Path Winter Final Dm

Front 1

when BMI > _____ is DM risk increased

Back 1

30- the minimum cut off for obesity

Front 2

what is the dx cirteria for DM

Back 2

Random blood glucose >200 x2 times

fasting blood sugar >126

>200 after standard CHO load

Front 3

what is a normal blood sugar
what is a normal post parandial

Back 3

normal 70-100, anything 101-124 is abnormal prediabetic
after meal <140

Front 4

if you have a blood sugar reading that spikes to like 204 when will you see increased glycosuria

Back 4

in like the next reading, there is a lag

Front 5

if you have a BMI >25 (still not obesity) and one of what 3 conditions do you do a screening A1C

Back 5

HTN
high risk ethnicity- indian, black, non hispanic whites, hispanic
hx of gestational DM

Front 6

what is normal A1c levels, what is preDM what is DM

Back 6

Normal: 5%

PreDM: 5.7-6.4%

DM >6.5

Front 7

what are the 3 contries w/high DM rates

Back 7

india
china
US

Front 8

what are all of the causes of DM

Back 8

1. Type I: ABSOLUTE deficit in insulin bc of b cell destruction. can be immune or idiopathic destriction. can only be treated w.insulin. NOT drugs to increase insulin

2. insulin resistance with RELATIVE insulin deficit

3. genetic defect of B cells dysfunction: MODY

4. secondary DM due to pancreatic destruction: chronic pancreatitis, cystic fibrosis, pancreatectomy,

5. glucocorticoids, protease inhibitors etc

6. endocrine problems (cushing, acromegaly, gluconoma, somatostatinoma)

7. infections: coxsackie B, CMV

Front 9

A 34 y/o man with moderately severe ulcerative
colitis has been on oral prednisone for 4 mon.
Which of the following symptoms is the most
likely adverse effect of his treatment?
A) Diabetes mellitus
B) Hyperpigmentation of the skin
C) Hypotension
D) Muscle hypertrophy
E) Sodium wasting

Back 9

prednisone is a corticosteroid, it can lead to sudden DM like SX

Front 10

what are some of the more unusual causes of DM

Back 10

1. genetic defects in MODY. B cell dysfunction

2. secodnary to pancreatic deficit: chronic pancreatitis, CF, hemochromatosis

3. endocrine problems: suching, acromegaly, glucaconoma, somatostatinoma

4. Infections: coxsackie B, CMV

5. Drugs: corticosteroids, protease inhibitors, thiazides, b adrenergic agonsits

Front 11

how does insulin get glucose into the cell

Back 11

binds R, then causes glut 4 to enter the membrane in sk mm and fat

*insulin is ANABOLIC

Front 12

whats the pathogenesis of DM I

genetic susceptible
clinical features of insulin resistance

Back 12

Pathogenesis DM I: abrupt onset after 90% of b pancreatic cells have been destoryed. autoimmune destruction.

Genetic: HLA DR3-DR4, DQ8 linkage insulin polymorphsim at VNTR tandem repeats, CTLA 4, for T cell regulation

Front 13

is DM I or II associated with VNTR.

what are the other genetic constituents assoicated with this

Back 13

Type I

Type I also associated with HLA DR3, DR4
CTLA4- gene that inhibits T cell response

Front 14

VNTR
HLA DR3 DR4. class 2 MHC on Chromosome 6
CTLA 4- T cell response

Back 14

all associated with DM I

recall NO HLA associations with DM II

Front 15

what is insulinitits

Back 15

Autoimmune destruction of b cells by T cells. DM 1 (CTLA4)

CTL T cells against b cells AG are GAD (glutamic decarboxylase)

Front 16

what is the pathogenesis of DM II

Back 16

also a genetic component
but also sedentary lifestyle and excess calories

Front 17

you have detected anti GAD, insulin, UCA512. does the pt have DM I or II

Back 17

I

Front 18

WHATS THE DEF OF... in DM II

1. Insulin resistance

2. B cell dysfunction

Back 18

: IR: decreased response of peripheral tissues to insulin. . get hyperglycemia after eating bc of insulin deficit

b cell dysfunction: insulin secretion in face of insulin resistance and hyperglycemia

Front 19

what is the effect of insulin on...

1. Striated mm

2. fat

3. liver

Back 19

1. sk MM: increase glucose uptake, increased glycogen synthesis, increased protein synthesis. Insulin is anabolic

2. fat: increase glucose uptake, increased lipogenesis, decreased lipolysis

3. liver: decreased gluconeogensisi, increased glycogen synthesis, increased lipogensis

Front 20

increased lipogenesisi is stim by insulin in what two tissues

increased glucose uptake is stim by insulin in what 2 tissues

Back 20

1. liver
2. fat


fat, sk mm

Front 21

DM I or II

1. onset adult
2. weight loss before dx
3. initial increase in insulin
4. AB to GAD, UCA512

Back 21

1. onset adult: II usually
2. weight loss before dx: I
3. initial increase in insulin: II
4. AB to GAD, UCA512: I

Front 22

DM I or DM II

1. non ketotic hyperosmolar coma
2. DKA w/o insulin
3. MHC mutations
4. CTLA 4
5. VNTR

Back 22

1. non ketotic hyperosmolar coma: DM II
2. DKA w/o insulin: I
3. MHC mutations: I
4. CTLA 4: I
5. VNTR: I

Front 23

type __ DM is associated with insulitis

type ___ DM is associated with amyloid

Back 23

I

II

Front 24

is genetics more in DM i or II

Back 24

II, II has NO HLA association

genetics then with sedentary lifestyle and excess calories

Front 25

increased risk of DM II with what kind of obesirty

Back 25

central- belly fat is BAD

Front 26

what are the 4 things associated with obesity related IR

Back 26

1. NEFA- nonesterified FFA
2. Adipokines: hyperglycemia is w.retinol binding protein 4
3. inflammation: TNF, IL6
4. PPARg (peroxisome proliforator activated receptor)

Front 27

tell me about PPAR g

Back 27

receptor in fat, determines fat differentiation

promotes adiponectin secretion

deposots non esterified FFA

mutation causes MONOGENETIC DM,

stim by thiazolidiones

Front 28

what genes are associated with DM II

Back 28

Tcf7L2
SCL3048
CDKN2A, CDKN2B

**thse are all obesity related genes, its NOT an HLA assocaittion as was seen in DM I

Front 29

adipokines, FFA, inflammation are all associated with what

Back 29

IR associated with DM II

Front 30

IR is seen with acanthosis nigricans T or F

Back 30

true
can also have androgen problems leading to polycystic ovary syndrome, anovulation, hirsutism

Front 31

how does insulin contribute to HTN

Back 31

retain water, expansion of blood volume, production of excess NE, SM proliforation in arterioles

Front 32

there is a dysfc in T reg which breakd down self tolerance.

this is the pathogenesis of DM I or II

Back 32

I

Front 33

IR in peripheral tisses w/failure of b cells to compensate

DM I or II

Back 33

DM II

obesity related factors as well
non esterified fatty acids
inflammatory mediators-

Front 34

in whiat disease do we see insulinitis- the T cell infiltrate

when do we see amyloid

Back 34

DM I, b cell depletion, islet atrophy

DM II, mild B cell depletion

Front 35

what is the pathogenesis of DM I

what is the pathogenesis of neonatal

Back 35

I: autoimmune destruction of B cells

Neonatal: gene mutation in ATP sensitive K channel in b cells, responds to sulfonylurea

Front 36

ok so when glucose binds to glut 2 in the b cells what happens, how is insulin released

Back 36

1. glucose means ATP can be made

2. ATP opens K channel (sulfonylurea) and K causes membrane depolarization to let Ca into the cell

3. once Ca is in the cell it causes insulin release

Front 37

MODY is what

**ON TEST

Back 37

Maturity onset DM of the young (MODY) its a monogenetic form of DM
Autosomal Dom inheritance w/high penetrance

early onset DM that is NOT associated with obesity, NO IR NO b cell AB

Front 38

what is the deal if your pt <25 has diabetes but is NOT obese, is NOT IR, and does NOT have AutoAB against b cells

Back 38

MODY- maturity onset DM of youth

**its a MONOGENETIC form of DM that is inherited AD

**MODY 2- glucokinase deficiency

Front 39

what is deficient in MODY 2

Back 39

glucokinase deficency

**catalyzes the RLE for glucose metabolism. increased blood glucose threshold for Insulin release. mild chronic hyperglycemia that does not worsen over time

Front 40

what is the monogenetic form of DM

Back 40

its MODY 2- defect in glucokinase. Glucose metabolism is inhibited in the RLE so more glucose needs to be in the blood than normal in order for insulin to be released.

