Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Endocrine II DF > Endocrine Pancreas Guerin > Flashcards

Endocrine Pancreas Guerin Flashcards

(74 cards)

Start Studying
1
Q

how can the islets of langerhans cells be differentiated

A

ultrastucturally and by their hormone content

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what do PP cells do

A

pancreatic polpeptide stimulates the secretion of gastric and intestinal enzymes
-inhibits intestinal motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

rare cell types in islets of langerhans

A

D1 cells: VIP
enterochromaffin cells: serotonin
-tumor of these can cause carcinoid syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what does VIP do

A

induces glycogenolysis and hyperglycemia

stimulates GI fluid secretion and causes secretory diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is fasting plasma glucose levels usually detemined by

A

hepatic glucose output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

insulin action on adipose tissue

A

increase glucose uptake
increase lipogeneisis
decrease lipolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

insulin action on liver

A

decreased clugoneogenesis
increased glycogen synthesis
increased lipogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

insulin action on striated muslce

A

increase glucose uptake
increase glycogen syn
increase protein syn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

mitogenic effects of insulin

A

initiation of DNA synthesis in certain cells and stimulation of their growth and differentiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what pathway intracellulary is responible for GLUT4 transport to the PM

A

PI3K/ATK

and CBL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

In the US diabetes is the leading cause of what

A

ESRD
adult onset blindness
non traumatic LE amputations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

populations at greatest risk for diabetes

A

NAH

native americans, africans, hispanics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

diagnosis of diabtes with fasting glucose of

A

126 or greater

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

diagnosis of diabetes: random plasma glucose

A

200 or greater (in pts with clasic hyperglycemis signs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

diagnosis of diabetes: 2 hour plasma glucose at ___ or greater during an oral glucose tolerance test with load dose of __

A

200 mg/dL

75 gm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

diagnosis of diabetes: HbA1C level at

A

6.5% or above

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

which of the diagnosis of diabetes does not need confirmation test on separate visit

A

random blood glucose test in pt with classic hyperglycemic signs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what can lead to transient hyperglycemia

A

acute stress

infections, trauma, burns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

impaired glucose tolerance (prediabetes)

fasting plasma glucose ___

2 hour plasma glucose with 75 gm OGTT ____

HbA1C level ___

will they develop overt diabetes?

increased risk for what?

A

100-125 mg/dL

140-199 mg/dL

5.7-6.4%

1/4 will over 5 years

increased risk for cardiovascular complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

genetic susceptibility in DM1

main ones

A

HLA gene cluster on chrom 6p21

  • 90-95% of caucasians with HLA-DR3 or DR4
  • DR3 or DR4 plus DQ8 has highest risk
    • DQA11301-DQB10302 alleles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

genetic susceptibility in DM1 other genes

A 
wasinsulin
polymorphism in CTLA4 and PTPN22
VNTR in promoter region of insulin gene
gene for immune regulators (AIRE)
   -cause autoimmune polyendocrinopathy syndrome, type 1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

