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Bio 252 > Endocrine disorders > Flashcards

Endocrine disorders Flashcards

1
Q

causes of hypersecretion

A
  • secretory tumor
  • increased trophic stimulation
  • defective negative feedback loop
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2
Q

causes of hyposecretion (and examples)

A
  • no trophic stimulation (atrophy)
  • receptor defect (nephrogenic diabetes insipidus)
  • immune disorder (autoimmunity)
  • suppressive therapy (overcorrection; hyper to hypo)
  • dietary deficiency (iodine for thyroid)
  • metabolism defect (missing enzyme)
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3
Q

In the islets of langerhans, beta cells produce ____ and alpha cells produce _____

A

insulin

glucagon

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4
Q

what is diabetes mellitus

A

defective insulin secretion and/or action

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5
Q

what are the 2 types of insulin deficiency

A
  • absolute deficiency (absent/little produced)

- relative deficiency (present but ineffective)

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6
Q

type 1 diabetes mellitus is what type of deficiency

A

absolute

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7
Q

what type of diabetes mellitus is early onset

A

type 1

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8
Q

what are the 2 types of type 1 diabetes mellitus and what are their cause and prevalance

A

1A: immune-mediated: 90-95%
1B: idiopathic: 5-10%

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9
Q

what % of diabetes mellitus is type 1

A

10%

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10
Q

what % of diabetes mellitus is type 2

A

90%

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11
Q

type 2 diabetes mellitus is what type of deficiency

A

relative

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12
Q

what is LADA

A

latent autoimmune diabetes in adults

type 1A manifesting in adults

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13
Q

what is MODY

A

maturity-onset diabetes in the young

type 2 in the young d/t poor lifestyle

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14
Q

diabetes mellitus is what type of genetic abnormality

A 
complex trait (multifactorial)
genetics + environment
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15
Q

type 1 diabetes mellitus has what type of risk

A

familial risk (10x)

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16
Q

causes of type 1 diabetes mellitus

A
  • defective insulin gene on chromosome 11
  • T cell hypersensitivity to beta cell Ag
  • defective MHC genes on chromosome 6
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17
Q

40% of type 1 diabetes mellitus is caused by

A

defective MHC genes on chromosome 6

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18
Q

the insulin gene on chromosome 11 codes for

A

a protein that regulates division and functioning of beta cells (therefore insulin secretion)

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19
Q

how does a defective MHC gene cause type 1 diabetes mellitus

A

beta cells are recognized as foreign, Ab’s target and destroy them

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20
Q

type 2 diabetes mellitus has a strong but ______ genetic involvement

A

unclear

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21
Q

50% of type 2 diabetes mellitus is caused by

A

a defective glucokinase gene on chromosome 7

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22
Q

the glucokinase gene codes for

A

a protein called glucokinase enzyme which is responsible for phosphorylation

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23
Q

what is phosphorylation

A

when glucose enters a cell and attaches to phosphate it becomes phosphorylated and cannot leave the cell

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24
Q

what are the criteria for prediabetes

A
  1. IFG (impaired fasting glucose) 6.1-6.9
  2. IGT (impaired glucose tolerance) 7.8-11
  3. HbA1C 6-6.4%
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25
Q

what is a fasting glucose test

A

testing after a 10 hour fast

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26
Q

what is a normal fasting glucose test range

A

3.5-5.5

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27
Q

what is a glucose tolerance test

A

fasting, oral glucose solution give, monitor BG for 2 hours

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28
Q

what does HbA1C measure

A

the 1C form of Hb

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29
Q

glucose binds HbA1C d/t

A

high affinity

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30
Q

what does metabolic syndrome predispose someone to

A

CVD

type 2 diabetes mellitus

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31
Q

parameters of metabolic syndrome

A
  • IFG
  • IGT
  • insulin resistance
  • hyperlipidemia
  • abdominal obesity
  • HTN
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32
Q

in type 1 diabetes mellitus with a defective MHC gene, Ab’s target

A

self-antigens on the surface of beta cells and islet cells

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33
Q

in type 1 diabetes mellitus with T cell hypersensitivity, T cells infiltrate ______ causing ______

