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Patho > Diabeetus > Flashcards

Diabeetus Flashcards

1
Q

Functions of insulin

A 
Stimulates taking GLUT4 transporters from vesicles and places them on the cell membrane
Antagonizes glucagon release
Signals that we are well fed and it's time to repair things
Acts as a growth factor
Stimulates protein synthesis
Increases amino acid uptake 
Trigger glycolysis (to make ATP)
Triggers glycogen synthesis
Stimulates fat storage (TG synthesis)
Acts as an appetite suppressant
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2
Q

Insulin receptor

A

The insulin receptor is a dimer. When insulin binds, the dimers come together, creating the active insulin receptor. It triggers a bunch of intracellular stuff that results in GLUT 4 receptors being placed on the cell membrane, as well as increase transport of amino acid, potassium, magnesium, and phosphate.

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3
Q

How does giving insulin and glucose lower K+ levels in the cell?

A

Causes a bunch of glucose to enter the cell, make a shit-ton of ATP, makes the Na/K/ATP pump run faster and bring more K+ into the cell.

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4
Q

These cells do not rely on insulin for glucose uptake

A

Neurons and cardiomyocytes
(they have insulin receptors, but probably serve more as a growth factor effect than serve to bring glucose into the cell)

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5
Q

What happens to glucose taken up by muscle cells?

A

Converted to glycogen or fat. Muscles can store glucose in either of these forms within the cell.

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6
Q

Can we convert fat into glucose?

A

NO. However, we can use the glycerol on a TG to make glucose.

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7
Q

Why are diabetics more prone to DKA than non-diabetics?

A

Because they make ketones at a VERY high rate

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8
Q

This organ tries to maintain BG levels between meals

A

Liver

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9
Q

These two cell types can ONLY use glucose

A

Brain and RBCs

However, the heart and skeletal muscle are able to burn fat.

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10
Q

Alpha cells make ____ and beta cells make ___. Delta cells make ____.

A 
Alpha = glucagon
Beta = insulin
Delta = somatostatin
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11
Q

Insulin secretion is stimulated by _____.

Glucagon secretion is inhibited by ____.

A

Glucose.

Insulin.

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12
Q

How is insulin released from beta cells?

A

GLUT 2 receptors on beta cells (always there) bring in glucose. Rate of uptake depends on glucose concentration. Once inside, a shit ton of ATP is made. This ATP acts as a signal to close the ATP-sensitice K+ channel. Because it is now closed, K+ builds up and results in depolarization. This depolarization activates voltage-sensitive Ca channels. Ca++ rushes in and causes release of insulin-filled vesicles.

Thus overall, increased glucose = increased ATP = increased insulin release.

Low glucose = low ATP = low insulin release.

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13
Q

What are ketones a sign of?

A

They are a sign that we’re burning fat.

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14
Q

What is more common, type 1 or 2 DM?

A 
Type 2 (90% of cases)
Type 1 (10% of cases)
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15
Q

What is MODY?

A

Maturity onset diabetes of youth
Basically, your B cells are there, but defective in either making insulin or releasing it. This form can be treated with oral hypoglycemics.

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16
Q

In the pregnant woman, is BG controlled by the fetus or the mother?

A

The fetus, because it is essential that the fetus receives enough glucose for development.

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17
Q

These endocrine disorders can cause diabetes

A

Cushing’s, acromegaly, or pheochromocytoma

because cortisol, GH, and NE all try to increase BG levels

18
Q

What is beta cell exhaustion?

A

The way that beta cells are killed in Type II diabetes

basically, so much intracellular glucose, that these high levels start killing the cells -> glycotoxicity

19
Q

Type 1 DM is due to a type __ hypersensitivity reaction

A

IV

20
Q

Do we see DKA in type 2 DM?

A

Not usually, because high insulin levels exist, which keeps glucagon low. Later in cell if B cells are destroyed, high glucagon can result in DKA.

21
Q

Diagnosis of DM

A

Fasting BG > 126

OR

BG > 200 after 2 hours during an OGTT

22
Q

Pre-diabetes is also called

A

Impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT). These are two different things.