environmental factors for diabetes type 1

A

possible viral infection but unknown which one

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

autoantigen target in B cell destruction for DM1

A

insulin
GAD (glutamic acid decarboxylase)
islet cell autoantigen 512

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

how much of islet B cell needs to be loss before get hyperglycemia and ketosis

A

90%, long period btwn initiation of autoimmune process and appearance of diseas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
inadequate insulin secretion (b cell dysfunction) in DM2
initially there is insulin hypersecretion to overcome resistance - from a combo of excess FFA (lipotox) - chronic hyperglycemia (glucotox) - abnormal incretin effect - amyloid deposition within islets, and genetics
26
insulin resistance in liver
failure to inhibit gluconeogenesis (endogenous glucose production) contributes to high fasting blood glucose levels
27
insulin reseistance in fat
failure to inhibit activation of HSL--> excess TG breakdown and excess circulating FFA
28
which adipokines decrease blood glucose by increasing insulin sensitivity and how are they effected in obesity
leptin and adiponectin | adiponectin levels are reduced in obseity and contribute to insulin resistance
29
PEP C and gluconeogensisis in central obesity
central obesity increases lipolysis of adipose tissue = excess FFA, which has DAG intermediate, which canc stop insulin signaling -insulin usually stops gluconeogensis by blocking PEP carboxykinase, so without insulin PEPC ramps up gluconeogeneisis
30
central obesity and inflammation
proinflammatory cytokines are secreted in response to excess nutrients like FFAs and glucose = insulin resitance and b cell dysfunction -excess FFas within macrophages and b cells can activate inflammasome = more proinflamm cytokines = insulin resitance
31
several mechanism for b cell dysfunction in overt diabetes in type 2
excess FFA compromise b cell function and attenuate insulin release (lipotox) impact of chronic hyperglycemia (glucotox) abnormal incretin effect = reduced GIP and GLP-1 that normally causes insulin release amyloid deposition wihtin islets, in people with long standing DM2 in 90% of pts
32
monogenic forms of diabetes, genetic defect in b cell function
no b cell loss b cell mass and or insulin production effecte4d was called MODY bc like DM2 but earlier onset gene mutation is in glucokinase, this is the RLS for oxidative glucose metabolism which in turn is coupled to insulin secretion within islet b cells -can also have defect in genes for ATP/K+ channel
33
monogenic forms of diabetes, genetic defects that impair tissue response to insulin 2 types -symptoms associated with each
insulin receptor mutations - acanthosis nigricans - women have polycysitic ovaries and elevated androgen levels -lipoatrophic diabetes :hyperglycemia with loss of adipose tissue in subcut fat :also have hyperTGemia, acanthosis nigricans, and fat deposition in liver
34
pregestational diabetes and pregnancy increased risk for
stillbirth | congenital malformations
35
gestational diabetes what is it how to fix what can develop
women develops impaired glucose tolerance and diabetes for first time during pregnancy - typically resolves after delivery - majority develop overt diabetes in next 10-20 yrs
36
poorly controlled diabetes later in pregnancy can cause
large for gestational age newborn | child at increased risk of developing obesity and diabetes later in life
37
classic triad in DM1 if severe get also see
polyuria, polydipsia, polyphagia when severe enough you get diabetic ketoacidosis too -also see weight loss and muscle weakness
38
DM type 2 can present with
fatigue, dizziness, or blurred vision
39
diabetic ketoacidosis is typically triggered by
failure to take insulin (most common) other stressors: infections, illness, trauma, drugs (epinephrine, blocks insulin action and stimulates glucagon secretion)
40
glucose level for diabetic ketoacidosis
250-600 mg/dL
41
how are ketone bodies formed
decreased insulin = increased HSL-->increased FFA-->in liver FA esteried to fatty acyl coA-->in liver mitochond oxidize this to produce acetoacetic acid and b-hydroxybutyric acid
42
clinical manifestations of diabeti ketoacidosis
``` fatigue nausea and vomiting ab pain fruity odor deep, labored breathing (kussmaul breathing) -can get CNS depression and coma ```
43
why is ketoacidosis less common in DM 2
bc of higher portal vein insulin levels that prevent unrestricted hepatic fatty acid oxidation and keeps formation of ketone bodies in check
44
what is this called when severe dehydration from sustained osmotic diuresis -in pts who don't drink enough water to compensate for urinary loss -what pts? when usually seek medical attention? hyperglycemia at what?
hyperosmolar hyperosmotic syndrome in type 2 DM older pts and disabled pts by stroke or infection seek attention when - severe dehydration - impaired mental status hyperglycemia 600-1200 mg/dL
45
signs and symptoms of hypoglycemia
