Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

SMUSPG-PHY1 > ENDO-INSULIN > Flashcards

ENDO-INSULIN Flashcards

1
Q

Why is blood sugar important?

A

Blood sugar essential for brain function in vertebrates, 40 % of it is used by brain

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

Describe the insulin responsibility

A

Stability of blood sugar

signals uptake and storage of carbohydrates, lipids and amino acids.

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

Is insulin catabolic or anabolic?

A

Anabolic

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

What did Banting and Best do to contribute to diabetes

A

1] Created diabetes in dogs by disabling pancreas,
2] Reversed diabetes in dogs WITH extracts of pancreatic products, discovered insulin,
3] Best discovered heparin

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

Describe how glucagon and adrenaline effect on cells in healthy people

A

Glucagon and adrenaline V cAMP V protein kinase A to phophorylate pyruvate dehydrogenase

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

Describe how insulin effect on cells in health people

A

Works in the opposite

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

Describe how insulin effect on cells in diabetes

A

DSFX-
type 1 -no insulin,
type 2- cells don’t respond to insulin_nothing stops glucagon and adrenaline from elevating glucose and ketones

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

What secretes insulin?

A

Beta cells of islets of langerhaan

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

Describe the insulin receptor.

A

Transmembrane
2 alpha,
2 beta subunits: auto phosphorylate intracellularly; Tyrosine kinase activity

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

What are the effects of intracellular insulin signalling?

A 
1] increase Glucose transport, 
2] protein synthesis, 
3] glycogen synthesis, 
4] inhibition of lipolysis, 
5] inhibition of hepatic gluconeogenesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the effect of carbohydrate metabolism of insulin

A

1] Uptake of glucose by facilitated diffusion hexose Transporters (GLUT4) incorporated in vesicles when insulin low;

2] Insulin promotes glycogen storage by activating hexokinase but inhibiting glucose 6-phosphatase

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

What tissues are non-insulin dependent?

A

Brain and liver

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

Why is phosphorylation important in glucose storage

A

keeps glucoses inside the cell (via hexokinase), because it makes it polar

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

Does glucose storage require ATP?

A

Yes, during phosphorylation into G6P

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

What are the effects of insulin on fats

A

When liver is saturated with glycogen, hepatocytes shunt glucose to fatty acid synthesis, exported as lipoproteins (HDL, LDL), Adipocytes use FA to synthesize triglycerides,

insulin inhibits enzymes that break down triglycerides

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

What are the effects of insulin on proteins

A

Insulin promotes incorporation of amino acids into cells, Protein degradation when insulin levels are low because body thinks a lack of sugar = lack of energy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the effects of insulin on Na/K pumps

A

increases potassium within cells

DKA- insulin admin will lower blood K levels
L/T CV, Death
GO SLOW will help

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What happens when there is high blood glucose?

Low Blood glucose

A

HIGH- Beta cells- release insulin and fat cells take in glucose

LOW- alpha cells- release glucagon and liver releases glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Define diabetes mellitus

A

Disorder of metabolism related to insulin deficiency or insensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Why does type 2 diabetes eventually look like type 1

A

State of pseudostarvation- sugar levels are high but cells don’t use/access appropriately -

resort to FA metabolism as if they were starving

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What does diabetes mellitus most commonly cause?

A

Blindness in adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What cell releases Insulin (lowers BG by increasing transport to muscle, liver, adipose)

A

beta cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What cell releases glucagon (increases BG by stimulating gluconeogenesis, glycogenolysis)

A

alpha cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What cell release somatostatin (delays intestinal absorption of Glu, inhibits GH, TSH)

A

delta cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What do Acinar cells release

A

exocrine digestive enzymes(amylase, lipase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is difference btwn type 1 and type 2 diabetes

A

Beta cell destruction by autoimmunity or idiopathic cause

disorder of insulin resistance, secretory disorder possible (90-95%

NO longer Juvenile or Adult onset.
Can both occur any age

27
Q

What are other causes of diabetes?

A 
genetic defects in beta function, 
insulin action, 
CF, 
Cushing, 
drug effects, 
infections, 
gestational
28
Q

What is the difference between DM type 1A and 1B

A

1A: immune mediated- MOST COMMON
1B: idiopathic

29
Q

Describe the pathophysiology of DM type 1

A

Lack of insulin -> Glucose accumulation in blood -> Ketoacidosis common due fatty acid metabolism

30
Q

Why are type 1 DM usually thin?

A

type 1 DM do not make insulin
Insulin inhibits lipolysis and FA metabolism
Thus rapeant lipolysis in TYPE 1, which predisposed to DKA

31
Q

What are the laboratory evaluation of type 1 DM?

A 
Testing by detection of autoantibodies to insulin (IAA), glutamic acid decarboxylase (GAD)
tyrosine phosphatase (IA-2)
32
Q

What is DM type 2?

A

Hyperglycemia + relative insulin deficiency (high, normal or low)

33
Q

What age is expected for onset of type 2 DM?

A

typically older

“adult onset” no longer endorsed

34
Q

Why are type 2 DM patients usually obese?

A

insulin inhibits FA metabolism,

also NO ketoacidosis

35
Q

What happens in pathophysiology of DM type 2?

A

Impaired beta function
Impaired insulin secretion,
Peripheral insulin resistance OR Increased glucose production (hepatic)

36
Q

Why does type 2 diabetes eventually look like type 1?

A

Initial hyperinsulinemia as response to insensitivity

Pancreas burnout fatigue of beta cells leads to low levels

37
Q

Describe relationship of diabetes to metabolic syndrome

A

1] High TG, 2] Low HDL, 3] HTN, 4] Inflammation, 5] Fibrinolysis, 6] Abn Vascular endothelium, 7] Macrovascular disease, 7] Central obesity

38
Q

What stimulates beta cell productions?

