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Pathophys > Endocrine 3b+c > Flashcards

Endocrine 3b+c Flashcards

1
Q

Specialized glands and tissue of the endocrine system secrete____

A

hormones

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2
Q

Hormones_____

A

secreted into the blood, travel throughout the body
-only exert an effect on cells w/ receptors
CONTROL AND COORDINATE BODY FXNS
overlap w NS

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3
Q

Hormones characteristics

A

-specific rate/rhythm of secretion: diurnal, cyclic, dependence on circulating levels
-operate via feedback mechanisms
-only affect target cells w/ receptors

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4
Q

hormones are classified by

A

chemical structure-lipid soluble or water soluble, target organ, origin

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5
Q

possible hormone effects

A

-after plasma membrane permeability or membrane potential by opening/closing ion channels
-stimulate the synthesis of regulatory molecules (proteins)
-activate or deactivate enzyme systems
-induce secretory activity
-stimulate mitosis

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6
Q

endocrine organs

A

hypothalamus, pituitary gland, pineal gland, thyroid gland, parathyroid glands, thymus gland, pancreas, adrenal glands, ovaries, testes

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7
Q

lipid soluble hormones

A

-steroids
-hydrophobic signals
-circulate w. carrier protein
-receptor inside cell
1/2 life: hours to days

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8
Q

water-soluble hormones

A

-peptides, amines, glycoproteins
-hydrophilic
-circulate unbound
-receptors on cell membrane
1/2 life seconds to mins

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9
Q

examples of steroid hormones

A

cortisol, aldosterone, testosterone, estrogens

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10
Q

how steroid hormones work

A
  1. hormone diffuses
  2. gene activated
  3. protein synthesis
  4. new protein alters cell activity
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11
Q

examples of peptide hormones

A

insulin, glucagon, thyroid hormone, epinephrine, growth hormone, oxytocin

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12
Q

how peptide hormones work

A
  1. hormone binds to receptor
  2. cyclic AMP generated (2nd messenger)
  3. enzyme 1 –> 2-> 3activated
  4. Final product alters cell activity
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13
Q

hypothalamic-pituitary axis

A

anatomically and functionally connected
-hypothalamus secretes inhibiting/releasing hormones
-regulation secretion from pituitary

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14
Q

hypothalamus is link between ___and____

A

nervous and endocrine syestem

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15
Q

Pituitary hormones- anterior

A

-thyroid stimulating hormone (TSH)
-adrenocorticotropic hormone (ACTH)
-Prolactin (PRL)
-Growth hormone (GH)
-Follicle-stimulation hormone (FSH)
-Luteinizing hormone (LH)

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16
Q

TSH

A

stimulates secertion of throid hormone

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17
Q

ACTH

A

-stimulates adrenal cortex to secrete glucocorticoids

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18
Q

PRL

A

after birth stimulates mammary glands to synthesize milk

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19
Q

GH

A

stimulates mitosis and cellular differentiation

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20
Q

FSH

A

stimulates secretion of ovarian sex hormones, development of ovarian follicles and sperm production

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21
Q

LH

A

Stimulates:
-ovulation
-corpus luteum to secrete progesterone
-testes to secrete testosterone

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22
Q

Pituitary hormones posterior

A

Antidiuretic hormone( ADH), Oxytocin (OT)

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23
Q

ADH

A

Antidiuretic hormone
-acts of kidney, incr water retention
-also called vasopressin bc it can cause vasoconstriction

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24
Q

OT

A

-stimulates uterine contradiction during childbirth, flow of milk during lactation
-promotes feelings of sexual satisfaction and emotional bonding between partners

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25
Q

Thyroid gland

A

-located below larynx in the throat
-two lobes joined by central mass (isthmus)
-follicles filled with colloid, lined with cuboidal

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26
Q

Thyroid gland produces:

A

Thyroid hormone and calcitonin

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27
Q

TH production

A

-iodine transport stimulated by TSH: TH made in colloid of the follicle, secreted from epithelium
-TH can be free-floating in plasma or protein-bound (albumin, transthyretin)
-is amine hormone BUT lipid solublae

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28
Q

Regulating thyroid hormone levels

A

-negative feedback mechanism
-TH secretion stimulated by TSH, TRH secretion, cold (in infants)
-TH secretion inhibited by: dopamine, somatostatin, stress, blood levels of TH

