Patholgoy - pancreas Flashcards

1
Q

polydipsia
polyuria
polyphagia
weight loss

A

DIABETES!!! mellitus

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

complication to worry about in DMI

A

DKA

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

complication to worry about in DMII

A

hyperosmolar coma

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

what else can rarely cause DM?

A

unopposed epinephrine or glucagon

steroid diabetes in pts on glucocorticoid therapy

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

what casues dehydration and acidosis in DM

A

decreased insulin or excess glucagon – dereased serugm glucose uptake — hyperglycemia, glycosuria, osmotic diuresis and electrolyte depletion
AND
decreased insulin or excess glucagon – increased protein catabolism – increased plasma aas, nitrogen loss in urine – hyperglycemia, glycosuria, osmotic diuresis, elevtrolyte deptiosn
AND
decreased insulin – increased lipolysis - increased plams free FAs, ketogeneiss, ketonuria, ketnonemia

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

what does noneyzmatic glycation cause

A

small vessel disease - diffuse thickening of basement membrane
retinopahy
glaucoma
neuropathy
nephrotpahty
large vessel disease: atherosclerosis, CAD, peripheral vascular occlusive disease, gangrene, cerebrovascular disae,

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

what is most common cause of fdeath in DM

A

MI

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

what does osmotoci damage cause

A

caratacts

neuropjaty - sensory, motor, autonomic

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

describe retinopathy in diabetes

A

hemorrhages
exudates
microaneurysms
vessel proliferation

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

at retina you see: hemorrhages, exudates, microanuerysms and veseels proliferation and you think?

A

diabetes

small vessel disease from nonenzymatic glycosylation

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

what casues osmotic damage in dm

A

sorbitol accumulation in organs with aldose reductase and low or absent sorbitol dehydrogenase

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

what is nephropathy in dm due to and describe please

A
small vessel diseas from nonenzymatic glycosylation
nodular glomerulosclerosis (kimmelsteil Wilson nodules) and pappilary necrosis and arteriolosclerosis -- hypertension and progressive proteinuria -- chronic renal failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

glaucoma due to in dm

A

small vessel non enzymatic glycosylation

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

cataracts due to in dm

A

osmotic damage

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

how to diagnose dm

A

fasting > 126
random with symptoms > 200
OGTT after two hours > 200
HBAiC > 6.5

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

DMI or DMII: autoimmune destrictuion fo beta cells

A

DMI

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

DMI or DMII: increased resistance to insulin with progressive pancreatic beta cell failure

A

DMII

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

DMI or DMII: insidious onset

A

DM II

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

DMI or DMII: sudden onset

A

DM I

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

DMI or DMII: < 30 years old

A

DM I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

DMI or DMII: > 40 years odl

A

DM II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

DMI or DMII: relatively weak genetic predisposition

A

DM I ; 50% concordance in identical twins

polygenic

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

DMI or DMII: relatively strong genetic predipsopstion

A

DM II; 90% concordance in identical twins

polygenic

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

DMI or DMII: polygenic

A

DM I

DM II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

DMI or DMII: association with HLA

A

DM I – HLA-DR3 and HLA-DR$

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

DMI or DMII: ketoacidosis

A

common DMI

rare DMII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

DMI or DMII: amyloid deposits

A

DMII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

DMI or DMII: polydipsia, polyphagia, polyuria weight loss

A

common in DMI

rare DMII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

histology of DM I

A

islet leukocytic infiltrate

30
Q

histology of DM II

A

islet amyloid polypeptide deposits/amyloidosis

31
Q

what causes diabetic ketoacidosis

A

increased insulin requirements from increased stress ie inefection

32
Q

what is pathogenesis of diabetic ketoacidosis

A

excess fat breakdown and increased ketogeneiss from increased free fatty acids – made into ketone bodies - beta hydroxybutyrate > acetoacetate

33
Q

why does DKA occur in type i

A

endogenous insulin in type II usually prevents lipolysis; absent completely in type I – lipogenesis all over the place

34
Q

s and sx of DKA

A
kussmaul respirations - rapid and deep breathing
nausea and vomiting
abdominal pain
psychosis/derlierum
dehydration
fruity breath odor - acetone
35
Q
rapid and deep breathing
n/v
ab pain
psychosis/delirium
dehydration
fruity breath
A

DKA

36
Q

labs in DKA

A

hyperglycemia
increased K
decreased HCO3 (increased anion gap metabolic acidosis)
increased blood ketones
leukocytosis
hyperkalemia - intracellular depletion though due to transcellualr shift out of cells when insulin is low

37
Q

what can happen from DKA

A

mucormycosis from rhizopus
cerebral edema
cardiac arrhtymias
heart failure

38
Q

cardiac arrhythmias
heart failure
cerebral oedema
mucormycosis

A

complicatinos of DKA

39
Q

how to treat DKA

A

IV insulin and fluids and K and glucose If necessary

40
Q

what is a glucagonoma

A

tumor of pancreatic alpha cells – overproduction of glucagon

41
Q

presentation of glucaognoma

A

depression
diabetes - hyperglycemia
DVT
dermatitis - necrolytic migratory erythema

42
Q

depression
hyperglycemia
DVT
necrolytic migratory erythema

A

glucagonoma

43
Q

glucagonoma maligi or benign

A

maligi

44
Q

what is an insulinoma

A

tu;mor of pancreatic cells - increased insulin

45
Q

presentation of insulinoma

A

hypoglycemia - letharyfy syncope fiplopia

46
Q

what is whipple triaf

A

decreased bloo glucose

symptosm of blood glusoe - lethargy, syncope, diplopia that are resolved with normalitio of glucose levels

47
Q

labs of insulinoma

A

lethargy/syncope/diplopia
low blood sugar
high C peptide vrs insulin o/d wehre C peptide is low

48
Q

what is most common pancreatic islet cell tumor

A

insulinoma

49
Q

insulinoma beigning or maligi

A

benign

50
Q

what is carcinoid syndrome

A

rare syndrome caused by carcinoid tumors of neuroendocrine cells

51
Q

where does tumor have to be to see carcinoid syndrome

A

not just in gi bc liver metabos serotonin

mets to liver ;)

52
Q

recurrent diarrhoea
cutaneous flushing
asthmatic wheezing

A

carcinoid syndrome

53
Q

labs in carcinoid syndrome

A

increase 5HIAA in urine

54
Q

complications of carconid syndrome

A

pellagra: dementia, diarrhoea, dermatitis

55
Q

how to treat carcinoid syndrome

A

serugery and octreotide

56
Q

rule of 1/3

A
carcinoid
1/3 are mets
1/3 present with second maligi
1./3 are multiple
mets, wieth second maligi and are multiple
57
Q

what is the most common malig in the small intestine

A

carcinoid tumors

58
Q

hypokalemia
diarrhoea
achlorhydria
normal anion metabolic acidosis

A

VIPoma

59
Q

what is zollinger Ellison syndrome

A

gastrin secreting tumor in duodenum > pancreas

60
Q

abdominal pain

diarrhoea/malabsoprtion

A

ZES

61
Q

PUD associated with ZES?

A

multiple tumors in duodenum and jenjun
suspect if multiple
past proximal duodenum
refractory to therapy and acid reducing efforts

62
Q

what is diagnostic test for ZES?

A

secretin stimulation test: gastrin levels reain high after administration fo secretion (because normally lowers)

63
Q

what is ZES associated with?

A

MEN I

64
Q

inheritance pattern of MEN sydnromes please

A

autosomal dominant

65
Q

type of tumors in MENI

A

pituitary tumors - prolactin or GH
parathyroid tumors
pancreatic - insulinoma, glucagonoma, VIPoma, ZES, etc

66
Q

MENI genetics

A

MEN1
menin
tumor suprresor

67
Q

MEN II a type of tumors

A

parathyroid hyperplasia
medullary thyroid
pheocrhomocytoma

68
Q

genetics of MEN IIa

A

ret gene for y kinase

69
Q

MEN IIb tumors please

A

pheochromocytoma
medullar carcinoma
oral and intestinal ganglioneruamatosis

70
Q

marfanoid habitus and MEN

A

men iib

71
Q

genetics of men IIb

A

ret gene

y kinase