dizziness, confusion, sweating, palpitations, tachycardia
46
chronic complication of diabetes | -diabetic macrovascular disease
large and medium sized muscular arteries - accelerated atherosclerosis (hallmark) - increased risk of MI, stroke, LE ischemia - HTN and dyslipidemia in type 2 DM - diabetics have increased PAI-1 = procoag = formation of atherosclerotic plaques
47
chronic complications of diabetes | microvascular disease
small vessels | retina, kidneys, and peripheral nerves
48
diabetic microangiopathy
diffuse thickening of basement memrbanes - capillaries are more leaky than normal to plasma proteins - seen in skin, muscle, retina, renal glomeruli and medulla - leads to diabetic nephropathy, retinopathy, and some neuropathy
49
diabetic neprhopathy first sign - marker for what - may develop
microalbuminuria over 30 mg/day but less than 300 mg/day - also marker for greatly increased CV mobidity and mortality - 80% of type 1 and 20-40% of type 2 over 10-15 yrs will develop overt nephropathy with macroalbuminuria and HTN
50
3 lesions in diabetic neprhopathy
glomerular lesions -capillary BM thickening, diffuse mesangial sclerosis, and nodular glomerulosclerosis renal vascular lesions, principally arteriolosclerosis pyelonephritis, including necrotzing papillitis
51
capillary basement membrane thickening - what % of pts - seen how - when begins - what else occurs
in virtually all diabetic nephropathy, only seen by electron microscopy begins 2 years after onset of type 1 also have thickening of tubular basement membranes
52
diffuse mesangial sclerosis - depositions are positive for what - progression of disese
PAS positive | as progresses, becomes nodular
53
nodular glomerulosclerosis - name of disease - where - progression?
kimmelstiel-wilson disease nodules of matrix (PAS positive) in periphery of glomerulus progression: nodules enlarge and obliterate glomerular tuft
54
arterioles in and tubes in diabetic nephropathy
hyalinosis of both afferent and efferent glomerular hilar arterioles glomerular and arteriolar lesions --> ischemia-->tubular atrophy and intersitital fibrosis
55
diabetic neuropathy distribution types
glove and stocking pattern (LE first) sensory and motor autonomic neuropathy: bowel, bladder, ED mononeuopathy: sudden footdrop, wristdrop, or isolated cranial nerve palsies
56
diabetic retinopathy other eye manifestations
from neovascularization from hypoxia induced overexpression of VEGF in the retina glaucoma and cataracts
57
diabetics have increased susceptibility to infections of the
skin, TB, pneumonia, and pyelonephritis
58
criteria for malignancy in pancreatic neuroendocrine tumors
can't predict behavior based on microscopic appearance bc bland criteria is metastases, vascular invasion, local infiltration
59
90% of insulin producing tumors are benign or malignant?
benign
60
60-90% of non insulin functioning and nonfunctioning NETs are what
malignant
61
genetic alterations in sporadic pancreatic NETs
``` MEN1 LOF: PTEN and TSC2 inactivating mutations in -ATRX -DAXX ```
62
most common clinical syndromes in PanNETs
hyperinsulinism hypergastrinemia MEN
63
classic clinical picture of insulinoma
hypoglycemic episodes if blood gluose under 50 mg/dL
64
morphology of insulinoma
small (less than 2 cm diameter) look like giant islets deposition of amyloid
65
hyperinsulinism not from insulinoma
focal or diffuse hyperplasia of islets (use to be called nesidioblastosis) - maternal diabetes - beckwith-wiedemann syndrome - rare mutations in B cell K+ channel protein or sulfonylurea receptor - mor common in neonates and infants from congenital malformation
66
other causes of hypoglycemia
abnormal insulin sensitivity diffuse liver disease inherited glycogenoses ectopic production of insulin by retroperitoneal fibromas and fibrosarcomas -induced by self injection of insulin
67
``` zollinger-ellison syndrome oversecretion of what location metastases? syndrome involved histology ```
``` hypersecrtion of gastrin in duodenum or pancreas >50% are locally invasive or have already metastasized at time of diagnosis -25% arise as part of MEN? -histologically bland ```
68
multifocal gastrinoma vs sporadic
MEN-1 syndrome is multifocal | sporadic is single
69
if you have unusual location of ulcer in the jejunum think what
zollinger-ellison syndrome
70
clinical course of ZE | metastases?
peptic ulcers in duodenum and stomach 50% have diarrhea pts with hepatic metastases-->eventual liver failure within 10 yrs
71
treatment of ZE
PPI | total resection
72
other rare pancreatic endocrine neoplasms - mild diabetes, skin rash (necrolytic migratory erythema) and anemia - in perimenopausal and postmenopausal women mostly
SAM is an a-cell tumor bc he is menospausal
73
other rare PanNETs -diabetes mellitus, cholelithiasis, steatorrhea, hypochlorhydria
D-cell tumor (somatostatinomas) | -D High school class
74
watery diarrhea, hypokalemia, achlorhydria | syndrome?
VIPoma WDHA syndrome

Endocrine II DF (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions