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LAST TEST!!! > L90- Diabetes > Flashcards

L90- Diabetes Flashcards

1
Q

Discuss Pro-insulin to Insulin cleavage and significance?

A

Pro-insulin secreted and cleavage occurs in 2 places resulting in bridged sulfa bonds and cleaved C-peptide released

*Cleaved C peptide is a bio-marker to see if patients are making their own insulin

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2
Q

Walk through how Insulin is secreted?

A

Glucose enters beta cell through GLUT-2

GK enzyme phosphorylates it to make G6P - rate limiting step

G6P enters Krebs cycle and transformed into ATP

Increased ATP closes inward rectifying K channel - changes Vm and Ca rushes into cell to release granules/veiscles which are pre-packaged w/ insulin

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3
Q

There are 3 main problems in the pathway for insulin release that can be seen and each leads to its own inherited insulin disorder. What are they?

A

1) MODY2 - problems w/ GK enzyme gene therefore decreased ability to convert glucose

2) MIDD - maternally inherited mitochondrial diabetes - mitochondrial gene change that leads to inherited diabetes and deafness

3) HHI - hereditary hyperinsulinemia - activating mutation of SUR1 or Kir6/2 transporters on cell surface so responsive regardless of status of energy stores leading to constant Vm depolarization and CA influx and insulin release

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4
Q

What are insulins effects on the liver?

A

Promotes glycogen synthesis and FA synthesis - building stores for later use

Stops Glycogenolysis, gluconeogenesis and ketogenesis

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5
Q

What are insulin effects on Adipose?

A

Promotes FA uptake and TG formation and storage

stops lypolysis

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6
Q

What are insulins effects on muscle?

A

Promotes protein synthesis and glycogen synthesis

stops proteolysis

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7
Q

What 2 systems have Insulin - indepennt effects when glucose is present?

A

Brain and RBCs take up glucose even when no insulin around

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8
Q

What happens in metabolism during overnight fasting state?

A

Blood sugar levels drop slightly but kept normal bc Liver constantly breaking down glycogen and making new glucose

+ Basal levels of insulin being released

slight lipolysis and breakdown of AA in muscle to be used in liver

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9
Q

What happens to metabolism after prolonged fasting?

A

Blood sugar levels fall, insulin low, rise of Glucagon

Increased lipolysis, breakdown of muscle into AA (alanine)

All goes to liver for gluconeogenesis and Ketone body production

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10
Q

What are normal levels of fasting glucose, OGTT (2 hours post glucose load) and Hba1c?

A

Fasting Plasma glucose < 100

OGTT 2 hours < 140

HbA1c < 5.7

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11
Q

What are 2 states of PRediabetes and how would you diagnose them? What is the biggest risk for these?

A

1) Impaired Fasting Glucose (IFG) - fasting levels are above normal but < 126 (100-125)

2) Impaired Glucose Tolerance Test - blood sugar level elevated 2hours after glucose but not above 200

Each has intermediate HbA1c levels of 5.7-6.4

Impaired risk for developing T2DM

**Increased risk developing CVD!!

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12
Q

How can you diagnose Diabetes?

A

Random plasma glucose > 200 regardless of time since last meal + Symptoms of DB (polyuria, unexplained weight loss etc)

or

Fasting plasma > 125, OGTT > 200, HbA1c > 6.5

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13
Q

Compare and contrast T1 vs T2 DM..

A

T1 DM: Autoimmune destruction of beta cells, Low-absent insulin levels, Ketosis prone, Thin people. less twin concordance, ICA/IAA/GAD antibodies, HLA ASSOCIATION (DR3, DR4, DQ)

Tx. INsulin

RF: Family Hx

T2 DM: Insulin resistance leading to defect in beta cell action and loss, High or low or normal insulin levles, No ketosis, Obese body type, no antibodies, no HLA, no Autoimmune endocrinopathies,

Tx: Diet/Exercise, pills, injectable meds or insulin

RF: FH, obseity, race, GDM

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14
Q

What is HbA1c test and why is it useful?

A

sugars bind to and glycosylate Hb in RBC and since RBCs lsat for 3 months is an accurate % of blood sugar levels for 3 month period

higher blood sugars then more HB glycosylated

< 5/7% normal

> 6.5% Diabetes

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15
Q

What cell types are found in pancreatic islets?

A

Beta cellls - insulin

Glucagon secreting cells (alpha?)

