Week 2 - Diabetes Seminar Flashcards
what is gluconeogenesis
- the production or conversion of glucose from non-carb sources, such as amino acids & lactic acids
what is glycogenolysis
- glycogen breakdown into glucose
what is glucose
- a simple sugar the body uses to produce energy
what is glucagon
- hormone secreted from the pancreatic alpha cells that increases bg
how is the liver involved in glucose regulation
- stores glycogen
how is the GI tract involved in glucose regulation (2)
- contains incretins, which are GI derived hormones
- these hormones are released in response to food intake & effect insulin & glucagon release
- also plays a role in glucose absorption
how are the kidneys involved in glucose regulation (3)
- filtrates glucose
- reabsorption of glucose
- SLGT-2 co-transporter
how is the pancreas involved in glucose regulation?
- beta cells –> release insulin
- alpha cells –> release glucagon
what slightly increases your risk of having type 1 diabetes?
- having a parent or sibling w type 1
researchers suspect that _____ and _____ okay a role in the development of type 1 diabetes
- our genes & enviro
list risk factors for type 2 diabetes (7)
- age > 40
- 1st degree relative w type 2 (genetics)
- member of high-risk population
- history of prediabetes
- history of GDM (type 4)
- history of delivery of a macrosomic infant
- presence of vascular risk factors
what is considered high-risk populations for typ2 diabetes
- african
- arab
- asian
- hispanic
- indigenous
- south asian
- low socioeconomic status
what is the cause of type 1 DM
- autoimmune
- destruction of beta cells leading to lack of insulin
what is the cause of type 2 DM
- progressive loss of beta cell function & cellular insulin resistance
which is more common: type 1 or 2 DM
- type 2 (90-95% of cases)
which is more common: type 1 or 2 DM
- type 2 (90-95% of cases)
how is type 1 DM managed/treated?
- cannot be managed with diet/exercise alone
- must be given insulin
how is type 2 DM managed/treated
- diet, exercise
- oral antihyperglycemics
- insulin
are the symptoms abrupt or gradual for type 1? type 2?
- type 1 = abrupt onset of symptoms
- type 2 = gradual
what age group is associated with diagnosis of type 1? type 2?
- type 1 = children/young adults, usually less than 35 years
- type 2 = often but not always adult onset, approx 55% older than 50
describe the physical structure of an indiv with type 1 vs type 2
- type 1 = usually underweight
- type 2 = often higher BMI
what condition may occur with type 1? type2?
- type 1 = prone to DKA
- type 2 = may develop hyperosmolar hyperglycemic syndrome (HHS/HHNC)
what would occur in a type 1 patient who does not receive exogenous insulin?
- death
what are the 4 acute clinical manifestations of hyperglycemia
- glucosuria
- polyuria
- polydipsia
- polyphagia
what BG is classified as hyperglycemia
> 11 mmol/L
what can cause hyperglycemia (10)
- circulating supply of insulin is insufficient
- or glucose cannot be effectively used for energy (insulin resistance)
- inappropriate glucose production by liver
- alteration in the production of hormone & cytokines by adipose tissues
- increased glucose intake
- meds (ex. corticosteroids, not taking diabetes meds)
- undiagnosed, untreated, or undertreated DM
- decreased activity
- stress (cause release of cortisol = CRH)
- infection, trauma, illness (increase CRH & effect BP which effects GFR which effects glucose reabsorption)
what might cause insufficient insulin?
- either insufficient insulin is being produced or none at all
what is insulin resistance?
