Diabetes Mellitus Type 1 Flashcards

1
Q

What are the four main types of hormones that the pancreas produces

A

Pancreatic Polypeptide
Insulin
Glucagon
Somatostatin

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2
Q

How does the pancreas function as an exocirne gland?

A

contains digestive enzymes that assist in digestion and absorption of nutrients in the small intestine
Also helps to break down carbs, proteins, lipids into chyme

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3
Q
What do the following cells secrete?
Alpha
Beta
Delta
Gamma
A

glucagon
insulin
somatostatin
pancreatic polypeptide

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4
Q

How does insulin work when glucose levels are high?

A

works by driving glucose into cells and inhibiting the secretion of glucagon

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5
Q

how does glucagon work when glucose levels are low

A

causes the liver to convert glycogen into glucose

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6
Q

How does insulin work to get glucose into the cell

A

insulin binds to cell membrane receptor which causes activation of GLUT4 a glucose transporter and allows glucose into the cell

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7
Q

What cells does glucose get transported into

A

Liver
Adipose tissue
Muscle

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8
Q

What happens to a patient who has DM?

A

Increase in Blood glucose levels
lack of insulin
Fat,Muscles,Live can not utilize blood glucose for energy
alternate energy sources are broken down for fuel

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9
Q

What are counterregulatory hormones

A

they undo insulins job

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10
Q

what are some counterregulatory hormones

A
Glucagon
Epinephrine
Norepinephrine
cortisol
Growth hormone
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11
Q

What inhibits the secretion of glucagon

A

high glucose levels and insulin

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12
Q

What stimulates glucagon

A

low glucose

strenuous exercise

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13
Q

What happens in the liver when glucagon is stimulated

A

stimulates glycogenolysis
breakdown of glycogen to glucose
Stimulates glycolysis and lipolysis- break down of lipids/triglycerides stored in fat tissues metabolized into free fatty acids which leads to ketogenic effect that decreases blood pH

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14
Q

In a healthy patient what are their defense mechanism against hypoglycemia

A

pancreas decreases its insulin output
Alpha cells in pancreas secrete counterregulatory hormone, glucagon to signal the liver to release more glucose, promotes glycogenolysis and glycolysis/lipolysis
Adrenal glands secrete epinephrine which act to signal the production of more glucose and refrain certain tissue from using glucose in bloodstream

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15
Q

What happens when epinephrine and glucagon fail to adequately raise blood glucose levels

A

the body releases cortisol and GH which work to increase blood glucose

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16
Q

What effects are seen in a patient with DM

A

After yrs of T1DM many lose these defenses against hypoglycemia
Not able to benefit from reducing bodies own secretion of insulin
Can not longer secrete glucagon
After many instances of hypoglycemia the epi response gets blunted
Results in defective glucose counterregulation and prone to bout of severe hypoglycemia
Causes hypoglycemia unawareness

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17
Q

what is the definition of Type 1 DM

A

chronic state of hyperglycemia due to an absence or deficiency of insulin

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18
Q

what is the definition of Type 2 DM

A

A combination of insulin receptor abnormalities and inadequate insulin secretion to compensate

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19
Q

Who is are the greatest risk for Diabetes

A
non-hispanic whites
Asian Americans
Hispanic
Non-hispanic blacks
Male-female ratio 1.5to1
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20
Q

when is T1DM most common

A

most common in children and young adults with a peak incidence before puberty 11-13
Can still develop in adults

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21
Q

What increases a patients odds of getting T1DM

A

autoimmune disease

Graves, Hashimoto, Addisons

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22
Q

What types of factors increase the risk of T1DM

A

Environmental factors can cause it to be expressed
Viral-which causes autoimmume response in which the immune attacks virus infected cells along with beta cells
Diet- response to antibodies in cows milk
Chemical/drugs-detroy
Trauma/pancreatitis

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23
Q

The majority of patients have susceptibility gene located on what region of which chromosome?