its DM that is NOT associated with obesity/IR/ or AB

Front 41

DD is a 26 y/o female with a history of type 1
DM since age 3. She is admitted with chest
pain. She has a daughter and the two live with
her mother. She has a boyfriend with whom she
recently has had “issues” as a consequence of
which, she has skipped some doses of insulin.
She smokes 4‐5 cigarettes a day and has a
history of illicit drug abuse that includes
cocaine and amphetamines but no IV drug use
or alcohol

Labs:

glucose, through the roof
BUN, Creat: high
Na: LOW
K:high
CO2 low

UA: + for cocaine and amphetamines

Family history: diabetes in a great grandmother
• Previous admission two weeks earlier was also
for chest pain. ECHO cardiogram revealed left
ventricular dysfunction and ejection fraction
consistent with congestive heart failure.
• She was nephrotic for a number of years and
now is on chronic dialysis for end‐stage renal
disease

what are some consequencs of DM

Back 41

1. HTN
2. Blurred vision
3. painful neuropathy
4. gastroparesis

Front 42

what are complications of DM that is NOT controlled

Back 42

1. Cardiomyopathy
2. retinopathy
3. vasculopathy
4. neuropathy
5. HTN

Front 43

why are there vascular complications associated with DM

Back 43

there is lots of sugar so we glycolsalate things. we get lots of AGE- advanced glycation end products

measured by HgA1c

Front 44

whats AGE

Back 44

its when sugar is added to protein non enzymatically, its more abundant in DM bc there is more sugar around

**involved in artherogenesis which in terms of DM leads to ===> microBV damage, nephropathy, and retinopathy

Front 45

AGE damages what 3 structures in DM

Back 45

1. small BV (AGE mediated)
2. nephron
3. retina (VEGF mediated)

**bc AGE is involved in atherogenesis

Front 46

ok so in DM we have 3 things that promote BV damage. what are they

Back 46

1. AGE
2. PKC activation
3. intracellular hyperglycemia that disturbc polyol path

Front 47

in DM there is activation of PKC, what does this lead to

Back 47

1. incresed VEGF!!! which causes retinopathy

Front 48

In DM we know we have AGE and we know age causes
1. AGE
2. PKC
3. Polyol activation

tell me what polyol activation does in the cell

Back 48

intracellular hyperglycemia will ACTIVATE polyol this damages....

nerve***
lens
BV

Front 49

nerves
kidney
eyes
BV (macro and microvascular) are all late stage of DM, how can we prevent this

Back 49

control the blood sugar!!!!!

Front 50

whats the pancreas like in late DM I and II

Back 50

I: decrease in size and number of islets, insulinitis, lots of lymphocyte infiltrate

II: amyloid replaces islets, subtle decrease in islet cell mass.

Front 51

what do the islet cells look like in infants born to DM moms

Back 51

increased islet cells

Front 52

insulinitis pancreas

amyloid pancreas

Back 52

DM I

DM II

Front 53

what do we mean, the "macrovascular" complications of DM

Back 53

ACCELERATED atherosclerosis

most common cause of death in DM is related to this atherosclerosis- MI, stroke, renal a stensois/HTN

Front 54

• A 59 y/o female presented to the ED with acute
onset of abdominal pain and bloody diarrhea
12 hours earlier. She has had no similar
episodes, no recent travel history and no known
contact with anyone with similar symptoms.
• Past history includes hypertension, hyperlipidemia
and type II diabetes mellitus for
which she takes medications.
• Her father had coronary artery disease and type
II DM; no family history of IBD or cancer

BP 151/91, fasting blood sugar 154, HbA1C7.8
• CT of abdomen shows fatty liver and colitis
at splenic flexure.
What is the likely cause of her:
‐ fatty liver?
‐ colitis?

Back 54

Fatty Liver: if poor contol of DM lots of lipolysis to free FA, these are sent to the liver

Colitis: its at splenic flexure which is watershed area, prbly its bc of ischemic bowel bc of all of the artherosclerosis seen in DM

Front 55

what might a LE exam look like for a person w/DM

Back 55

gangrene (wet or dry)
lack of hair

BOTH are regulated by the artherosclerosis and decreased blood flow that is seen in DM

Front 56

why do most ppl w/DM II die

Back 56

MI- HUGE atherosclerosis

DM as a risk factor for MI carries same amt of risk as previous MI!!!


all of this damage is mediated by AGE that activates endo and released cytokines and growth factors, also PKC actibation with is prothrombotic

Front 57

is the risk of MI asscoiated with DM due to obesity

Back 57

NO!

obesity/metabolic syndrome is INDEPENDENT risk for atherosclerosis

in DM we have AGE nad PKC as additional risks

Front 58

what are the MICROangiopathies associated with DM complications

Back 58

1. thickening of BM in capillaries (skin, mm, retina, renal glomeruli, placenta, nerves etc)

-causes protein to leak from capillaries: retinopathy, nephropathy, neuroopathy

Front 59

what contributes to the pathogenesis of DM

retinopathy
nephropathy
neuropathy

Back 59

the MICROvascular damage. the BM thicken adn protein leaks out, and causes eye/kidney/nerve prblem

Front 60

will we see thickend or thined BM in ppl w/DM

Back 60

thick!!! thick BM in capillaries

esp in:
retina
nephron
nerves

**thickening causes MICROvascular damage nad protein leakage

Front 61

A 60 y/o patient complains of polydipsia, polyuria and polyphagia. A histologic slide of the patient’s kidney biopsy is shown. Which of the following findings will most likely be
apparent on renal biopsy?
A) Amyloid deposits
B) Crescent formation
C) Nodular glomerulosclerosis
D) Segmental sclerosis

Back 61

NODULAR glomerulosclerosis

**recall microvascular damage leads to BM thickening
*amyloid is seen in the pancreas in DM
**cresencts are seen in rapidly progressing nephritis

Front 62

what happens to the morphology of a DM kidney

Back 62

nodular glomerulosclerosis

THIS IS A MUST KNOW PIC. sclerosis of the glomerulus

Front 63

what is the most common cause of renal failure in adults

does this cause nephritic or nephrotic

Back 63

DM!!!!! nodular glomerularsclerosis

nephrotic

Front 64

whats Kimmelstiel Wilson leasion

Back 64

its the kidney lesion seen in DM

-glomerular lesion produces NEPHROTIC syndrome

Front 65

we know DM will cause renal failure, will it cause infection in kidney

Back 65

you bet! pyelonephritis with risk for papillary necrosis

Other forms of renal damage w/DM
-hyaline arteriolosclerosis in afferent/efferent steriole
-artherosclerosis
-glomerular nodular sclerosis
-kimmelstiel wilson lesion
- end stage is small and shrunken

Front 66

where is arteriolosclerosis seen

Back 66

in DM kidney- afferent/efferent look like malignant onion skin

Front 67

what is the most important thing to prevent renal failure associated with DM

Back 67

HTN control

use ACE inhibitors

Front 68

is there albumin in the urine of the DM pt

Back 68

ya, small amts. its first sign of nephrpoathy

**correlates with increased risk of cardiovascular disease,

Front 69

will tx w/ACE inhibotors just take care of renal problems in pts w/DM

Back 69

no, also decreases cardiovascular risks

Front 70

tell me about the ocular complications of late DM

Back 70

1. retinopathy, retinal hemorrhage, detachment and blindness (neurovascularization bf of VEGF)

2. Cataracts: polyol path

3. GLaucoma:

Front 71

when you do a fundoscopic exam on a person w/DM what might you see

Back 71

exudates
hemorrhage
AV nicking
NEOVASCULARIZATION

Front 72

what happens to the lens in DM

Back 72

cataracts, gets cloudy and hard. bc of polyol path

Front 73

is glaucoma associated with DM

Back 73

oh ya, cupping of optic disc

Front 74

An autopsy is performed on an 8 y/o child with recent onset of diabetes mellitus who had died following an automobile accident. Which
of the following autopsy findings would favor the Dx of type I diabetes as contrasted to type 2?

