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Bio 252- atherosclerosis > Endocrine disorders > Flashcards

Endocrine disorders Flashcards

1
Q

2 Basic problems for endocrine disorders

A

hyperfunction

hypofunction

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2
Q

Hyperfunction

A

increase in hormone secretion/action

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3
Q

Hypofunction

A

decrease or no hormone secretion or action

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4
Q

Hypofunction etiology

A
  • dietary deficiency
  • metabolic defect
  • no trophic stimulation cause atrophy
  • receptor defects (distorted or damaged shape)
  • suppresive therapy (surgery/Tx for hypersecretion)
  • immune disorders (anitbodies bind to receptor sites)
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5
Q

Hyperfunction etiology

A
  • excessive trophic stimulation
  • defect in negative feedback loop leads to no suppression
  • Secretory tumor ( tumor cells will be same so have same secretion)
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6
Q

ectopic tumor

A

located somewhere else ex. cell in lung that secretes hormone

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7
Q

non functioning tumor

A

destroys normal secretory cells that can lead to hypofunction

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8
Q

commonest endocrine disorder, affects approx

A

diabetes mellitus (2.5 mil)

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9
Q

diabetes mellitus has ______ or ________ insulin defects

A

absolute or relative

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10
Q

absolute insulin defects

A

no insulin produced

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11
Q

relative insulin defects

A

insulin produced not able to recognize

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12
Q

Diabetes mellitus is a complex disease that affects

A

protein metabolism, lipid metabolism and carbohydrate metabolism

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13
Q

Diabetes melliuts has defective

A

insulin secretion or action which leads to widespread metabolic defects (proteins, carbohydrates & lipids)

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14
Q

Diabetes melliuts is ________ if uncontrolled

A

life threatening

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15
Q

Impact of diabetes

A

Cardivascular, occular, renal, nueroimplications

these will develop approx 10 yrs, with better management takes longer to dev, with bad management happens sooner

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16
Q

classification of diabetes has 2 types

A
  • type 1

- type 2

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17
Q

Type 1 affects

A

10 % of individuals with diabetes

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18
Q

Type 2 affects

A

90% of individuals with diabetes

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19
Q

Type 1 is __________ insulin deficiency

A

absolute, destruction of cells that create insulin (beta cells)

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20
Q

Type 1a

Type 1b

A

1a (immune mediated 90-95%)

1b (idiopathic destruction of beta cells 5-10%)

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21
Q

Type 2 beta cells are

A

intact and it is relative insulin deficiency

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22
Q

Etiology of both type 1 and type 2

A 
complex trait (polygenic + environmental) 
enivormental ex. viral infection & obesity
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23
Q

Type 1 has

A

juvenile onset (early onset)

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24
Q

LADA

A

progressive form of type 1

latent autoimmune diabetes in adults

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25
Q

MHC genes

A

-majorhistocompatability complex code for cells to be able to identify as self to immune system

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26
Q

Type 1 etiology (genes) & others

A
  • MHC genes on chromosome 6 (40%)
  • Insulin gene on chromosome 11 (10%) -function division of beta cells
  • T cell hypersensitivity to Beta cell antigen
  • familial risk (increase x10)
27
Q

Type 2 is Mo

A

mature happens later in life

28
Q

MODY

A

maturing onset diabetes in young -this is a growing condition

29
Q

Type 2 etiology

A

-50 % due to glucokinase gene on chr 7

30
Q

Glucokinase

A

adds phosphate to glucose catalyze by enzyme glucokinase. therefore glucose cannot stay in cell and moves out

31
Q

Prediabetes

A

metabolic stage before onset of DM

32
Q

prediabetes has an imparied

A
  • impaired fasting glucose
  • Abnormal oral glucose tolerance test
  • increase
33
Q

several characteristics of Metabolic syndrome

A
  • abdominal obesity w > 88 m >102
  • HTN
  • hyperlipidemia (increase LDL, Low HDL, High triglycerides)
  • impaired fasting glucose
  • Impaired glucose tolerance
  • Insulin resistance (insulin present but can’t do job)
34
Q

insulin resistance

A

absence of hypoglycemic response to hyperglycemia in the presence of insulin

35
Q

Type 1 diabetes is a progressive autoimmune destruction of

A

beta cells up to 90 % of cells are destroyed

36
Q

type 2 diabetes beta cells

A

intact, but dysfunctional no autoimmunity

37
Q

Type 2 diabetes, relative insulin deficiency from:

