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CMS200 > Week 3- Diabetes > Flashcards

Week 3- Diabetes Flashcards

1
Q

what is diabetes mellitus

A

A metabolic disease that involves abnormally elevated blood glucose levels

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2
Q

diabetes mellitus as one of the leading causes of mortality

A

Reduces lifespan by 5-15 years and the all-cause mortality rate is twice as high as for those without diabetes

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3
Q

what % in US and Canada have diabetes

A

10-15%

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4
Q

subtypes of diabetes mellitus

A

type 1 and type 2

maturity-onset diabetes of the young, gestational diabetes, secondary causes due to endocrinopathies/steroid use, etc.

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5
Q

type 1 diabetes- which cells are effected?

A

Due to the destruction of pancreatic islet beta cells – typically secondary to an autoimmune reaction

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6
Q

age most common to get T1D

A

4-6 or 10-14 yrs

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7
Q

causes of T1D

A

One-third of the disease susceptibility is due to genetic factors, with two-thirds attributed to environmental factors

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8
Q

genetic factors for T1D? what’s most common?

A

HLA

The HLA locus (HLA-DR3, -DR4, -DQ) confers about 40% of the genetic risk to developing Type 1 diabetes, while the 5’ polymorphic region of the insulin gene adds 10%

  • Most patients will have circulating antibodies to islet cells, glutamic acid decarboxylase 65, insulin, tyrosine phosphatase IA2, and zinc transporter 8
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9
Q

environmental factors for T1D

A

less prevalent near the equator

migration?

breastfeeding is protective

hygiene hypothesis- public health and immune system dysregulation and develop autoimmune

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10
Q

what % and who doesnt have the typical pancreatic beta cell autoimmunity in T1D

A

Approximately 5% of patients have no evidence of pancreatic beta cell autoimmunity = the subgroup of “idiopathic type 1 diabetes” (also known as “type 1B”)

Most of these individuals are of Asian or African descent

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11
Q

symptoms of T1D

A

Excessive urination (polyuria) and thirst (polydipsia)
Blurred vision
Weight loss
Parasthesias
Altered level of consciousness

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12
Q

is screening recommended for T1D?

A

no

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13
Q

T2D eitology/ causes

A

Due to the non-autoimmune loss of pancreatic B cell function or development – leading to impaired insulin sensitivity (“insulin resistance”)

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14
Q

T1D vs T2D cause

A

T1D: Due to the destruction of pancreatic islet beta cells – typically secondary to an autoimmune reaction

T2D: Due to the non-autoimmune loss of pancreatic B cell function or development – leading to impaired insulin sensitivity (“insulin resistance”)

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15
Q

onset of T2D

A

adults, but rising in kids

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16
Q

what % is T2D

A

More than 90% of patients with diabetes in the U.S. have Type 2 diabetes

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17
Q

who has higher prevalence of T2D (race and other risk factors)

A

Prevalence is 2-6x higher in persons of Black (12.9%), South Asian (14.4%), Arab/west Asian (9.4%), Native American (34.8%), Pima Indian, or Hispanic American (4.5%) backgrounds (Sapra 2023)

Other risk factors include: obesity, first-degree relative with Type 2 diabetes, cardiovascular disease, hypertension, HDL cholesterol <35mg/dL (0.91mmol/L) and/or triglycerides >250mg/dL (2.8mmol/L), acanthosis nigricans, polycystic ovary syndrome, gestational diabetes or delivery of baby >9lb

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18
Q

genetic factors in T2D

A

Epidemiologic studies looking at monozygotic twins >40 years of age have shown that when Type 2 diabetes develops in one twin, in 70% of cases the second twin will also develop Type 2 diabetes within a year

  • Genome studies have identified 143 risk variants and regulator mechanisms for Type 2 diabetes, including loci that code for proteins involved in beta cell function/development (TCF7L2), insulin secretion (e.g., CDKAL1, SLC30A8), fat mass and obesity risk (FTO, MC4R), and insulin resistance (PPARG)
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19
Q

T2D envrioenmtnal factors

A

visceral obesity –> insulin resistance (subcutaneous fat is less correlated)

metabolic obesity= visceral fat without overt obesity

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20
Q

adipocytes and immune system in T2D

A

Adipocytes secrete abnormal levels of adipokines (e.g., adiponectin and resistin) that can impair insulin signaling

  • The release of TNF-alpha and IL-6 by macrophages and other immune cells activated in adipose tissue can also impair insulin signaling
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21
Q

T2D diagnosis - when do you see symptoms?