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29
Q

Thyroid hormone effects

A

-determines basal metabolic rate (BMR)
-enhances effect of SNS( bc of incr adrenergic receptor production)
-promotes glucose catabolism, lipolysis

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30
Q

thyroid hormone effects in children______and in adults_____

A

children: critical for nervous, muscular, skeletal development
adults: normal functioning of nervous, muscular, CV, GI, reproductive syestems

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31
Q

Types of thyroid dysfunction

A

hyperthyroidism (thyrotoxicosis)
hypothyroidism (myxedema)
goiter
thyroid nodule
abnormal thyroid fxn test

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32
Q

Hyperthyroidism

A

overproduction/ secretion of TH
-enlargement of gland (adenomas, neoplasia)
-pituitary or hypothalamic dx
-overdose of thyroid meds
-excessive hormone release due to TSH receptor autoantibody–> graves dx (type 2 hypersensitivity)

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33
Q

Graves dx patho

A

-autoantibodies that stimulate TSH receptor in thyroid gland-persistent TSH “signal”-> excessive release of T3 and T4
–> Formation of autoantibodies by B cells
- thyroid-stimulating immunoglobulins (TSIs)
-Thyroid-stimulation antibodies (TSAbs)

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34
Q

Graves dx may develop into ___

A

hypothyroidism
-gland ablation (radiotherapy) or removal (sx)
-creation of more autoantibodies–> destroy gland
-creation of autoantibodies that block TSH receptor

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35
Q

Graves dx manifestations

A

Increased metabolism-increased appetite, weight loss, hyperthermia
-trachycardia and incr CO
-increased gluconeogenesis and lipolysis
-restlessness, agitation, anxiety
-exophthalmos- orbital connective tissue inflam/ weakening
-pretibial edema

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36
Q

Thyrotoxicosis

A

-thyrotoxic crisus, thyroid storm
-dramatic rise in TH, potentially lethal: undiagnosed graves dx
-hyperthermia
-trachycardia, heart failure
-delirium
-vomitting, diarrhea-> dehydraitons

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37
Q

Hyperthyroidism tx

A

-diminish production, secretion, or action of TH
antithyroid drugs
radioactive iodine therapy (destroy thryoid cells)
sx removal of adenoma or part of thyroid gland
excessive tx –> hypothyroidism

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38
Q

Hypothyroidism

A

underproduction/ secretion of TH
-Hypoplasia of thyroid gland (congenital)
-iodine deficiency
-pituitary or hypothalamic dx or injury
-tx for hyperthyroidism
-autoimmune destruction of thyroid follicles
–>hashimotos

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39
Q

Hashimoto patho

A

autoantibodies destroy follicle cells:
-Thyroglobulin (Tg Ab)
-Thyroidal peroxidase (TPO Ab)
-TSH receptor-blocking (THS-R block Ab)
low levels of T3 and T4

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40
Q

Hypothyroidism manifestations

A

decreased metabolism:
-hyperthermia, cold intolerance
-weight gain despite decr appetite
bradycardia and decr CO
increased cholesterol
muscle cramps, weakness, stiffness
decrease GI motility
myxedema (skin puffiness) and hair loss
lethargy, forgetfulness, depression

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41
Q

Hypothyroidism in children

A

cretinism- abnormal nervous syestem development- mental retardation
-slowed skeletal growth/maturation
-delayed puberty
+ all the other reg manifestations

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42
Q

Goiter

A

enlargement of thyroid gland
-typical lack of dietary intake of iodine
-reduced thyroid hormone secretion
-incr TSH secretion–> thyroid hyperplasia
(can also occur due to hyperthyroidism)- TSH-R stim Ab stimulates gland, leading to hyperplasia

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43
Q

Adrenal glands

A

-sits atop kidneys

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44
Q

Adrenal cortex produces-

A

corticosteroids:
-aldosterone (mineralocorticoids)
-cortisol (glucocorticoids)
-androgens (gonadocorticoids)

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45
Q

Adrenal medulla produces____

A

amines
-epinephrine, norepinephrine

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46
Q

Mineralocorticoids

A

regulates electrolytes(primarily Na+ and K+) in ECF
-Importance of Na+: affects ECF volume, blood volume, blood pressure, level of other ions
-importance of K+: sets RMP of cells

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47
Q

_____the most potent mineralocorticoids

A

Aldosterone
-Na+ reabsorption and water retention
-K+ excretion
Net result: increase blood volume and BP

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48
Q

Regulating aldersterone

A

stimulated by:
-decr blood volume and BP (RAAS)
-INCR K+ in blood
-ACTH release from PITUITARY GLAND
Inhibited by:
-ANP release from atria (incr blood volume and BP)

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49
Q

Hyperaldosteroniam pathogen

A

-neoplasm or hyperplasia of adrenal cortex
-excess renin secretion:
kideny dx/injury
heart failure
excessive laxative/ diuretic use

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50
Q

Hyperaldosteronism manifestations

A

-Na+ and water retention/ K+ and H+ excretion
-Hypertension- and organ damage that comes. w/ it
-tiredness, weakness, nocturia (low K+)
-metabolic alkalosis (H+ moves into cells to replace K+)
-renin levels decreased (primary) or increased (secondary)

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51
Q

Hyperaldosteronism tx

A

ALDOSTERONE RECEPTOR BLOCKERS
-removal of adenoma

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52
Q

Glucocorticoids

A

-keep blood sugar levels relatively constant
-maintain blood pressure by increasing the action of vasoconstrictors

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53
Q

cortisol the most significant bc:

A

-enhances breakdown of protein/fat to make glucose (gluconeogenesis + lipolysis)
-inhibits inflammation
-suppresses immune syestem
intended for surviving acute stress

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54
Q

Cortisol mechanism of action

A

bind to cytosolic receptor –> act as transcription factor
-promote breakdown of fat and protein
-promote synthesis of glucose (liver)

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55
Q

Cortisol- suppress immune activity

A

-reduce circulating lyphocytes, monocytes, eosinophils, basophils
-inhibit production of IL-2
-interfere with antigen processing
-decrease WBC migration into tissue

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56
Q

Regulating cortisol

A

-negative feedback mechanisim
-release stimulated by:
acth RELEASED FROM PITUITARY
emotional stress, bodily injury
-release inhibited by:
Fall in ACTH level

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57
Q

ACTH released:

A

-ACTH released in a diurnal pattern
peak between 6-8am
low between 12-2am

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58
Q

Hypercortisolism

A

-neoplasm of pituitary, adrenal cortex
overuse of corticosteroid medications

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59
Q

Cushing’s

A

redistribution of fat to face (“moonface”) and upper back (“buffalo hump”)

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60
Q

Hypercortisolism manifestation

A

-immune supression (inhibit transcription of pro-inflammatory genes)
-elevated blood glucose –> insulin resistance
-obesity / redistribution of fat
-muscle wasting (excessive breakdown of protein)
-loss of collagen (thin skin, poor wound healing)
-polydipsia and polyuria
-increased bone remodeling (weakening of bone tissue)
-hypertension (mechanism unclear)

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61
Q

Corticosteroids used for treating autoimmune conditions –>prolonged use leads to______

A

adrenal atrophy

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62
Q

Stopping corticosteroid tx:

A

-CRH/ ACTH signals suppressed
-Adrenal gland unresponsive –> adrenal insufficiency
-takes time to re-establish physiologic cycle of hormone release

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63
Q

Hypercortisolism tx

A

-sx/ radiation to treat tumor
-medication to block affects of cortisol

64
Q

Hypercortisolism w/o tx leads to:

A

infections
complication from HTN

65
Q

Hypocortisolism

A

-destruction/ dysfunction of adrenal cortex
~80% autoimmune
~TB infection
-deficient pituitary/ hypothalamic activity

66
Q

Addison’s

A

-anti-adrenal antibodies
-decrease cortisol
-increase ACTH

67
Q

Hypocortisolism patho autoantibodies

A

-adrenal cortex Ab (ACA)
-Steroid 21 hydroxylase Ab (21-oh Ab)
-other organs often targeted (thyroid, parathyroid, gonad, pancreas)
lymphocyte infiltration
destruction of cortex -> replacing cortical cells fibrous stroma

68
Q

Hypocortisolism patho

A

-basal cortisol secretion is normal at first
-no increase in cortisol in response to stress, injury, trauma
-eventful destruction of tissue -> basal cortisol levels fall
-ACTH and CRH levels increase (because no negative feedback)

69
Q

Hypocortisolism manifestation

A

-anorexia, weight loss
-GI issues; nausea, vomiting, diarrhea
-hyperpigmentation of skin (ACTH hypersecretion)
-hyponatremia
-prone to hypoglycemia (impaired gluconeogenesis); fasting can lead to coma quickly
-hypotension –> vascular collapse

70
Q

Hypocortisolism tx

A

-glucocorticoid/ mineralocorticoid replacement therapy
-extra Na+
-additional cortisol for stressors: infection, sx, trauma

71
Q

Pituitary gland

A

“master gland” of endocrine system

72
Q

ADH stimulates thirst, causes water retention from ____

A

collecting duct of kidneys

73
Q

increase in blood osmolarity

A

simulates release of ADH

74
Q

Diabetes insipidus

A

insufficient ADH
-Polydipsia (abnormal thirst)
-Polyuria (dilute and large volume of urine)
-Nocturia (waking at night to pee)
dilute hypotonic urine- 10-20L/day

75
Q

Diabetes insipidus : Central

A

disease of pituitary, hypothalamus
-head injury
-intracranial tumor collecting duct of kidneys

76
Q

Diabetes insipidus: Nephrogenic

A

kidneys unable to respond
-inherited defect
-renal damage from drugs

77
Q

DI pathogen: Central

A

initial edema/ shock from injury -> inhibit ADH release
-once healed -> ADH secretion resumes

78
Q

DI Patho: Nephrogenic

A

-familial: defect in ADH receptor or aquaporin channel
-drug-induced: receptors sensitive to lithium and fluoride salts (reversible if exposure stops)

79
Q

DI manifestation

A

-normal blood volume
-hypernatremia-> cell shrinking due to loss of osmotic balance
decreased responsiveness to stimuli
seizures
coma

80
Q

Pancreas

A

exocrine and endocrine organ just behind stomach
-digestive enzymes, bicarbonate-> dudenum
-glucagon, insulin, somatostatin -> blood stream

81
Q

pancreatic hormones

A

-glucagon
-insulin

82
Q

glucagon

A

secreted by A or alpha (a) cells
-released between meals when blood glucose decreases
-liver stimulates glucogenesis, glycogenolysis
-adipose stimulates lipolysis, release of free fatty acids

83
Q

insulin

A

secreted by B or beta cells
-secreted during and after meal when blood glucose and amino acid levels rise
-stimulates cells to absorb nutrients ->lowering blood glucose
-promotes synthesis of glycogen(liver, muscle), lipid (adipose) and protein
-suppresses use of already stored fats

84
Q

hyperglycemic hormones raise blood glucose

A

glucagon
growth hormone
epinephrine/ norepinephrine
cortisol

85
Q

Hypoglycemic hormones lower blood glucose

A

insulin
GIP (gastric inhibitory peptide), GLP-1 (glucagon-like peptide) (indirectly)

86
Q

insulin is produced and secreted in response to_____

A

-increase blood glucose, amino acids, free fatty acids
-GI hormones (GIP, GLP)

87
Q

proinsulin made of 3 peptides:

A

ABC
-C peptide cleaved
-A-B peptides =active insulin
-C peptide in blood an indirect measurement of insulin synthesis

88
Q

Factors that inhibit insulin release:

A

decrease blood glucose
epi and ne
somatostatin

89
Q

action of insulin

A

facilitates glucose transport into cells (not all)
incr glucose use and storage as glycogen
incr uptake of amino acids
incr uptake of free fatty acids and glycerol
stimulates production of lipids and proteins
incr uptake K+, mg2+, phosphate

90
Q

GLUT receptors

A

GLUT1: brain cells
GLUT2; liver, kidney, intestinal, pancreatic cells
GLUT3: brain cells
all ^ insensitive to insulin
GLUT4: muscle and adipose cells highly sensitive to insulin

91
Q

Diabetes insipidus

A

-hyposecretion of ADH or kidney insensitivity to ADH
-characterized by intense thirst and heavy urination

92
Q

Diabetes mellitus

A

dysfxn of endocrine pancreas
-affects metabolism of fat, protein and carbohydrates

