Endocrine Diabetes

Front 1

What blood glucose value following a OGTT (75g is diagnostic of Diabetes? What value would represent prediabetes?

Back 1

>200 mg/dL 2 hours after a OGTT 75 g… 140-200=pre-diabetes

Front 2

What is the screening protocol for GDM?

Back 2

at 6-7 mos --> 50 g glucose load --> if > 140 mg/dL give formal OGTT of 100 g… if > 190 after 1 hour, > 165 mg/dL after 2 hrs, or > 145 mg/dL after 3 hrs

Front 3

What is the peak age of presentation for DM-1?

Back 3

puberty

Front 4

What is the greatest health risk from DM-1?

Back 4

ketoacidosis

Front 5

T/F adult onset of DM-1 is more severe than childhood onset

Back 5

FALSE

Front 6

which form of DM (1 or 2) involves "insulinitis"?

Back 6

type 1

Front 7

which form of DM (1 or 2) involves "familial inheritance"?

Back 7

type 2 (common)

Front 8

which form of DM (1 or 2) involves "HLA DQ> DR"?

Back 8

Type 1

Front 9

which form of DM (1 or 2) involves "twin concordance in high proportions"?

Back 9

type 2

Front 10

which form of DM (1 or 2) involves "ICA, ICA-512 and GAD"?

Back 10

Type 1

Front 11

Which has a greater risk of DM-1 a father with DM or a mother… Which has a greater risk of DM-1 DQ or DR?

Back 11

increased risk: father with DM and DQ>DR (both both are related)

Front 12

In DM-1, what causes "insulinitis"?

Back 12

Insulinitis: lymphocytes infiltrate the islets --> Ab and T cells directed against Islets

Front 13

Which islet antibodies are most prognositic of DM in young people and older people?

Back 13

ICA-512 = young predictor… GAD=predictor in adults… other Ab: ICA and IAA

Front 14

What is the Honeymoon period in acute onset of DM-1 in children. How does this differ from adult onset?

Back 14

DM acute onset --> hyperglycemia --> ketoacidosis --> insulin Rx --> honeymoon period (asymptomatic)… In adults this period is longer

Front 15

What is believed to be the etiology of DM-1?

Back 15

virus… unkn

Front 16

What are the 3 main sites of insulin resistance?

Back 16

1) prereceptor phase… 2) receptor phase… 3) post receptor binding phase

Front 17

What is a cause of pre-receptor insulin resistance?

Back 17

Ab-directed at insulin (perhaps abnormal insulin structure)

Front 18

What are 5 common causes of receptor phase defects that cause reduced insulin affinity --> leading to insulin resistance?

Back 18

DM-2, obesity, steroid use, OC or acromegaly

Front 19

Give one cause of post receptor insulin resistance.

Back 19

inability of GLUT-4 to translocate

Front 20

What type of receptor is found on the insulin receptor?

Back 20

Tyrosine kinase --> protein kinase insulin activated--> tyrosine phophorylation

Front 21

What effect does insulin deficiency have on receptor and post receptor defects?

Back 21

aggravate them

Front 22

What effect does increased glucagon have on insulin resistance?

Back 22

glucagon increases insulin resistance

Front 23

What are the two subtypes of insulin resistance? (see hint)

Back 23

Type A=PCOS… Type B: AI (Lupus)

Hint 23

Match the insulin resistance subtype (A or B) to the description: Associated with PCOS (symptoms), Associate with AI (e.g., Lupus)

Front 24

T/F visceral obesity and insulin resistance can lead to dyslipidemia with or with out DM and is associated with metabolic syndrome (--> increased risk of CV dz)

Back 24

TRUE

Front 25

T/F decreased ß cell mass is all that is required for the development of DM2.

Back 25

False - requires insulin resistance and insulin deficiency

Front 26

Amyloid deposits are associated with which type of DM?

Back 26

Type 2

Front 27

T/F In type II DM, insulin is still secreted when stimulated by amino acids, pancreatic lipases and ∂ adrenergic stimulation.

Back 27

FALSE - NOT pancreatic lipases and NOT ∂ adrenergic stimulation. TRUE- stimulated by amino acids, gut hormones and ß adrenergic stimulation.

Front 28

What is MODY and how is it characterized?

Back 28

MODY is autosomal dominant inheritance of TYPE 2 DM, where a there is a pure insulin secretory lesion and insulin resistance is not a primary defect

Front 29

What is the pathophysiology of ketoacidosis in type I DM?

Back 29

decrease in insulin --> hyperglycemia --> dehydration and hyperosmolarity --> osmotic diuresis --> volume depletion --> release of counter regulatory hormones --> glucagon stimulates ketogenesis --> increased counter reg hormones --> insulinune resistance --> UGLY CYCLE

Front 30

What are the 3 main components to DKA?