A) Amylin deposits in pancreatic islets
B) Tubular glycogen deposit (Armanni‐Ebstein l.)
C) Insulitis
D) Kimmelstiel Wilson nodules
E) Proliferative retinopathy

Back 74

insulinitis*** DM I


amyloid in pancreas is DM II

Kemmelstien wilson is in kidney
both DM I nad II are retinal proliforation

Front 75

what all are the manifestations of neuropathy in DM

Back 75

1. sensory, motor loss
-IMPOTENCE
2. LE most affected-ulcers, 2 infection
3. CHARCOT JOINTS: lysis of injured bone

Front 76

why might a DM not be able to feel a rock in their shoe

Back 76

neuropathy

**neuropathy can even lead to cognitive dysfunction

Front 77

are GI compliants common in pts w/DM

Back 77

OH YA!!!
constipation >diarrhea
NV, heart burn, abd pain
GB dysfunction, delayed emptying

Front 78

why do pts w/DM have GI complaints

Back 78

lots of reasons

one is amylin (DM II) decreases stomach emptying
microangiopathy etc etc

Front 79

whats gastroparesis

Back 79

delayed gastric emptying in the ABSENCE of obstruction

abd pain, early satiety, fullness, bloating, etc etc

**common in DM

Front 80

what kinds of infections are common in DM

Back 80

fungal- mucormycoses-broad hyphea
ulcers
TB
pneumonia
PYELONEPHRITIS

Front 81

list ALL of the complications of DM

Back 81

1. stroke- infarct/hemorrhage
2. HTN
3. Artherosclerosis, nephrosclerosis, arteriolsclerosis, hyaline arteriolosclerosis, pyelonephritis
4. pyelonephropathy
5. autonomic neuropathy
6. retinopathy, cataracts, glaucoma,
7. MI
8. Gasteroparesis
9. islet (insulitis in DM I) (Amyloid in DM II)
10. peripheral vascular artherosclerosis
11. gangrene
12. infection

Front 82

ok you have a new onset of DM, is it I or II

8 yo male, loosing weight but eating tons! parents think its growth spurt, peeing bed.

Back 82

I

**its onset is mostly in kids
**catabolic state--> weight loss and polyphagia

**will be ketotic from FA oxidation

HYPOnaturemic

Front 83

what is the renal threshold for polyuria

Back 83

blood sugar >160

acts as osmotic diuretic and we get polyuria

Front 84

what hormones are released in DM I what lead to more hyperglycemia

Back 84

1. glucagon
2. GH
3. EPI

Front 85

when do we see ketoacidosis, DM I or II

Back 85

I

Front 86

what happens to Na in DM I

Back 86

decreases, be we have that polyuria/glycouria pulling all the Na out

this dehydrating effect also leads to increased H ion conc--> acidosis

K is high and Na is low

Front 87

what can ppt an episode of glucose intolerance in DM I

Back 87

minor dietary change, infection, stress, vomit, exercise

Front 88

what are some signs of ketoacidosis assoc w/DM I

Back 88

kussmal breaths, deep rapid. blos off CO2 from acidosis

K will be high!

Front 89

what is the ONLY appropriate tx for DM I

Back 89

insulin REPLACEMENT, none of this stuff that increases insulin secretion will work

diet, exercise

Front 90

what effect does insulin deficiency have on

fat
sk MM
liver

Back 90

FAT: lipolysis to free FA, this --> polyphagia

SK MM: catabolism of protein, no more glycogen being made, no glucose uptake

LIVER: gluconeogensis --> hyperglycemia, ketoscidosis

get dehydrated

Front 91

what is the typical presentation of DM II

Back 91

polyphagia, polyuria, polydipsia
weight loss (more common in DM I)
WEAKNESS
obese
still have SOME insulin so protect against ketoacidosis

Front 92

who gets a hyperosmolar nonketotic coma

Back 92

DM II- severe DEHDRATION

usually seen in old folks

Front 93

if you have JUST been dx with DM II whats the BEST thing you can do

Back 93

LOOSE WEIGHT 10%
-exercise, diet

Front 94

what do the following drugs do

1. sulfonylurea,glitinides
2. metformin
3. thoazolidinedioes

Back 94

1. sulfonylurea,glitinides: stim release of insulin

2. metformin: decrease glucose production by liver

3. thoazolidinedioes: decrease IR

Front 95

what drugs stim release of insulin

what drugs decrease glucose production by liver

what drugs decrease IR

Back 95

aulfonylurea, glitinides

metformin

thiazolidinediones

Front 96

whats sitagliptin and exenatide

Back 96

drungs for DM II that enhance Insulin releaes

Front 97

whats the other name for glycohemoglobin

Back 97

HgA1c- gives us an average blood sugar level for the past 3 months

**falsely decreased in sickle cell adn thalassemia

Front 98

what groups of preggers get tested for gestational DM

Back 98

ALL at 24-28 weeks

**its the most common pregnancy related disease

Front 99

ok so all women get screened for gestational DM at 24-28 weeks, who is at increased risk

Back 99

if you gain a ton of weight
hx of large babies
hx miscarriage
fx of DM II
UR + for glucose

Front 100

whats the dx criteria for getational DM

Back 100

Fasting >105
190 at 1 hr
165 at 2 hrs

**lower requirements than normal dx

Front 101

what are the complications of the fetus when mom has gestational DM

wht about delivery

Back 101

1. predispose for obesity
2. stupid
3. metabolic syndrome/DM II as adult
large baby (ILGF- anabolic, growth)


Delivery:
dystocia (hard to deliver), fracture, nerve palsies, pre-eclampsia bc babe is HGUE

Front 102

are babies born to moms w/gest DM more or less likely to be still born. what about some other things

Back 102

more likely to be still born

cardiac, neurotube defects

islet cell HYPERPLASIA

increased risk of hyaline membrane disease

Front 103

what cells in the pancreas make

insulin
glucagon
somatostatin

Back 103

insulin- beta, most numerous
glucagon- alpha
somatostatin- delta (suppresses release of other two)

Front 104

whats the deal with pancreatic endocrine tumors

Back 104

rare, occur in adults
located along length of pancreas
carcinoid, single or multiple lesions, benign or malignant,

mets to LN, invades vasculature/viscera

Front 105

what is the most common islet cell tumor

Back 105

insulinoma

**will have LOW fasting glucose, HIGH serum C peptide

Front 106

what are the sx of whipples triad

Back 106

1. hypoglycemia
2. CNS- confusion, unconscious, that are ppt by fast/exercise, releived by glucose

**Hyperinsulinemia!!!

Front 107

your pt has LOW fasting glucose, high c prtein. what can cause this

Back 107

insulinoma- insulin secreting tumor of islet cella

**Insulin: glucose ration >0.3

Front 108

besides insulinoma what else can cause hypoglycemia

Back 108

1. end stage liver diseae
2. drugs

Front 109

A 23 y/o nursing student with no significant
past medical history comes to the ED with
light‐headedness, nausea, vomiting and
tremors.
On PE, the patient with tachycardic and
diaphoretic. Lab studies show a blood glucose
level of 30 mg/dL. The patient’s symptoms
resolve after she drinks a cup of orange juice.

Which of the following tests should be ordered
to determine whether the student’s condition
was self‐induced?
A) Serum ß‐chain and insulin levels
B) Serum C‐peptide and insulin levels
C) Serum insulin only
D) Serum preproinsulin
E) Serum proinsulin level

Back 109

EPI is elevated bc she is trying to make glucose- epi --> tremor,

Serum C peptide is normal if self induced. if we are kicking out the insulin C peptide will also be high.

exogenous insulin will NOT increase C peptide

Front 110

A 42 y/o female has a 3 year history of episodic
confusion and syncope; she is often belligerent
and hallucinating.
• She was admitted for a 72 hour fast that was
stopped at 36 hours when diagnostic results were
achieved.
• What is the diagnosis?

glucose 35
Insulin 64 (high)
C peptide (6.2 high)
Insulin: glucose 1.82

Back 110

with I:G ration >0.3 we can dx in INSULINOMA- tumor in islet cells of pancreas

Front 111

This patient has recurrent episodes of syncope,
lethargy, headaches and weakness over the past
year. Episodes are generally with fasting early in
the a.m. or later in the day when she has been w/o
food for hours.
• She was admitted after being found
unconscious by her husband. Paramedics
drew blood and administered IV glucose. She
immediately became alert and oriented, but
became disoriented 1 hour later

serum glucose was 10 adn 35
insulin 34 (high)
C peptide (3.4- high)

Back 111

insulinoma?
she had pancreatic tumors, and sx resolved but she became insulin dependent DM bc so much of the pancreas was removed

Front 112

A 28 y/o man is evaluated for recurrent peptic
ulcer disease, apparently refractory to
pharmacologic intervention. Serum gastrin is
markedly elevated. These findings are most
characteristic of which of the following?
A) Cushing syndrome
B) Glucagonoma
C) Whipple triad
D) Zollinger‐Ellison syndrome
E) Acromegaly