93
Q

DM characterized by

A

hyperglycemia thqat results from:
secr in insulin secretion
decr in cell response to insulin
incr in hormones that oppose insulin

94
Q

Diabetes dx

A

NORMAL: 90-100 mg/dL glucose and A1c , 6%
Diabetes: Hb1c >or =6.5 %
fasting blood glucose > or = 126 mg/dL
2 hr plasma glucose > or = 200 mg/dL
random plasma glucose . or = 200 mg/dL

95
Q

HbA1c is

A

glycated hemoglobin:
-perm attachment of glucose to hemoglobin
-% Hb glycation proportionate to blood glucose level

96
Q

Glycosylation

A

(glucose attatches to protein by enzyme)
-post-translation modification
-regulated by enzyme activity
-confers (+) biological properties to proteins

97
Q

glycation

A

nonenzymatic attachment
a form of protein damage: impairs fxn and stability

98
Q

Type 1 DM

A

little or no insulin secretion
loss of beta cells in the pancreas
-autoimmune:
body’s immune cells destroy beta cells
genetic predisposition + environmental trigger
-non-immune
secondary to other condition (pancreatitis)
idiopathic (no autoantibodies detected)

99
Q

type 1 dm mechanism genetic factors:

A

unclear; may involve class ll human leukocyte antigen (HLAll)

100
Q

type 1 dm environmental factors

A

-childhood infection ( enteroviruses, H.pylori)
-changes in gut microflora
-cow’s milk
-exposure to toxins

101
Q

type 1 dm creation of autoantibodies

A

GAD65 (glutamic acid decarboxylase 65)
ZnT8 (zinc transporter)
IA2 (tyrosine phosphate-IA2)
–>Targetting pancreatic beta cells

102
Q

by the time symptoms of t1dm occurs 90% of _____have been destroyed

A

beta cells

103
Q

T1DM Symptoms

A

hyperglycemia
polydipsia- thirst
polyuria- peeing more
glucosuria- glucose in urine
polyphagia- hunger
weight loss
muscle wasting

104
Q

acute complications with t1dm

A

diabetic ketoacidosis (DKA) with type 1 or 2

105
Q

Diabetic ketoacidosis

A

type of metabolic acidosis
T1DM dx is usually occurs after first episode of DKA
-brought on by stress (trauma, infection, lack of insulin)

106
Q

DKA presents with:

A

-lethargy
-labored breathing (kussmaul)
-fruity breath (acetone)
-hyperglycemia
-dehydration
-decr K+ (diuresis and vomiting)

107
Q

Chem of DKA

A

-DECR IN insulin, incr in glucagon
-adipocytes release FFAs as energy source
-liver metabolizes FFAs to ketones->acetone, acetoacetic acid, beta-hydroxybutyric acid

108
Q

Ketones ___blood pH

A

LOWER: BICARB BUFFERING SYSTEM QUICKLY overwhelmed
-hyperventilation and incr in H+ excretion in kidneys to compensate
-extra glucose pulls water/elertrolytes into kidney tubule-> polyuria dehydration

109
Q

tx of t1dm

A

goal: to regulate blood glucose w/o episodes of hyper or hypoglycemia
-daily insulin
-self monitoring of blood glucose
-meal planning
-exercise
yearly screening for complications

110
Q

Type 2 dm

A

chronic hyperglycemia
-insulin resistance (cells do not respond to insulin)
-improper beta cell fxn
causes by complex genetic, epigenetic, and environmental interactions

111
Q

dm + obesity=
dm + obesity + htn=

A

diabesity
metabolic syndrome

112
Q

T2DM effects

A

genetic -> obesity <- diet, inactivity
leads to adipokines, incr ffas, inflamm cytokine, decr activity of ghrelin
leads to insulin res and decr in beta cell mass n fxn
hpoinsulinemia, incr of glucagon

113
Q

t2dm risk factors. causes

A

age, fam hx, genetic sus
inherited defects: B-cell fxn, insulin molecule, insulin receptors
obesity, htn, inactivity
metabolic syndrome: includes central obesity, dyslipidemia, htn, hyperglycemia

114
Q

DM type 2 pathogenesis: insulin resistance

A

-resistance: diminished response of insulin-sensitive
contributors:
-abnormal insulin molecule
-high amount of insulin antagonists
-down-regulation of insulin receptor
-decr in activation of intracellular pathways
-alteration of GLUT proteins
-obesity

115
Q

insulin resistance

A

down-regulation of insulin receptor, abnormal insulin molecules, alteration of GLUT proteins
decr activation of intracellular pathways, high amount of insulin antagonists= glucagon

116
Q

Obesity

A

imbalance of energy intake and expenditure leads to expansion of adipose tissue (can be healthy or not)
inflammation or metabolic dysfxn

117
Q

Healthy expansion of adipose tissue

A

incr in adipogenesis
decr cell volume
incr insulin sensitivty
decr inflammtion

118
Q

Unhealthy expansion of adipose tissue

A

decr in adipogenesis
ince cell hypertrophy
decr insulin sensitivity
incr low grade inflammation
incr mo infiltration
CAN LEAD TO LIPOTOXIXITY- insulin res

119
Q

____and_____affecting energy expenditure likely contribute to unhealthy expansion

A

genetic , endocrine

120
Q

effect of obesity

A

-alterations in adipokines
-elevated serum free fatty acids and ectopic lipid deposits
release of inflamm cytokines from adipose tissue
-decr insulin-stimulated mitochondrial activity
-hyperinsulinemia and decr insulin receptor espression

121
Q

adipokines-

A

hormones secreted by adipose cells:
adiponectin, leptin

122
Q

Adiponectin

A

-compliments effects of insulin
-inversely correlated with body weight
-obesity decr adiponectin levels; contributes to insulin res

123
Q

Leptin

A

-acts on recptor in hypothalamus
-decr food intake (signals satiety), incr energy expenditure
-scretion incr as adipocyte number and size incr
can lead to leptin resistance

124
Q

leptin resistance

A

obese individuals have larger/more adipocytes
-incr serum levels of leptin
BUT are insensitive to its effects
promotes over-eating, excessive weight gain
-attributed to inherited defect in leptin receptor

125
Q

Serum FFA and lipid deposits

A

-2 types of fat: visceral and subcutaneous
-Visceral (central) fat accumulation leads to adipocyte dysfxn
FFA metabolism is distributed-> dyslipidemia
inappropriate (ectopic) lipid deposition-detected by biomarkers in blood

126
Q

release of inflamm cytokines from adipose tissue

A

chronic low grade inflamm
-released from intra-abdominal adipocytes or nearby mo:
TNF-a and IL-6
Acute phase reactants (fever, attract neutrophils)

127
Q

two main effects on inflamm response in dm 2

A

1)induce insulin resistance: TNF-a phosphorylates insulin receptor, making it unresponsive to insulin
2)perpetuate associated conditions
-atherosclerosis
-fatty liver
-dyslipidemia

128
Q

decreased mitochondrial activity

A

-insulin induces glucose uptake
-glucose used in cell respiration (in mitochondria)
cells(skeletal muscle, liver) become res to effects of insulin-> glucose not taken up effectively -> cell respiration and oxidative phosphorylation(makes ATP) become dysfxn -> leads to less ATP synthesis, more ROS production

129
Q

effects of hyperinsulinemia

A

insulin receptors become desensitized due to the persistent presence of insulin
-insulin ‘signal” no longer processed by cells
-receptor expression downregulated
-hyperinsulinemia associated with increased risk for CAD, HTN

130
Q

obesity has profound effects that induce_____

A

insulin resistance

131
Q

Chronic DM complications

A

CV dx: micro and macrovascular
retinopathy
nephropathy
neuropathy
bladder dysfxn

132
Q

Mucrovascular dx

A

dx of capillaries
-hyperglycemia alters cell metabolism
characteristic:
-EC hyperplasia
-thickening of extracellular matrix
-thrombosis
changes in capillary beds-> less tissue perfusion
leads to hypoxia and ischemia in tissues receiving blood from diseased capillaries

133
Q

Intracellular effects of hyperglycemia

A

oxidative stress
incr in activation of polyol pathways
-metabolic pathways, leads to accumulation of sorbitol
-exhausts NADPH (req for neutralizing ROS)
incr activation of protein kinase C
-IC signaling protein inappropriately activated (cell proliferation)
incr glycation =AGE
-glucose irreversibly bound to things
incr activation of hexosamine pathways
-excess glucose directed to hexosamine pathway
-results in glycation (dysfxn) of signaling proteins
-contributes to oxidative stress

