ENDOCRINE Flashcards

1
Q

Four major cells found in pancreas

A

Beta - insulin
alpha - gluccagan
delta - somatostatin
PP - pancreatic polypeptide that stimulates secretion of gastric and intestinal enzymes, inhibit intestinal motility

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

two minor cells

A

D1 cells - VIP

Enterochromaffin cells - serotonin

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

zollinger ellison syndrome

A

gastrinomas usually in small intestine and pancreas
present with chronic diarrhea and duodenal ulcer
increase thickness of oynthnic mucosal fold due to in rease in parietal cells
hyperplasia of mucous neck cells
dysplastic nodules or rare carcinoid tumours

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

what conditions are somatostatinomas associated with

A

DM
cholelithiasis
steatorrhea
hypochlorhydria

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

carcinoid tumor

A

from enterochrommafin cells

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

which muscle is the major insulin responsive site for PP glucose utilization

A

skeletal muscle

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

hyperglycemic in diabetes result from

A

defect in insulin secretion
defects in insulin action
both commonly

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

normal range for blood glucose

A

70 - 120mg dl

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

rbs value for diabetes

A

A random glucose > 200 mg/dL, with classical signs and symptoms

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

fbs value

A

A fasting glucose > 126 mg/dL on more than one occasion

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

ogtt value

A

An abnormal oral glucose tolerance test (OGTT), in which the glucose is > 200 mg/dL 2 hours after a standard carbohydrate load

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

primary diabetes

A

Type I – IDDM / Juvenile – 10%.

Type II – NIDDM /Adult onset – 80%.

MODY – 5% maturity onset of diabetic of the young - Genetic

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

secondary DM

A

Islet destruction

IPED

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

type 2 diabetes

A

combination of peripheral resistance to insulin and inadequate secretory response by the pancreatic b cells(relative insulin deficiency)

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

where is preproinsulin synthesized

A

RER

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

Which transport protein mediate uptake of glucose by pancreatic b cells

A

GLUT2

Insulin independent

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

mitogenic pathway of insulin responsible for

A

mitogenic effects of insulin and insulin like growth factors

Cell growth, proliferation, gene expression

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

metabolic effects on insulin mediated by

A

PI3K

synthesis of lipids, proteins, glycogen, cell survival and proliferatio

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

GLUT 4

A

insulin dependent

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

type 1 dm mediated by which lymphocytes

A

t lymphocytes

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

gene implicated in type 1 dm

A

hla - dr3 dr4

6p21

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

insulin resistance

A

to effects of insulin on glucose uptake, metabolism, and storage

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

abnormalities in insulin signalling pathway

A

Down-regulation of the insulin receptor
Decreased insulin receptor phosphorylation and tyrosine kinase activity
Reduced levels of active intermediates in the insulin signaling pathway
Impairment of translocation, docking, and fusion of GLUT-4-containing vesicles with the plasma membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q
adipokines like
leptin
adiponectin
resistin
retinol binding protein  1
A

Leptin - acts on CNS receptors to induce satiety
Adiponectin – Cause hypoglycemia,
Resistin – induce hyperglycaemia
Retinol binding protein 4 – induce hyperglycaemia

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

how is ppary activated and how does it work

A

activated by thiazolidinediones

PPARγ binds to DNA and activate transcriptin of genes that increase storage of free fatty acids in adipocytes

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

monogenic forms of diabetes

A

MODY

primary defect in B cell function that occurs without B cell loss

affecting either b cell mass and or insulin production

genetic

mitochondrial diabetes
diabetes associated with insulin gene or insulin receptor mutations

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

short term complicatioons

metabolic

A

Hypoglycemia
Diabetic Ketoacidosis
Non Ketotic hyperosmolar diabetic coma
Lactic acidosis

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

long term complications

angiopathy

A

Angiopathy, Retinopathy, Nephropathy, Neurophathy

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

Macrovascular disease

A

mi, stroke, lowee extremity gangrene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

microvascular disease

A

retinopathy, nephropathy, neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what are the infections due to

