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ENRP Exam 2 > pathology of the endocrine pancreas - hillard > Flashcards

pathology of the endocrine pancreas - hillard Flashcards

1
Q

B cells secrete what?

what is its major effect

A

beta cells secrete insulin and the major effects are to lower blood glucose and increase glucose in tissues (fat and muscle)

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2
Q

a cells secrete what and what is its major effect

A

glucagon and its major effect is to increase blood glucose by glycogenolysis

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3
Q

delta cells secrete what cells and what is the major effect

A

somatostatin

and it causes decreased insulin and decreased glucagon

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4
Q

PP cells secrete

major effect

A

pancreatic polypeptide

decreased intestinal motility and increase intestinal enyzmes

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5
Q

D1 cells secrete what

major effect

A

increase blood glucose a lot and cause by glyconeogenosis

cause a watery diarrhea

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6
Q

enterochromaffin cells secrete what

major effects

A

serotonin

regulate mood/mental states
“carcinod syndrome- flushing, tachycardia, diarrhea)

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7
Q

diabetes is very common and affects the _ system the _, peripheral _ and kidney

it results in too much _ in the blood to due issues in insulin production or response

A

cardiovasculae

nerves

glucose

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8
Q

type 1 diabetes is more frequently seen in _ and is caused by _ descruction of pancreatic _ cells leading to hyperlgycemia, it often requires _ for treatment

A

children

autoimmune

beta

insulin

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9
Q

type 2 diabetes is seen in adults is caused by _ _ to insulin, it is most frequently seen in _ adults

A

peripheral resistance

obese

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10
Q

diabetes is present if

HbA1c=
fasting plasma glucose=
oral glucose tolerance test 2 hours=
randmon plasma glucose =

A

HbA1c=6.5
fasting plasma glucose= 126
oral glucose tolerance test 2 hours=200
randmon plasma glucose = 200**

all tests must be repeated a second time on a different day to confirm

2 times- expect random plasma glucose

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11
Q

hemoglobin A1c is used to determine _ blood glucose levels over the last _ months

HGBA1c

A

average

2-3

hemoglobin AB1c is the glycosylated form of hemoglobin becuase glucose binds to hemoglobin

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12
Q

type 1 diabetes is a type _ hypersentitivity reaction and is caused by a _ cell autoimmune reaction against _ cells

_ _ are created

A

type 4

T

Beta cells

islet autoantibodies

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13
Q

in type 1 diabetes T cells attack beta cell antigen: what antigens

A

insulin and glutamic acid decarboxylase

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14
Q

in order to diagnose type 1 diabetes you must test the presence of?

A

autoantibodies (islet)

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15
Q

what HLA types are associated with type 1 diabetes

A

HLADR3, 4, 8

breakdown in self tolerance to islet autoantigens

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16
Q

stages of type 1 diabetes

A

stepwise progression

presymptomatic normoglycemia

non-symptomatic elevated blood sugar levels

symptomatic diabetes

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17
Q

typw 2 diabetes pccurs due to _ resistance which prevents peripheral tissues from adequattely responding to insulin couples with _ cell dysfunctino

A

insulin

b cell

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18
Q

the most important risk factor for type 2 diabetes is?

A

obesity

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19
Q

how does obesity drive type 2 diabetes

A

it causes insulin resistance by increasing free fatty acids, inflammatory cytokines, and adipokines which inhibit peripheral response to insulin

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20
Q

what type of diabetes causes type 2 diabetes

A

central belly fat wrapped around abdomnial organs due to the portal vein being able to carrier free fatty acids to the liver causing insulin resistance in the liver and preventing glucose uptake

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21
Q

other than obesity what caused T2DM

A

sedentary lifestyle
genetics
high caloric intake
sleep disturbances

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22
Q

what adipokin is decreased in obesity

A

adiponectin

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23
Q

what is the purpose of adiponectin

A

it is beneficial in insulin utilization (it is decreased in obesity)

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24
Q

excess _ _ _ in obesity will inhbit the peripheral reponse to insulin but are also proinflammatory and secrete cytokines like _

A

FFA

IL-1

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25
Q

in T2DM the initial reposne to an increased peripheral resistance is beta cells _ insulin production but eventually there is beta cell _ and ultimately failure

A

increase

dysfunction

failure= T2DM

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26
Q

histologically _ deposition is seen in T2DM as a result of _ secretion

A

amyloid

amylin

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27
Q

what is amylin

A

this is a amyloid polypeptide that is released from beta cells along with insulin and help to inhibit glucagon secretion and delay gastic eating

28
Q

histology of type 1 diabetes

A

insulitis (infiltrate of T cells in the islet)

29
Q

describe the effects of insulin on adipose tissue

striated muscle

liver

A

increase in glucose uptake in striated muscle like the heaty and in adipose tissue

increases protein sythesis increases fat synthesis (lipogenlysis) glcogen synthesis

decreases gluconeogensis in the liver

30
Q

insulin is an _ hormone

A

anabolic

causes complex molecules to form from simpler ones

31
Q

what type of fat is associated with obesity

A

white adipose

brown adipose increases glucose uptake/utilization

32
Q

what are the 3 p’s of diabetes

how do they occur

A

polyuria- glucose in pee, water follows it creating an osmotic diuresis

polydipsia- urine water loss + increased blood glucose depeltes intracellular water and triggers thrist receptors

polyphagia- type 1 and later type 2; no insulin and there is fat/muscle breakdown

33
Q

diabetic ketoacidosis is seen in _ and is severe _ def

A

type 1 diabetes

insulin

34
Q

what causes DKA

what is released? what does this do

A

stress like infection or trauma

epinephrine is release and increased glucagon and blcoks insulin action

35
Q

pathogensis of DKA

A

no insulin causes peripheral glucose to not be utilized

liver breaks down glycogen to create more glucose

fat is broken down to FFA and are metabolized by the liver to form acidotic ketone bodies

ketones and glucose spill into the urine and cause osmotic diuresis causing severe dhydration and ketocidosis

36
Q

symptoms of DKA

A

fatigue, can lead to coma, fruity breath, deep labored breathing

37
Q

what causes the fruity breath in DKA

A

ketone metabolism and acetone formation

38
Q

ketones end up in the urine and a _ test can detect them, confirmatory tests involve checking the urine for?

A

nitroprusside

beta-hydroxyurea

39
Q

what causes kussmal breathing in DKA

A

the body attempts to neutralize the metabolic acidosis by exhaling off CO2

40
Q

what is hyperosmolar nonketotic hyperglycemic syndrome

A

this is a complication of type 2 diabetes especially in the elderly where there is prolonged insulin deficiency

this causes increased hepatic gluconeogenis, and glycogenolysis causing really high glucose

glucose greater than 600
no ketone bodies
and severe dehydration
can cause AMS and coma

41
Q

what is matuirty-onset diabetes of the young (MODY)

what does it resemble

A

this is a monogenic diabetes that affects glucokinase of the beta cell

it resembles T2DM

there are no autoantiboies and is nonketotic

42
Q

what is glucosekinase

A

a rate limiting enxyme in oxidative glucose metabolism that leads to the secretion of insulin

43
Q

during pregnancy early on there is an increase in _ sensitivity that allows for a reservoir of energy supply. Later on _ _ block the effects of insulin and create insulin resistance this is because they want glucose in the blood to be able to cross over to the baby

A

insulin

placental hormones

44
Q

in pregnancy maternal weight gain or underlying risk factors can cause insulin resistance to precipiate a state of?

A

gestational diabetes

45
Q

how does th ebaby appear in a person with gestational diabetes

A

macrosomia

difficult birth (shoulder dystocia_

c section

congenital malformations (still birth)

46
Q

describe the pathogensis of hyperglycemia

A

glucose causes advanced glycation of end products. End products have a vast majority of effects that cause the endothelium to become activated and allow for athersclerosis and vascular damage to occur

47
Q

what other pathways contibute to hyperglycemia effects other than the glycationof end products

A

polyol pathway- loss of antioxidant production

hexosamine pathway- increase in oxidative stress

activation of protein kinase c (PKC) - increases growth factors and procoagulant activity

48
Q

advanced glycation end products produces

A

vascular damage and athersclerosis

49
Q

major complications of diabetes

A

athersclerotic disease (MI, cerebral infacrt, PVD–>gangrene)

retinopathy/ocular

neuropathy/peripheral neuropathy

nephropathy- ateriorsclerosis, pyelonephritis

infections- UTI, dental carries, candida

50
Q

what fungal infection is common in diabetes

A

candida

51
Q

describe the macrovascular athersclerotic disease in diabetes

brain
kidney
bowel
heart
peripherally

A

brain: can cause hemmorage or stroke

kidney: can cause renal artery stenosis and activation of the RAS system

bowel: can cause mesenteric ischemia

heart: chronic heart disease, MI

peripherally: claudication and ganreenoug necrosis

52
Q

diabetic retinopathy and occular pathology is common and causes _ loss and diminished _

it can be divided into proliferative and nonproliferative: what are these

it can also cause _ and _ (end stages)

A

vision

sight

proliferative: formation of new vessels on the retina

non proliferative: anurysems in small vells and microhemorrhage; lipid leak

cataracts and glaucoma

53
Q

diabetic peripheral neuropathy is a _ , _ , _neuropthy

A

distal

symmetric

polyneuropathy

54
Q

symptoms of diabeteic peripheral neuropathy

A

numbness

loss of pain sensation

55
Q

diabetic peripheral neuropathy is in a _ and _ distibution

A

glove and stocking

56
Q

one of thedirect affects of peripheral neuropathy is injury to the _

A

foot

57
Q

loss of sensation in the foot can lead to _ and infection

A

trauma

58
Q

peripheral vascular disease in the foot leads to decreased _ and a _ foot (ulceration)

A

healing

diabetic

59
Q

inflammationof the bones of the foot in diabetic neuropathy can lead to severe deformity of _ and joint and leads to a _ foot ( midfoot collapse/rocker bottom)

A

bones

charcot foot

60
Q

diabetes can cause _ kidney disease

A

chronic

61
Q

symptoms of chronic kidney disease

A

extermity edema, puritis, hypertension, bone fractures ( decresed calcitriol) and hypocalcemia

encephalopathy

62
Q

what are the three principal vascular lesions in diabetic kidney nephropathy? in diabetes

A

renal vascular lesions

pyelonephritis

golmerular lesions

63
Q

what are the renal vascular lesions in diabetic kidney nephropathy

A

athersclerosis thar causes renal atery stenosis and hypertension

hyaline ateriorsclerosis: from chronic hypertension and diabetes ( nephroclerosis of the kidney giving a grnaular nodular apperance)

64
Q

what infection is increased in the kidney in a diabetic patient

A

pyelonephritis

**fevers, chills, flank pain, hematuria

65
Q

_ _ is strongly associated with diabetic induced pyelonephritis

A

papillary necrosis

66
Q

what does a diabetic glomerulus look like?

A

diffuse mesanglial slcerosis (increase in mesangium)

capillary basement membrane thickening

and PAS stained nodules (large) kimmelstiel wilson

ENRP Exam 2 (13 decks)

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