A

Many patients have an insidious onset of hyperglycemia and are initially asymptomatic. Diabetes is recognized only after glycosuria or hyperglycemia is discovered on routine lab testing.

At the time of diagnosis, patients may already have some level of neuropathic or cardiovascular complications

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22
Q

T2D - whos effected?

A

lower income, not finished university, permanatley unable to work

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23
Q

skin conditions of T2D

A

Chronic skin conditions:
* Vulvovaginal candidiasis in females
* Balanoposthitis in males
* Acanthosis nigricans
* Eruptive xanthomas
* Lipemia retinalis

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24
Q

other T2D symtpoms

A

weight, pregnancy complication

Weight gain
* Overweight or obese
* Centripetal fat distribution
* Waist circumference >40 inches for men, >35 inches for women

Obstetrical complications
* Consider Type 2 diabetes in women who have delivered babies over 9 lb (4.1 kg) or have had polyhydramnios, preeclampsia, or unexplained fetal losses

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25
Q

is screening recommended for T2D?

A

yes

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26
Q

screening test for T2d? what factors if patient has will you decide to test in?

A

Screen asymptomatic adults with a body mass index ≥25 kg/m2, and one or more additional risk factors (American Diabetes Association, ADA) from previous lab results:
* A1C > 5.7%
* Impaired glucose tolerance
* Impaired fasting glucose

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27
Q

clinical features of diabetes SLIDE 30 chart

A

xx

ie.
polyuria and thirst in both T1D and T2D but moreso in T1D

nocturnal eneuresis is common in T1d but not in T2D

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28
Q

metabolic syndrome

A

insulin resistance –> higher risk of diabetes and CVD

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29
Q

gestational diabetes- what %

A

8% in 2020

prevalence increases with higher BMI

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30
Q

screening time for gestational diabetes? what is the test?

A

24-48 weeks gestation with non fasting 50g glucose challenge test

If blood glucose >140 mg/dL (7.8 mmol/L), then perform a 3- hour fasting 100g glucose challenge test to confirm (Diagnostic)
* Positive if there is at least one abnormal value (≥180, 155, 140 mg/dL for 1-, 2-, and 3-hour fasting glucose levels, respectively)

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31
Q

what is the value of blood glucose to DIAGNOSE gestational diabetes

A

> 140mg/dl blood glucose

then 3 hours test

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32
Q

2 step test for gestational diabetes

A

One-step testing: a single fasting 75g oral glucose tolerance test

Two-step testing: a non-fasting 50g oral glucose tolerance test, followed by a 3-hour fasting 100g glucose tolerance test if the result passed the threshold of 130-140 mg/dL

Diagnosis of gestational diabetes is more common in one-step screening (16.5%) than two-step screening (8.5%) – but no statistically significant differences in perinatal or maternal complications

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33
Q

what is better; 2 step or 1 step test for gestational diabetes

A

the two-step testing produces equivalent benefits and fewer harms than the one-step testing approach

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34
Q

risks of gestational diabetes

A

To reduce maternal and fetal complications: preeclampsia, caesarean delivery, congenital malformations, macrosomia, childhood or adolescent obesity, nerve palsy, bone fracture, jaundice, and infant death

gestational hypertension, development of T2D later in life, being overweight in childhood, birth defects, shoulder dystocia

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35
Q

who to screen for gestational diabetes?

A

Screen women in their first trimester if risk factors are present, such as obesity, advanced maternal age or >35 years of age, history of gestational diabetes, family history of diabetes, belonging to a high-risk ethnic group

Screen asymptomatic patients at or after 24 weeks’ gestation

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36
Q

manage gestational diabetes after birth

A

test 6-12 weeks postpartum

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37
Q

the types of diabetes that kids can get?

A

Type 1 diabetes
Type 2 diabetes
Maturity-onset diabetes of the young (MODY)

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38
Q

how many kids have diabetes

A

20% in 12-18 yrs old have pre diabetes

200,000 kids in US have diabetes

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39
Q

risk factors in kids with T2D

A

obesity, excess adipose tissue (especially when centrally distributed), and family history

Socioeconomic position, area of residence, and environmental factors may also play a role (e.g., quality of and access to health care, toxic stress, structural racism)

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40
Q

races for kids that are likely to get T2D

A

Prevalence is highest in American Indian/Alaska Native, Black, Hispanic/Latino, and Hawaiian/Pacific Islander youth

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41
Q

complications of T2D in kids

A

ketoacidosis, hyperglycemic hyperosmolar state

macrovascular (atherosclerosis)
microvascular (retinopathy, nephropathy, neuropathy)

renal disease, retinopathy, peripheral neuropathy,

hypertesnion, dyslipidemia, NAFLD

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42
Q

screening for T2D in kids

A

evidence insufficient….

screen if overweight or have history of Type 2 diabetes in a first- or second-degree relative, belonging to a high-risk ethnic group, acanthosis nigricans, hypertension, hyperlipidemia, or polycystic ovarian syndrome (ADA)

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43
Q

maturity onset diabetes of the young (MODY- what is it?

A

A non-insulin-dependent form of diabetes, typically diagnosed at ≤25 years of age

1-5% of all patients with diabetes have the MODY type

Often misdiagnosed as Type 1 or 2 diabetes

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44
Q

who to suspect MODY in?

A

non obese if diagnosed with diabetes under 30 yrs old

strong family history of diabetes

Preserved pancreatic beta cell function 3-5 years post- diagnosis (detectable serum C-peptide levels with a serum glucose level >144 mg/dL and no laboratory evidence of pancreatic beta cell autoimmunity)

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45
Q

what is the most common reason for MODY? what genes?

A

autosomal dominant disease (50% of offspring affected)

14 subtypes (MODY1 to MODY14), with MODY1 to MODY3 accounting for 95% of cases

The subtypes are distinguished by their gene mutations:
* MODY1 (HNF4A): rare
* MODY2 (GCK): less rare
* MODY3 (HNF1A): most common, 30-50% of cases
* Remaining subtypes are very rare

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46
Q

what is the most common gene mutation for MODY?

A

MODY3 (HNF1A): most common, 30-50% of cases

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47
Q

what does MODY 1 and MODY3 have similar to type 1 and 2 diabetes

A

MODY1 and MODY3 have progressive hyperglycemia and vascular complication rates similar to patients with Type 1 and Type 2 diabetes

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48
Q

how dangerous is MODY 2?

A

MODY2 has mild stable fasting hyperglycemia with low risk of diabetes-related complications. These patients generally do not require treatment, except in pregnancy.

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49
Q

screening for MODY

A

genetic testing and refer to endocrinologist

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50
Q

prevalence of diabetes in older people

A

> 65 yrs have 20% diabetes

16% are unaware that they have diabetes based on glycosylated hemoglobin, fasting plasma glucose, or oral glucose tolerance testing

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51
Q

most common type of diabetes in older

A

T2D

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52
Q

older adults: diabetes increases risk of…

A

mortality and cardiovascular and microvascular complications, as well as other geriatric conditions (e.g., cognitive impairment, frailty, unintentional weight loss, polypharmacy, and functional impairment)

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53
Q

screening for diabetes in older adults recommendation?

A

no current recommendations

-screening for quality of life and life expectancy

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54
Q

secondary causes of diabetes

A

Secondary causes include: exocrine pancreas diseases, endocrinopathies, drug- or chemical-induced insulin resistance, and other genetic diseases

Any disorder that damages the pancreas can result in diabetes (e.g., liver cirrhosis, hemochromatosis, hemosiderosis)

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55
Q

slide 56 secondary causes of diabetes chart

A

xx

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56
Q

4 diagnostic tests for diabetes

A

Fasting plasma glucose levels (FPG)

Oral glucose tolerance test (OGTT)

Glycated hemoglobin (HbA1c)

Additional tests (urine, self-monitoring, continuous glucose monitoring, autoantibody)

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57
Q

fasting plasma glucose in diabetes

A

100-125 mg/dl = prediabetes
>126 (8 hours after fasting)= diagnostic

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58
Q

pros and cons of fasting plasma glucose

A

Pros: may identify one-third more undiagnosed cases than A1c

Cons: fasting is required

59
Q

oral glucose tolerance test- when to perform?

A

Perform if FPG (fasting plasma glucose) is <126 mg/dL (7.0 mmol/L) but diabetes is still suspected

60
Q

how to prepare for oral glucose tolerance test

A

Preparing for test: minimum 150-200g of carbohydrates per day for 3 days prior, then fasting after midnight before test day

Morning of test: 75g of glucose consumed within 5 min; blood samples collected at 0 and 120 min post-ingestion

61
Q

oral glucose tolerance test values for normal and diagnosis

A

<100mg/dl (and <140 for 2 hour value) is normal

126mg/dl (and 2 hour value of 200mg/dl) is diagnostic

62
Q

pros and cons of oral glucose tolerance test

A

Pros: may identify one-third more undiagnosed cases compared to HbA1c

Cons: fasting is required; false-positives in malnourishment, bedridden, infection, and severe emotional stress

63
Q

what is glycated hemoglobin (HBA1C) diagnostic for

A

type 1 and type 2 diabetes

64
Q

what is HbA1C (glycated hemoglobin) measure? over what time frame?

A

Refers to the percentage of glycosylation of the hemoglobin
A1c chain due to hyperglycemia over the previous 3 months
* HbA1c circulates within red blood cells, which have a lifespan of up to 120 days

Since the HbA1c value is weighted to more recent glucose levels (i.e., in the previous month), measurements should be repeated at 3- to 4-month intervals

65
Q

what are the values for pre-diabetes and diagnosis in HBA1C

A

5.7-6.4% = pre-diaebetes
6.5%= diagnosis

66
Q

pros and cons of HBA1C

A

Pros: no fasting is required; lower variability than FPG and OGTT; provides an estimate of glucose control for the preceding 2-3 months

Cons: substantial individual variability; affected by Hb variants/traits and the specific assay used; falsely lowered by conditions that decrease RBC age (e.g., hemolytic anemia, acute blood loss); falsely elevated by conditions that increase the RBC age (e.g., prior splenectomy, aplastic anemias)

67
Q

nonglycemic factors that may interfere with A1C measurements chart

A

SLIDE 65

malnutrition, pregnancy, vitamin E and C, HIV, chronic liver disease, hyperbilirubinemia, iron deficiency anemia, renal failure…

68
Q

CRITERIA FOR DIAGNOSIS OF DIABETES CHART SLIDE 66

A

for FBG, plasma glucose, HbA1c

69
Q

additional testing for diabetes

A

Urine (glucose and ketones)
Self-monitoring glucose measurements
Continuous glucose monitoring systems
Autoantibody
Genetic testing (MODY)

70
Q

urine testing

A

urinalysis reagent test strips (colour differs showing glucose concentrations and ketones presence)

high ketones= diabetic ketoacidosis

71
Q

what is non diabetic (renal) glycosuria and what test can it be seen in

A

in urine testing

its a benign asymptomatic condition where glucose appears in the urine despite a normal amount of glucose in the blood

72
Q

self monitoring glucose measurements measures??

A

A capillary blood sample is collected on a blood glucose monitor strip, then inserted into a blood glucose meter for an output glucose reading

73
Q

pros and cons of self monitoring glucose measurements

A

Pros: Capillary blood glucose measurements performed by the patient can be extremely useful – particularly in Type 1 diabetes where greater metabolic control is needed

Cons:
* The strips have limited lifespans and improper storage can affect the function
* Increases/decreases in hematocrit can decrease/increase the measured glucose values
* Meters and test strips are calibrated for glucose concentrations ranging from 60 mg/dL (3.3 mmol/L) to 160 mg/dL (8.9 mmol/L) and the accuracy is not as accurate for glucose levels outside this range
* Impaired circulation to the fingers (e.g., Raynaud disease) will artificially lower glucose measurements (pseudohypoglycemia)

74
Q

continuous glucose monitoring (CGM) systems- what do they measure?

A

Measure glucose concentrations in the interstitial fluid

A small disposable subcutaneous sensor is worn under the skin (often on the stomach or arm) to measure glucose concentrations continuously, every few minutes, for 7-14 days

75
Q

pros and cons of continuous glucose monitoring (CGM) systems-

A

Pros: improved glycemic control in Type 1 diabetes and gestational diabetes to prevent complications, such as hypoglycemia and diabetic ketoacidosis; improved glycemic control also translates to HbA1c levels

Cons: costly for the patient, unless covered by private health insurance

76
Q

DIAGNOSTIC SENSITIVITY AND SPECIFICITY OF AUTOIMMUNE MARKERS IN NEWLY DIAGNOSED TYPE 1 DIABETES (CHART ON SLIDE 73)

A

Islet cell antibodies
glutamic acid decarboxylase
insulin
tyrosine phsophatase
zinc transporter 8

77
Q

diabetic dyslipidemia –> lipid profile

A

high TG
low HDL

  • Presence of smaller-density LDL particles: carry abnormal amounts of free cholesterol and are more susceptible to oxidation and atherogenesis

-diabetes as risk for coronary disease
- want LDL <100mg/dl

78
Q

diabetic complications

A

Diabetic nephropathy
Diabetic neuropathy
Diabetic retinopathy
Diabetic foot ulcers
Diabetic ketoacidosis (DKA) Hyperosmolar hyperglycemic state (HHS)

79
Q

what is the most common complication of diabetes and a major cause of death in T1D

A

diabetic nephropathy

80
Q

how much of end stage renal disease cases in the USA are due to diabetes

A

1/3

81
Q

what type of diabetes is end stage renal disease more common in

A

T2D

Though patients with Type 1 diabetes have a higher chance of developing nephropathy after 20 years, ESRD is more prevalent in Type 2 diabetes due to the larger population of patients diagnosed with Type 2
* Develops in 30% of patients with Type 1 and 40% of patients with Type 2 (Hussain et al. 2020)

82
Q

what happens in diabetic nephropathy (which markers)

A

Initial presentation of albuminuria, then urea and creatinine accumulation in the blood as kidney function declines

  • Transient albuminuria can occur in short-term hyperglycemia, exercise, UTI, heart failure, and acute febrile illness
83
Q

what are the types of diabetic neuropathies

A
  • Peripheral (Distal symmetric polyneuropathy and Isolated peripheral neuropathy)
  • Autonomic
84
Q

what is the most common type of diabetic neuropathy

A

distal symmetric polyneuropathy

85
Q

what is the presentation of distal symmetric polyneuropathy

A
  • Most common, particularly in longer nerves (e.g., foot)
  • Loss of function in a “stocking-glove” pattern
  • Sensory changes (dulled vibration sense, pain, temperature) that are bilateral, symmetric, and range from mild to severe
  • May result in clawing of the toes, altered biomechanics of the foot, calluses, and ulcerations
86
Q

what is the presentation of isolate peripheral neuropathy

A
  • Due to vascular ischemia or traumatic damage
  • Mononeuropathy (one nerve) or mononeuropathy
    multiplex (several nerves)
  • Commonly affects the cranial and femoral nerves, leading to motor abnormalities
  • Sudden onset with subsequent recovery of all or most function
87
Q

what is isolate peripheral neuropathy from

A

vascular ischemia or traumatic damage

88
Q

what nerves are commonly affected in isolated peripheral neuropathy

A

cranial and femoral

89
Q

what systems are effected in autonomic neuropathy

A

many… Occurs primarily in patients with long-standing diabetes, and affects many visceral functions….
ie.
cardiovascular
gastrointestinal
genitourinary

90
Q

CV, GI, and genitoruinrary complications in autonomic neuropathy

A
  • Cardiovascular: orthostatic hypotension
  • Gastrointestinal: nausea, vomiting, postprandial fullness, reflux/dysphagia, constipation/diarrhea/both, and fecal incontinence. Gastroparesis in Type 1 diabetes.
  • Genitourinary: incomplete bladder voiding, erectile dysfunction
91
Q

what is diabetic retinoatpathy and what % of people will have? what’s it from?

A

A microangiopathy of the retina that nearly all patients with diabetes will eventually have

25%

The result of long-standing diabetes, abnormal blood glucose levels,
and inadequate arterial blood pressure control
* The risk of retinopathy increases substantially beyond a HbA1c value of 6.5%

92
Q

what are the subdivisions of diabetic retinopathy

A

non-proliferative (early stages) and proliferative (final and most severe stage) retinopathy

93
Q

does proliferative retinopathy have higher prevelane in type 1 or 2 diabetes

A

Proliferative retinopathy ultimately develops in both Type 1 and Type 2 diabetes, but has a slightly higher prevalence in Type 1 diabetes (25% after 15 years’ duration)

94
Q

what is the recommended screening for diabetic retinopathy

A

annual routine eye exam (ADA)

95
Q

what is cataracts

A

glycosylation of lens protein

  • Incidence is twice as high in patients with diabetes, and at a younger age
96
Q

what is glaucoma

A

increased ocular pressure that damages the optic nerve

  • Occurs in approximately 6% of patients with diabetes
97
Q

diabetic retinopathy symtptoms

A

cataracts (glycosylation of lens protein)

glaucoma (increased ocular pressure damages optic nerve)

dry eye syndrome

macular edema

98
Q

diabetic foot ulcers: prevalence? what’s comorbid? what else can it cause?

A

Lifetime risk may be as high as 19-34% (Altkorn, 2020) * Nearly all patients with ulcers have neuropathy

If left untreated, foot ulcers can progress to soft tissue infection (50% of ulcers), gangrene, and limb loss (15-20% of moderate-severe infections)

The 5-year mortality rate is 30%, and >70% for those with a major (above foot) amputation

Ulcers precede 80% of lower extremity amputations among people diagnosed with diabetes. There are approximately 1.6 million amputations per year worldwide.

99
Q

what populations are diabetic foot ulcers more common in

A

Higher rates among Black, Hispanic, and Native American populations, and within low socioeconomic status and rural areas

100
Q

what are the 2 types of foot ulcers/ what points do they tend to occur at?

A

Tend to occur at pressure points:

  • Venous ulcers = above medial/lateral malleolus
  • Arterial ulcers = on toes, metatarsal heads, shins
101
Q

what is a strong predictor of non healing diabetic foot ulcers

A

Peripheral arterial disease is a strong predictor of nonhealing ulcers (>50% of patients have peripheral arterial disease)

102
Q

by the time a foot ulcer is discovered what is it usually associated with

A

osteomyelitis

By the time the ulcer is discovered, it is typically advanced and with associated osteomyelitis

Osteomyelitis: inflammation of bone, usually the result of
an infection

  • Develops in up to 20% of patients with mild foot infections and in 50-60% of patients with moderate to severe infections
103
Q

characteristics of osteomyelitis diagnosis in patients with diabetic foot ulcers: highest LR+??? chart of slide 90

A

ESR > 70 mm/h
bone exposure
ulcer area >2cm2
positive probe to bone

104
Q

risk factors for diabetic foot ulcer

A
  • History of foot ulcer or lower extremity amputation
  • Absence of protective sensation due to peripheral
    neuropathy
  • Peripheral arterial disease
  • Foot deformity
  • Pre-ulcerative callus or corn
  • Obesity
  • Visual impairment
  • Poor glycemic control leading to impaired wound healing
  • Diabetic nephropathy (especially patients on dialysis)
  • Smoking
  • Poor footwear
105
Q

what are the 3 classifications of diabetic foot ulcers

A

mild, moderate and severe

106
Q

what is a mild diabetic foot ulcer

A
  • At least 2 of the following: local swelling/induration, erythema >0.5 cm around ulcer, local tenderness or pain, local warmth, purulent discharge
  • Involves skin and subcutaneous tissue, with no involvement of deeper tissues or systemic signs
  • Erythema extends ≤2 cm from the ulcer
107
Q

what is a moderate diabetic foot ulcer

A
  • Signs of local infection, PLUS
  • Erythema extends >2 cm from the ulcer or a deep structure is
    involved (abscess, osteomyelitis, septic arthritis, fasciitis)
  • No systemic inflammatory response signs (SIRS)
108
Q

what is a severe diabetic foot ulcer

A

Local infection, PLUS at least 2 SIRS criteria
* Temperature >38°C or < 36°C
* Pulse rate >90 bpm
* Respiratory rate >20 breaths/min or PaCO2 <32 mmHg
* WBC >12,000 or <4000 cells/mcL, or ≥10% band forms

109
Q

what is a SIRS in a severe diabetic foot ulcer

A

systematic inflammatory response signs

i.e. temp, pulse, respiratory, WBC&raquo_space;

110
Q

how many people heal from diabetic foot ulcer vs get them again

A

Approximately 30-40% of diabetic foot ulcers heal by 12 weeks

Recurrence after healing is 42% at one year; 65% at 5 years

111
Q

how often should patients with neuropathy get regular foot exams?

A

Patients with neuropathy should be given regular foot exams

  • Educate patients on the need for daily visual inspection of feet
  • Examine the feet of low-risk patients at least annually
  • Examine the feet of high-risk patients at every visit
112
Q

SCREENING AND FOLLOW-UP FOR DIABETIC FOOT ULCER RISK AND ACTIVE COMPLICATIONS OF DIABETIC FOOT DISEASE

A

CHART ON SLIDE 97

113
Q

what are the 3 tests for foot uclers

A
  1. femmes weinstein monofilament test
  2. tuning fork
  3. Ipswich touch test

Semmes-Weinstein 5.07 monofilament test to assess for the absence of pressure sensation at minimum 3 sites per foot (LR+ 11-16)

128-Hz tuning fork to assess for the absence of vibratory perception (LR+ 16-35)

Ipswich Touch Test to assess the patient’s ability to perceive light touch from examiner’s index finger applied to 6 or 8 pre- specified sites on the feet (LR+ 10-15)

114
Q

what is diabetic ketoacidosis cause by

A

Most often caused by infection (e.g., pneumonia, urinary tract infection, sepsis), inadequate or noncompliance with (insulin) treatment, new-onset diabetes, or cardiovascular disease (e.g., MI)

May also be precipitated by other conditions (e.g., hyperthyroidism, pancreatitis, pregnancy), alcoholism, starvation, or medications that can cause metabolic acidosis (e.g., atypical antipsychotic agents, corticosteroids, glucagon, sympathomimetic agents)

115
Q

most common cause of diabetic ketoacidosis (DKA)

A

infection

CVD, not taking insulin, new onset diabetes

116
Q

is diabetic ketoacidosis (DKA) more common in type 1 or 2

A

T1D

117
Q

what are the three key features of diabetic ketoacidosis

A

hyperglycemia, ketosis, acidosis

118
Q

what symptoms are usually present in diabetic ketoacidosis?

A

The three key features are: hyperglycemia, ketosis, and acidosis

Patients usually present with: polyuria, polydipsia, polyphagia, weakness, and Kussmaul’s respirations. Often there is “fruity” (acetone) breath.

Nausea and vomiting (50-80% of patients), coffee-ground emesis usually from hemorrhagic gastritis (25% of vomiting patients)

Abdominal pain (30% of patients) may be a symptom or part of the precipitating causes of DKA (e.g., appendicitis or cholecystitis)

Body temperature is usually normal/low, even in the presence of an infection

Often signs of dehydration, such as dry mucous membranes, tachycardia, and hypotension (10% of patients)

Consciousness ranges from alert to confused to comatose state (<20% of patients)

119
Q

how severe is diabetic ketoacidosis

A

Mortality rate of 1.2-9%
LIFE-THREATENING

120
Q

what labs are done for diabetic ketoacidosis

A
  • Plasma glucose
  • Electrolytes with calculated anion gap and effective osmolality
  • Phosphorus
  • Blood urea nitrogen and creatinine
  • Beta-hydroxybutyrate or serum ketones
  • Complete urinalysis with urine ketones by dipstick
  • Arterial blood gas or venous pH level
  • Complete blood count with differential
  • Electrocardiography
121
Q

what plasma glucose concentration and bicarbonate level are needed to diagnose diabetic ketoacidosis

A

plasma glucose concentration of >250 mg/dL, pH <7.30, and bicarbonate level ≤18 mEq/L

Patients should be monitored closely and frequently: blood glucose evaluated every 1-2 hours until patient is stable; blood urea nitrogen, serum creatinine, sodium, potassium, and bicarbonate levels monitored every 2-6 hours depending on the severity of DKA

Cardiac monitoring may be warranted for patients with significant electrolyte disturbances

122
Q

complications of diabetic ketoacidosis

A

Commonly: hypoglycemia, hypokalemia, and recurrent hyperglycemia (must monitor carefully)

Hyperchloremia is also common, though a transient finding

Rare: cerebral edema

123
Q

cerebral edema is a rare complication of diabetic ketoacidosis; what are the symptoms?

A

(more common in young patients,
comprises 0.7-1.0% of children with DKA)

  • Early signs of headache, confusion, lethargy
  • May also have papilledema, hypertension, hyperpyrexia, diabetes insipidus
  • Typically improve mentally with initial treatment but then suddenly worsen
  • In severe cases may have seizures, pupillary changes, respiratory arrest with brain-stem herniation. At this point, the mortality rate is >70% and only 10% of patients recover without sequelae
124
Q

managing diabetic ketoacidosis in kids

A

When managing children/adolescents with DKA, greater care must be taken in administering electrolytes, fluids, and insulin based on the weight of the patient and the increased concern of high fluid rates inducing cerebral edema

Though less common, DKA can also occur in children with obesity and Type 2 diabetes

125
Q

the complication of cerebral edema in diabetic ketoacidosis is most common in?

A

young patients

126
Q

older patients and diabetic ketoacidosis

A

With older patients, no specific guidelines are available

Less likely to be on insulin prior, previous episode of DKA

Typically require more insulin to treat DKA, patients have longer hospital stays and higher mortality rate (22% for age >65 years verses 2% for age <65 years)

Causes of death include: infection, thromboembolism, MI

127
Q

who is most frequently affected by hyperosmolar hyperglycemic state (HHS)

A

Most frequently affects older adults with Type 2 diabetes

128
Q

what are some precipitating factors to hyperosmolar hyperglycemic state (HHS)

A

infections (e.g., pneumonia, urinary tract infection, sepsis), medications, non- compliance with diabetic medications, undiagnosed diabetes, substance abuse, and other coexisting diseases (e.g., MI, cerebrovascular accident, pulmonary embolus, mesenteric thrombosis)

129
Q

what are the symptoms of hyperosmolar hyperglycemic state (HHS) and what other diabetic related condition does it present similarly to?

A

Presents similarly to DKA: excessive thirst, elevated blood glucose, dry mouth, polyuria, tachypnea, tachycardia

Also typically display weakness, visual disturbance, or leg cramps; and eventually develop lethargy, confusion, hemiparesis, seizures, or coma

130
Q

what is the mortality rate of hyperosmolar hyperglycemic state (HHS)

A

Mortality rate is 10-50%
Emergent concern

131
Q

what are the lab findings in hyperosmolar hyperglycemic state (HHS)

A

elevated plasma glucose concentration of >600 mg/dL, elevated serum osmolarity of >320 mOsm/kg of water, pH >7.30, and mild/absent ketonemia

132
Q

in comparison to diabetic ketoacidosis what is the difference in findings in hyperosmolar hyperglycemic state (HHS)

A

There is an absence of excessive urinary ketones (compared to in DKA) since insulin is still being produced by pancreatic beta cells

133
Q

what are the complications of hyperosmolar hyperglycemic state (HHS)

A

Vascular occlusions (e.g., mesenteric artery occlusion, MI, low-flow syndrome, disseminated intravascular coagulopathy) and rhabdomyolysis

Overhydration may lead to adult respiratory distress syndrome and induced cerebral edema – rare but often fatal in children and young adults. Correcting hyperosmolarity slowly may prevent cerebral edema.

134
Q

CHART FOR DIAGNOSIS OF DKA VS HHS ON SLIDE 112

A

i.e. plasma glucose and arterial pH and serum bicarbonate much higher in HHS

urine and serum ketones and beta-hydroxybutryate high in DKA

135
Q

symptoms when to consider diabetes diagnosis

A

polyuria, polydipsia, fatigue, blurry vision, weight loss, poor wound healing, numbness, tingling

136
Q

screening for diabetes

A

creen for abnormal blood glucose and Type 2 diabetes in ages 40-70 and overweight/obese – and repeat testing every 3 years if results are within normal limits (USPSTF)

Diagnostic testing for individuals with clinical history (signs and symptoms, risk factors) indicative of diabetes

–>screen if overweight or obese

The American Diabetes Association recommends annual screening for Type 2 diabetes in patients:
* ≥45 years of age
* <45 years of age with major risk factors
* If test results are normal, then to repeat testing at least every 3 years

137
Q

recommendation for annual screening for T2D if meet what criteria

A
  • ≥45 years of age
  • <45 years of age with major risk factors
  • If test results are normal, then to repeat testing at least every 3 years
138
Q

what age is the screening of diabetes questionable for

A

older than 70

Ceasing diabetes screening after age 70 will avoid overdiagnosis and unnecessary treatment

most have pre diabetes

upon follow up of meeting pre diabetic criteria 6 years later they become normoglycemic

139
Q
A
140
Q

cardiovascular complications in diabetes

A
  • Heart disease (coronary atherosclerosis, MI) * Hypertension
  • The ADA recommendation is to maintain a systolic BP <140 mmHg and diastolic BP <90 mmHg (<130/<80 mmHg in younger patients)
  • Peripheral vascular disease
141
Q

skin and mucous membrane complications in diabetes

A
  • Candida infections
  • Vulvovaginitis
  • Eruptive cutaneous xanthomas
  • Necrobiosis lipoidica diabeticorum
  • Diabetic dermopathy
142
Q

bone and joint complications in diabetes

A
  • Diabetic cheiroarthropathy, adhesive capsulitis, carpal tunnel syndrome, Dupuytren contraction
  • Increased risk of fractures
  • Diffuse idiopathic skeletal hyperostosis (DISH)
  • Bursitis
143
Q

co management for diabetes

A

Nutritionists and diabetes educators: lifestyle modifications, at-home glucose management

Ophthalmologist, neurologist, podiatrist, nephrologist: regular screenings to prevent vascular complications

Endocrinologist: for complex presentations or unresponsive to initial treatments

144
Q
A

CMS200 (22 decks)

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