Pancreatic Disease Flashcards by Wasim Alkahlout

What are the different types of diabetes

T1DM
T2DM
MODY
LADA - Latent autoimmune diabetes of adults

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What is MODY?

MATURE ONSET DIABETES of the Young
non-insulin dependent diabetes which showed autosomal dominant inheritance
β cell dysfunction characterised by non-kenotic diabetes and absence of pancreatic auto-antibodies
MODY ~ HNF1-alpha gene = causes diabetes by reducing insulin synthesis

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What is LADA

Latent Autoimmune Diabetes in Adults

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Polydipsia
Polyuria + Nocturia
Ketosis
Rapid weight-loss
Young
BMI <25
FHX autoimmune disease

These are a presentation T1DM

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Which genes are associated with T1DM

HLA DR3/HLA DR4

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What is the pathogenesis of T1DM?

Autoimmune disease - ICA
TYPE 4 HYPERSENSITIVITY
Islet cells antibodies attack islet b cells resulting in absolute INSULIN deficiency
=
Low cellular glucose
Hyperglycemia
Hyperkalemia

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What does insulin do?

Stimulates:
Increase GLUT4 reeceptor on cell surface thus increasing glucose uptake into cells
Glycogenesis (glycogen storage in hepatocytes)
Lipogenesis glucose > fatty acids (storage in adipocytes)

Inhibits
Glycogenolysis
Gluconeogenesis
Lipolysis
Ketogenesis - Too much can cause DKA

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How may a patient with T1DM look like?

YOUNG, LEAN AND WHITE

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DX T1DM

HbA1C >48 or 6.5%
Fasting >7
Random >11

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Tx T1DM

BASAL-BOLUS REGIMEN

Basal - Slow acting
glargine/detmire

Bolus - Fast Acting
Novorapid (Aspart)

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What do you do if patient medication isnt working and has lead to persistent and disabling hypoglycaemia

MIX INSULIN REGIMEN
and if hba1c cant be controlled at all and is above >69
consider continuous infusion pump

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What are the macrovascular complication of Diabetes?

Cardiovascular - IHD, HF, PVD
Cerebrovascular disease- Stroke

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what are the microvascular complications of diabetes?

Neuropathy:
Mononeuropathy/polyneuropathy - (Stocking glove neuropathy)
Autonomic neuropathy
Retinopathy
Diabetic Nephropathy
Cataracts

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What is the main acute complication of T1DM?

DKA - Diabetic ketoacidosis

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How Does T1DM lead to DKA?

through two mechanism:
Due to absolute def of insulin there is unrestrained GLUCONEOGENESIS - which causes hyperglycaemia and subsequently osmotic diuresis (increased URINATION)

ALSO due to unrestrained lipolysis and subsequently fatty acid oxidation (ketogenesis) - excess ketone bodies which cause ketoacidosis

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How would someone with DKA present

MEDICAL EMERGENCY
Patient will have Reduced GCS
Reduced tissue turgor
Haematologically unstable - High HR, Low BP
N/V

+ Signs:
Kussmaul’s Breating - Deep laboured breathing
Pear drop breath - Acetone / nail varnishy smell

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What is the diagnostic criteria for DKA involve?

Diagnostic criteria includes:

Plasma ketone >3mmol/l
RPG>11mmol/l
Blood pH <7.35 - Acidosis
Blood Bicarbonate > 15 mmol

Other observation include:
Urine dipstick: ketonuria/glucosuria
Serum U/E - Up urea / creatinine
hyperkalaemia

How is DKA mananged?

ABC management
IV fluids
IV insulin
restore electrolytes (e.g. K+)

in Hypoglycemia what do you give to patients?

Initially a fast acting carb - Glucose tablets
then a long acting carb - Bread

If reduced GCS - IV glucose / IM glucagon

What is the pathology of T2DM

AND ASSOCIATED RF

Peripheral insulin resistance (Down GLUT4 expression)
+/- partial insulin insufficiency

RF:
Steroids/Cushing’s
Chronic pancreatitis

T2DM risk factors

Lifestyle: obesity, sedentary, high calorie or alcohol excess
Higher prevalence in Asian men
Above 40 years old (late onset)
Hypertension

presentation of T2DM

30+, Obese, HTN, Asian
px/ Triad
Polydipsia
polyuria + Nocturia
Wt gain / Then wt loss later on
Glucosuria
Acanthosis nigrican (dark thick velvety skin at body folds/creases)

1st line management of T2DM

Lifestyle changes for allll

Tx T2DM

1st - Metformin Biguanide
2nd - + Sulphonyl urea
+ DPP4 Inhibitors
+ Pioglitazone

If contradications (CKD/HF/CVD) - Use SGLT2 Inhibitors

Metformin MOA and SE

Decrease gluconeogenesis and Increases insulin sensitivity (up GLUT 4) Thus increases glucoses reuptake into cells SE - Decreased B12 absorption - peripheral neuropathy GI disturbances CI- CKD

Sulphonylurea E.g Glicazide MOA / SE

Acts on B cell to promote insulin secretion SE - Wt Gain/ Hypoglycemia/ GI disturbance

Pioglitazone MOA / SE

Reduces peripheral insulin resistance / Increases glucose metabolism SE - Bone fracture/ Wt Gain CI - HF

DPP4i e.g sitagliptin MOA / SE

Inhibits dipeptidylpeptidase-4 to increase insulin secretion adn reduce glucagon secretion

SGLT2 inhibitor

Inhibits sodium-glucose 2 co-transporter to reduce glucose reabsorption and increase urinary glucose excretion SE: DKA, Uti, Back Pain

What are the glucose range for OGTT?

OGTT - Oral glucose tolerance test Give 75mg of fast acting glucose than after 2 hours take blood glucose level Normal range - <7.8mmol/l Prediabetic 7.8-11 mmol/L DM>11mmol/l

What are the glucose range for FPG?

First measure taken at OGTT is considered FPG Normal <6 Prediabetic -6.1-6.9 DM >7

What does it mean if someone has impaired fasting glucose IFG

Prediabetic patient w/ hepatic insulin resistance FPG- 6.1-7mmol/l (Prediabetic range) OGTT- <7.8 - Normal

What does it mean if someone has impaired glucose tolerance IGT

Prediabetic patient w/ muscle insulin resistance OGTT - 7.8-11 FPG<6mmol/l - Normal

What is the main acute complication of T2DM?

Hyperosmolar Hyperglycaemic State - HHS This in turns causes severe osmotic diuresis

What causes hyperosmolar hyperglycaemic state?

Excess gluconeogenesis and lipolysis result in hyperglycaemia.-> Osmotic diuresis However sufficient insulin to prevent ketogenesis (DKA)

What are the diagnostic criteria for HHS?

Urine dipstick - Glucosuria High plasma osmolality profound hyperglycaemia (glucose ≥30 mmol/L [≥540 mg/dL]), hyperosmolality (effective serum osmolality usually ≥320 mOsm/kg volume depletion in the absence of significant ketoacidosis (pH ≥7.3 and bicarbonate ≥15 mmol/L [≥15 mEq/L]),

HHS TX

IV fluids Insulin (at low rate of infusion) Restore electrolytes LMWH

Describe Insulin release?

Glucose in blood bind to low affinity GLUT 2 receptors on beta pancreatic cells. So at high glucose conc->inward glucose movment -> metabolism and atp production results in K+ chanels closing - > depolarisation-> calcium influx -> insulin vescile exocytosed

What does HbA1c represent?

Measure of glycated haemoglobin over the previous 3 months Measures: >48mmol/L or >6.5% or greater is diagnostic but less is not definitive

When cant we use HbA1C

Anything that affects Anyone younger than 18 pregnant or 2 month post partum (gestational diabetes) sx of diabetes less than 2 months Anything that affects glucose levels: Acutely unwell - infection associate hyperglycaemia Hyperglycaemia induce medications - corticosteroids Anything that affects RBC Acute pancreatitis CKD HIV Anemias