Back 112

increased gastrin seen in ZE

**whipple tirad is confusion adn hypoglycemia associated with hyperinsulinemia

Front 113

what is zollinger ellison syndrome

Back 113

tumor in duodenum or pancreas that secreted GASTRIN

common sx is to have peptic ulceration,

Front 114

63‐year‐old woman with a 4 1/2‐year history
of diabetes mellitus presented with an
ulcerating
rash, primarily on the shins, groin, and face
(Panel A); cheilitis (Panel B); and glossitis. (CIRCUMORAL RASH)
Her symptoms had been worsening for 4 years
despite specialized wound care. In addition,
she noted concurrent weight loss, depression,
abdominal pain, and intractable nausea. She
was

Abdominal computed tomography was
performed, and glucagon levels were measured.
An enhancing, lobulated mass measuring 7 cm
in diameter was found in the tail of the
pancreas,
and the patient's fasting glucagon level was
890 pg/ml (normal, 0 to 80).
• Mass was resected. 1 day later, the rash had
faded; 4 wks later, glucose levels (while taking
no medication) were normal, and the necrolytic
migratory erythema had completely resolved

Back 114

the infection caused the DM,

**in DM you get infectinos but NOT that circumoral rash we saw- but super common in GLUCAGONOMA- HUGE glucacon increase

Front 115

what is characteristic in a glucagonoma

Back 115

DM
migratory necrotizing skin erythema- circumoral

**HIGH plasma glucagon!!!!! glucagon from alpha cells

Front 116

nasty skin lesions are seen in...

1, DM
2. Insulinoma
3. Glucagonoma

Back 116

glucagonoma

Necrotizing Skin Erythema

classic to have the rash perianal or perioral

Front 117

A 59 y/o woman with no prior medical history
presents to the physician with marked hyperglycemia,
diarrhea and weight loss. A CT scan
of the abdomen reveals a pancreatic mass. A
trial period on an oral hypoglycemia agent has
not helped reduce her glucose levels. On PE,
she has a perioral necrotizing rash. Which of
the
following is the most likely diagnosis

A) Corticosteroid therapy
B) Glucagonoma
C) Insulinoma
D) Type I diabetes mellitus
E) VIPoma

Back 117

glucagonoma

Front 118

what is the abnormal lab value that gives away a somatostainoma from delta cells

Back 118

low Cl!!!

also will have high serum somatostatin

Front 119

whats associated with VIPoma

Back 119

watery diarrhea
hypokalemia
achlorhydria (low gastric acid)

Front 120

watery diarrhea, hypokalemia, achlorhydria are associated with what

insulinoma
glucagonoma
VIPoma
Somatostatinoma

Back 120

VIPoma

Front 121

A 12 year old y female presents to the ER with
fatigue, weight loss, polydipsia, polyuria,
vomiting and drowsiness. On exam she has a
blood pressure of 90/55, pulse rate 110/min,
cold extremities and deep, sighing respiration
(Kussmaul respiration).

Urine showed glucose +4, Ketones + 3.
plasma glucose 600. Na Low, K high, bicarb LOW, pH low

Back 121

DM I- in ketoacidosis

Front 122

Patient was diagnosed with type I at age 12
and treated with twice daily insulin.
• At age 37, she presents to the ER with acute
substernal chest pain that radiates to the neck
and down the left arm. Pain is associated with
nausea and sweating. Cardiac enzymes are
increased, total CK 500 U/L (38‐120) with
CK‐MB 25 (0‐3 ng/mL). EKG shows ST
segment changes and Q waves consistent with
myocardial infarction. She is hospitalized 7d.

At age 39, she presents with generalized
edema without evidence of cardiac failure.
• There is muscle weakness and loss of sensation
in both lower extremities on neurologic exam.
• There is bilateral visual impairment. The retina
by ophthalmoscope reveals microaneurysms
in retinal vessels.
• Lab results: elevated BUN and creatinine; 2+
glucose and 4+(massive) protein in the urine.

Back 122

MI

Front 123

This 50 y/o man has been treated 15 years for
hypertension and is currently on 3 meds.,
calcium channel blocker, ACE inhibitor and a
diuretic. He has always been slightly overweight,
5’11”, 205#, and has had diabetes mellitus for
10 years.
• Fundoscopy shows arteriolar narrowing,
microaneurysm formation, and moderate
proliferative retinopathy.

BUN high
Creat high
cholesterol high
HDL low
fasting glucose high
HbA1c high
Apecific gravity low
proteinuria- NO glucose or ketones

Back 123

DM II

- UA gluccose bc sugar was <160

HTN is BAD for DM- treat it!!! (ACEi)