A

HLA region on chromosome 6

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24
Q

Which is the highest risk for type 1 DM in the US borne by individual who express which allele

A

DR3 and DR4 allele

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25
Q

what do DQ+Dr both code for

A

antigens expressed on the surface of macrophages and B lymphocytes

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26
Q

what are DQ alleles associated with?

A

increased risk for type 1 DM

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27
Q

What causes the destruction of the beta cells in Type 1 DM?

A

lymphocytic infiltration

loss of the insulin-productin beta cells of the islets of langerhans in the pancreas, leading to insulin deficiency

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28
Q

what is type 1a immune mediated destruction of beta cells

A

T-cell mediated autoimmune attack

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29
Q

what happens with beta cell pathophysiology?

A

as beta mass declines, insulin secretion decreases until the available insulin no longer is adequate to maintain normal blood glucose levels

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30
Q

How much os the beta cell need to be destroyed for diabetes to be diagnosed

A

80-90%

31
Q

How is the pathology of the beta cells reversed

A

exogenous insulin to reverse this catabolic condition, prevent ketosis, decrease hyperglucagonemia and normalize lipid and protein metabolism

32
Q

when patients are diagnosed with T1DM have which antibodies circulating at diagnosis

A

Islet cell antibody (ICA)
Insulin auto-antibodies (IAA)
Antibody to glutamic acid (GAD 65)
antibody to tyrosine phosphatases (IA-2 and IA2-B)

33
Q

what happens when glucagon levels are high

A

breakdown of fats lipolysis leads to ketoacidosis which produces energy for cellular function

34
Q

what are symptoms of diabetic ketoacidosis?

A

N/V
Thirst/polyuria
Abdominal pain
SOB

35
Q

what are physical exam findings of diabetic ketoacidosis

A
presents in less than 24hrs
Tachycardia
Dehydration/hypotension
Tachypnea/kassmaul
respiration/respiratory distress
abdominal tenderness
lethargy
obtundation
cerebral edema/ coma
36
Q

What events take place in a patient during DKA

A

there is a lack of insulin which elevated glucagon. There is a osmotic diuresis causes polyuria, dehydration, polydipsia. The body starts lypolysis for fuel which cause ketone bodies to form causing metabolic acidosis. This triggers counter regulatory hormones.

37
Q

what are the classical clinical presentation of T1DM

A

polyuria, polydipsia, polyphagia, unexplained weightloss

38
Q

what are some other symptoms associated with T1DM other than the polys

A

Fatigue, Nausea, Blurred vision
Paresthesia
Hypotension/Orthostatic hypotenstion

39
Q

When can you take a fasting blood glucose level

A

at least 8 hours after eating

40
Q

when can you take a post prandial blood glucose

A

2 hours after a meal

41
Q

how many readings of 126mg/dl are needed to be diagnosed as diabetic

A

2 consecutive positive readings

42
Q

what is the function of the HbA1C do

A

provides an average blood sugar control over the 120 day period (life cycle of RBC)

43
Q

when do you need to screen for diabetes in patients?

A

high risk patients with a relative with type 1 DM which will be screened for anti-islet antibodies before ago of 10years

44
Q

According to ADA recommendations when should you test a patients HbA1c

A

it is used to diagnose type 1DM only when the condition is suspected but the classic symptoms are absent

45
Q

What are microvascular complications with DM

A

nephropathy
neuropathy
retinopathy

46
Q

what are the macrovascular complications with DM

A

coronary artery disease
peripheral arterial disease
Cerebrovascular accident

47
Q

what types of additional lab studies would you want to order

A
lipid panel
Renal function (Bun,Cr, GFR, urinalysis)
EKG/carotid ultrasound
peripheral pulse
podiatric assessment
opthalmic assessment
48
Q

what are the primary goals of type 1 DM

A

prevent acute illness
Hyper/hypoglycemia
prevent long term complication of macro/microvascular

49
Q

what are the types of rapid acting insulin

A

lispro (humalog)

aspart (Novolog)

50
Q

what are short acting regular insulin

A

Humulin R

Novolin R

51
Q

What are intermediate acting NPH

A

Humulin N
Novolin N
Humulin L
Novolin L

52
Q

what are long acting insulin

A

ultralente

glargine (lantus)

53
Q

What are the benefits of rapid acting insulin?

A

pts can eat sooner
flexible dosing schedule allows patients to adjust their insulin to their eating habits
used with long acting or intermediate insulin
hypoglycemia is common

54
Q

What is the short acting insulins function

A
used 30 min before meal
used in a sliding scale for 
DM or Hospital patients with out DM for stressful situations, infections, MI, perioperative period
Can be given IV
diabetic ketoacidosis
hyperkalemia
55
Q

What is the most common form of insulin treatment for T1DM

A

intermediate acting insulin
give 2x/day
given in combo with regular or lispro for tighter glucose control

56
Q

What is the benefit of long acting insulin and when should it be given

A

no peaks
best for basal coverage controls blood sugar levels between meals and sleeping
best given at bed time with recurrent uncontrolled fasting hyperglycemia
less nocturnal hypoglycemia

57
Q

how many injections will insulin therapy require

A

3-6x/day
requires self monitoring readings
preferred regimens
ultra-short acting and long acting

58
Q

What are the ADA’s recommendations for diet

A

cholesterol 300mg/day
sat fats<10% of total daily calories
unsaturated fats of total daily calories

59
Q

what are the important things for T1DM to do with their diet

A

eat snacks and meals at regular intervals or smaller portions more regularly
Avoid dehydration

60
Q

what are the most common lipid abnormalities

A

hypertriglyceridemia and lover levels of HDL are most common

61
Q

What do children and adolescents with T1DM have a higher risk of what type of other diseases

A

athersclerosis

heart disease

62
Q

What should diabetics be put on to get their lipids under control

A

statins

63
Q

how can exercise be helpful treatment for T1DM

A

improves utilization of carbs and lipids

Might predispose to hypoglycemic episodes

64
Q

how would you council your patients who are T1DM that are going to exercise

A

start slow and work up to moderate exercise
check glucose prior to exercise and every 30 min during exercise
may need to reduce insulin before and after exercise

65
Q

What are the surgical interventions for pancreatic transplantation indications

A

for T1DM only
serious and progressive DM complications
Old pancreas is left in place because it still makes digestive enzymes
A kidney-pancreas transplant is an operation to place both a kidney and pancreas at the same time in someone who has kidney failure related to T1DM

66
Q

Pancreatic islet allo-transplantation?

A

is a procedure in which islets cells from the pancreas of a deceased organ donor are purified, processed and transferred into another person
experimental procedure as of now

67
Q

What is the function of self monitoring glucose levels.

what are the pros and cons

A

achieve tight glycemic control and to monitor asymptomatic hypoglycemic episodes
patient is in control
must trust patient

68
Q

what is the threshold for hypoglycemia

A

50mg/dl dangerous level

69
Q

what are symptoms of hypoglycemia

A
confusion
letharhy
seizure
coma
focal neurological symptoms
autonomic hyperactivity
70
Q

what are treatments for avoid hypoglycemia?

A
decrease insulin or oral hypoglycemic doses
increase snacks
educate your patient about hypoglycemia
Carry packs of sugar/candy
Glucagon
71
Q

how would you treat a person with extreme hypoglycemia

A

IV bolus 50% dextrose or 1mg Glucagon IM

72
Q

what is the somogyi effect

A

nocturnal hypoglycemia followed by rebound am hyperglycemia
body responds to the low blood sugar by releasing hormones that raise the blood sugar level, may cause a high sugar level in the morning

73
Q

what can cause the smogyi effect

A

a person who takes insulin doesn’t eat regular bedtime snack, the persons sugar level drops during night
hypoinsulinemia

74
Q

what is the dawn phenomenon?

A

end result of a combination of natural body changes that occur during the sleep cycle to prepare a person to wake up
the counterregulator hormones work against insulin during bedtime where insulin may be wearing out which causes hyperglycemia in the morning