Somatostatin secreting cells

Pancreatic Polypeptide producing cells

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16
Q

What are the stages in development of T1DM?

A

See graph

Genetic Susceptibility + Precipitating event (like infection)

IMmunologic abnormalities but normal insulin

Decreased insulin but normal glucose

Diabetes but still have C-peptide

No C-peptide

17
Q

Discuss the process in the development of T2 DM?

A

Genetic susceptibility + Enviro + Aging (less beta cel lregenration)

Insulin resistance - increased insulin

Impaired glucose tolerance

18
Q

Name some races very susceptible to T2DM?

A

PIMA INDIANS

AA and Hispanics

19
Q

What is gestational Diabetes? Why must you treat it?

A

Diabets that onsets during pregnancy and resolves after

associated with increased maternal/fetal morbitidity - BABIES AND PLACENTAS are larger

Treatment reduces risk of Csection, should dystonia, nerve damage and birth injuryies in genreal

40% women develop T2 DM within 10 years

20
Q

What is MODY? how is it inherited?

A

Maturity Onset Diabetes of Youth

Mutations in GK gene result in inability of beta cell to sense increased glucose and so less insulin released and on average higher blood sugar levels

Autosomal Dominant

21
Q

What is MIDD? inheritence?

A

Maternally inherited Diabetes and Deafness

Rare

caused by A to G mutation in mitochondrial DNA

22
Q

What are some syndromes of extreme insulin resistance?

A

PCOS w/ severe hyperandrogenism

Acanthosis nigricans

Hereditary Insulin reistance

23
Q

What is HEreditaary Hyperinsulininemia?

A

Mutations in SUR1/KIR6.1 genes

ACtivating mutations cause insulin release no matter what

24
Q

What are secondary causes of Diabetes?

A

Pancreatic Diseases:

  • Hemochromatosis - infiltration
  • Pancreatitis
  • Pancratic cancer
  • Cystic Fibrosis - ducts clogged

Other Endo disorders that prevent insulin rom working

  • Cortisol excess
  • Acromegaly - GH excess
  • CAtecholamine excess

Drug Induced

  • Niacin
  • Beta blockers
  • Thiazides

STatins increase risk of development of T2

25
Q

What are symptoms of Hyperglycemia?

A

Poluryia and polydispia

nocturia

polyphagia

weight loss

confusion, fatigue, blurred vision

vulvovaginitis

poor wound healing

Or asymptomatic!

26
Q

What happens in DKA? Tx?

A

Life-threatening condition where insulin deficiency leads to ecxessive lipolysis, unrestrained FA oxidation to produce ketones (Beta-Hydroxybutyrate, Acetoacetate, Acetone)

Metabolic Acidosis, Dehydration, Electrolyte disturbances

DKA Treatment: IV Fluids and INsulin

27
Q

What is a Hyperosmolar Hyperglycemic state? Tx?

A

occurs in state of relative reduction of insulin secretion in T2DM

  • stress or infection –> Insulin deficiency and Osmotic Diuresis - loss of electrolytes and dehydration and protein catabolism
  • Hyperosmolarity
  • Decreased renal perfusion and shock!!1

TX IV Fluid an dINsulin

28
Q

Distinguishing DKA from HHS:

A

DKA: Glucose > 250 pH < 7.35

  • positive serum ketones and increased anion gap

HHS: Glucose > 600 and pH > 7.3

Bicarbonate > 15

Eosm > 320

(Eosm = effective osmolarity = 2(Na+K)+blood glucose/18

29
Q

What are complications from diabetes?

A

Retinopathy

Nephropathy

Amptutations

Vascular Disease

30
Q

What are the 2 principle forms of diabetes related retinal disease?

A

Non-Proliferative: Macular edema (hard exudates and cholesterol leavage from BV), blot hemorrhage, microaneurism, Cotton Wool spots, fluid in layers of retina

Proliferative: Retinal detachment from new vessels pulling it forward

(TX for new vessels - Bevacizumab!)

31
Q

What kidney changes occur in Diabetic Neprhopathy?

A

Thickening of Glomerular BM and Hypertrophy

Increased Mesangial ECM and reduced podocytes

32
Q

What are signs / symptoms of Diabetic neuropathy?

A

Peripheral - distal symmetric stocking and glove, motor neuropathy, CN 3, 4, 6, 7

Autonomic - orthostatic hypotension, resting tachycardia, GI neuropathy, Urinary bladder atony, ED

LAST TEST!!! (17 decks)

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