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Patho > DM > Flashcards

DM Flashcards

1
Q

Defintion: a group of common ____ disorders and share the ___ of ____ that affects multiple ___ _____

A

metabolic disorders
phenotype
hyperglycemia
organ systems

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2
Q

Types of diabetes are caused by ___ and ___

A

genetics and environmental factors

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3
Q

Factors that can contribute to hyperglycemia are: (3)

A
  • reduced insulin secretion
  • decrease glucose utilisation
  • increased glucose production
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4
Q

What are some consequences of diabetes?

A
  • adlult blindness
  • amputation
  • end stage renal disaes (ESRD)
  • CV disease
  • burden on helath care system and those affected
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5
Q

Broad categories of DM

A

type 1 and type 2

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6
Q

some other categories of diabetes

A

MODY
Gestational DM

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7
Q

Which diabetes do we need insulin to survive and which is it just to control glucose levels with?

A

type 1 - survive
type 2 - control

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8
Q

Where are the three diagnostic measuring tools and what does each one stand for?

A

FPG - fasting blood glucose
OGTT - oral glucose tolerance test
HbA1c - average glucose levels over past 1 -2 months

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9
Q

The diagnostic range for normal glucose homeostasis - values?

A

FPG < 5.6 mmol/L
OGTT < 7.9 mmol/L
HbA1c < 5.7 %

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10
Q

The diagnostic range for impaired glucose homeostasis - values?

A

FPG 6.1-6.9 mmol/L
OGTT 7.8 -11 mmol/L
HbA1c 5.7-6.4%

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11
Q

The diagnostic range for DM - -values?

A

FPG > 7.00
OGTT > 11
HbA1c >= 6.5

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12
Q

What lab values are recommended to use for screening purposes?

A

FPG
HbA1c

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13
Q

what are some screening recommendations?

A

aboe 45 screen every 3 years or if BMI is over 25

  • can be asptomatic and unaware
  • can have for a decade without knowning
  • if we find pre-diabetes values we can maybe prevent DM
  • early tx can alter course of DM
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14
Q

Talk about glucose hometostias. like when we have too much glucose vs when we have low levels

A

too much - message send to pancreas and brain - B isletes cells produced (insulin produced) - fat and msucle take in glucose form the blood

Too little - message sent to brain and pancrease - glucagon relase by al[ha cells, liver relases glucose into blood

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15
Q

Role of incretins? what stimulates them?

A

incretins are used for hormonal regulation

they are stimulated by the ingestion of food in the gut

The kinds of incretins are:
1. glucose-dependent insulinotropic polypeptide (GIP)
2. Glucose 0like peptide 1 (GLP-1)

They:
- stimulate insulin production and inhibit glucagon
- promote proliferation of beta cells and inhibit apoptosis
- GLP-1 delays gastric emptying and increases satiety

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16
Q

what delays gastric emptying and increases satiety

A

GLP-1

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17
Q

If we have low arterial glucose comment on what happens along the brain pathway (already covered pancreas pathway)

A
  • stimulate pituitary hormone, growth factor, ACTH Adrenal cortex and then cortisol levels
  • increases sympathoadrenal outflow so adrenal medullae produce more ephedrine and sympathetic postganglionic neurons increase norepinephrine and acetylcholine

Epinphrine - stimulates liver whihc causes increase glucose and arterila glucose

norepehinre and acetycholine cause ingestion and less glucose clearance whihc causes increase in arterial glucose

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18
Q

Hypoglycemia activates what 3 responses in Dm and in Dm people?
What are the results of these?

A

pro-inflammatory, pro-coagulant, pro -atherothrombotic

Results:
1. increase platelet aggregation
2. increase intravascular aggreagtion
3. decreased arterial vasodilation mechanisms

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19
Q

Where is insulin produced?

A

in the pancreas by beta cells of the islets of langerhans

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20
Q

What are some other pancreatic cells and their functions?

A

alpha - glucagon production
delta - produce somatostatin
F - produce pancreatic polypeptide

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21
Q

Synthese and insulin production

A

2 insulin chain with high molecular weight are synthesise and called preproinsulin

after this is sequestered in the lumen of the endoplasmic reticulum they are cleaved by porteases into insulin and C-peptide in the scretory glands of beta- cells

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22
Q

Insulin scretion

A

glucose enters the beta cell via GLUT

via glucokinase, ATD is generated

ATP then blocks the ATP-sensitive K+ channel meaning that K is effluxed out of the cell.

The cell is then depolarized and ca enter via a calcium voltage-dependent channel.

This stimulates insulin exocytosis from the cell

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23
Q

Insulin receptor and action

A

Insulin attaches to receptor and tyrosine kinase intrinsic activity is stimulated

the receptor autophsophoryaltes

Actiavting PI-3 kinase

then GLUT4 translocates from inside of cell to cell surface

Glucose is taken up by sketal muscle or fat

24
Q

What are the effects of insulin on the body sepcifically on carbohydartes,

A

carbohydrates (muscle, adipose tissue and liver) :
- increase in glucose uptake, oxidation, storage
- increase in glycogon synthesis
- decrease in gluconeogenesis
- decrease in glycogenolysis

25
Q

What are the effects of insulin on the body sepcifically on AA and proetins

A

AA and proetins (muslcle):
- increase in aa uptake and protein synthese
- decrease in aa release

26
Q

What are the effects of insulin on the body sepcifically on lipids

A

Lipids (adipose tissue and liver):
- increase in triglyceride synthesis
- decrease in free fatty acid and glycerol
- decrease in oxidation of FFa to ketoacids (liver)

27
Q

what kind of activty does inuslin produce in the body?

A

anabolism effects (conservative)

28
Q

Type 1 DM is the reuslt of what? whats the consquence?

A

autoimmunity against pancreatic beta cells

consquence: Complete or near total inuslin loss

29
Q

Immunogenic Markers of T1D

A

Islet cell autobodies (ICA) :

GAD, insulin, IA-2/ICA-512 and ZnT-8

Present in 85% of people diagnosed with T1d

5-10% for T2D

3-4% in first degree relative

30
Q

ICA combined with what helps us predict DM. and what are the predictions?

A

ICA with IV GTT:
- 50 % will get Dm in 5 years
- 70% t1d in 10 years
- 80% Dm in 15 years

31
Q

Etiology of T1D can be ___ or ____

A

immune-mediated or idiopathic

32
Q

What autoimmune markers or HLA association offer protective or put you are risk?

A

Class II MHC genes (HLA region on chromosome 6)
Haplotype: 301, 302, 201 - strong risk
Haplotype: 102, 602 = protective factors

33
Q

what environmental factors can cause T1D?

A
  1. Molecular mimicry - rubella, Coxsakievirus, protein (GAD), bovine milf proteins
  2. Vit D defieincy
  3. microbiome
34
Q

Age for T1D

A

usualy before 20

35
Q

do all have evidence for islet-directed autoimmunity?

A

no, some but not all

36
Q

Those that lack immunologic and gentic markers have what assumptions amde for them (3)?

A
  • insulin defeiceny is due to unknonw, nonimmune mechanisms
  • are prone to ketosis
  • many are of afriacn american or asian heritage
37
Q

humoral and cellualr abnormallities in T1D

A
  • islate cells antibodies, avticated lymphocytes, T lymphocytes, cytokines release within the insulitis
38
Q

Explain what happens when we don’t have enough insulin?

A

no beta cells
no insulin availble to cells
no glucose entering cells
glucose acucmulates in blood
- cells satrve (less ATP prpduction) -less energy = tired = difficulty concenrtraion
compensetory mec is activated

39
Q

Compensatory Mechanisms for hyperglycemia

A

Catecholamines release Ne/Ep which increase glycogenolysis in liver

Cortisol released promotes gluconeogeneis

Increased ICP
- dehydration

kideney increases (GFR)
- polyuria
-glusaria

Thirst center
- polydipsia

40
Q

complications of chronic hyperglycemia

A

HTN, CVD, ESRD, stroke

  • effects are vascular or neuropathic
41
Q

Vascular complications categorized as what?

A

Macrovascular
- leads to CVD and stroke

and microvascular
- retinophathy and nephropathy

42
Q

Expand on microvascular complications

A
  • hyperglycemia disrupts platelt function and gorwth of basment membrane
  • thickening of basement membrane may improve glycemic control
  • risk factors of microvascualr complications include HTn nad smoking
43
Q

Some overall complications of t1D

A
  • increased risk of infection
  • rapid growth of gersm
  • reduce defense agaisnt gersm
    (poor skin helaing or affects to WBC that can’t get to site to bind due to altered blood suppple or due to phagocytic fucntion of cells)
44
Q

Diabeteic ketoacidosis

A

increased lipolysis, FFA, ketoacids, ketosis, and ketoacidosis

45
Q

How do we manage DKA?(4)

A
  1. insulin
  2. water sodium and potassium replacemnt
  3. bicarbonate replacemnt
  4. normalization of glucose level s
46
Q

insulin therapies?

A
  1. BID
  2. Continouse sc insulin infusion (pump)
  3. Multple daily insulun injectiosn (MDII)
47
Q

T2D gentic compont?

A

yes

48
Q

Definiton: T2D a ___ ___ disease with strong ____ componet

A

polygenetic, multifactorial disease with a genetic component

49
Q

Cause of T2D, contributing factors?

A

Fro every knonw, one unknonw

obesity contributes

50
Q

Defect in ___ for T2D

A

defect in insulin resistacne - change in number or seniticity of insulin receptos leads to developing insulin resistacne

51
Q

what is T2D characterized by?

A
  1. impaired insulin secretion
  2. excesscive haptic glucose production
  3. abnormal fat metabolism
  4. systemic low - grade inflammation
  5. overprodution and secrtaion for glucagon - therefore more glucose over production
52
Q

DM and FFA, Lipotoxicity, inflammation, amylin

A

with obesity FFA increase

  • lipotoxicity: decrease signalling in IRs pathway so less adiponectin and leptin levels
  • inflammtion: PPAR(Y) by TNF
  • Amrylin deposition may cause decreased insulin secretion
53
Q

MODY 3 vs MODY 5

A

MODY 3
- respond to sulfonylureas
- mutation in HNR-1 alpha

MODY 5
-minmial repsonse to sulfonylureas so insulin required
- mutation in HNF -1 beta

54
Q

T2D ketoacidosis?

A

no

55
Q

Managment of t2d

A
  1. diet and excerise
  2. oral hypoglymic
  3. two OH
  4. OH and insulin
  5. Insulin
  6. insulin plus TZD

Patho (8 decks)

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