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Adv Patho > Endocrine Exam 3 > Flashcards

Endocrine Exam 3 Flashcards

1
Q

What are the key components of the endocrine system?

A
  1. glands that secrete Hormones
  2. Target organs that have cell receptors for hormones
  3. Hormone/receptor reaction that stimulates a chemical reaction
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2
Q

Water solubles hormones are made from

A

Protein hormones made from amino acids,

soluble in water; they are stored; most hormones are water soluble

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3
Q

Water solubles hormones have receptor locations where

A

on the cell surface

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4
Q

Water solubles hormones, examples

A

ADH (vasopressin), insulin, epinephrine,

growth hormone

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5
Q

Lipid soluble hormones are made from

A

Steroid hormones made from cholesterol,

soluble in fat not water

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6
Q

Lipid solubles hormones acts on

A

Cross the cell membrane and interact

with genes inside the cell; receptor site is inside cell

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7
Q

Lipid solubles hormones time to reaction

A

Made on demand, persistent effect

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8
Q

Lipid solubles hormones, examples

A

Ex. Estrogen, androgens, steroids

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9
Q

What types of feedback loops regulate hormones and how do they work?

A
  1. Negative feedback:
    •Most common
    •Increased level of hormone inhibits further release
  2. Positive feedback:
    •Surges of hormones
    •Increased level of hormone stimulates further release
  3. Cyclic variations:
    •Periodic variation in hormone release
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10
Q

How can we assess diabetes?

A

Hemoglobin A1c >6.5%
Fasting Plasma Glucose >126 mg/dl
Random plasma Glucose >200mg/dl

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11
Q

What role does obesity play in insulin resistance?

A
  1. Adipokines (leptin and adiponectin) are produced by white adipose tissue and obesity changes levels&raquo_space;decrease insulin synthesis and increase insulin resistance
  2. Elevated free fatty acid increase TG and cholesterol&raquo_space;disrupted intracellular insulin signaling, decreased tissue response to insulin, + pro-inflammatory
  3. Obesity causes release of inflammatory cytokines&raquo_space;induce insulin resistance and contribute to fatty liver, dyslipidemia, and atherosclerosis
  4. Alter oxidative phosphorylation in cellular mitochondria&raquo_space;insulin resistance and changes in energy metabolism
  5. Obesity associated with hyperinsulinemia and decreased insulin receptors
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12
Q

Describe general underlying pathophysiology of chronic DM complications:

A
  1. Oxidative stress&raquo_space; increaseed ROS
  2. Polyol pathways
    - alternate pathways for glucose metabolism
    - when activated you have increased intracellular osmotic pressure and oxidative injury in blood vessels
  3. Protein kinase C» increased insulin resistance, cytokine production, angiogenesis&raquo_space; microvascular complications
  4. Glycation&raquo_space; glucose binds irreversibly to collagen, proteins in RBC, vessel walls and interstiitium&raquo_space; advanced glycation end products with abnormal cell proliferation and inflammatory changes
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13
Q

Diabetic Retinopathy

A

ETIOLOGY:
chronic hyperlgycemia

CLINICAL MANIFESTATIONS:
VISION LOSS AND BLINDNESS

PATHO:
•Damage to vessels, vasoconstriction, platelet aggregation, hypoxemia,
•Non-proliferative: thickening of retinal capillary membrane and increased
membrane permeability with vein dilation and microaneurysm formation
•Preproliferative: retinal ischemia with areas of poor perfusion and infarcts
•Proliferative: Angiogenesis and fibrous tissue formation in the retina or optic disc

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14
Q

Diabetic Nephropathy

A

ETIOLOGY: due to hypertension d/t hypelglycemia

CLINICAL MANIFESTATIONS:
cardiovascular disease, stroke, peripheral artery disease
-Glomerular enlargement, glomerular basement membrane thickening

PATHO:
•Hyperglycemia&raquo_space; polyol pathway, protein kinase C and inflammation&raquo_space;advanced glycation end products

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15
Q

Infections

A

ETIOLOGY:
impaired tissue oxygenation, high glucose levels, impaired immune responses, decreased sensation, delayed healing

CLINICAL MANIFESTATIONS:

PATHO:

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16
Q

Coronary Artery Disease

A

ETIOLOGY:
HPTN, DM1 associated with microalbuminuria, DM2 metabolic syndromes
• HPTN  increased risk for CAD and stroke
• MI more deadly in DM patients

CLINICAL MANIFESTATIONS:

PATHO:

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17
Q

Stroke

A

ETIOLOGY: Ischemic and lacunar strokes risk increased r/t autonomic nervous system neuropathy associated a-fib and platelet coagulopathy

CLINICAL MANIFESTATIONS:

PATHO:

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18
Q

Peripheral Arterial Disease

A

ETIOLOGY:
Atherosclerosis of LE with increased risk for ulcers, gangrene and amputation BTK

CLINICAL MANIFESTATIONS:

PATHO:

19
Q

FUNCTIONS OF THE ENDOCRINE SYSTEM

A
  • Growth and sexual maturation
  • Energy production and energy utilization by cell = metabolic rate
  • Glucose homeostasis
  • Fluid and electrolyte balance
  • Circulatory function
20
Q

What hormones are made in the anterior pituitary(6)

A
  1. Adrenocorticotropin (ACTH or corticotropin)- Controls secretion of adrenal cortex hormones
  2. Thyroid stimulating hormone (TSH or thyrotropin): Controls secretion of thyroxine and triiodothyronine by thyroid gland
  3. Growth hormone (GH)
  4. Prolactin (PRL); Promotes mammary gland development and lactation
    5; Follicle Stimulating Hormone (FSH)
  5. Luteinizing Hormone (LH)
21
Q

NAME 6 HYPOTHALAMIC HORMONES that CONTROL

ANTERIOR PITUITARY SECRETION

A
  1. Thyrotropin releasing hormone (TRH)
  2. Corticotropin releasing hormone (CRH)
  3. Growth hormone releasing hormone (GHRH)
  4. Growth hormone inhibitory hormone (GHIH) or Somatostatin
  5. Gonadotropin releasing hormone (GRH)
  6. Prolactin inhibitory hormone (PIH)
22
Q

What hormones are made in posterior pituitary?

A

Antidiuretic hormone (AHD / vasopressin)

Oxytocin

23
Q

3 hormones from thyroid

A

T4
T3
calcitonin

24
Q

3 hormones from adrenal

A

aldosterone (mineralocorticoids)
cortisol (glucocorticoids)
adrenal androgens

25
Q

2 hormones from medulla

A

epinepherine

norepinepherine

26
Q

4 hormones from pancreas

A

insulin
glucagon
amylin
somatostatin

27
Q

1 hormone from parathyroid

A

parathyroid hormone

28
Q

1 hormone from pineal gland

A

melatonin

29
Q

hormone receptors are ______

A

proteins

30
Q

When T4 enters the bloodstream, it is converted to___

A

T3

31
Q

SYNTHESIS OF THYROID HORMONE

A

•Iodides from dietary iodine are pumped from blood into thyroid gland
•Thyroid stimulating hormone (TSH) regulated the iodide pump activity based on
concentrations of circulating thyroid hormone
•The ER synthesize thyroglobulin protein
•Thyroxine (T4) and triiodothyroxine (T3) from from iodination of tyrosine on the thyroglobulin
•T4 and small amounts of T3 remain bound to thyroglobulin and are stored in gland follicles
•Thyroid hormones are secreted from the follicles after cleavage from thyroglobulin by proteinases
•TSH regulates the release of the thyroid hormone