A

microangiopathy and ischemia
immmunosuppression
hyperglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

distinct metabolic pathways involved in long term diabetic complications

A

Formation of Advanced Glycation End Products

Activation of Protein Kinase C

Intracellular Hyperglycemia with Disturbances in Polyol Pathways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

key things in ages

A

non enzymatic
intracellular glucose derived dicarbonyl precursors
amino intracellular and extracellular proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

cross linking between polypeptides

A

collagen type one in large vessels

type 4 in basement membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

result of crosslinking

A

decreased elasticity of vessel - shear stress and endothelial injury

decreased endothelial cell adhesion and increases fluid filtration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

AGE proteins

A

resistant to proteolytic digestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

age modified matrix

A

trap non glycated plasma or interstitial proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

age receptors on which cell

A

endo cell
mesangial cell
macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what does binding to plasma proteins to RAGE do

A

activation and nuclear translocation of nfkb

40
Q

biologic effect off AGE receptor signalling

A

Release of cytokines and growth factors from macrophages and mesangial cells (insulin-like growth factor-1, TGF-β, platelet-derived growth factor, VEGF);

Increased endothelial permeability;

Increased procoagulant activity on endothelial cells and macrophages

Enhanced proliferation and synthesis of extracellular matrix by fibroblasts and smooth muscle cells.

41
Q

which tissues do not require insulin for glucose transport

A

nerve
lense
kidney
blood vessels

42
Q

Potential mechanisms of microvascular damage and malfunction in the polyol pathway include

A

Sorbitol-induced osmotic stress due to accumulated sorbitol,
Altered or decreased Na/K-ATPase activity,
myo-inositol depletion with impaired phosphatidylinositol metabolism,
Increased prostaglandin production, and
Alterations in protein kinase C isoform activity

43
Q

cotton wool spots

A

diabetic retinopathy

44
Q

proliferative retinitis

A
neovascularisation
haemorrhagic
fibroplasia
retinal detachment
laser cauterization
45
Q

protein kinase c

A
Production of VEGF
vasoconstriction
    vasoconstrictor endothelin – 1
     vasodilator Enos
Fibrogenesis – TGF B
Procoagulant	
Pro inflammatory cytokine
46
Q

Hormones that trigger biochemical signals upon interacting with cell-surface receptors are classified into two

A

peptide hormones - growth and insulin

small hormones - adrenaline

47
Q

binding of these hormones to cell surface receptors leads to

A

an increase in intracellular signaling molecules, termed second messengers, such (cAMP);
production of mediators from membrane phospholipids, such as inositol 1,4,5-trisphosphate or IP3;
shifts in the intracellular levels of ionized calcium.

48
Q

example of hormones that diffuse across plasma membrane to bind to ic receptors

A
progesterone
estrogen
glucocortic
steroids
thyroxine
49
Q

weight of pineal gland

A

100 - 180mg

50
Q

cell in pineal and function

A
epithelial like
pphotosensory
neuroendocrine
melatonin
jet lag
51
Q

name of tumor in pineal gland

A

of embryogenic origin
rare pinealomas
pineacytomas
pineablastomas

52
Q

where adenohypopyhsis is derived from

A

rathke pouch

adeno about 80 % of gland

53
Q

which of the releasing factors are inhibitory

A

PIF
dopamine
somatostatin

54
Q

3 Major cells types based on appearance in h e stainin

A

acidophils - bright pink
GP

Basophils - purple
thyroid stim, acth, gondo

chormophobes - pail stainining
not assted with specific hormone secrn

55
Q

5 cell types based on antibodies

A

somatotrophs - GH half of all hormone producing

lactotroph/ mammotrophs - prolactin

cortico - ACTH MSH

thyrotrophs - TSH

gonadotrophs - FSH, LH

56
Q

Cells in neurohypophysis

A

pituicytes..modified glial cells

57
Q

adh produced in response to

A

Increased plasma osmotic pressure,
Reduced left atrial distention,
Exercise and certain emotional states