IFG is BG of 100-125 after overnight fast.
IGT is BG of 140-199 after 2 hours during an OGTT.

23
Q

___% of Americans have pre-diabetes

A

40%

Most of these people will go on to develop full-on DM. But! There is a lot you can do to prevent developing DM!

24
Q

Hypoglycemia dx and s/s

A

BG < 70

Mild:
Hunger, shakiness, paleness, sweating, anxiety, blurry vision

SEVERE:
Extreme tiredness, confusion, combativeness, dazed appearance, seizures, unconsciousness, coma, DEATH

25
Q

Formula for filtered load

A

Concentration x GFR

26
Q

Tmax reabsorption for glucose

A

300mg/min

27
Q

Can the brain burn ketones?

A

Yes, but it takes a few days for it to switch gears and be able to use this source

28
Q

Basic problem with DKA

A

Often happens due to insufficient exogenous insulin, or is the first sign of DM. Also, anything that raises stress can increase risk of DKA.

Not enough insulin causes excessive glucagon. This causes increased glucose release from the liver and life-threatening levels of hyperglycemia (can cause brain damage). High glucagon also causes ffas to be converted to ketones for energy, causing ANION GAP acidosis. The high glucose also causes osmotic diuresis and hypovolemia and electrolyte disturbances. They hay also have N/V, contributing to the dehydration and electrolyte disturbances. There will be glucose and ketones in the urine!

29
Q

How does HONKS occur

A

Similar to DKA, but in Type II patients. Some sort of stressor increases BG levels. This causes osmotic diuresis and extremely high BG levels and osmolarity. Insulin is present in this syndrome however, so ketones are not produced, and person does not become acidotic.

30
Q

What normally happens to glycosylated proteins in our body?

A

They are eaten by macrophages. In diabetes, macrophages can’t keep up, and levels of glycosylated proteins increase.

31
Q

Chronic complications of DM

A 
Retinopathy
Cataracts
Glaucome
HTN
CVA
CAD/MI
PVD
Gangrene
Peripheral and autonomic neuropathies
Gastroparesis
32
Q

Unchecked BG causes production of

A

Advanced glycosylation end-products (AGEs)

33
Q

Production sequence of AGEs

A

Glucose + protein => Schiff Base => Amadori Product => AGE

HbA1C looks for Amadori Products
AGEs are what macrophages clear
Progression to AGE is irreversible

34
Q

How does DM cause kidney failure?

A

A fuck-ton of macrophages hang around the glomerulus, eating up AGEs. Macrophages being active here damage the glomeruli

35
Q

HgA1C looks for these products

A

Amadori products

36
Q

Damaging chemical properties of AGEs

A

They cross-link polypeptides of same protein (collagen)
They trap non-glycosylated proteins (LDL, Ig, complement)
They resist proteolytic digestion
Induce lipid oxidation
Inactivate NO
Bind nucleic acids

37
Q

AGEs bind to these receptors and induce

A

AGE receptors (RAGE) on monocytes and mesenchymal cells, causing:

1) Monocyte emigration
2) Increased vascular permeability
3) Cytokine and growth factor secretion
4) Procoagulant activity
5) Enhanced cellular proliferation
6) Enhances ECM production

38
Q

Normal HbA1C is ____ and we want diabetics to be less than ____

A

4-5

7

39
Q

Should the goal of DM II be lifestyle modification or HbA1C reduction?

A

Life-style modification!!!

40
Q

Two phases of diabetic retinopathy

A

Background retinopathy- early phase, retinal arteries are weak and form small, dot-like microhemorrhages, causing patchy vision loss

Proliferative retinopathy- the retina is now become ischemic. New and fragile vessels proliferate to compensate, but these hemorrhage easily.

41
Q

How to prevent type II DM

A

Diet

  • Weight loss increases insulin sensitivity (more space in those fat cells!)
  • Omega 3s seem to help decrease incidence and complications of type 2 DM

Exercise

  • Exercising muscle doesn’t need insulin for glucose uptake
  • Single bout of aerobic exercise increases insulin sensitivity for 48-72 hours

Patho (14 decks)

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