Back 30

ketonemia, hyperglycemia and vol depletion

Front 31

Which of the following are keto acids? Acetoacetate, ß hydrobutyrate, acetone

Back 31

Acetoacetate, ß hydrobutyrate

Front 32

What role does GH play in ketoacidosis?

Back 32

GH --> increased HSL activity --> increase lipolysis --> FFA available --> ketone substrate --> ketoacidosis

Front 33

What is suspected in Young African Americans children or young adult that have DM onset with ketoacidosis?

Back 33

It is an Autosomal dominant disorder --> DM-2 = atypical DM

Front 34

What is a more common form of ketoacidosis for DM-2 patients?

Back 34

Non ketotoic hyperosmolar coma

Front 35

What is the difference between Non ketotoic hyperosmolar coma and ketoacidosis?

Back 35

Non ketotoic hyperosmolar coma has more severe hyperglycemia and dehydration.... and NO KETONES

Front 36

In DM-1, why are you more likely to see hypoglycemia after 5 years?

Back 36

After 5 years glucagon levels don't rise with hypoglycemia, thus they are dependent on epinephrine for glucose counter regulation… CNS symptoms --> shakiness, hunger, palplatations

Front 37

In terms of Glucose regulation, what happens after 10 year of DM-1?

Back 37

Epi fails to rise with decreased blood glucose --> low blood glucose --> comoa, seizure, confusion, blurred vision

Front 38

What are the 4 types of DM sequelae?

Back 38

diabetic retinopathy, diabetic nephropathy, macrovscular disease, and diabetic neuopathy

Front 39

What are the two types of diabetic retinopathy?

Back 39

non-profusion of retinal capillaries (non proliferative) --> weak capillary walls, with microaneurisms --> rupture and leak… b) Proliferative: retinal veins dilate… formation of new vessels (more advanced) --> non resolving vireous hemorrhage --> blindess, retinal detachment, macular edema (blindness... rx with panretinal laser)

Front 40

What are two pathologic finding of diabetic nephropathy?

Back 40

glomerular basement membrane thickening, and expansion of mesangial matrix (with kimmelsteil-wilson bodies).

Front 41

What happens as a result of glomerular basement membrane thickening, and expansion of mesangial matrix seen in diabetic nephropathy?

Back 41

glomerular HTN --> proteinuria --> systemic HTN in end stage renal failure

Front 42

What is the Rx for diabetic nephropathy?

Back 42

Angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blocker (ARB)

Front 43

What can happen as a result of macrovascular disease due to DM?

Back 43

increase risk of CAD --> atherosclerosis (due to HTN, hyperlipidemia, central obesity, hyperglycemia, and diabetic nephropathy)

Front 44

Besides sensory or sensorimotor impairment, what can happen as a result of diabetic neuropathy?

Back 44

bladder dysfunction, orthostatic hypotension, sexual dysfunction, diarrhea and constipaiton

Front 45

What is the best way to prevent diabetic complications?

Back 45

Rx hyperglycemia

Front 46

What are the 3 mechanisms associated with diabetic complications?

Back 46

non-enzymatic glycosylation end products (HbA1C), Polyol pathway, Activation of protein kinase C.

Front 47

What is the pathophysiology behind AGEs? (hint: renal)… Rx?

Back 47

hyperglycemia --> non-enzymatic glycosylation end products --> irreversible --> diabetic nephropathies and decrease renal fx --> AGE taken up by ® --> release of cytokines and growth factors --> increased renal matrix, proteins and increase vascular permeability... (2) AGE inhibitors

Front 48

What is the pathophysiology behind the Polyol pathway? (2) Rx?

Back 48

hyperglycemia -(aldo reductase)-> increase in Sorbitol --> sorbitol doesn't diffuse out of the cell, which causes osmotic changes and damages the cell --> closely related to damage to the eyes (lens, retina), arterial and endothelial cells, and peripheral nerve damage... (2) Aldos reductase inhibitors

Front 49

What is the pathophysiology behind the Protein Kinase C pathway (DM)? (2) Rx?

Back 49

Hyperglycemia --> increase in DAG --> increase in PKC --> diabetic complications…. Rx: PKC inhibitors

Front 50

Match the drug mechanism of action with the drug ( sufonylurea, metformin, ∂ glucosidase inhibitor, thiazolidinediones, meglitnides, insulin, incretins, amylinmimetics): increase sensitivity of peripheral tissue to insulin

Back 50

thiazolidinediones - increase sensitivity of peripheral tissue to insulin

Front 51

Match the drug mechanism of action with the drug ( sufonylurea, metformin, ∂ glucosidase inhibitor, thiazolidinediones, meglitnides, insulin, incretins, amylinmimetics): increase insulin secretion, eventually K+ channel closes