A

islets of Langerhans, causing insulitis

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34
Q

what is insulitis

A

inflammation of the islets of Langerhans

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35
Q

what are the 4 types of relative insulin deficiency in type 2 diabetes mellitus

A
  • delayed secretion
  • target cell problem
  • insulin resistance
  • hepatic glucogenesis
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36
Q

in type 2 diabetes insulin levels are

A

normal, high, or low

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37
Q

in type 1 diabetes, insulin levels are

A

low and none at all

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38
Q

how is degree of damage determined in type 2 diabetes mellitus

A

amyloid deposits in the islets of Langerhans

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39
Q

in type 2 diabetes mellitus, increased hepatic glucose output is caused by

A

a perceived lack of glucose d/t mutated glucokinase preventing phosphorylation

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40
Q

in type 2 diabetes mellitus, there is decreased glucose uptake due to

A

mutated glucokinase preventing phosphorylation

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41
Q

insulin deficiency (absolute/relative) causes

A

impaired glucose utilization and increased hepatic glucogenesis d/t a perceived lack of glucose

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42
Q

when hyperglycemia occurs, ____ is exceeded causing ______

A

the renal threshold for glucose causing glucosuria

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43
Q

glucosuria causes what to increase

A

osmotic pressure in the filtrate

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44
Q

increased osmotic pressure in the filtrate causes increased ________, causing ____

A

fluid movement to the filtrate, causing polyuria

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45
Q

polyuria causes ____ and ____

A

dehydration and polydipsia

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46
Q

once above the renal threshold everything else will be ___

A

excreted

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47
Q

impaired glucose utilization by cells will cause

A

increased mobilization and use of lipids and proteins

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48
Q

mobilization and use of lipids and proteins will increase what

A

metabolites in the blood (ketones)

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49
Q

elevated levels of ketones cause

A

ketonuria

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50
Q

manifestations of diabetes mellitus

A 
3 P's:
- polyuria
- polydipsia
- polyphagia
type 1: weight loss
type 2: obesity
complications
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51
Q

why does type 1 diabetes mellitus cause weight loss

A

d/t glucose not being stored

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52
Q

why is insulin not take PO

A

because it is a hormone and also a protein that will be broken down by enzymes in the stomach

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53
Q

hypoglycemia is more frequent in type _ DM because

A

1

they are taking insulin injections

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54
Q

causes of hypoglycemia

A
  • insulin overdose/mismanagement
  • missed meal
  • overexertion (depletion of glucose/glycogen stores)
55
Q

hypoglycemia = < __ mmol/L

56
Q

neurons rely on _____ for energy but do not require _____

A

glucose

insulin

57
Q

severe hypoglycemia = < _ mmol/L

58
Q

treatment of mild hypoglycemia

59
Q

treatment of severe hypoglycemia

60
Q

a byproduct of lipid metabolism is

61
Q

the breakdown of free fatty acids from _____ stores in _____ tissue produces _______

A

triglyceride
adipose
ketones

62
Q

formation of glucose from a non-carbohydrate source is called

A

gluconeogenesis

63
Q

diabetic ketoacidosis can cause _____ shock d/t ______

A

hypovolemic shock d/t dehydration

64
Q

diabetic ketoacidosis presents as

A

intoxication

65
Q

hypoglycemia affects _____ function and activates the ____

A

cerebral function

ANS

66
Q

hypoglycemia coma is caused by

A

glucose deprivation in the brain

67
Q

treatment of hypoglycemic coma

A

1mg glucagon IM/SC

20-50mL 50% glucose IV

68
Q

requirements for diabetic ketoacidosis

A
  • hyperglycemia
  • ketosis
  • metabolic acidosis
69
Q

the breakdown of lipids is called

70
Q

lipolysis forms

A
  • free fatty acids

- glycerol

71
Q

FFA are metabolized by the ____ and release ____

A

liver

ketones

72
Q

diabetic ketoacidosis usually occurs in type _ DM

73
Q

HHS usually occurs in type _ DM and ____

A

2

the elderly

74
Q

why does ketoacidosis not occur in type 2 DM

A

because insulin is present so there is no lipolysis

75
Q

hyperosmolar hyperglycemic state is a state of

A

elevated blood glucose and elevated glucose concentration

76
Q

HHS is caused by

A
  • excessive CHO intake

- persistently elevated insulin resistance

77
Q

other ways HHS can occur are

A
  • MI
  • severe infection
  • pancreatitis
78
Q

in HHS, hyperglycemia –> ________ –> cellular efflux –> _________ –> fluid loss –> _______

