bg, gluconeogenesis, lipolysis, protein breakdown, glucogenolysis, Ketone production

Question 3

Insulin secretion stimulated by ___

Glucagon secretion inhibited by___

Answer 3

Stim by glucose

Inhib by insulin

Question 4

Glucose uptake by __ transporter leads to cell depolarization ___ influx and release of __

Answer 4

Glut 2
Calcium
Insulin

Question 5

After just eating what happens to levels

Answer 5

Bg and insulin high. Insulin takes up gluc, gluc falls, glucagon goes up. FFA goes up, shift to FA metab. Ketone bodies go up. Glycogen up while ins up, down in between meals

Question 6

Type 1 dm: % and what it is

Type 2 dm: % and what it is

Answer 6

1 10%, autoimmune destruction of B cells

2 90%, insulin resistance

Question 7

MODY

Incidence, what it is

Answer 7

<1% total. Genetic defect in insulin production or release. 2% of <15 y/o diabetics

Question 8

Endocrine disorders that lead to dm

Answer 8

Cushing, acromegaly, pheochromocytoma

Question 9

Clinical appearance dm 1

Answer 9

IDDM. <20 y/o onset. Normal wt. decreased insulin. Anti islet cell antibodies. Ketoacidosis common

Question 10

Clinical appearance dm 2

Answer 10

NIDDM. >30 typically. Obese. Increased insulin. No anti islet antibodies. Ketoacidosis rare

Question 11

Genetics dm 1

Answer 11

<50% concordance in twins, HLA D linked

Question 12

Genetics dm 2

Answer 12

> 90% concordance, no Hla assoc

Question 13

Pathogenesis dm 1

Answer 13

Autoimmunity, immunopathic mechanisms, severe insulin deficiency

Question 14

Pathogenesis dm 2

Answer 14

Insulin resistance and relative insulin deficiency

Question 15

Islet cells dm 1

Answer 15

Insulitis early. Atrophy and fibrosis. B cell depletion

Question 16

Islet cells dm 2

Answer 16

No insulitis. Focal atrophy and amyloid deposits. Mild B cell depletion

Question 17

Clinical dx of dm based on glucose tolerance test

Answer 17

Fasting bg >126 (normal <100) or plasma glucose >200 after 2 hrs during an ogtt

Question 18

Gestational diabetes dx during glucose test

Answer 18

Fasting of 95, 1 hr of 180, 2 hr 155, 3 hr 140

Question 19

Glucose levels are normally ___ in pregnancy so the cutoff levels in dx of diabetes are ___

Answer 19

Lower, lower

Question 20

GD: when it usually occurs, what it does to baby

Answer 20

Occurs 24-28 weeks in pregnancy. Glucose can cross placenta and go to baby. Baby has higher risk of htn and cv disease

Question 21

What is pre diabetes

Answer 21

Impaired fasting glucose/glucose tolerance. IFG- bg 100-125 after an overnight fast. IGT- bg 140-199 after a 2 hr glucose tolerance test

Question 22

Macrovascular diseases assoc w dm

Answer 22

CAD, stroke, PAD

Question 23

Microvascular diseases assoc w dm

Answer 23

Diabetic retinopathy, nephropathy, cardiomyopathy

Question 24

Hypoglycemia
Level
S/s mild

Answer 24

<70. Hunger, shaky, pale, blurry vision, sweating, anxiety

Question 25

Hypoglucemia severe s/s

Answer 25

Extremely tired, confused, dazed, seizures, unconsciousness, coma, death

Question 26

DKA
Could result in
How it happens
Due to

Answer 26

Brain damage
Ketosis from breakdown of fat and protein for energy when glucose not present
Due to untx dm (esp IDDM), non compliance w meds, illness, infection

Question 27

S/s DKA

Answer 27

Fruity breath, kussmail breathing (rapid and deep), dehydrated, nv, abd pain, alt loc, weak, parasthesia, severe hyperglycemia, electrolyte abn, metabolic acidosis, ketones in urine

Question 28

How to calc filtered load

Answer 28

Bg 80 x gfr 125 = glucose that is reabsorbed (300)
Bg 300 x gfr 125= 375-300
75 mg/min not reabsorbed

Question 29

1 mM of glucose = ___ mg/dl

Answer 29

18

Question 30

Acetyl coA is converted to ketones for use by:

Answer 30

Brain, heart, liver, kidneys

Question 31

Ketone bodies include

Answer 31

Acetoacetate, acetone, b-hydroxybutyrate

Question 32

HHS vs DKA
Glucose
Na
PH

Answer 32

Glucose higher in HHS
Na high HHS low DKA
Ph mildly low HHS, very low DKA

Question 33

HHS vs DKA 
HCO3
Osmolality 
C peptide 
Anion gap

Answer 33

Bicarb higher HHS
Osmolarity higher HHS
C peptide high hhs low DKA
Anion elevated in DKA

Question 34

What is AGEs

Answer 34

Glucose binds to amino group. Higher bg more schiff products. Macrophages break them down to keep us healthy. Higher bf- more macrophages, chronic inflammation and vascular damage. Inc w age

Question 35

What happens in diabetic nephropathy

Answer 35

Leaky glomerular capillaries. Microalbuminuria, proteinuria. Glomerulosclerosis, tubulointerstitial fibrosis. Renal failure, htn, cv disease.

Question 36

Diabetic nephropathy
Dm= leading cause of __ __
Type at risk
Greatest rate of progression seen in

Answer 36

Kidney failure
Both
Poor control of bp

Question 37

Diabetic nephropathy
Main tx
What happens after transplant

Answer 37

BP <130/80 and use ace and arb.

Often req dialysis, even after transplant those w diabetes do worse than without