58
Q

pituitary disoders manifest as

A

hypo
hyper
local mass effect

59
Q

hyperpituitarism

A

Pituitary adenoma – most common cause
not always functional

Pituitary hyperplasia

Carcinoma of the anterior pituitary

Paraneoplastic syndromes

60
Q

pituitary adenoma occur in which type of MEN

A

MEN 1

61
Q

mutations in pituitary adenoma

A

GNAS 1 for g protein
ras ongnene
cmyc oncogene

62
Q

gs alpha bound to what in inactive state

A

gdp

63
Q

cAMP acts as which type of stimulus and regulated by

A

mitogenic

GTPase

64
Q

alpha subunint of gs encoded by

which chromosome

A

GNAS gene

20q13

65
Q

there is no GNAS mutation in which trophs

A

lacto
thyro
gondo

66
Q

gnas mutation is more where

A

somato

cortico minor

67
Q

micro of pituitary adenoma

A

uniform cells in diffuse sheet with absence of supporting reticulin sheet

68
Q

hypopituitarism

A
Pituitary masses
Pituitary surgery or radiation
Pituitary apoplexy
Ischaemic necrosis or Sheehan’s syndrome (post partum necrosis)
Genetic abnormalities
69
Q

adrenals mass

A

4g each

70
Q

adenoma and carcinoma of adrenals..which is heavier

A

Carcinoma

71
Q

types of adrenal hyperplasia

A

diffuse less heavier

nodular

72
Q

what avors malignancy in adenocortical neoplasms

A

anaplasia

mitotic activity

73
Q

adenoma
carcinoma

seen in

A

hyperaldosteronism
cushing

virilizing neoplasm

74
Q

can the functional status of adrenal cortical adenom be predicted from gross or micro app

A

no

75
Q

xtic of neoplastic cells in adrenal cortical adenoma

A

vacuolated due to presence of intracytoplasmic lipid

76
Q

necrosis seen in adenoma or carcinoma

A

carcinoma

77
Q

forms of cushing syndrome

A

pituitary
adrenal
paraneoplastic
iatrogenic

78
Q

deficiency in congenital adrenal hyperplasia

A

21 - hydroxylase

recessive

leads to virilization

79
Q

micro features in congenital adrenal hyperplasia

A

hyperplastic acessory nodules

lipid depleted cutp[;as,

80
Q

hypoadrenalism causes

A

pimary
acute - waterhouse friderichsen..sudden withdrawal from steroids
chronic - Addison

secondary
acth def

81
Q

kidney in waterhouse

A

dark
hemorrhagic
shrunken
cortical architecture not discernible

82
Q

causes of addison disease

A
autoimmune - most common cause
tuberculosis
metastatic..lung and breast
fungal
amyloidosis
hemachromatosis
83
Q

cells secreting catecholamines in pheochromocytoma

A

chromaffins

84
Q

are pheochromocytoma sporadic

A

yeah 90%

85
Q

presentation in pheochromo

A

hypertension
tachycardia
sweating
anxiety

86
Q

is hypertension correctable in pheo

A

yes

87
Q

when is malignancy established in pheo

A

metasasis only

88
Q

nest with alveoli pattern known as zelllballen

A

micro of pheo

89
Q

xtic in MEN

A
Inherited
proliferative
multifocal
asymptomatic stage of hyperplasia
younger age
agrresive 
recur
90
Q

MEN 1

A

Pituitary
parathyroid
pancreatic islets

91
Q

mutant gene locus in MEN

A

11q13 menin

92
Q

MEN 2A

A

Parathyroid
Adrenal..pheo
Thyroid

93
Q

mutant gene locus in MEN 2A

A

RET protooncogene

94
Q

variant of MEN 2A

A

familial medullary thyroid cancer

95
Q

MEN 2B

A

adrenal pheo
thyroid
extraendo..mucocutaneous ganglinoneuromas and marfanoid habitus

96
Q

mutant gene locus

A

RET protooncogene