Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pathophysiology > Endocrine System > Flashcards

Endocrine System Flashcards

1
Q

Thyroid Hormones- T3

A

virtually affects every cell
triiodothyronine- 2 tyrosines with 3 bound iodines
-4x more potent than T4
-present in lower concentrations than T4
-shorter half-life than T4 (T1/2= 1.5 days)
iodine must be present in diet approx= 100 mcg/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Thyroid Hormones- T4

A

affects every cell in the body
thyroxine (2 tyrosines and 4 bound iodine)
serves as a precursor to T3
must be present in the diet at approx = 100 mcg/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Thyroid Disorders

A

more common between ages 20-40, females>males

  • hyperthyroidism: elevated levels of thyroid hormone in blood- T3 and T4: HIGH and TSH: LOW
  • hypothyroidism: decreased levels of thyroid hormone in blood- T3 and T4: LOW and TSH: HIGH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Effects of Thyroid Stimulating Hormone (TSH) on Thyroid Follicular Cells

A
  • growth of thyroid follicular cells
  • increased iodide uptake and thyroglobulin iodination, and thyroid hormone synthesis
  • thyroid hormone release into blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Physiological Effects of Thyroid Hormone

A
  • fetal growth and brain development
  • increased oxygen consumption and heat production
  • increased rate and force of heart contraction
  • increased beta adrenergic receptor
  • increased red blood cell production
  • increased bowel motility
  • increased bone turnover
  • increased speed of muscle contraction and relaxation
  • maintain normal CNS function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Endocrine System

A

major organ system by which cells and tissue communicate- hormones are secreted directly into circulation and exert their effects by binding in or on target cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Hormones

A

secreted from glands, bind to receptor, and initiate action
-homeostatic regulation of: growth, reproduction, metabolism, energy, fluid and water balance
negative feedback!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Hormone Receptors

A

proteins that bind hormones with high affinity and specificity- each receptor has a domain that recognizes a specific hormone and a domain that generates a signal once a hormone binds
-cells have a mechanism for release to stop physiological response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Endocrine Glands include…

A
  • hypothalamus
  • pituitary
  • thyroid
  • parathyroid
  • pancreas
  • adrenal
  • ovary
  • testis
  • placenta
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hypothalamus

A

“central relay system”!

  • gather signals from the central nervous system to send information via hormones and neurotransmitters
  • influence many vital functions, such as: arterial pressure, thirst, temperature regulation, body weight, emotions, sleep, instinct
  • hypothalamic-pituitary axis: controls action of thyroid gland, adrenal glands, gonads, growth hormone, prolactin, oxytocin, vasopressin (ADH)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Endocrine Homeostasis

A

goal= maintain homeostasis

  • excess hormone downregulates number of receptors, decreased receptor availability diminishes tissue response to excess hormone
  • hormone depletion upregulates receptors, enhance receptor availability increase tissue response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What leads to hormone excess/deficiency and possible outcome?

A 
CONTROL MECHANISM FAIL= excess/deficiency
leads to:
-abnormal metabolism
-water imbalance
-blood pressure abnormalities
-growth and reproductive issues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Anterior Pituitary Adenomas

A

excess hormone secretion impacts hormone axis (mostly in adults), most common: lactotroph adenoma, excess prolactin (PRL)
classified as:
-microadenomas are <10mm
-macroadenomas are >10mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is Hyperprolactinemia/Lactotroph Adenoma?

A

increased prolactin (PRL) secretion, caused by prolactinoma or in some cases medication (antipsychotics, antidepressants, or metoclopramide), which results in gonadal dysfunction (decreased bone mineral density and also, excess prolactin inhibits normal secretion of LH and FSH, lack of ovulation, estrogen deficiency)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Result of Hyperprolactinemia in males and females and treatment options

A

-Females: amenorrhea, galactorrhea (increased/abnormal milk production), infertility
-Males: decrease libido, impotence
treatment includes:
-microadenoma: dopamine agonist (cabergoline)
-macroadenoma: surgery, radiotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Somatotroph adenoma/Excess GH- difference in children and adults

A

excess GH secretion

  • children/adolescent: anti-insulin, long bone and muscle growth, gigantism
  • adults: anti-insulin, acromegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Acromegaly

A

signs/symptoms: cardiomegaly(hypertension), barrel chest, male sexual dysfunction/female menstrual disorders, increase size in hands and feet, degenerative arthritis
treatment: somatostatin analog (inhibits GH secretion) or surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Corticotroph Adenoma

A

overproduction of adrenocorticotropic hormone (ACTH) which functions to stimulate adrenal cortex to produce cortisol (stress hormone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Cushing Syndrome

A
  • adrenal gland excess: too much cortisol, caused by: iatrogenic (corticosteroids), ACTH producing pituitary adenoma, adrenocortical tumor
  • clinical findings: central obesity, purple striae, weight gain, moon facies, cervical fat pad (“buffalo hump”), acne, thinned skin, bruises easily, muscle weakness, fatigue, hypertension, neurological disturbances
  • diagnosis: 24-hour urinary free cortisol, salivary cortisol, overnight dexamethasone suppression test, serum ACTH
20
Q

Diabetes Insipidus (DI)

A
  • inadequate release of antidiuretic hormone (ADH/vasopressin)
  • polyuria, polydipsia, dilute urine (but normal glucose)
  • causes: genetics (mutation in vasopressin II, vasopressin V2 receptor, or aquaporin genes), brain tumors which compress posterior pituitary, or idiopathic (unknown cause)
21
Q

What is the hormone involved in Diabetes Insipidus and treatment options

A

ANTIDIURETIC HORMONE (ADH deficiency)
ADH normal functions, include:
-secreted in response to high solute concentration in blood
-causes aquaporin water channels to increase in renal collecting duct
-increases renal water reabsorption, more water in blood
Treatment: ADH/vasopressin

22
Q

Hypothyroidism- types, signs/symptoms, diagnostic, treatment

A
  • primary: most common! failure of the thyroid gland
  • secondary: failure of the pituitary or hypothalamus
  • Hashimoto’s thyroiditis (with or without goiter (enlarged thyroid gland)- depends on stage of disease): autoimmune disease, CHRONIC INFLAMMATION, antibodies to thyroid peroxidase, thyroglobulin and TSH receptors
  • signs/symptoms: decreased/absent T3 and T4, slow pulse, decreased cardiac output, hypotension, lowered body temperature, cold intolerance, dry skin, weight loss, hair loss, muscle cramps, edema of face and eyelids, constipation, menstrual irregularities
  • diagnostic tests: measure FT4 and TSH in blood
  • treatment: daily thyroid hormones
23
Q

Hyperthyroidism (Graves Disease): Signs/Symptoms

A

-signs/symptoms: palpitations, tachycardia, nervousness, tremor, hyperkinesia, diarrhea, excessive sweating, intolerance to heat, weight loss, lack of appetite, ophthalmopathy, profound muscle weakness, goiter (enlarged thyroid gland)

24
Q

Pathophysiology of Graves Disease and Treatment

A
  • IgG antibodies bind to TSH receptor on plasma membrane of thyroid follicular cells- antibodies are TSH AGONIST= increase thyroid hormone secretion and proliferation of thyroid follicular cells- goiter (enlarged thyroid gland)
  • increased FT4 and decreased TSH
  • treatment: anti-thyroid medication, destruction of thyroid tissue with radioactive iodine
25
Addison's Disease Pathophysiology
- insufficient glucocorticoid (cortisol), mineralocorticoid (aldosterone), and androgen production from adrenal cortex - autoimmune disease: lymphoid infiltrates in adrenal gland, circulating antibodies, abnormalities of cellular immunity
26
Function of Glucocorticoid
CORTISOL - stress hormone, stimulates gluconeogenese, increases blood glucose, causes vasoconstriction and raises blood pressure - without this the vascular system is unable to respond to catecholamines, and hypotension or shock occurs
27
Function of Mineralocorticoid
ALDOSTERONE - stimulates Na+ reabsorption in kidney, increases fluid retention, raises blood pressure - stimulates K+ excretion in urine
28
Addison's Disease Signs/Symptoms and Treatment
OCCURS WHEN 90% OF ADRENAL CORTEX IS DESTROYED - signs/symptoms include: profound weakness, anorexia, GI symptoms, hypotension, electrolyte imbalance, personality changes - treatment: glucocorticoid and mineralocorticoids (hydrocortisone or fludrocortisone)- higher doses needed at time of stress
29
Cushing Syndrome Cause
Increased glucocorticoid (cortisol) concentration - ACTH dependent: hypersecretion of ACTH due to pituitary corticotroph adenoma, ectopic ACTH production by a malignant tumor - ACTH independent: adrenocortical adenoma or carcinoma, chronic corticosteroids treatment for immunologic or inflammatory diseases
30
Cushing Syndrome Signs/Symptoms and Treatment
- signs/symptoms: obesity in face, neck, trunk, abdomen, muscle wasting and severe weakness, hypertension which could lead to congestive heart failure, glucose intolerance, irritability, depression, paranoia, women may have increased facial hair while med may experience ED and decreased libido - treatment: surgery, discontinue corticosteroid therapy, medication that blocks cortisol production
31
Pheochromocytomas Pathophysiology, Signs/Symptoms, Treatment
mostly in young or middle-aged adults, sporadic or due to genetic mutations, 10% are malignant - neuroendocrine tumor that usually arises in the adrenal medulla, secrete excessive amounts of catecholamines (epinephrine, norepinephrine, and metabolites) - urinary or plasma samples to test concentration of catecholamine metabolites - catecholamine excess, leads to: hypertension (moderate to severe), cardiac arrhythmias, angina, myocardial infarct, pallor, anxiety, sweating, abdominal pain, vomiting, 5 P's (palpitations, perspiration, pallor, pain, pressure) - treatment: surgery, beta-adrenergic receptor antagonists
32
Type 1 Diabetes Mellitus
review endocrine system 3
33
Islet Cell Types and Hormones: alpha cells
glucagon, proglucagon
34
Islet Cell Types and Hormones: beta cells
insulin, proinsulin, C peptide, amylin
35
Islet Cell Types and Hormones: delta cells
somatostatin
36
Glucagon
- synthesized in pancreatic islet alpha cells - secretion inhibited by glucose, insulin, amylin, somatostatin, and GLP-1 - liver is principle target causing glycogenesis, gluconeogenesis, ketone bodies- fasting blood glucose comes mainly from liver
37
Incretin Hormone: GLP-1
produced in the intestinal epithelial endocrine L-cells by differential processing of proglucagon
38
Incretin Hormone: GIP
gastric inhibitory peptide, secreted in the proximal small intestine in the presence of nutrients in the gut
39
Type 2 Diabetes Mellitus
review endocrine system 4
40
Metabolic Syndrome Risk Factors or Pathophysiology
combination of medical disorders that increase risk of developing cardiovascular disease and diabetes - risk factors: age, obesity, sedentary lifestyle, insulin resistance, stress - implicated conditions: hypertension, dyslipidemia, diabetes, polycystic ovarian syndrome (PCOS), non-alcoholic fatty liver disease (NAFLD), dementia, hyperuricemia - adipocytes of the visceral fat increase plasma levels of TNFalpha, which cause production of inflammatory cytokines and triggers cell signaling by interaction with TNFalpha receptors (leads to insulin resistance), increase in adipose tissue leads to increase of immune cells within- plays role in inflammation
41
Diagnosis of Metabolic Syndrome and Treatment
``` -central obesity (BMI>30kg/m2) and two of the following: -raised triglycerides -reduced HDL -raised blood pressure -raised fasting plasma glucose treatment: healthy nutrition, active lifestyle, treatment of associated disorder ```
42
Complications of Obesity
endothelial dysfunction, hepatic steatosis, premature puberty, hypogonadism, obstructive sleep apnea, restrictive lung disease, bone and joint disease, cardiovascular disease, stroke, digestive disease, cancer
43
Causes of Obesity
- genetic: 77% heritability - physiologic: enhanced response to food cues, diminished response to satiety signals, lower metabolic rate - social/cultural - behavioral: eating in absence of hunger, rapid eating, low level of physical activity
44
Leptin
- hormone secreted by adipocytes - key hormone in management of long-term energy homeostasis - receptors located in liver, skeletal muscles, pancreas, hypothalamus, and brain stem which regulates satiety, energy expenditure, neuroendocrine function - obese individuals may have leptin resistance and elevated serum leptin levels
45
Adipose Tissue
not simply a passive storage depot for lipids but are composed of adipocytes, preadipocytes, vascular cells and macrophages, produce and secrete variety of bioactive molecules known as: adipokines, maintain energy balance and regulates insulin sensitivity, blood pressure, lipid metabolism, hemostasis, and immune response

Pathophysiology (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions