Endo Part 9

Front 1

in DKA, insufficient insulin =>

(2)

Back 1

1. high glucose

2. ACID FORMATION

Front 2

DKA is associated more with:

Back 2

DM1

Front 3

HHS =

Back 3

Hyperglycemic Hyperosmolar State

(~~high rate of mortality)

Front 4

3 c.c.'s of both DKA and HHS:

Back 4

1. omit insulin

2. inadequate insulin

3. inf.

Front 5

in HHS, insufficient insulin =>

(3)

Back 5

1. severe hyperglycemia

2. very high serum osm

3. *DEHYDRATION*

Front 6

nl serum osm =

Back 6

285-295

Front 7

HHS ~~

Back 7

DM2

Front 8

insulin binding =>

(2)

Back 8

1) rapidly-occurring metabolic effects

2) slower mitogenic effects

Front 9

the rapidly-occurring metabolic effects of insulin fall into 2 classes:

Back 9

1. anabolic effect

2. anti-catabolic effects

Front 10

***anabolic effects of insulin => ***

Back 10

creation of large-mlcl storage forms of energy

i.e. glucose => glycogen in the liver and muscle,

and FFA's and ketones => TG's

Front 11

there are NO GLUT4 r's in the liver

Back 11

only in muscle and fat

Front 12

significance of no GLUT4 r's in the liver:

Back 12

check

Front 13

anti-catabolic effects of insulin =

Back 13

PREVENT breakdown of glycogen, TG's

- that's why you need basal levels of insulin always

Front 14

the process of breaking down glycogen and TG's in the fasting state is:

Back 14

CONTROLLED in a nl pt

- in DKA, the process is UNCHECKED; occurs more than normal in the fasting state

Front 15

glucose from muscle glycogen goes to:

Back 15

muscle ONLY

Front 16

features of DKA:

(5)

Back 16

1. usually ~~ established DM1, s/ts new onset DM1

2. rarely, DM2

3. any age (but young > old)

4. SHORT time to presentation (DAYS)

5. RAPID development of symps and signs

Front 17

**precipitatants of DKA = **

(3)

Back 17

absolute OR relative deficiency of insulin

1. insulin omission

2. insulin reduction

3. increased insulin requirement

Front 18

what could increase your insulin requirement?

(4)

Back 18

1. inf

2. steroids (meds)

3. cocaine

4. high anti-insulin hormones (glucagon, cortisol, cats)

Front 19

pathogen of DKA: lack of insulin = high amount of:

Back 19

anti-insulin hormones

=> inc. FFA's from adipose, inc. AA's from muscle

=> **both go to liver for GNG**

(not to mention concurrent ketone production =>=> metabolic acidosis)

Front 20

excess GNG =>

Back 20

hyperglycemia

=> osmotic diuresis

=> dehydration, electrolyte losses

Front 21

both EPI and glucagon increase:

Back 21

GNG at the liver

Front 22

effect of GH and cortisol at fat/muscle:

Back 22

inhibit GLUT4's from going to the memb.

=> keep BG high

Front 23

Unchecked ketogenesis =>

Back 23

ketosis

=> inc. AG metabolic acidosis

Front 24

body's defenses against acidosis:

(3)

Back 24

1. ketone bodies are excreted and buffered in the urine

2. serum bicarb, bone, and intracellular proteins buffer hydrogen ions

3. hyperventilation
=> CO2 is blown off

Front 25

ketone bodies can be present (initially in the urine without high blood levels, then later in higher concentrations in the blood) WITHOUT:

Back 25

actual fall of arterial pH

Front 26

4 characteristic blood gases of DKA:

Back 26

1. Low bicarb

2. Low pCO2

3. Low arterial pH

4. inc. AG

Front 27

the AG is the sum of “measured cations” minus “measured anions”

BUT, “total cations” must equal “total anions”

Thus, the NORMAL AG represents:

Back 27

**unmeasured anions in the blood**
(negatively-charged phosphates and sulfates)

- ***in DKA, the unmeasured anions are ketone bodies***

Front 28

***formula for AG:***

Back 28

Na+ – [Cl + HCO3]

- should be <= 12

Front 29

****why the AG is so important for DKA:****

(2)

Back 29

1. best indicator of severity of the DKA

2. best indicator of successful treatment
(i.e. “closing” or normalization of the AG)

Front 30

if ketones are not strongly positive in diluted serum, but AG is high, consider diagnoses other than DKA, like:

(4)

Back 30

1. high Lactate

2. Alcohol (ethanol, methanol, ethylene glycol)

3. Salicylate

4. Renal failure

Front 31

clinical manifestations of DKA:

(13)

Back 31

1. Thirst

2. Polyuria

3. profound weakness

4. tachy

5. hypotension

6. orthostasis

7. dry membranes

8. poor skin turgor (tissue rigidity)

9. abd pain, n/v

10. Kussmaul respirations (rapid, shallow)

11. “fruity” breath

12. relative hypothermia

13. serum and urine ketones+,

Front 32

7 features of HHS:

Back 32

1. ~~older pts

2. known OR untreated OR unrecognized DM2

3. longer pre-coma phase than in DKA

4. insidious development

5. greater severity of obtundation at presentation

6. dehydration presenting with a shock-like state

7. severe hyperglycemia (much more than in DKA)

Front 33

4 effects of severe hyperglycemia:

Back 33

1. dehydration

2. electrolyte loss (Na+, Cl, K+, P)

3. hyperosmolality

4. hypotension

Front 34

obtunded =

Back 34

dull, deadened

Front 35

**HHS is often confused for:**

Back 35

stroke

~~slurred speech, one-sided weakness

Front 36

lots of different things can induce HHS, but the m.c. med =

Back 36

corticosteroids

Front 37

compared to DKA, HHS has more-severe:

(4)

Back 37

1. dehydration

2. hyperglycemia

3. hypernatremia

4. hyperosmolality

(HHS ketogenesis is minimal, insufficient to produce a medically-significant met. acid.)

Front 38

obtundation of HHS ~~

Back 38

severity of hyperglycemia/hyperosmolality

(definitely not due to minor met. acidosis)

Front 39

clinical course of HHS:

(4)

Back 39

1. may be complicated by seizures, vascular thromboses, or embolism

2. treatment requires more free water and greater volume replacement than DKA

3. K+ replacement req'd

4. treatment after recovery in many cases may be oral agents or diet

Front 40

HHS ~~ older pts who:

Back 40

already have a lot of other issues going on

- that's why mortality is higher

Front 41

*treatment of DKA, HHS is about the same, just different in:*

Back 41

degrees

Front 42

3 main components of treatment for DKA, HHS:

Back 42

1. fluids

2. electrolytes

3. insulin

Front 43

7 elements of therapy for both DKA and HHS:

(more thorough)

Back 43

1. Fluids, including NaCl

2. IV insulin infusion until AG closes

3. K+ replacement

4. eventually free water

5. eventually glucose

6. no clear role for bicarb

7. VIGILIANT AND FREQUENT CLINICAL AND LABORATORY ASSESSMENT

Front 44

***you HAVE to keep giving insulin until:***

Back 44

ketones are gone

- which means you have to keep giving glucose too, b/c of the insulin you're giving

Front 45

caveat of K+ with treatment of DKA, HHS:

(4)

Back 45

1. life-threatening hypokalemia can develop during insulin treatment

2. K+ re-enters cells under the influence of insulin therapy

3. the small extracellular compartment experiences a precipitous drop of K+ concentration

4. => Anticipatory replacement during treatment of DKA is almost always required
- i.e. start replacing K+ once serum K+ normalizes, BEFORE it falls below reference range

Front 46

a sharp drop of serum P can occur during insulin treatment;

Back 46

it is uncommon that treatment is required for this

Front 47

DKA and HHS exist along a spectrum;

Back 47

DKA would occur before HHS, which can occur with normal insulin secretion/action

Front 48

pre-discharge education:

(4)

Back 48

1. which symps to report

2. glucose testing

3. urine acetone testing

4. “sick-day rules”
- DM1 pts should not omit insulin when ill, and may even need to increase insulin doses

Front 49

BEE = basal energy expenditure =

Back 49

e/t except for physical activity and thermic effect (energy expended after eating)

- highly variable

Front 50

3 features of CCK:

Back 50

1. from duodenal I cells

2. responds to lipids and proteins

3. anorexigenic

Front 51

anorexigenic =

Back 51

promoting fullness/NOT eating

=> decreases hunger, increases satiety

Front 52

features of GLP-1:
(glucagon-like peptide)

(4)

Back 52

1. from intestinal L-cells after meals

2. anorexigenic

3. inhibits GI motility/secretions

4. => major component of “ileal brake”, which regulates transit of nutrients in the GI tract

Front 53

remember that GLP-1 Mimetics cause:

Back 53

wt loss

Front 54

features of PYY:
(peptide-tyrosine-tyrosine)

(6)

Back 54

1. L-cells,

2. stimulated by food intake (esp. lipids)

3. and by nut. presence in the ileum

4. secretion proportional to calories
- larger meals significantly increase release

5. freely crosses BBB

6. anorexigenic

Front 55

features of ghrelin:

(4)

Back 55

1. from endocrine cells of the fundus and duodenum

2. orexigen (stimulates hunger)

3. can be released in anticipation eating

4. fasting increases its plasma levels

Front 56

what does the Hypothalamic arcuate nucleus (ARC) do?

Back 56

monitors and integrates signals including nutrient levels, food intake, fat stores, energy expenditure, and metabolic rate

Front 57

2 neuropeptides of central control of eating:

Back 57

1. POMC

2. NPY

Front 58

role of POMC at the ARC:

Back 58

decreases food intake

=> promotes wt loss

Front 59

role of NPY at the ARC:

Back 59

stimulates feeding and wt gain

Front 60

what is FTO?

Back 60

the fat mass and obesity-associated gene

Front 61

3 specific prot.-energy malnutrition:

Back 61

1. Kwashiokorkor

2. Marasmus

3. Marasmus-Kwashiorkor Mix

Front 62

Kwashiokorkor =

Back 62

*acute* prot. malnutrition

~~**bellies**

- may be secondary to illness

Front 63

Marasmus =

Back 63

**chronic** kcal and protein malnutrition

~~ severe deprivation of food over time

- characterized by wasting

Front 64

Marasmus-Kwashiorkor Mix ~~

Back 64

wasting with edema

Front 65

"adiposity rebound" =

Back 65

natural increase in fat as child grows up

- the earlier adiposity rebound occurs, the more likely child will be obese

Front 66

metformin + lifestyle was not as good as:

Back 66

metformin + rosiglitazone

=> even kids should get combo therapy (+ lifestyle changes)

Front 67

3 types of eating disorder:

Back 67

Anorexia Nervosa (AN)

Bulimia Nervosa (BN)

Eating Disorder Not Otherwise Specified (EDNOS)

Front 68

approach to anorexia nervosa:

(2)

Back 68

1. refeed at 30-40 kcal/day, eventually weight gain at 70-100

2. be careful for Refeeding Syndrome

Front 69

a slightly-higher prot. intake may help:

Back 69

decrease binging

- helps you feel full faster

Front 70

gut microbiome is important; effects include:

(4)

Back 70

1. altering calories absorbed from ingested foods

2. metabolizing nutrients (e.g. choline)

3. metabolites

4. altering organ function (e.g. liver)

Front 71

whole grains are good,

Back 71

refined grains are bad

Front 72

get enough milk to:

Back 72

get enough Ca2+

Front 73

physical activity guidelines for ages 6-17 =

Back 73

at least 60 mins daily,

moderate to vigorous

Front 74

physical activity guidelines for ages 18-64 =

(3)

Back 74

1. avoid inactivity

2. at least 150 mins/week moderate
75 mins/week, vigorous

3. for more extensive benefits: 300 mins/week moderate or 150 mins/week vigorous

Front 75

physical activity guidelines for >65:

Back 75

do as many activities as allowed

Front 76

4 common deficiencies in adults:

Back 76

1. Vit. D

2. Ca2+

3. K+

4. dietary fiber

Front 77

common deficiencies in children and adolescents:

(5)

Back 77

1. Vit E

2. Ca2+

3. K+

4. fiber

5. Mg2+

Front 78

3 common deficiencies in vegans:

Back 78

1. Vit B12

2. Ca2+

3. iron

Front 79

2 other nutrients that vegetarians and vegans may lack:

Back 79

1. methionine

2. creatinine

Front 80

2 common deficiencies in preg:

Back 80

1. iron

2. folic acid

Front 81

2 common deficiencies in older adults:

Back 81

1. Vit D

2. Vit B12

Front 82

daily vitamin supplements may be needed for:

(3)

Back 82

1. vegetarians

2. vegans

3. anyone on an "extreme," long-term diet

Front 83

4 myths about wt loss:

Back 83

1. Small sustained changes produce large, long-term weight changes

2. Setting realistic goals in obesity is helpful

3. Large, rapid weight loss is better than slow, gradual weight loss

4. Assessing stage of change is important
Physical education classes in their current form are important to address childhood obesity

Front 84

obesity as defined by % body fat:

Back 84

>25% in men,

>33% in women

- other measures = BMI, waist circumference

Front 85

even MODEST wt loss can have drastic effects;

Back 85

multiple comorbidities decreased with 5-10% loss

Front 86

what falls with wt loss?

Back 86

metabolic rate

Front 87

how many net kcals do you have to burn to lose 1 lb per week?

Back 87

500 kcal deficit per day

Front 88

only RIGOROUS exercise induces:

Back 88

wt loss by itself

- but exercise in general does change body composition

Front 89

wrt exercise, strive for:

Back 89

30 minutes of aerobic exercise 5-7 times per week.

Front 90

drug treatment of obesity is only an:

Back 90

adjutant,

not a replacement for diet and exercise

Front 91

when is it appropriate to give drugs for obesity?

(2)

Back 91

1. appropriate if BMI > 30

2. consider if BMI >27 and complications

Front 92

therapy considered effective if:

(3)

Back 92

1) 2 kg weight loss during the first month

2) 5% fall by 3-6 months

3) 10-15% is good response, >15% is excellent

Front 93

3 features of Phentermine:

Back 93

1. reduces food intake by causing early satiety

2. VERY effective

3. may increase blood pressure

Front 94

Sibutramine not used b/c of:

Back 94

CV risk

Front 95

features of Orlistat:

(2)

Back 95

1. inhibits pancreatic lipase such that ~30% of ingested fat is not digested/absorbed

2. also improves lipids and BG

Front 96

***SE's of Orlistat:***

(2)

Back 96

1. cramps, flatus, fecal incontinence, oily spotting
(really unpleasant)

2. malabsorption of fat-soluble vits

Front 97

Qsymia = two drugs,

Back 97

Phentermine / Topiramate

- both given at much lower doses, which improves their synergy and lowers SE's

Front 98

SE's of Qsymia =

(6)

Back 98

1. paresthesias

2. dizziness

3. insomnia

4. dry mouth

5. constipation

6. fetal toxicity

Front 99

action of Belviq =

Back 99

reduce appetite

via 5HT2C r's

Front 100

6 SE's of Belzviq:

Back 100

1. H/A

2. dry mouth

3. dizziness

4. fatigue

5. n/v

6. diarrhea

Front 101

gastric bypass works - it:

Back 101

keeps the pounds off, decreases M/M

- risks as with any surgery, so use as last resort

Front 102

one major contraindication of gastric bypass =

Back 102

serious psychological dz

Front 103

who should consider gastric bypass?

(3)

Back 103

1. BMI > 40

2. BMI > 35 and comorbidities

3. failed medical management

Front 104

one risk of gastric bypass =

Back 104

Nutritional deficiencies

- Iron, Thiamine, B12, Ca2+, Vit. D

Front 105

2 gastric surgeries that don't work:

Back 105

1. bypassing the ilium and part of the colon

2. restrictive rather than cutting out