32
Q

PHYSIOLOGIC FUNCTIONS OF

THYROID HORMONE

A
  • Regulates protein, fat and carbohydrate metabolism
  • Regulates cell metabolic rate
  • Regulates body heat production
  • Maintains growth hormone secretion and skeletal muscle maturation*
  • Affects CNS development (fetal 2 years of age)*
  • Maintains cardiac rate, force and output
  • Maintains secretion of GI tract
  • Affects RR and oxygen utilization
33
Q

what does growth hormone do

A
  • Growth of body tissues
  • Metabolic effect
  • Fat utilization
  • Glucose utilization
  • Protein building
  • Bone and cartilage growth
  • Helps body assemble and build new tissues
34
Q

METABOLIC EFFECTS OF GH

A
  • Increased protein synthesis by cells
  • Increased mobilization of fatty acids from adipose (ketosis)
  • Increased serum fatty acid level
  • Increased use of fatty acids for energy production by cells
  • Decreased rate of glucose metabolism by cells and decreases glucose utilization (conserves carbohydrates)
  • Decreased glucose uptake by skeletal muscles
  • Increased insulin secretion and glucose production by liver
35
Q

GH PROMOTES PROTEIN BUILDING

A
  • Enhances amino acid transport through cell membranes
  • Increases nuclear transcription of DNA
  • Enhances RNA translation and protein synthesis by ribosomes
  • Decreases catabolism (breakdown) of proteins and amino acids
36
Q

GH STIMULATES BONE AND CARTILAGE

GROWTH

A

•Increases deposition of protein by chondrocytic and osteogenic cells
•Increases rate of chondrocyte and osteocyte reproduction
•Induces conversion of chondrocytes to osteocytes for new bone deposition, so
cartilage can convert to bone
** Most important role of GH in children

37
Q

CONTROL OF INSULIN SECRETION

A
  • Increased serum glucose stimulates secretion of insulin
  • Plasma insulin concertation increases 10-20-fold within 3-5 minutes after an acute elevation in serum glucose (eating)
  • First insulin peak serum concentration is 5-10 minutes after insulin is formed from pre-insulin and pro-insulin
  • Second peak insulin serum concentration is at 15 minutes as additional insulin is made
  • Plateau phase 2-3 hours
  • Reduction of serum glucose concentration turns off insulin synthesis and secretion
38
Q

OTHER CONTROLS OF INSULIN

SECRETION

A

•Excess serum amino acids (arginine, leucine, and lysine) – promote protein
synthesis
•Gastrin, secretin, and gastric inhibitory peptide secretion – anticipation of increased serum glucose levels
•Growth hormone, cortisol, estrogen and progesterone
•Parasympathetic nerve activation

39
Q

GLUCAGON

A
  • Opposes the effect of insulin / increase serum glucose concentration
  • Stimulates glycogenolysis
  • Increases gluconeogenesis from amino acids
  • Activates adipose cell lipase to liberalize fatty acids for conversion to glucose
  • Increases myocardial contractility
  • Increased renal blood flow by dilating afferent arterioles
  • Enhances bile secretion
  • Inhibits gastric acid secretion
40
Q

SOMATOSTATIN

A
  • Acts locally on islet cells to decrease production of insulin and glucagon
  • Decreases stomach, duodenum, and gallbladder motility
  • Decreases secretion of digestive enzymes and absorption by the GI tract
  • Extends the period of time nutrients and energy enter blood from digestion
41
Q

Glucocorticoids: cortisol

A
  • Carbohydrate, protein and fat metabolism
  • Stress response
  • Inflammation and immune response
  • Membrane stability
  • Intravascular volume and blood vessel tone
42
Q

Mineralocorticoids: aldosterone

A
  • Electrolyte regulation
  • Increased absorption of sodium and secretion of potassium
  • Increases intravascular fluid volume
  • Stimulates Na and K transport in sweat glands, salivary glands and intestinal epithelial cells
43
Q

CORTISOL AND INFLAMMATION

A
  • Increased cortisol production during times of stress
  • Anti-inflammatory properties
  • Stabilizes lysosomal membrane
  • Decreases capillary membrane permeability
  • Prevents migration of WBCs and phagocytosis of damaged cells
  • Reduces IL-1 lowers fever
  • Suppresses T-lymphocyte production
  • Blocks allergic response

Adv Patho (23 decks)

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