A

hyperosmolarity
glucosuria
dehydration

79
Q

acute complications of diabetes

A
  • hypoglycemia
  • diabetic ketoacidosis
  • hyperosmolar hyperglycemic state
80
Q

chronic complications of diabetes

A
  • microvascular (nephropathy, retinopathy, neuropathy)
  • macrovascular (atherosclerosis, CAD, MI, CVA, PVD)
  • infections
81
Q

chronic complications of diabetes are due to

A

altered metabolites and vascular damage

82
Q

chronic complications of diabetes occur

A

10-15 years post-onset

83
Q

increased blood glucose will cause proteins to become ______ and _______

A

glucosylated

dysfunctional

84
Q

microvascular damage involves

A

capillaries

85
Q

macrovascular damage involves

86
Q

causes of vascular damage in diabetes mellitus

A
  • altered metabolism
  • glycosylated proteins
  • proliferation of anaerobic bacteria
  • poor healing
87
Q

glycosylated proteins deposit on the ___________ causing

A

endothelial surface

impaired function of the trans-capillary exchange, platelet aggregation and decreased perfusion

88
Q

Hb not offloading oxygen properly (decreased delivery) is an example of a _____ ______ becoming dysfunctional

A

glycosylated protein

89
Q

why does proliferation of anaerobic bacteria occur in diabetes

A
  • thrives in low oxygen conditions

- damaged vessels cause impaired perfusion (low oxygen)

90
Q

poor healing in diabetics is due to

A

damaged vessels have low perfusion

delivery of defense cells and oxygen is low and waste removal is slow

91
Q

5 things oral hypoglycemics do

A
  • stimulate the release of insulin
  • increase tissue response to insulin
  • decrease hepatic glucogenesis
  • delays breakdown and absorption of CHO
  • blocks DPP-4 enzyme (increases release of insulin after a rise in BG)
92
Q

what hormones does the thyroid release

A

T3 (triiodothyronine)

T4 (thyroxine)

93
Q

iodine is required for the synthesis of

A

thyroid hormones

94
Q

why is T4 given instead of T3 for hypothyroid treatment

A
  • T4 is naturally converted to T3 in the body (allows natural process to occur)
  • the half-life of T4 is longer than T3
95
Q

how does T4 become T3

A

when T4 contacts blood cells, iodine is removed and becomes T3

96
Q

what hormones does the adrenal medulla secrete

A

epinephrine and norepinephrine

97
Q

what groups of hormones does the adrenal cortex secrete (and an example of each)

A
  • glucocorticoids (ex. cortisol)
  • mineralocorticoids (ex. aldosterone)
  • androgens (ex. testosterone, DHT)
98
Q

what hormones does the hypothalamus release

A
  • oxytocin
  • ADH
  • thyroid releasing hormone (TRH)
99
Q

what hormones does the posterior pituitary synthesize

A

none

it stores oxytocin and ADH until triggered to release them

100
Q

what hormones does the anterior pituitary synthesize

A
  • thyroid-stimulating hormone (TSH)

- adrenocorticotropic hormone (ACTH)

101
Q

what disease is an example of hyperthyroidism

A

Grave’s disease

102
Q

what disease is an example of hypothyroidism

A

Hashimoto’s thyroiditis

103
Q

a toxic goiter has what type of secretion

A

hypersecretion

104
Q

an endemic goiter has what type of secretion

A

hyposecretion

105
Q

a toxic goiter will present as what

A

a nodular gland

106
Q

iodine deficiency causes

A

decreased levels of T3/T4 and compensatory high levels of TSH

107
Q

what are the 3 hallmarks of Grave’s disease

A
  • hyperthyroidism
  • goiter
  • exophthalmos
108
Q

what are protruding eyes called (as in Grave’s disease)

A

exophthalmos

109
Q

what do 1st, 2nd, and 3rd degree hypothyroidism affect

A

1: thyroid
2: pituitary
3: hypothalamus

110
Q

what are the 2 main steps in hashimoto’s thyroiditis

A
  • Ab’s recognize and block TSH receptors (preventing TSH binding) leading to decreased T3/T4 levels
  • lymphocytes infiltrate and destroy the gland
111
Q

what are the 2 main steps in Grave’s disease

A
  • TSAb’s (thyroid stimulating antibodies) target TSH receptors and mimic TSH, increasing stimulation and T3/T4 release
  • increased TH release triggers the negative feedback loop and decreases TSH release
112
Q

what is the main complication of hyperthyroidism

A

thyrotoxicosis

113
Q

3 things glucocorticoids do

A
  • decrease inflammation
  • suppress the immune response
  • altered metabolism of proteins and fats
114
Q

6 things Cushing’s syndrome causes

A
  • gluconeogenesis (protein catabolism)
  • hyperglycemia & insulin resistance
  • HTN & hypokalemia
  • fat deposits
  • infection
  • male sex characteristics in women
115
Q

3 causes of adrenal hypersecretion

A
  • cortical tumor
  • anterior pituitary tumor
  • ectopic secretory tumor
116
Q

what is dexamethasone and what is it used to diagnose

A

a potent glucocorticoid (steroid)

Cushing’s Syndrome

117
Q

how is dexamethasone used to diagnose Cushing’s

A

administration will trigger the negative feedback loop and decrease ACTH release, therefore cortisol should decrease
if upon admin ACTH levels do not decrease, it is being released from somewhere else (ectopic tumor)

118
Q

why does hyperpigmentation occur with addison’s disease

A

low aldosterone levels will not trigger the negative feedback loop… increased levels of ACTH release
when ACTH is broken down the intermediate is MSH (melanocyte stimulating hormone)
increased levels of MSH stimulate melanocytes which are responsible for melanin secretion which causes pigment

119
Q

ADH is also known as

A

vasopressin

120
Q

Is Conn syndrome hypo or hypersecretion and of what

A

hyperaldosteronism

121
Q

what are 3 manifestations of Conn syndrome

A
  • HTN
  • hypokalemia
  • alkalosis
122
Q

what type of secretory disease is Addison’s Disease

A

hypoaldosteronism

123
Q

what are 2 causes of Addison’s disease

A

classic autoimmunity

increased steroid treatment causing decreased ACTH

124
Q

what are 5 manifestations of Addison’s disease

A
  • hypotension
  • hyperkalemia
  • appetite and weight loss
  • hyperpigmentation
  • weakness and fatigue
125
Q

which pituitary disorder involves ADH hypersecretion

A

Syndrome of inappropriate ADH (SIADH)

126
Q

what does SIADH cause

A

water retention causing dilutional hyponatremia

127
Q

diabetes insipidus is hypo or hyper secretion of what

A

hyposecretion of ADH

128
Q

someone with diabetes insipidus is unable to do what

A

concentrate their urine d/t a lack of aquaporins

129
Q

2 manifestations of diabetes insipidus

A
  • polyuria

- polydipsia

130
Q

2 types of diabetes insipidus

A

neurogenic (central)

nephrogenic

131
Q

neurogenic diabetes insipidus is a defect in what

A

the synthesis or release of ADH

132
Q

nephrogenic diabetes insipidus happens because the ______ don’t respond to _____

A

kidneys don’t respond to ADH

133
Q

complications of diabetes insipidus

A

dehydration (low BP, high HR, headache, kidney damage)

134
Q

what are 2 drugs that can be given to someone with diabetes insipidus

A

ADH

a thiazide diuretic

Bio 252 (15 decks)

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