- when body tissues do not respond to the action of insulin
what causes insulin resistance (3)
- unresponsive insulin receptors
- insufficient number of receptors
- both
what occurs when insulin is not effective, causing the entry of glucose into the cell to be impeded? (2)
- hyperglycemia
2. hyperinsulinema
list clinical manifestations of hyperglyemia (6, but some are grouped together if they fit together)
- 3 P’s (polyuria, polydipsia, polyphagia)
- glycosuria
- nocturia
- abdominal cramps, NV
- weakness, fatigue, headache
- blurred vision
what BG is considered hypoglycemia
< 4mmol
what causes hypoglycemia (5)
- too much insulin in proportion to the available glucose in the blood
- lack of food intake/NPO
- excessive physical activity
- med reaction (ex. too much insulin)
- alcohol (ETOH) consumption
what clinical manifestations are first seen in hypoglycemia? what next? why?
- when BG drops below 4, the autonomic nervous system gets activated –> glucagon & epi ate produced to increase BG = autonomic symptoms
- if BG continues to drop, the brain does not get adequate glucose & we see CNS symptoms bc cognitive functioning is affected
symptoms in hypoglycemia related to activation of the autonomic system are called
- neurogenic
symptoms in hypoglycemia related to decreased cognitive functioning are called
- neuroglycopenic
at what BG level will we see SNS vs CNS symptoms in hypoglycemia?
- neurogenic < 3.5
- neuroglycopenic < 2.8
list neurogenic (autonomic SNS) symptoms seen during hypoglycemia (8)
- shaky. trembling
- nausea
- hungry
- increased HR & palpitations
- sweaty
- anxiety
- cold, clammy, moist, skin
- irritability
list neuroglycopenic (CNS) symptoms seen during hypoglycemia (7)
- confusion, difficulty concentrating
- weakness, drowsiness
- disorientation
- lose consciousness
- have a seizure
- vision changes
- difficulty speaking
BG of 4-7mmol is considered ______
euglycemia
what are vascular risk factors (which means they will be risk factors for type 2)
- TG >1.7
- HTN
- overweight
- abdominal obesity
- smoking
- high cholestrol
what gives us an average blood glucose over 90-120 days
glycosylated hgb (HbA1C)
a fasting BG of _____, post prandial BG of ___, or A1C of ____ is considered prediabetes
- fasting –> 6.1-6.9
- A1C 6-6.4%
- post prandial = 7.8-11
list 4 factors that increase BG
- food
- stress
- glucocorticoids
- CRH
list 3 factors that decrease BG
- alcohol
- exercise
- insulin
when is doubt, should you treat hypoglycemia or hyper
- hypo
what is meant by glycemic target
- what you want the BG to be while managing BG
should each persons gylcemic target be the same? why or why not?
- no it is individualized for everyone
- need to consider activity levels, life expectancy, etc.
what is considered a critical high vs critical low BG
- critical high = 33
- critical low = 2.8
what is the normal BG range prior to meal intake? 2hr after meal intake>
- before = 4-6
- after = 5-8
what is BG range prior and after meals for someone with DM
- before = 4-7
- after = 5-10
what does DKA stand for
diabetic ketoacidosis
who is at risk for DKA
- type 1 diabetics
what does HHNS stand for? who is at risk for it?
- hyperosmolar hyperglycemic nonketotic syndrome
- type 2
what is the acronym for treatment of DKA
Fluids
Insulin
Glucose monitor
Potassium (bc insulin pushed it into cell)
Infection (monitor for)
Chart fluid balance
Ketones (monitor in blood or glucose)
what should we consider when taking a pt’s health hisotry?
- medical history
- meds
- social & family history
- OPQRSTU of symptoms
- ROS/H2T
DM is diagnosed with one of….
- A1C > 6.5%
- fasting (8h) BG >7mmol
- random glucose >11
- two hour oral glucose tolerance test >11
how is blood glucose maintained within normal levels when we expend more glucose thru exercise? (3)
- release of glucagon
- liver will release glucose
- gluconeogensis (production of glucose from non-carbs)
how is blood glucose maintained within normal levels when physical activity is decreases? (3)
- glycogen formation
- insulin
- increase glucose uptake into tissue
what is the primary chronic complication of hyperglycemia
- angiopathy
list 4 chronic manifestations of hyperglycemia
- neuropathy
- microangiopathy
- macroangiopathy
- infection
why might infection be more likely w hyperglycemia? (3)
- more glucose for microbes
- immunity effected with long-term hyperglycmia
- impaired blood flow = delayed healing
what are 2 types of microangipathy
- retinopathy
2. nephropathy
what will we want to assess for regarding retinopathy
- blind spots
- blurred vision
- just overall vision changes
what will we want to assess for regarding nephropathy
- albuminuria
- proteruria
- assess ins & outs
- assess BUN, creatine
what will we want to assess for regarding macroangiopathy
- bp
- HR
- EKG
- lipid levels
- peripheral perfusion
- pulses/HR
what might we assess for regarding neuropathy
- distal extremities
- if they have feeling in their extremities
- numbness, tingling
- with autonomic neuropathy assess for fixed, resting tachy
what might we assess for regarding infection
- temo
- CBC, WBC
- CWCM
- lesions?
- drainage
why/how do diabetic foot ulcers occur?
- diabetes = increased risk of infection
- decreased blood flow
- lack of feeling due to neuropathy makes it hard to identify
describe assessment of the CNS for DM
- LOC
- sensation (especially in the distal extremities)
describe assessment of the CVS for DM
- cap refill
- CWCM
- HR
- BP
- temp
describe assessment of respiratory system for DM
- kussmal respiration
- lung sounds? crackles (due to infection or fluid backup from HF)
- fruity breath
describe GI/GU assessment for DM
- NVD
- diet
- appetite
- kidney function
- urinary habits
describe integumentary assessment for DM
- assess for sores & ulcers
describe MSK assessment for DM
- weakness
- activity level
- look for muscle wasting (type 1)
list 4 long term complications of hypoglycemia
- hypoglycemia unawareness syndrome
- loss of consciousness/neurologicsl changes (seizures)
- coma
- death
what is it called if someone has a diabetes & cardiac risk?
- metabolic syndrome
list 3 risk factors diabetes & heart disease share
- high bp
- overweight
- high cholestrol
a glycated hemoglobin (A1C) level above 7% is associated with… (3)
- high risk of microangiopathy
- high risk of macroangiopathy
- infarctions
when is insulin required?
- when a patient does not have sufficient insulin to meet metabolic demands
why must injection sites for insulin be rotated?
- to prevent lipodystrophy
what does insulin administartion require close monitoring of? why?
- BG levels
- have to watch for hypoglycemia
- & doses are often based of BG reading
what is an alternate use of insulin? why?
- for hyperkalemia
- it pushes K+ into the cells
what is the somogyi effect regarding insulin therapy
- morning rebound hyperglycemia due to mid-night hypoglycemia
- due to giving insulin hs which will peak in the middle of the night
- this will then cause the release of CRH in the middle of night leading hyperglycemia
what is the dawn phenomenom regarding insulin therapy
- morning hyperglycemia but NO hypoglycemia in the night
- due to GH release during the night, which decreases peripheral uptake of glucose
what should educate your patient on regarding diabetes
- closely & how to monitor BG
- always have access to a simple sugar
- the signs of hypo vs hyper
- how to inject insulin
- storing of insulin
- age & developmental considerations
how should insulin be stored?
- unopened = firdge
- the one you are using tho should be stored at room temp
what do anti-hyperglycemics do?
- improve the use & production of insulin & glucose in the body
- target things like insulin resistance & decreased insulin production
what type of DM are anti-hyperglycemics used for?
- type 2
what is a risk associated with some anti-hyperglycemics?
- hypoglycemia
why are anti-hyperglycemics only used for type 2?
- bc they rely only the body having some insulin, which type 1 does not
what is the first line treatment for type 2 DM
- lifestyle changes in diet & exercise
true or false: insulin’s only role in our body is to allow glucose to enter cells
false, also:
- puts K+ into cells
- storage of glycogen
