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3.1 cards > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Pancreatic cells
alpha -________
Beta - ________
Delta - _____

A

Islet Cell - alpha in the middle and beta around
Alpha = glucagon
Beta = insulin
Delta = somatostatin

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2
Q

Mnemonic for causes of pancreatitis

A

I GET SMASHED

I: idiopathic
G: gallstone; common bile duct/obstruct Ampulla of Vater —> obstruction- backflow causes lysis of pancreatic cells – pancreatitis
E: ethanol (-OH)
S: steroids
M: mumps (paramyxovirus) EBV CMV
A: Autoimmune as PAN & SLE
S: Scorpion sting – tityus trinitatis-trinidad/ snake bite
H: hypercalcemia, hyperlipidemia, hypertriglyceridemia and hypothermia
E: ERCP (endocopic retrograde cholangio pancreatography)
D: drugs (SAND-steriods & sulfonamindes, azathioprine, NSAIDS, diuretics, duodenal ulcers)

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3
Q

Overall action of insulin

A

A- Promotes synthesis of energy reserve —> anabolic action
B- Released by B-cell due to increased glucose in the blood
C- Inhibit carbohydrate degredation
G- Inhibit gluconeogenesis
U- Stimulates uptake of glu, aa, FFA into cells, reduces concentration in blood

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4
Q

Action of insulin in adipose

A

put glu in, stop fat breakdown and increase fat production
Increase glucose uptake
Increase Lipogenesis
Reduced Lipolysis

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5
Q

Insulin action on liver

A

glycogen (Sugar storage), increase fat production, reduce sugar production
Increase glycogen synthesis
Increase lipogenesis
Reduce gluconeogenesis

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6
Q

Insulin action on striated muscle

A

Take up glu, make glycogen (sugar storage) and protein
Glucose uptake
Glycogen synthesis
Protein synthesis

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7
Q

Counter-hormones to insulin

A

GAC
Glucagon (liver only)
Adrenaline (liver and muscle)
Cortisol

Muscle = increase proteolysis
Adipose = increase lipolysis
FFA for energy

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8
Q

T2D basic pathway

A

Genetic predisposition + obesity lifestyle factors —> insulin resistance —> compensatory B cell hyperplasia (Normoglycemia) —> B cell failure (impaired glu tolerance) —> B-cell fail (Diabetes)

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9
Q

Cause of Insulin resistance

A

Increased hepatic glu production
Reduced peripheral glu uptake and utilisation
Dyslipidemia
All increase demand for insulin

IR = hyperglycemia + hypertriglyceridermia

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10
Q

Insulin resistance to T2D

A

Initially increase demand = increase size

In susceptible B cell w/ genetic risk = failure for B cell to compensate and increased glu and FFA —> glucolipotoxicity

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11
Q

Beta cell dysfunction and growth genes

A 
HNF1a
HNF4a
Kir6.2
TCF7L2
Mitocondrial
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12
Q

Insulin receptor is a type of

A

Tyrosine kinase

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13
Q

Rapid and long-term role of insulin signalling

A

Rapid = glu uptake via GLUT 4 translocation, enzyme activation
Long term = enzyme synthesis, cell growth

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14
Q

Termination of Insulin receptor signalling

A

Protein phosphatases like PTEN and PTPN1 dephosphorylate residue on the receptor or downstream kinases

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15
Q

-Ive feedback of insulin signalling is modulated by

A

IRS protein on Ser residue terminates Insulin signalling
IRS protein on Ser residue is phosphorylated by downstream kinases in insulin pathway.
IRS detaches from receptor and changes docking of signalling protein + its degredation —> terminates insulin action

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16
Q

Cause of hyperlipidemia in diabetes

A

Excess glu in liver (GLUT2)

Glu in liver turns to TG by increased hepatic de novo lipogenesis

17
Q

Effects on IR on lipid metabolism and liver

A

Overall increased FFA and TG

  1. increased lipolysis and reduced Fat storage = increase FFA
  2. Reduced VLDL and cylomicron clearance due to reduced LPL activity = increase TG
  3. In liver excess TG production
    —> fatty liver
18
Q

Diabetes is defined by

A

Insulin deficiency

Glucagon excess

19
Q

Role of glu on glucagon

A

Normally Glu reduced glucagon release

Alpha cell still release glucagon

20
Q

Role of GLP-1 in insulin secretion

A

GLP-1 = from gastrointestine

  1. Acts on GLP-1 receptor on B-cell to increase glu dependant insulin release via ACh, MR and cAMP
  2. Suppress Glucagon release
21
Q

Impact of high Glu

A

High glu but blocked from going into cell

  1. Cell uses FFA oxidation to produce Ketone body —> acidosis
  2. Glucouria —> polyuria —> dehydration —> polydypsia
22
Q

Metabolic syndrome in IR- what causes the inflammatory state in insulin resistance

A

Excess energy —> adipose = hypertrophy and hyperplasia , vascular doesn’t keep up —> necrosis, apoptosis and pro-inflammatory response

23
Q

Kinases inhibiting Insulin’s action

A

JNK

IKKb

24
Q

Release of kinase inhibiting action of insulin is mediated by

A
  1. Hyperlipidemia and hyperglycemia causing mitocondrial dysfunction and oxidative stress
  2. Necrotic debris, inflammation and saturated fatty acids activating kinases
25
Q

FFA effect on vasculature

A

Increase constriction
Reduce relaxation
(Via Adrenaline)

26
Q

Presentation of Type 1 Diabetes

A

Weight loss
Muscle weakness
Increase appetite (polyphagia)
Polyuria (osmotic diuresis), polydipsia (plasma osmolality stimulates thirst)

Increased chances with other autoimmune - graves, hashimoto, Addison’s , coeliac

Freq skin infection + thrush

27
Q

What are the values for diagnosing diabetes

A

HbA1c >6.5 %

Fasting flu >7.0 and random >11.1

Oral tolerance (2 hr) >11.1

28
Q

Complication of T1D

A

Ketoacidosis

29
Q

Presentation of T2D

A 
Often aymptomatic, 
Mild metabolism - polydipdia, polyuria
Often in obese people 
Tiredness/malaise/fatigue
Nocturia 
Freq skin infection and Freq thrush
30
Q

How do you test for peripheral Neuropathy

A

Reflex - tendon reflex

Sensation (cotton wool, 10g monofilament, neurotip)

31
Q

Who do you screen for T2D

A
    • people w/ impaired fasting glu or impaired glu tolerance
    • age >40 yr
    • Age >30 w family hx, obesity or hypertension
    • Age >20 in high prevalence ethnic group - ATSI, Pacific Islander
    • previous gestational diabetes, history of large babies
    • long term steroid use or atypical antipsychotic
    • PCOA esp overweight
    • CVD + other risk

Screen every 3 years from 40

3.1 cards (13 decks)

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