134
Q

macrovascular dx

A

majority of diabetics succumb to coronary artery dx, atherosclerosis, aneurysm, stroke, peripheral artery dx

135
Q

macrovascular dx mediated by____-

A

advanced glycation end-products (AGE)

136
Q

aDVANCED GLYCATION END-PRODUCTS (AGE):

A

Attach to the receptor for AGE (RAGE)
promotes: oxidative stress
inflammation
endothelial cell dysfxn
VSM dysfxn
hyperlipidemia

137
Q

Retinopathy

A

leading cause of blindness worldwide
already present in dm by time of diagnosis
-retina most metabolically-active structure in the body
vulnerable to changes in metabolism caused by hyperglycemia
-occurs in 2 stages: nonproliferation and proliferative

138
Q

Nonproliferative retinopathy

A

microaneurysms )loss of supportive cells)
-incr capillary permeability:
heard exudates (fat)
edema
-ischemia and infarction
soft exudates
-hemorrhages

139
Q

proliferative

A

neovasculation, ischemia causes release of VEGF

140
Q

nephropathy

A

DM most common cause of end-stage renal dx/ kidney failure
-occurs more often in T1
-higher prevalence of T2 make up 50% of ESRD pts
-progressive changes in glomerular fxn that take many yrs to develop
-kidneys eventually fail

141
Q

nephropathy, characteristic changes to ___

A

glomerulus
-enlarges
-basement membrane thickens
-mesangial cell sproliferate
-loss of podocytes : incr permeability
proteins lost in urine: proteinuria
-resistance to bloo dflow(changes to arterioles)
decr GFR

142
Q

___made worse by renal dysfxn
controlling____ a key part of slowing progression of nephropathy

A

HTN

143
Q

Neuropathy 3 types

A

-distal symmetric
-autonomic
-transient asymmetric (specific nerves/plexuses)

144
Q

Neuropathy characteristics

A

demyleniation
nerve degeneration
slowed conduction

145
Q

in neuropathy :

A

sensory deficit precedes motor deficit
begins distally, moves proximally
-attributes to metabolic and vascular dysfxn from hyperglycemia:
polyol pathways in neurons
microvascular dx-> ischemia
autoantibodies (sometimes)
neurotrophic factors defects (cannot repair damage)

146
Q

Vascular dysfxn and neuropathy both contribute to ______

A

gangrene (body tissue death)

147
Q

diabetic bladder dysfxn

A

mojority of DM pts experience bladder dysfxn
not life-threatening but severely impacted quality of life

148
Q

dm bladder dysfxn casued by

A

hyperglycemia/glucosuria
-impaired metabolism
-oxidative stress
significant incr in urine voule (full of glucose)
-leads to tissue remodeling
-hypertrophy of smooth muscle (bc bladder working harder)
-decr in contractility

149
Q

t2dm tx

A

primary tx-changing habits to reduce body weight
-diet, decr caloric intake
-exercise :decr postprandial blood glucose and triglyceride and cholesterol levels
-incr HDL (good cholesterol) levels

150
Q

reduction in body weight can ____

A

sometimes reverse insulin resistance

151
Q

if lifestyle changes do not decr hyperglycemia and HBA1c levels _____

A

pharm tx

152
Q

Biguanides

A

metformin; 1st line drug for dm
decr hepatic glucose production
decr glucose absorption in gut
incr insulin sensitivity (liver, muscles, adipose)

153
Q

Glitazones

A

activate transcription factor-> glucose homeostasis
-anti-inflamm, incr insulin sens, decr FFS and LDLS

154
Q

Sulfonylureas

A

depolarizes pancreatic B-cells
stimulate insulin release

155
Q

a-glucosidase inhibitors

A

prevent digestion of carbohydrates in intestines
naturally occurring in some foods (green teas, maitake mushrooms), not effective on its ownp

156
Q

peptide mimetics

A

glucagon-like peptide (GLP) agonist (Ozempic)
gastric inhibitiry peptide (GIP) analog
incr insulin secretion
decr appetite
slow gastric emptying

157
Q

Glycosurics

A

SGLT2 inhibitors
-inhibits glucose uptake in kidney tubule
decr glucose reabsorption and incr glucose exretion

Pathophys (11 decks)

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