A
  • Insulin resistance
  • Deranged secretion (may have less secretion than needed)
  • Defective target cell response
  • hepatic glucogenis
38
Q

Type 2 diabetes has has ____, _____ or _____ in insulin levels

A

normal, increase or decrease

39
Q

need insulin to move _____ into cells

A

glucose

40
Q

Patho of Type 1 & Type 2 Diabetes

A
  • insulin deficiency
  • impaired glucose utilization & increase in hepatic gluconeogenesis
  • Hyperglycemia (11-67mmol/L)
  • renal threshold exceeded
  • glucosuria
  • increase in osmotic pressure in filtrate
  • fluid enters filtrate
  • polyuria
  • dehydration
  • polydipsia (
41
Q

Manifestations of diabetes

A
  • polyuria & (frequencey)
  • Polydipsia
  • Polyphagia
  • wt loss (type 1)
  • obesity (type 2)
  • complications
42
Q

polyuria

A

excessive peeing

43
Q

polydipsia

A

excessive thirst

44
Q

polyphagia

A

excessive hunger, hungry all the time (losing all calories in urine)

45
Q

glucosuria

A

Increased glucose in urine

46
Q

The 3 acute complications of diabetes (life threatening):

A
  • Diabetic ketoacidosis (DKA)
  • Hyperosmolar hyperglycemic state (HHS)
  • Hypoglycemia leading to Hypoglycemic coma
47
Q

Diabetic ketoacidosis usually happens in type _____

A

1

48
Q

Diabetic ketoacidosis

A
  • severe insulin deficiency (can’t take glucose into cells)
  • glucagon excess (hormone that breaks glycogen in glucose)
49
Q

3 main features of diabetic ketacidosis

A
  • hyperglycemia
  • ketosis (formation of ketones)
  • metabolic acidosis
50
Q

glucogenesis

A

formation of carbohydrate from non-carbohydrate sourve

51
Q

Hyperosmolar hyperglycemic state is more common in

A

Type 2 and elderly

52
Q

Hyperosmolar hyperglycemic state is due to

A
  • increase in insulin resistance

- excessive increase in carbohydrate intake (or if don’t take oral meds)

53
Q

Hypoglycemia usually in type

A

1

54
Q

Hypoglycemia due to

A
  • insulin overdose (double dose of insulin or oral meds)
  • missed meal
  • overexertion
55
Q

Hypoglycemia is a blood glucose level of

A

less than 4 mmol/L

56
Q

Hypoglycemia causes

A

altered cerebral function and activation of ANS

57
Q

Treatment of Hypoglycemia

A
  • 15g - 20g Carbohydrates po

- inject glucagon

58
Q

Hypoglycemic coma

A
  • brain depends exclusively on glucose for metabolic needs
  • brain cells are insulin independent
  • brain deprived of glucose
  • loss of consciousness
59
Q

Brain cells are_____independent

A

Brain cells are insulin independent (can take in glucose without insulin)
erythrocytes are also insulin independent

60
Q

Treatment of Hypoglycemic coma

A
  • 1mg glucagon subcut or IM

- 20-50 ml 50 % glucose IV

61
Q

chronic complications of diabetes are due to

A

metabolic changes & vascular damage

62
Q

Chronic complications of diabetes

A
  • microvascular
  • macrovascular
  • CAD & MI
  • CVA (stroke)
  • PVD
  • infections (particularly foot & UTI)
63
Q

Microvascular complications of diabetes

A
  • retinopathy
  • nephropathy
  • neuropathy
64
Q

glycosylated protiens

A

glucose + protien

Bio 252- atherosclerosis (37 decks)

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