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Endocrine > Pancreatic Disease > Flashcards

Pancreatic Disease Flashcards

1
Q

What are the different types of diabetes

A

T1DM
T2DM
MODY
LADA - Latent autoimmune diabetes of adults

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2
Q

What is MODY?

A

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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3
Q

What is LADA

A

Latent Autoimmune Diabetes in Adults

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4
Q

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

A

These are a presentation T1DM

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5
Q

Which genes are associated with T1DM

A

HLA DR3/HLA DR4

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6
Q

What is the pathogenesis of T1DM?

A

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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7
Q

What does insulin do?

A

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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8
Q

How may a patient with T1DM look like?

A

YOUNG, LEAN AND WHITE

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9
Q

DX T1DM

A

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

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10
Q

Tx T1DM

A

BASAL-BOLUS REGIMEN

Basal - Slow acting
glargine/detmire

Bolus - Fast Acting
Novorapid (Aspart)

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11
Q

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

A

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

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12
Q

What are the macrovascular complication of Diabetes?

A

Cardiovascular - IHD, HF, PVD
Cerebrovascular disease- Stroke

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13
Q

what are the microvascular complications of diabetes?

A

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

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14
Q

What is the main acute complication of T1DM?

A

DKA - Diabetic ketoacidosis

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15
Q

How Does T1DM lead to DKA?

A

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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16
Q

How would someone with DKA present

A

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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17
Q

What is the diagnostic criteria for DKA involve?

A

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

18
Q

How is DKA mananged?

A

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

19
Q

in Hypoglycemia what do you give to patients?

A

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

If reduced GCS - IV glucose / IM glucagon

20
Q

What is the pathology of T2DM

AND ASSOCIATED RF

A

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

RF:
Steroids/Cushing’s
Chronic pancreatitis

21
Q

T2DM risk factors

A

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

22
Q

presentation of T2DM

A

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)

23
Q

1st line management of T2DM

A

Lifestyle changes for allll

24
Q

Tx T2DM

A

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

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

25
Q

Metformin MOA and SE

A

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

26
Q

Sulphonylurea E.g Glicazide MOA / SE

A

Acts on B cell to promote insulin secretion

SE - Wt Gain/ Hypoglycemia/ GI disturbance

27
Q

Pioglitazone MOA / SE

A

Reduces peripheral insulin resistance / Increases glucose metabolism

SE - Bone fracture/ Wt Gain
CI - HF

28
Q

DPP4i e.g sitagliptin MOA / SE

A

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

29
Q

SGLT2 inhibitor

A

Inhibits sodium-glucose 2 co-transporter to reduce glucose reabsorption and increase urinary glucose excretion

SE: DKA, Uti, Back Pain

30
Q

What are the glucose range for OGTT?

A

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

31
Q

What are the glucose range for FPG?

A

First measure taken at OGTT is considered FPG

Normal <6
Prediabetic -6.1-6.9
DM >7

32
Q

What does it mean if someone has impaired fasting glucose IFG

A

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

33
Q

What does it mean if someone has impaired glucose tolerance IGT

A

Prediabetic patient w/ muscle insulin resistance

OGTT - 7.8-11
FPG<6mmol/l - Normal

34
Q

What is the main acute complication of T2DM?

A

Hyperosmolar Hyperglycaemic State - HHS

This in turns causes severe osmotic diuresis

35
Q

What causes hyperosmolar hyperglycaemic state?

A

Excess gluconeogenesis and lipolysis result in hyperglycaemia.-> Osmotic diuresis

However sufficient insulin to prevent ketogenesis (DKA)

36
Q

What are the diagnostic criteria for HHS?

A

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]),

37
Q

HHS TX

A

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

38
Q

Describe Insulin release?

A

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

39
Q

What does HbA1c represent?

A

Measure of glycated haemoglobin over the previous 3 months

Measures: >48mmol/L or >6.5% or greater is diagnostic but less is not definitive

40
Q

When cant we use HbA1C

A

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

Endocrine (9 decks)

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