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Pathophysiology and Pharmacology 2 > Diabetes > Flashcards

Diabetes Flashcards

FML

1
Q

Pancreas Components

A

exocrine (80) acini glands

endocrine (20) islets of langerhans

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2
Q

Islets of Langerhans components/secretions

A

alpha cells: glucagon
beta cells: insulin
delta cells: somastatin
f cells: pancreatic polypeptide

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3
Q

Insulin primary FX

A

synthesis of glycogen/protein in liver/muscle
suppression of gluconeogenesis/glycogenlysis/lipolysis
glycolysis/glucose transport

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4
Q

Insulin Release Process

A

BG increases –> insulin released –> BG lowers

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5
Q

Glucagon Release Process

A

BG decreases –> glucagon released –> BG raises

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6
Q

Endocrine Hormones Fueling Metabolism

A 
Glucagon
cortisol
growth hormone
epinephrine
norepinephrine
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7
Q

Post-absorptive (fasting) State

A

provides glucose for brain/nervous tissue
higher ratio of glucagon to insulin
hepatic glycogenolysis/gluconeogenesis
muscle oxidizes ffa

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8
Q

Absorptive State

A

insulin levels rise
stimulates glucose uptake into tissues
excess glucose stored as glycogen

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9
Q

Starvation State

A

glucagon levels elevated
hepatic gluconeogenesis
brain oxidizes ketones for energy

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10
Q

Type 1 Diabetes DKA

A

increased mobilization of free fatty acids –> increased hepatic synthesis of ketones
diabetic ketoacidosis

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11
Q

Type 2 Diabetes DKA

A

ketone bodies not sufficient for DKA

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12
Q

Type 2 Diabetes

A

can’t produce/respond to insulin

can’t use energy in food as well

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13
Q

Type 1 Diabetes

A

lack of insulin secretion (total or partial)
auto-immune (pancreatic beta cells destroyed)
no oral meds

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14
Q

Hyperglycemia acute symptoms

A

increased thirst/urination

weight loss

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15
Q

Monogenic DM

A

neonatal diabetes

maturity-onset diabetes of oung

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16
Q

Gestation DM onset/TX

A

during pregnancy
dietary TX, oral meds, exogenous insulin
hyperglycemia can lead to fetal/maternal complications

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17
Q

Prediabetes DX

A

impaired fasting glucose (100-125)
impaired glucose intolerance (144-199)
increased hemoglobine

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18
Q

Diabetes (nonpregnant) DX

A

Hemoglobin >6.5% increase
random serum glucose >200
FAsting serum glucose >126

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19
Q

Most common Type 1 DM

A

T-cell mediated autoimmune against beta cells

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20
Q

Type 1 DM etiology

A

childhood disease
genetic predisposition
viruses
cow’s milk proteins

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21
Q

Type 1 DM pathogeneisis

A

environmental triggers immune response
autobodies develop (honeymoon period)
insulin production ceases

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22
Q

Type 1 DM s/s

A 
hyperglycemia (fasting BG >126 x2)
polyuria
polyphagia (hunger)
polydipsia
glucosuria
weight loss
fatigue
n/v
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23
Q

Insulin aspart

onset/peak/lasts/admin

A

rapid acting
(15 min onset) (1-3 hr peak) (lasts 3-5 hrs)
SQ 5-10 min AC
must eat within onset

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24
Q

Insulin regular

onset/peak/lasts/admin

A

short-acting
(30-60 min onset)(2-5 hr peak)(lasts 5-8 hr)
SQ 30-60 min AC
Iv for DKA (only IVP)

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25
Q 
Insulin isophane (NPH)
onset/peak/lasts/admin
A

intermediate acting
(onset 1-2 hr)(peak 4-12 hrs)(lasts 12-18 h)
SQ 30 min before 1st/last meals
NEVER IVP

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26
Q

insulin detemir

onset/lasts/admin

A

long-acting
gradual onset over 24 hr (lasts 24 hrs)
SQ HS

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27
Q

Insulin glargine

onset/lasts

A

long acting
gradual over 24 begining at 1 H
lasts 24 hrs

28
Q

Use of combination insulin

A

long-acting+short-acting
use body’s natural levels to enhance control
should not cause hypoglycemia

29
Q

Insulin that can’t be mixed

A

glargine

30
Q

Hyperglycemia Med Induced

A

corticosteroids
NSAIDS
diuretics

31
Q

Hyperglycemia ICU PT Targets

A

140-180

32
Q

Hyperglycemia non-ICU PT Targets

A

<140 fasting

<180 random

33
Q

Metabolic Syndrome

A 
adipose tissue is an endocrine organ that produces hormones
insulin resistance
ab obesity
increased LDL/BP/artery disease
Waste circumference >35/40
Lifestyle changes
34
Q

Type 2 DM insulin resistance physiology

A

unresponsive to insulin (b/c of receptors) –> blood glucose ^ –> pancrease secretes more insulin (hypersecretion) = beta cell exhaustion/death

35
Q

Type 2 DM TX

A 
lifestyle change
antidiabetic drugs (lower BG)
insulin
36
Q

Type 2 TX goals

A

pre-prandial BG <110

HBA1C <6.5

37
Q

Biguanides action/pro

A

decreases hepatic production of glucose/reduces insulin resistance
does not cause hypoglycemia
1st line med
METFORMIN

38
Q

Biguanides Side effects

A

minor, GI-related
lactic acidosis
increased risk for renal disease/liver disease/severe infection/shoc/hypoxemia

39
Q

Sulfonylureas MOA/ex/SE

A

glyburide/glipizide/glimepiride
stimulate release of insulin from pancreatic islet cells/increase receptors
hypoglycemia

40
Q

Alpha-Glucosidase Inhibitors (ex/MoA/SE)

A

ACARBOSE/MIGLITOL
block enzymes in small intestines from breaking down CHO (delayed digestion)
GI SE most common
No hypoglycemia (unless w/ Insulin/sulfonylurea)

41
Q

Meglitinides (ex/MoA/Duration/SE/Cont)

A 
NATEGLINIDE/REPAGLINIDE)
stimulates insulin from pancreatic islet cells
short duration (2-4 hrs)
well-tolerated
hypoglycemia
hepatic/renal disease
42
Q

Thiazolidinediones (ex/MoA/optimal BG)

A

PIOGLITAZONE, ROSIGLITAZONE
decrease insulin resistance/inhibit hepatic gluconeogenesis
3-4 months

43
Q

Thiazolidineiones SE/Contra

A

Fluid Retention/headache/weight gain
CHF, pulmonary edema, bladder cancer
NO hypoglycemia

44
Q

Incretin Enhancers (MoA)

A

mimic hormones released in response to food (signal insulin secretion/stop glucagon production)
reduce food intake (feeling of fullness)
protect beta cells from injury

45
Q

Incretin Enhancers (agonists/inhibitors)

A

(-glutides, -enatide)

-gliptins

46
Q

Hypoglycemia Medical Emergency Levels

A

<60

47
Q

Hypoglycemia s/s

A

hunger, sweating, palpitations, tremors, anxious, difficulty speaking, visual disturbances, atypical behavior, confusion, ,seizures

48
Q

Hypoglycemia TX

A 
glucose
fast-acting simple CHO (juice,)
glucagon (to convert glycogen to glucose)
(5% Dextrose)
(50% Dextrose if unconscious)
49
Q

Somogyi Phenomenon

A

Hypoglycemia @ night (undetected)

Hyperglycemia in the morning

50
Q

Somogyi Phenomenon s/s

A

night sweats, headaches, nightmares

51
Q

Somogyi Phenomenon DX

A

BG 0200, 0200, 0600

52
Q

Somogyi PHenomenon TX

A

complex carbs @ bedtime

may need to change insulin

53
Q

Dawn Phenomenon and DX

A

Hyperglycemia in AM
Most common in Adolescents/YA
Testing @ HS, 0200, 0400, fasting

54
Q

Dawn Phenomenon TX

A

based on testing if below 60 = reduce insulin
if above 120 increase insulin
snack @ bedtime

55
Q

DKA patho

A

can be first sign of DM
absolute/relative insulin deficiency (most common with Type1)
not enough insulin = hyperglycemia = polyuruia, polydipsia, polyphagia = acidosis (fat breakdown)

56
Q

DKA causes

A 
infection
skipping insulin
new onset T1DM
surgery
trauma
pregnancy
57
Q

DKA TX

A

supportive, IV insulin, IV fluids, IV electrolyte replacements

58
Q

DKA progression

A

hyperglycemia > dehydration > hemoconcentration > peripheral circulation failure > shock > hypotension > anuria > coma/death

59
Q

Hyperglycemia Hyperosmolar Syndrome Patho

A

severe hperglycemia and coma
DKA - ketosis/acidosis/Kussmaul’s breathing
just enough insulin

60
Q

Hyperglycemia Hyperosmolar Syndrome Etiology

A

T2 DM

excessive unreplaced fluid losses w/hyperglycemia

61
Q

Hyperglycemia Hyperosmolar Syndrome s/s

A

r/t hyperglycemia, dehydration, hyperosmolality
neuro
vascular thromobosis

62
Q

Hyperglycemic Hyperosmolar Syndrome DX

A 
glucose >600
osmolality >320
profound dehydration 
alteration in consciousness
Bicarbonate >18
pH >7.3
63
Q

Hyperglycemic Hyperosmolar Syndrome TX

A

Support
IV Insulin
IV Fluids
IV Electrolytes

64
Q

DKA DX

A

usually younger
BG >250
Serum Ketones
Bicarbonate <18

65
Q

Diabetic Neuropathy Pathogenesis

A

incrreased polyol pathway –> NA retention > edema > myelin swelling > nerve degneration

66
Q

Diabetic Neuropathy s/s

A 
GI disturbances 
Nerve disturbances
diarrhea
neurogenic bladder
impotence
distal polyneuropathy
67
Q

Diabetic Neuropathy TX

A

depends

Gabapentin can help

Pathophysiology and Pharmacology 2 (27 decks)

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