A

Central obesity causes increased FFA- omentum favors

fasting and postprandial_ Stimulate beta cell production, leads to lipotoxicity

Cause insulin resistance and glucose underutilization at periphery

39
Q

Describe the effects of insulin resistance in the Free Fatty Acid Theory
????

A

FFA + TG reduce hepatic insulin sensitivity, leading to gluconeogenesis because liver perceives a state of starvation and starts producing glucose even though you have high glucose levels,

Diverts of FFA to non-adipose sites

40
Q

What is the incidence rate of gestational diabetes mellitus?

A

1-14% of pregnancies

41
Q

Your PT is over 35 and obese, with 5+ children, what are other risk factors for gestational diabetes mellitus?

A 
Hx of DM
glycosuria, 
stillbirth,
obesity,
 maternal age (above 35), G5+
42
Q

What are the fetal risk factors of gestational diabetes mellitus?

A 
macrosomia 
shoulder dystocia,
hypoglycemia
hypocalcemia, 
polycythemia,
hyperbilirubinemia
43
Q

What is the treatment of gestational diabetes mellitus

A

Tx with insulin, not PO meds

44
Q

What are the MC symptoms of DM?

A

polyuria-Loss of water in urine d/t osmotic activity of glucose

polydipsia-thirst from cellular dehydration

polyphagia- usually sx type 1

45
Q

What are other signs and symptoms of diabetes mellitus

A 
1] Wt loss with type 1, 
2] Blurred vision >300
3] Fatigue, 
4] Paresthesias (affects the longest nerves first), 
5] Skin infections- fungus
6] Lipemia
46
Q

Why do DM have blurred vision?

A

sugar in the lens blood vessels
will draw fluid into blood
distort the shape of the lens due to dehydration

47
Q

What is the normal fasting blood glucose?

A

100 mg/dL

48
Q

What is the fasting blood glucose in pre-diabetic and diabetic?

A

Pre diabetes Impaired: 100-125 mg/dL,

DM: DX 126 mg/dL

49
Q

What is the normal 2hr GT?

A

140 mg/dL

50
Q

What is the normal 2hr GT

A

<140 mg/dL

51
Q

What is diagnosis of DM on random glucose plasma?

A

200 mg + symptoms

52
Q

What is considered diabetic using HbgA1c?

A

A1C above 6.5 = dx of DM,

elderly pts to be below 6.5 when 7 is probably ok

53
Q

List the tests used for diagnosis of diabetes

A

1] Blood sugar (FBS*, RBS) – fasting or random,

2] GTT (Glucose tolerance drink,

3] Glycated Hemoglobin (Hgb A1C),

4] UA – detect sugar in urine (180mg of glucose to be detectable by dipstick)

54
Q

How do you manage diabetes?

A

1] Diet and Exercise,
2] Routine blood testing,
3] Insulin,
4] Oral medications for type 2

55
Q

What is the best management of diabetes?

A

Don’t mess around with more than 2 of the oral diabetes meds; insulin pump is the best!

56
Q

What is the best management of diabetes?

A

best and most effective way to manage blood sugar. Don’t mess around with more than 2 of the oral diabetes meds; insulin pump is the best!

57
Q

What are acute complications of diabetes?

A

1] DKA (beta-hydroxybutyrate, acetoacetate, acetone),
2] Hyperosmolar Hyperglycemia- fluid draw in to blood vessel
3] Hypoglycemia

58
Q

What are acute complications of diabetes

A

1] DKA (beta-hydroxybutyrate, acetoacetate, acetone), 2] Hyperosmolar Hyperglycemia, 3] Hypoglycemia

59
Q

What is worse than DKA, in a dehydrated, infectious person with H/o of DM?

A 
Hyperglycemia Hyperosmolar Non-ketotic Syndrome
1] BG usually >600, 
2] Hyperosmolarity, dehydration, depressed sensory from brain
3] acute pancreatitis, 
4] severe infection, 
5] MI, 
6] NO Ketoacidosis, 
7] Prognosis worse than DKA
60
Q

What syndrome is a result of Fatty acid metabolism produces ketones?

A 
Diabetic Ketoacidoisis
Fatty acid metabolism produces ketones, 
Used by brain and muscle; 
With acidosis, Na dumped (LOW blood), K retained (HIGH)
>GLU >500
61
Q

Who is affected by diabetic Ketoacidosis?

A

type 1,

occur late in 2,

diabetic when they get sick with something else, kidney or bladder infxn, PNA.

Excess metabolic demand tips them over

62
Q

What presentation of diabetic Ketoacidosis?

A 
dehydrated, 
N/V, 
fruity odor, 
Kussmaul breathing-initallly rapid shallow, worsen l/t deep labored, gasp,
abdominal pain, 
mentation changes,
 hyperglycemia, 
hyperkalemia
63
Q

What leads to prolonged blood sugar extremes? What cause it?

A

Diabetic Coma

caused by
1] DKA (usually type I),

2] Diabetic hyperosmolar syndrome (sugar in urine draws water from body, BS>600),

3] Hypoglycemia (can be due to excessive insulin)

64
Q

Describe a diabetic coma

A

Result of prolonged blood sugar extreme, caused by 1] DKA (usually type I), 2] Diabetic hyperosmolar syndrome (sugar in urine draws water from body, BS>600), 3] Hypoglycemia (can be due to excessive insulin)

SMUSPG-PHY1 (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions