Diabetes Flashcards
pathopys. of T2DM
- a progressive disorder of insulin resistance within the body, leading to eventual deterioratino of the B cells in the pancreas and increased blood glucose & impaired hepatic production of glucose
Early Phase: an insulin resistance pattern occurs (a result of metabolic syndrome)
- pancreas initially HYPERSEcretes the insulin (thinking i need to make more to get it into the cells)
- but even with high levels of insulin, the cells (in muscle, fat and liver) stop responding to insulin and they wont take up any glucose (or a very small level)
- overtime though, the cells wear out and cant make insulin anywhere
the FIRST sign of insuin resistance and T2DM is the LOSS of the post-prandial insulin spike after meals; the body is unable to do that = post-pradial hyperglycemia
Later on: the body is unable to produce insulin at all: leading to a state of fasting hyperglycemia as there is no insulin response at all to lower blood glucose
Additionally…
- loss of insulin means theres not regulation of glucagon release: thus glucagon released: breaks down stores glucose & results in even more hyperglycemia
- lack of insulin also triggers the liver cells to think they need to form more glucose: through gluconeogensis which results in a resting state of hyperglycemia
What is the Dawn Phenomenon
- patho & significance
- the AM hyperglycemic spike which results due to the NATURAL secretion of counter-regulatory hormones at 3am = trigger a raised glucose in the serum
- this phenomenon is common in those with DM, and sleep apnea
- see blood sugars as high as 150-200s
Counter-regulatory hormones
- cortisol
- glucagon
- growth hormone
- catecholamines (noreip and ei)
What is the Somogyi Effect
- AM reactive hyperglycemia as a result of an overnight hyPOglycemic event
- sOmOgyi = hypOglycemia Overnight
example of the effect
- pt takes their insulin at bedtime, develops low blood sugar overnight, so the counter regulatory hormones trigger an increase in blood sugar resulting in hyperglycemia in the morning
screen by asking bed partner; are thye sweaty, shakey, pale and signs of hypoglycemia overnigh that you noticed
Etiology of T2DM
- individual factors
- risk factors
Etiology = multifactoral
- Genetics: plays a HUGE role and links of family history make someone significantly more likely to develop it
- environmental factors
- sedintary lifestle, eating habits and body habitus (apple shaped)
Risk Factors
- OBESITY and central adiposity
- family history
- CVD
- sedintary lifestyle!!!
- latino/hispanic, asian, islander (underrepresented pop.) are more at risk
- signs of insulin resistance (impaired fasting glucose)
- HTN
- dyslipidemia
- history of gestational diabetes
- history of large baby devleiry ( > 9lbs)
- PCOS
Medications which may induce or increase the risk of T2DM
Medical Conditions which may cause T2DM
- atypical antipsychotics!!!: the risperidone, etc. (not the haldol and first-gens)
- chronic oral steroid use (prednisone) for immune conditions
- OCPs
- statin use ?
Medical Conditions
- OSA: increased cortisol production = hyperglycemia
- cushings disease: increased cortisol
- acromegaly
Patho of Type 1 DM
an immunologic destruction (auto-immune) of the beta cells in the pancreas leading to complete lack of insulin release
- lack of insulin release leads to a lack of glucoses abiity to enter ANY cells: making the cells resort to other energy production (ketoacidosis occurs due to the byproducts) and DKA can occur
- hyperglycemia will occur and death withinout the introduction of exogenous insulin
- some thought of environmental triggers (viruses, toxins, etc.) can trigger the occurance of the destruction to occur
- genetic link: auto-immune mutation then the insinulating event happnes
Risk Factors for T1DM
- viral infection: coxackie, mumps, rubella
- family history of T1DM (not as strong as T2DM)
- family history or personal hsitory of other autoimmune disease
- scandinavian or northern european decent
- early diagnosis: like age 4-6 or 10-14 most commonly
Key Aspects of a pt. which may clue you into thinking they have Type 1 DM
- auto-immune personal hx or family hx.
- GAD65, low peptide -C levels
- younger age dx. (before 18)
- fair skin, northern european
- small body habitus
- failed oral diabetic medications
- requiring basal and bolous insulin
- presentation of DKA at first signs can be extremely common
Key Aspects of pt. presenation which may clue you into thinking they have T2DM
- obese body habitus
- family hx. of T2DM
- metabolic syndrome (HTN, high lipids, obese, central adiposity)
- meds causing insulin resisatnce
- older age (40s-60s)
- PE significant for: acanthosis nigricans or skin tags (acrocordons)
- presenation of HHS/HHNK:
What is LADA
- etiology
- presentation
- diagnosis
- treatment
LADA: latent autoimmune diabetes of adulthood
Etiolgy: an insidious onset of type 1 DM where the beta cells are slowly, over time destoryed leading to a much later presentation of full blown T1DM
Presentation
- over 18: slender body habitus with no signs or fam hx. of T2DM
Diagnosis
- pts have + GAD65/anti-islet cells AB but with normal C=peptide (because they are making some insulin….. for now)
Treatment
- the pts. will slowly over time need to become insulin dependent
- pts. with varying BMI will need insulin at different times in life
- if the BP spike is out of proportion to the baseline of BS for the pt. start them on insulin!!!!
