Diabetes physiology review Flashcards

1
Q

= storage hormone and ‘puts away’ excess sugars into fats and glucogon

A

Insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Proinsulin = C-pep + insulin ; when you see increasing C peptides and insulin levels = _____

Vs someone overinjecting insulin only see elevated insulin levels, not C peptide

A

endogenous source

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Insulin stimulated glucose uptake in skeletal + heart msl, fat tissue

A

Glut 4:

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

: B-cell gluose sensor; transports out of intestinal an renal epithelial cells; on B islet cells, liver, sm intestine and kidney

A

Glut 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Insulin effects:

A

tissue uptake and sequestration of glucose, Fas, AAs and decrease in plasma levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Control of insulin secreation: Gluose**, AA, FA,…

Amplified by :

Inhibited by :

A

GI hormones

somatostatins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

High levels of AA act on the Alpha cells to produce______ in the pancreas

A

Glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

High levels of Glucose, Insulin, SST, Ketones and FFA_____ release of Glucagon by Alpha cells

A

inhibit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Secreated from gut in response to feeding::: Acute- increases insulin response to glucose

A

GLP: glucagon like peptides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

= islet cell destruction

= insulin resistance

A

Type I: T1DM= islet cell destruction

Type 2: T2DM = insulin resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

= principal stimulus for insulin release from pancreatic β-cell.

A

Glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

also stimulates release of insulin; acts in other places as well but as more AMPLYFING effect thus not great for drug therapy

              à promotes feeling full, slows gastric emptying, inhibits glucagon secreation
A

**GLP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

: chronic metabolic disorder w/ characteristic complications + hyperglycemia

              disease of metabolism: usually insulin/glucagon/SST from pancrease--\>

when this system becomes disrupted can lead to it

A

Diabetes mellitus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

. Diagnosis of Diabetes Mellitus

HbA2c > or =____

         Fasting plasma glucose \>/= \_\_\_

 2 hr pl glucose \>/=\_\_\_\_ w/ glucose tolerance test

Random glucose >/= ___mg/dL

A

6.5%

126

200

200

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

measure of glycosylated hemoglobin at the terminal valine of the beta chain. Glucose is non-enzymatically attached to proteins. w/ higher concentration and the longer the exposure to glucose, more glycosylation occur

A

HbA1c:

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Dx of Pre-diabetes:

Fasting plasma glucose:

2hr pl glucose= ____ after 75 g oral glucose tolerance test

A1c of _____

A

Fasting plasma glucose: 100-125

2hr pl glucose= 140-199 after 75 g oral glucose tolerance test

A1c of 5.7 -6.4%

17
Q

Short term complications of diabetes mellitus left untx

A

elctrolycte abnormal, fatigue, poor wound healing, impaired immune, prolonged hospital stay, increase inpatient morbidity and mortality, diabetic ketoacidosis, hyperosmolar hyperglycemic state, tx related hypoglycemia

18
Q

retinopathy, nephropathy, neuropathy; damage to small nutrient vessels; see micro hemorrhages causing accumulation of excudates in the retina; lots of vascular leakage into macular area

A

All long term complication related to Microvascular diabetes mellitus complications

19
Q

CAD and peripheral vascular disease; blindness, kidney fail, amputation, heart attack, stroke

A

Macrovascular complications form long term diabetes mellitus

20
Q

What is the pathogeneis of diabetes mellitus complications

A

Pathogenesis of DM complications:

accumulation of advanced glycosylation end products, accum sorbitol, disrupt hexosamine path, disruption of protein kinase C path, activation of poly ADP-ribose, increased oxidative stressà all this shit accumulates

21
Q

: autoimmine B cell destruction with lack of insulin

: insulin resistance with relative insulin deficiency

A

Type 1

Type 2

22
Q

What happens in gestational diabetes?

A

Gestational: insulin resistance with B cell dysfunx; Pregnancy is an insulin resistance state; the placenta secretes hormones which cause insulin resistance in the mother, so that nutrients can be directed to the growing fetus

23
Q

Type 2 DM Pathophysiology:

A

insulin resistance and impaired insulin secretion.

24
Q

Initially, due to genetic predisposition and poor lifestyle, patient develop insulin resistance: how does the pancreas respond to this?

A

At this time the pancreas increases insulin secretion to maintain good glycemic control in the face of the insulin resistance. Over time, insulin secretion wanes and hyperglycemia and diabetes mellitus develops.

25
Q

Prior to developing diabetes mellitus type 2, patients with obesity demonstrate insulin resistance, requiring more insulin release to maintain normal glucose levels. This insulin resistance is more pronounced in patient with

A

truncal adiposity

26
Q

potent and sensitive marker for T1DM is increased levels of______ that primes CD4 cells to help other shit differentiate into Pancrease B cell attack monsters

A

GAD65

27
Q

What is the ‘natural’ history or timeline for people with T1DM

A

. Natural history: have genetic predispositionà overtime will get insults to B cells and accumulate injuryà move into prediabets as insulin production decreaeses and when pts present with diabetes often have lost 80% function

28
Q

What lab values are seen in untreated T1DM ?

A

hypOnatremic

hypOkalemic

low bicarb

29
Q

Why do se we hyponatremia in T1DM that are untreated?

A

d/t osmotic dilution of plasma from hyperglycemia (causes water to leach out)

30
Q

Low “carbon dioxide” or bicarb: d/t________: Insulin deficiency and increased plasma concentrations of glucagon, cortisol and epinephrine increase glucose production, lipolysis and ketogenesis which collectively contribute to the development of both the hyperglycemia and the ketoacidosis

A

ketoacidosis

31
Q

Sytmptoms of T1DM

A

increased thirst (polydipsia), increased urination (polyuria), bedwetting (enuresis), weight loss, increased hunger (polyphagia), and fatigue

32
Q

How do we Dx T1DM in kids?

Fasting blood sugar > ____ mg/dL x 2 or

random BG >____mg/dL.

Oral glucose tolerance test that peaks over___

A

126

200

200

33
Q

what are twom markers we see for diabetic ketoacidosis?

A

increased levels of acetoaceteate and B-hyprocxybutyrate

34
Q

Insulin Overdose; see hypoglycemia of glucose >___

what syptoms do we see?

A

70

See adregeneric symptoms: tachycardia, dizzy, sweaty and hunger.

35
Q

How do we tx hypoglycemia:

mild

moderate

severe

A

Tx with oral fast acting carbs: juice and recheck 15 mins

Moderate hypoglycemia: neuroglycopenic symptoms: confusion, combativeness, poor coordination, slurred speech. Tx w/ fast acting carbs like frosting or sugar gel

Severe: stupor, seizure, coma; get Glucagon injections once EMS is called

36
Q

T1DM in adults: latent______ diabetes of Adults

5-15% of adults with DM express anti-islet autoantibodies and progress relatively fast (3 years) to insulin-requiring diabetes

____alleles seen as link

A

autoimmune

HLA