Back 51

Meglitinides - increase insulin secretion, eventually K+ channel closes

Front 52

Match the drug mechanism of action with the drug ( sufonylurea, metformin, ∂ glucosidase inhibitor, thiazolidinediones, meglitnides, insulin, incretins, amylinmimetics): closes the K+ channel --> depolarizes the cell membrane --> Ca influx --> insuin and C-peptide released

Back 52

sufonylurea - closes the K+ channel --> depolarizes the cell membrane --> Ca influx --> insuin and C-peptide released

Front 53

Match the drug mechanism of action with the drug ( sufonylurea, metformin, ∂ glucosidase inhibitor, thiazolidinediones, meglitnides, insulin, incretins, amylinmimetics): decreases hepatic glucose production and increase peripheral uptake of glucose (does NOT increase insulin secretion)

Back 53

Metformin - decreases hepatic glucose production and increase peripheral uptake of glucose (does NOT increase insulin secretion)

Front 54

Match the drug mechanism of action with the drug ( sufonylurea, metformin, ∂ glucosidase inhibitor, thiazolidinediones, meglitnides, insulin, incretins, amylinmimetics): Decreases starch and polysaccharide absorption in the intestines

Back 54

∂ glucosidase inhibito - decreases starch and polysaccharide absorption in the intestines

Front 55

Match the drug mechanism of action with the drug ( sufonylurea, metformin, ∂ glucosidase inhibitor, thiazolidinediones, meglitnides, insulin, incretins, amylinmimetics): retards gastric emptying, suppression of glucagon, and suppresion of appetite (co secreted with endogenous insulin)

Back 55

amylinmimetics - retards gastric emptying, suppression of glucagon, and suppresion of appetite (co secreted with endogenous insulin)

Front 56

Match the drug mechanism of action with the drug ( sufonylurea, metformin, ∂ glucosidase inhibitor, thiazolidinediones, meglitnides, insulin, incretins, amylinmimetics): increases secretion of GLP and GIP

Back 56

Incretins - increases secretion of GLP and GIP

Front 57

Match the drug EFFECTS with the drug ( sufonylurea, metformin, ∂ glucosidase inhibitor, thiazolidinediones, meglitnides, insulin, incretins, amylinmimetics): counter indicated with renal failure --> acidosis, recommended to start at low doses to avoid GI problems

Back 57

Metformin (biguanide) - counter indicated with renal failure --> acidosis, recommended to start at low doses to avoid GI problems

Front 58

Match the drug EFFECTS with the drug ( sufonylurea, metformin, ∂ glucosidase inhibitor, thiazolidinediones, meglitnides, insulin, incretins, amylinmimetics): causes massive weight gain, may be related to PPARgamma

Back 58

Thiazolidinedioines - causes massive weight gain, may be related to PPARgamma

Front 59

Match the drug EFFECTS with the drug ( sufonylurea, metformin, ∂ glucosidase inhibitor, thiazolidinediones, meglitnides, insulin, incretins, amylinmimetics): not for pregnant women, not during breast feeding, causes hypoglycemia, weight gain, in long term use it loses its effectivenes,

Back 59

Sulfonylureas - not for pregnant women, not during breast feeding, causes hypoglycemia, weight gain, in long term use it loses its effectivenes

Front 60

Match the drug EFFECTS with the drug ( sufonylurea, metformin, ∂ glucosidase inhibitor, thiazolidinediones, meglitnides, insulin, incretins, amylinmimetics): short acting, doesn't cause hypoglycemia

Back 60

Meglitinides - short acting, doesn't cause hypoglycemia

Front 61

which drug is the same as Biguanide?

Back 61

Metformin = biguanide

Front 62

Match the Insulin (Lispro/aspart), Glargine, NPH< Regular) drug with the onset, peak and duration: very short onset, peak 1-2 hrs, duration 3-4 hrs

Back 62

Lispro/aspart: very short onset, peak 1-2 hrs, duration 3-4 hrs

Front 63

Match the Insulin (Lispro/aspart), Glargine, NPH< Regular) drug with the onset, peak and duration: 2-4 hrs onset, peak 2-3 hrs, duration 6-8 hrs

Back 63

Regular: 2-4 hrs onset, peak 2-3 hrs, duration 6-8 hrs

Front 64

Match the Insulin (Lispro/aspart), Glargine, NPH< Regular) drug with the onset, peak and duration: Onset 2.4 hours, peak 4-10 hours, duration, 14-18 hrs

Back 64

NPH: Onset 2.4 hours, peak 4-10 hours, duration, 14-18 hrs

Front 65

Match the Insulin (Lispro/aspart), Glargine, NPH< Regular) drug with the onset, peak and duration: Onset 2 hrs, peak -none, duration 24 hrs

Back 65

Glargine: Onset 2 hrs, peak -none, duration 24 hrs