Other Classifications of DM
steroid induced
- this is a diagnosis for those on CHRONIC or LONGTERM steroid use which results in hyperglycemia
- this is NOT a short corse of steroids spiking the glucose
MODY (maturity onset diabetes of youth)
- eary DM in a genetic atuo. dominat pattern
- non-obese white with no antibodies and not needing insulin
Gestational DM
- from pregnancy and makes mom more likely to develop T2DM afterwards
What is Pre-Diabetes
the KEY point for intervention in pt. education to prevent DM!!!! if you can at this point
A1c 5.8-6.4%
Or fasting glucose 101-125
a point of insulin resistance development priot to overt dx. of DM
Treatment
- pt. education
- lifestyle modification!!!! lost weight by 5-10% is best
- change diet to mediterranean
- 150 mins. of CV intense exercise weekly
- check BS 1x daily
for those with extremely high risk or high A1c can be acceptable to begin metformin at this stage
Treatment
- rerduce risk of other diseae states (CVD risk) and llifestly changes
- HTN control: ACE/ARB
- HLD: statin thearpy
Diabetes: Pt. Presentation
most times: your pt. will come in asymptomatic: thus you MUST be on the look out
the 3 ps: polyuria, polydypisa, polyphagia
- fatigue
- anorexia
- mental status change (in HHS with hyperglycemia)
- weight loss: in VERY uncontrolled : peeing out the sugar, no cells getting any glucose leads to loss
- vision changes (thickened lens or microvas. comp)
- paresthesias of the feet and extremities
- recurrent UTo ro mycotic infection: increase glucose in urine
how is DM diagnosed
- labs
how is pre-diabetes diagnosed
specifics on the A1C
one of the following is significant enough for a diagnosis of DM
- signs of DM (3 ps, weight loss) + random plasma glucose level of > 200
- a fasting glucose > or equal to 126 on 2 checks
- oral glucose test > 200 = not commonly done
- A1C = or > 6.5% = (most commonyl done becuase no need to fast)
Pre-Diabetes
- an A1C 5.8-6.4%
- a fasting glucose ** 101-125**
A1C specifics
- preferred screening method & good for long term monitoring of DM
- measures 3 month glucose contorl: by measuring teh glycosylation of the red blood cells via an irreversible bond of the glucose and protein on the RBC: proportional to the glucose lvel (aka how much glucose the rbc has been swimming in)
- an A1c level can be impacting by severe anemia, hemoglobopathies and hemoylic anemia: in this cause a serum frutosamine can be used
Diabetic Monitoring of sugar
monitoring for T1DM
monitoring for T2DM
a hallmark of DM management: glucose must be monitored
- a blood glucose level must be checked regardless of type of DM and regardless of teh A1c level: blood glucose gives exact NOW measurement of glucose in the serum
Type 1 DM
- AM check, before meals & at bedtime (4 times a day)
Type 2 DM
- AM check, before meals, and before bed if sugars not controlled
GM (gestaional)
- AM check, before meals, 2 hours after meals, at bedtime
DM Complications
major complications are revolved around macrovascular and microvascular issues
Macrovascular: secondary to large vessel disease
- CAD
- stroke
- PAD
Microvascular: smaller vessel: but still significant lifestyle implications
- retinopathy
- nephropathy
- neuropathy
other complications (secondary to those above usually)
- foot and leg ulcers (ischemic and neurologic issues)
- skin issues (acnthosis nigricans, necrobiosis, skin tags)
- MSK abnormalities
- infections
- hypoglycemia
Macrovascular Complications
- what disease and why
- how do you approach treatment
CAD/CVD = leading to an MI event
atherosclerosis of the ICA: stroke
PAD of LE: leading to gangrene and ischemic ulcers
Patho: not entirely known but…
- LDL cholesterol is fragmented: possibly due to glucose: making it easier for it to oxidize and become a plaque & CVD risk increaed dramatically
Treatment Approach
- treat those with DM just like someone who had a previous MI (same CVD risk)
- use ASCVD risk score calculator: but DM pt. will need to be treated
Treatment of CVD risk in those with DM
smoking cessation: a MUST
- prevent CAD/CVD SECONDARY (already had one) with low dose asprin daily
- prevent/treat HTN: ACE/ARB treatment
this helps with albuminuria too and kidney protection
goal BP: < 130/80 - Lipid management: treating pt. regardless of cholesterol level
advise with lifestyle management
age 40-75 without ASCVD risk: moderate intensity statin
age 40-75 with ASCVD risk: high intensity statin so rousuvisatin or atorvostatin can be high dose
(age less than 40 requires a convo)
Microvasculariation Complications of DM
Retinopathy
screening, types & treatment
Screening
T1DM: 5 years after diagnosis or those with visual changes
T2DM: at time of diagnosis
Types of retinopathy
1. non- proliferative = early stage of the disease, microanyuresums, dot hemorrhages, exudates & retinal edema
2. proliferative = new capillary gorwth, fiberous tissue creation, retinal hypoxia leading cause of blindness & risk of vitreous hemorrhae and retial detachment high
Treatment
- laser photocoag.
- VEGF injection
- control the DM
- stok smoking
- treat the HTN
- yearly eye checks at minimum
Microvascular Complication of DM
Nephropathy
patho, labs, screening, treatment
leading cause of ESRD is DM
Patho
- hyperglycemia leads to hyperfilteration in the kidneys (because there gets to a point where the body can no longer reuptake the glucose: tmax thus the glucose begins to spill into the urine; where glucose goes (solute) the fluid will follow & creates hyper filteration of other substances out with it
- additionally: the glucose deposits within the basement membrane of the glomeruleus and creates a thickened membrane –> leads to damage to the podocytes & eventuall proteinuria results
Labs
- microalbuminuria is the first sign of nephropathy = leading to CKD
- microalbuminuria: 30-300
- macroalbuminuria: > 300
Screening
yearly urine studies for albumin
Treatment
- glycemic control
- HTN control
- ACE/ARB
because the ACEII works at the efferent arteriole: blocking the action of ACEII (through ACE) which was trying to increase filteration secondary to the hyperglucose but spilling protein
